SECOND EDITION
Nutritional
Assessment
of Athletes
© 2011 by Taylor and Francis Group, LLC
SECOND EDITION
Nutritional
Assessment
of Athletes
Edited by
Judy A. Driskell
Ira Wolinsky
Boca Raton London New York
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© 2011 by Taylor and Francis Group, LLC
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© 2011 by Taylor and Francis Group, LLC
Dedication
We would like to dedicate this book to Sylvia Wood, Project Editor
at CRC Press, Taylor & Francis Group LLC. Sylvia worked with
us and the chapter contributors for almost two decades. She
made sure that the books and each of the associated chapters
were correctly formatted, grammatically correct, appropriately
referenced, and copyrights obtained if needed. She was hardworking, responsible, and easy to work with. She played a major
role in helping us and the chapter contributors publish quality
books and chapters. On January 26, 2010 she lost her years-long
struggle with cancer. We miss her and her dedicated service.
© 2011 by Taylor and Francis Group, LLC
Contents
Preface.......................................................................................................................ix
The Editors................................................................................................................xi
Contributors ........................................................................................................... xiii
SECTION I Dietary Assessment of Athletes
Chapter 1
Estimation of Food and Nutrient Intakes of Athletes ..........................3
Robert J. Moffatt, Virginia B. Tomatis, Donna A. Harris, and
Ashley M. Deetz
Chapter 2
Evaluation of Nutrient Adequacy of Athletes’ Diets.......................... 51
Nanna L. Meyer and Melinda M. Manore
SECTION II Anthropometric Assessment of Athletes
Chapter 3
Physique Assessment of Athletes: Concepts, Methods, and
Applications........................................................................................ 73
Gary J. Slater, Helen T. O’Connor, and Fiona E. Pelly
Chapter 4
Body Composition and Gender Differences in Performance........... 121
Peter R.J. Reaburn, Ben J. Dascombe, and Xanne Janse de Jonge
SECTION III Physical Activity Needs Assessment
of Athletes
Chapter 5
Laboratory Methods for Determining Energy Expenditure of
Athletes............................................................................................. 151
Robert G. McMurray
Chapter 6
Field Assessment of Physical Activity and Energy Expenditure
among Athletes................................................................................. 183
Nuala M. Byrne, Sarah P. Shultz, and Andrew P. Hills
vii
© 2011 by Taylor and Francis Group, LLC
viii
Chapter 7
Contents
Molecular Aspects of Physical Performance and Nutritional
Assessment ....................................................................................... 213
Yousef I. Hassan and Janos Zempleni
SECTION IV Biochemical Assessment of Athletes
Chapter 8
Assessment of Lipid Status of Athletes ............................................ 235
Richard B. Kreider, Jonathan M. Oliver, and Amy F. Bragg
Chapter 9
Assessment of Protein Status of Athletes......................................... 255
Benjamin F. Miller and Matthew M. Robinson
Chapter 10 Assessment of Vitamin Status of Athletes ....................................... 289
Mark D. Haub, Helena B. Löest, and Kelcie L. Hubach
Chapter 11 Assessment of Mineral Status of Athletes ....................................... 311
Henry C. Lukaski and Angus G. Scrimgeour
Chapter 12 Assessment of Hydration of Athletes ............................................... 341
Fiona E. Pelly, Gary J. Slater, and Tanya M. King
SECTION V Clinical Assessment of Athletes
Chapter 13 Clinical Assessment of Athletes....................................................... 377
Khursheed N. Jeejeebhoy and Farida M. Jeejeebhoy
Index ...................................................................................................................... 395
© 2011 by Taylor and Francis Group, LLC
Preface
Through our books and researches, we are pleased to have played a small part in
the recent, and rapid, growth of the science of sports nutrition, a phenomenon that
continues unabated. Taken together, our series of monographs, edited volumes, and
textbooks form an exhaustive and comprehensive corpus on the subject of sports
nutrition, including assessment. These books have been very well received and we
are proud. You have in your hands the latest book on the subject, the second edition of Nutritional Assessment of Athletes. Since the irst edition, there have been
important advances in critical areas of nutritional assessment and these are included.
In-depth discussions of important topics of interest to health and nutrition professionals as well as the motivated layman and the weekend athlete are presented. As
before, the volume covers a wide span of nutritional assessment and brings you the
latest authoritative information from experts. As such, it may be used as a resource
and a textbook.
Judy A. Driskell, Ph.D., R.D.
Professor
University of Nebraska
Ira Wolinsky, Ph.D.
Professor Emeritus
University of Houston
ix
© 2011 by Taylor and Francis Group, LLC
The Editors
Judy A. Driskell, Ph.D., R.D., is professor of
nutrition and health sciences at the University of
Nebraska. She received her B.S. degree in biology from the University of Southern Mississippi
in Hattiesburg. Her M.S. and Ph.D. degrees were
obtained from Purdue University. She has served
in research and teaching positions at Auburn
University, Florida State University, Virginia
Polytechnic Institute and State University, and
the University of Nebraska. She has also served
as the nutrition scientist for the U.S. Department
of Agriculture/Cooperative State Research
Service and as a professor of nutrition and food
science at Gadjah Mada and Bogor Universities
in Indonesia.
Dr. Driskell is a member of numerous professional organizations, including the
American Society for Nutrition, the American College of Sports Medicine, the
International Society of Sports Nutrition, the Institute of Food Technologists, and the
American Dietetic Association. In 1993 she received the Professional Scientist Award
of the Food Science and Human Nutrition Section of the Southern Association of
Agricultural Scientists. In addition, she was the 1987 recipient of the Borden Award
for Research in Applied Fundamental Knowledge of Human Nutrition. She is listed
as an expert in B-complex vitamins by the Vitamin Nutrition Information Service.
Dr. Driskell co-edited the CRC book Sports Nutrition: Minerals and Electrolytes
with Constance V. Kies. In addition, she authored the textbook Sports Nutrition and
co-authored the advanced nutrition book Nutrition: Chemistry and Biology, both
published by CRC. She co-edited Sports Nutrition: Vitamins and Trace Elements,
irst and second editions; Macroelements, Water, and Electrolytes in Sports Nutrition;
Energy-Yielding Macronutrients and Energy Metabolism in Sports Nutrition;
Nutritional Applications in Exercise and Sport; Nutritional Assessment of Athletes,
irst edition; Nutritional Ergogenic Aids; Sports Nutrition: Energy Metabolism and
Exercise; Nutritional Concerns in Recreation, Exercise, and Sport; and the current book, Nutritional Assessment of Athletes, second edition, all with Ira Wolinsky.
She also edited the books Sports Nutrition: Fats and Proteins and Nutrition and
Exercise Concerns of Middle Age, published by CRC Press. She has published almost
200 refereed research articles and 20 book chapters as well as several publications
intended for lay audiences and has given numerous presentations to professional and
lay groups. Her current research interests center on vitamin metabolism and requirements, including the interrelationships between exercise and water-soluble vitamin
requirements.
xi
© 2011 by Taylor and Francis Group, LLC
xii
The Editors
Ira Wolinsky, Ph.D., is Professor Emeritus of
health and human performance at the University
of Houston. He received his B.S. degree in chemistry from the City College of New York and his
M.S. and Ph.D. degrees in biochemistry from the
University of Kansas. He has served in research
and teaching positions at the Hebrew University,
the University of Missouri, the Pennsylvania
State University, and the University of Houston,
as well as conducted basic research in NASA life
sciences facilities and abroad.
Dr. Wolinsky is a member of the American
Society for Nutrition, among other honorary
and scientiic organizations. He has contributed
numerous nutrition research papers in the open literature. His major research interests relate to the nutrition of bone and calcium and trace elements and to sports
nutrition. He has been the recipient of research grants from both public and private
sources. He has been the recipient of several international research fellowships and
consultantships to the former Soviet Union, Bulgaria, Hungary, and India. He merited a Fulbright Senior Scholar Fellowship to Greece in 1999.
Dr. Wolinsky co-authored a book on the history of the science of nutrition,
Nutrition and Nutritional Diseases. He co-edited Sports Nutrition: Vitamins and
Trace Elements, irst and second editions; Macroelements, Water, and Electrolytes
in Sports Nutrition; Energy-Yielding Macronutrients and Energy Metabolism
in Sports Nutrition; Nutritional Applications in Exercise and Sport; Nutritional
Assessment of Athletes; Nutritional Ergogenic Aids; Sports Nutrition: Energy
Metabolism and Exercise; Nutritional Concerns in Recreation, Exercise, and Sport;
and the current book, Nutritional Assessment of Athletes, second edition, all with
Judy Driskell. Additionally, he co-edited Nutritional Concerns of Women, two
editions, with Dorothy Klimis-Zacas; The Mediterranean Diet: Constituents and
Health Promotion with his Greek colleagues; and Nutrition in Pharmacy Practice
with Louis Williams. He edited three editions of Nutrition in Exercise and Sport. He
also served as the editor for the CRC Series on Nutrition in Exercise and Sport, the
CRC Series on Modern Nutrition, the CRC Series on Methods in Nutrition Research,
and the CRC Series on Exercise Physiology.
© 2011 by Taylor and Francis Group, LLC
Contributors
Amy F. Bragg, M.S., R.D.
Department of Athletics
Texas A&M University
College Station, Texas
abragg@tamu.edu
Nuala M. Byrne, Ph.D.
School of Human Movement Studies
Institute of Health and Biomedical
Innovation
Queensland University of Technology
Kelvin Grove, Queensland, Australia
n.byrne@qut.edu.au
Ben J. Dascombe, Ph.D.
Faculty of Science and Information
Technology
University of Newcastle
New South Wales, Australia
Ben.Dascombe@newcastle.edu.au
Xanne Janse de Jonge, Ph.D.
Faculty of Science and Information
Technology
University of Newcastle
New South Wales, Australia
x.jansedejonge@newcastle.edu.au
Ashley M. Deetz, B.S.
Department of Nutrition, Food and
Exercise Sciences
Florida State University
Tallahassee, Florida
amd04f@fsu.edu
Judy A. Driskell, Ph.D., R.D.
Department of Nutrition and Health
Sciences
University of Nebraska
Lincoln, Nebraska
jdriskell@unl.edu
Donna A. Harris, M.S.
Department of Nutrition, Food and
Exercise Sciences
Florida State University
Tallahassee, Florida
dah08e@fsu.edu
Yousef I. Hassan, Ph.D.
Department of Nutrition and Health
Sciences
University of Nebraska
Lincoln, Nebraska
youhassan@yahoo.com
Mark D. Haub, Ph.D.
Department of Human Nutrition
Kansas State University
Manhattan, Kansas
haub@k-state.edu
Andrew P. Hills, Ph.D.
School of Human Movement Studies
Institute of Health and Biomedical
Innovation
Queensland University of Technology
Kelvin Grove, Queensland, Australia
a.hills@qut.edu.au
Kelcie L. Hubach, B.S.
Department of Human Nutrition
Kansas State University
Manhattan, Kansas
khubach@ksu.edu
Farida M. Jeejeebhoy, M.D.,
F.R.C.P.C., F.A.C.C.
Division of Cardiology
Peter Munk Cardiac Centre
University Health Network
University of Toronto
Toronto, Ontario, Canada
farida.j@sympatico.ca
xiii
© 2011 by Taylor and Francis Group, LLC
xiv
Khursheed N. Jeejeebhoy, M.B.B.S.,
Ph.D., F.R.C.P., F.R.C.P.C.
Department of Medicine
St. Michael’s Hospital
Toronto, Ontario, Canada
khushjeejeebhoy@compuserve.com
Tanya M. King, B.Sc. Hons.,
M.Nutr.Diet.
Nambour General Hospital
Nambour, Queensland, Australia
Tanya_King@health.qld.gov.au
Richard B. Kreider, Ph.D.,
F.A.C.S.M., F.I.S.S.N.
Department of Health and Kinesiology
Texas A&M University
College Station, Texas
rkreider@hlkn.tamu.edu
Helena B. Löest, M.S.
Department of Plant and Environmental
Sciences
New Mexico State University
Las Cruces, New Mexico
hloest@ad.nmsu.edu
Henry C. Lukaski, Ph.D.,
F.A.C.S.M., F.N.S.C.A.
HYGEA Consults International, LLC
and
Departments of Medicine and of
Physical Education, Exercise Science
and Wellness
University of North Dakota
Grand Forks, North Dakota
henry.lukaski@und.nodak.edu
Melinda M. Manore, Ph.D., R.D.,
C.S.S.D.
Department of Nutrition and Exercise
Sciences
Oregon State University
Corvallis, Oregon
melinda.manore@oregonstate.edu
© 2011 by Taylor and Francis Group, LLC
Contributors
Robert G. McMurray, Ph.D.
Department of Exercise and Sport
Science
University of North Carolina
Chapel Hill, North Carolina
exphys@email.unc.edu
Nanna L. Meyer, Ph.D., R.D.,
C.S.S.D.
Beth-El College of Nursing and Health
Sciences
University of Colorado at Colorado
Springs
Colorado Springs, Colorado
nmeyer@uccs.edu
Benjamin F. Miller, Ph.D.
Department of Health and Exercise
Science
Colorado State University
Fort Collins, Colorado
bfmiller@cahs.colostate.edu
Robert J. Moffatt, M.P.H., Ph.D.
Department of Nutrition, Food and
Exercise Sciences
Florida State University
Tallahassee, Florida
rmoffatt@mailer.fsu.edu
Helen T. O’Connor, Ph.D., A.P.D.
Discipline of Exercise and Sport
Science
University of Sydney
New South Wales, Australia
helen.oconnor@sydney.edu.au
Jonathan M. Oliver, M.Ed.
Department of Health and Kinesiology
Texas A&M University
College Station, Texas
joliver@hlkn.tamu.edu
Fiona E. Pelly, Ph.D., A.P.D.
School of Health and Sport Sciences
University of the Sunshine Coast
Maroochydore, Queensland, Australia
fpelly@usc.edu.au
xv
Contributors
Peter R.J. Reaburn, B.H.M.S. (Ed.)
Hons., Ph.D., Grad. Cert. Flex.
Learn.
Department of Health and Human
Performance
Central Queensland University
Rockhampton, Queensland, Australia
p.reaburn@cqu.edu.au
Matthew M. Robinson, M.S.
Department of Health and Exercise
Science
Colorado State University
Fort Collins, Colorado
matthew.robinson@rams.colostate.edu
Angus G. Scrimgeour, Ph.D.
Military Nutrition Division
U.S. Army Research Institute of
Environmental Medicine
Natick, Massachusetts
angus.scrimgeour@us.army.mil
Sarah P. Shultz, Ph.D., A.T.C.
School of Human Movement Studies
Institute of Health and Biomedical
Innovation
Queensland University of Technology
Kelvin Grove, Queensland, Australia
sarah.shultz@qut.edu.au
© 2011 by Taylor and Francis Group, LLC
Gary J. Slater, Ph.D., A.P.D.
School of Health and Sport Sciences
University of the Sunshine Coast
Maroochydore, Queensland, Australia
gslater@usc.edu.au
Virginia B. Tomatis, M.S.
Department of Nutrition, Food and
Exercise Sciences
Florida State University
Tallahassee, Florida
vbt08@fsu.edu
Ira Wolinsky, Ph.D.
Department of Health and Human
Performance
University of Houston
Houston, Texas
ira.wolinsky@gmail.com
Janos Zempleni, Ph.D.
Department of Nutrition and Health
Sciences
University of Nebraska
Lincoln, Nebraska
jzempleni2@unl.edu
Section I
Dietary Assessment of Athletes
© 2011 by Taylor and Francis Group, LLC
of Food
1 Estimation
and Nutrient Intakes
of Athletes
Robert J. Moffatt, Virginia B. Tomatis,
Donna A. Harris, and Ashley M. Deetz
CONTENTS
1.1
1.2
1.3
1.4
Introduction ......................................................................................................4
Methods of Assessing Food Intake...................................................................4
1.2.1 Diet Records .........................................................................................5
1.2.2 Twenty-Four Hour Dietary Recall ........................................................5
1.2.3 Food Frequency Questionnaires ...........................................................6
1.2.4 Issues with Nutrition Assessment .........................................................6
1.2.4.1 Misreporting ..........................................................................7
1.2.4.2 Snacking.................................................................................8
1.2.4.3 Openness in Reporting ..........................................................9
1.2.4.4 Time Frame for Determination of Nutrient Status ................9
1.2.4.5 Dietary Assessment vs. Clinical Testing ...............................9
1.2.5 Exchange Lists System ....................................................................... 10
1.2.6 Dietary Assessment Abroad ............................................................... 11
Special Issues with Assessing Food Intake in Athletes.................................. 13
1.3.1 Periodization of Training and Dietary Periodization ......................... 13
1.3.2 Fluid Intake ......................................................................................... 16
1.3.3 Vegetarian Diets and Assessment .......................................................20
1.3.4 Gastrointestinal Issues and Assessment ............................................. 21
1.3.5 Supplements ........................................................................................ 23
1.3.6 Traveling .............................................................................................25
1.3.6.1 Jet Lag ..................................................................................25
1.3.6.2 Dining Out and Eating on the Road.....................................25
1.3.7 Weight Management ...........................................................................26
Translation of Dietary Assessment into Analysis ........................................... 30
1.4.1 Internet Web Sites ............................................................................... 30
1.4.2 Special Considerations When Choosing Software ............................. 32
1.4.3 Databases ............................................................................................ 35
1.4.4 Recipes ................................................................................................ 37
1.4.4.1 New Foods ........................................................................... 37
3
© 2011 by Taylor and Francis Group, LLC
4
Nutritional Assessment of Athletes, Second Edition
1.4.4.2 Default Assumptions ............................................................ 38
1.4.4.3 Ethnic Foods ........................................................................ 38
1.4.5 Fluids and Hydration .......................................................................... 39
1.4.5.1 Sports Drinks ....................................................................... 39
1.4.5.2 Water .................................................................................... 41
1.4.5.3 Other Beverages ................................................................... 41
1.4.5.4 Fluid Hydration Status ......................................................... 41
1.4.6 Supplement Analysis .......................................................................... 42
1.5 Conclusions ..................................................................................................... 42
References ................................................................................................................44
1.1
INTRODUCTION
To ensure optimal performance it is vital to understand all aspects of an athlete’s
preparation, including the diet. If a full understanding of the athlete’s nutritional status is to be learned, it is critical that this assessment be accurate and complete. This
chapter examines the use of the dietary assessment as well as the proper analysis of
dietary reports with a special emphasis on the athletic population.
There are various methods available to assess the nutritional status of an individual. It is often helpful to combine multiple methods to obtain a more comprehensive
and accurate assessment. Sports dietitians should be aware of special considerations
regarding the nutritional assessment of athletes, such as misreporting, snacking,
luid intake, and weight management. In addition, it is important that nutritional
assessment be individualized according to the type of athlete and periodization
(cycles) of training, as well as the location in which training and/or competition may
take place.
Once the assessment has been obtained, dietary analysis should be performed to
translate food intake into nutritional recommendations for individuals and populations. There are several options available to analyze food intake, such as an escalating variety of software programs and databases. Special considerations should
be taken into account when choosing a food analysis method, such as the cost and
output of the software as well as the quality of the nutritional database. New and
ethnic foods, along with luid and supplement analysis, are important components
that should be included in the dietary analysis process.
In consideration of the issues stated above, this chapter addresses the following:
(1) methods of assessing food intake, (2) special issues with assessing food intake in
athletes, and (3) translation of dietary assessment into analysis.
1.2
METHODS OF ASSESSING FOOD INTAKE
The ability of the sports nutritionist to determine an athlete’s dietary intake and
to consequently analyze his or her nutrient status is important. Reliable and accurate ways to assess food intake using food diaries, 24-hour dietary recalls, and food
frequency questionnaires serve to assess food and nutrient intake in various ways.
© 2011 by Taylor and Francis Group, LLC
Estimation of Food and Nutrient Intakes of Athletes
5
The use of a speciic method can be determined by the purpose of the assessment
and other factors such as time and ability of the patient or athlete to record or recall
speciic intake.
Although these methods have the capability of being accurate and reliable when
used properly, the dietitian must be aware of several issues that may arise and lead to
decreased accuracy in analysis.
This section discusses the various methods of food intake and nutrient analysis.
1.2.1
DIET RECORDS
A diet record consists of the all the food and beverages a person consumes in certain amount of time. Three-day diet records are most often used (preferably two
weekdays and one weekend day) to determine an individual’s daily food and beverage consumption. Seven-day food dairies are more time consuming but may afford
a more complete picture of the diet. It should be noted that diet records lasting an
extended amount of time are not always as accurate as more concise diet records.1
This is due to the fact that individuals may absent-mindedly forget to write down
the information daily or may ind the task tedious and redundant. The 7-day diet
record is one of the most common approaches when assessing an individual’s diet.1
In general, the more information collected and the more details provided, the more
accurate the conclusions.
After completion of the food diary it is important that the record be analyzed
by a trained nutrition practitioner and preferably a registered dietitian. To ensure
completeness and further accuracy regarding speciic portion sizes, this is best conducted with the athlete.
When providing an individual with the task of assembling a diet record, a clear
description of what items should be recorded as well as instruction on how to record
the information should be provided. The individual should also be told what information will be drawn from the diet record. Reviewing speciic tips on creating a diet
record and the details that need to be present will assist the dietitian in subsequent
visits and during analysis. As discussed later in this chapter, snacking and misreporting are issues that need to be considered when asking an individual to complete a
diet record.
1.2.2
TWENTY-FOUR HOUR DIETARY RECALL
Twenty-four hour dietary recalls are often used as a quick nutrition assessment and
many times can used on an impromptu basis to determine an individual’s daily
intake. A dietitian will ask an individual to list the foods and beverages that he or
she has consumed within the past 24 hours. When doing so, it can be advantageous
to irst review with the individual the past day’s events, which then can be used to
help recall speciics about dietary consumption.2 The 24-hour dietary recall can be
performed by two different methods. The irst is when the dietitian asks the individual to start from the beginning of the previous day and provide in detail all of
the food and beverages consumed from the beginning of the day before. The second
method starts with the current day and works backward. For example, the individual
© 2011 by Taylor and Francis Group, LLC
6
Nutritional Assessment of Athletes, Second Edition
would be questioned on what he or she ate prior to this visit and then work back over
the past 24 hours. Both methods allow the dietitian to use the individual’s activities
as a way to assist in recalling his or her dietary intake. A 24-hour dietary recall can
take approximately 15 to 30 minutes to perform; however, it can take considerably
longer if the individual has had mixed dishes or different foods.1,2 Both quantity and
food preparation play a major role when performing a 24-hour dietary recall. An
advantage of this method is that it can be done in person or over the telephone in a
brief amount of time.
A main concern with a 24-hour dietary recall is its misrepresentation of the usual
diet. It is important to ask the individual if the diet consumed within the last 24
hours is a normal diet or if it was a variation from the norm. As one might expect,
the 24-hour recall is also very dependent on the individual’s short-term memory.2
A further complication in recalling food relates to its preparation, and accuracy is
likely to be less if the diet was not prepared by the individual.
1.2.3
FOOD FREQUENCY QUESTIONNAIRES
Food frequency questionnaires can assist in determining, on average, the amount of
a speciic macro- or micronutrient an individual consumes. It too is highly dependent
upon the individual’s memory and ability to estimate the quantity of a particular
food or food group. A list of foods is given to the individual and he or she is asked to
determine how often each food was consumed during a speciic period, usually ranging from one day to several months. A limitation of food frequency questionnaires
is its speciicity to certain populations.1 Overreporting can be a major factor in this
type of diet analysis.3 Table 1.1 provides a brief description of the dietary analysis
methods and their applications, along with advantages and disadvantages of each.
1.2.4
ISSUES WITH NUTRITION ASSESSMENT
A nutrition and dietary assessment is an integral part of determining the nutritional
and health status of an athlete. The focus of a dietary assessment is to attain the
most accurate report on the type, amount, cooking method, and time of consumption
for all food and beverages. The ability to properly assess the nutrient intake of an
individual entails precise reporting. Choosing the correct assessment method for the
athlete being examined ultimately promotes accuracy when analyzing the record.4
However, there are many factors to consider when beginning an assessment. One
must consider the time available to perform the assessment, the amount of money
available, and the reason for the assessment, such as trying to determine speciic
nutrient intakes or looking for a sign of deiciency. Some of the most important issues
that the dietitian needs to be aware of and that will affect an accurate assessment
include under- and overreporting food intake, the ability of an athlete/client to be
open in reporting, descriptive explanations of food intake, reporting all snacks and
beverages, and determining the proper assessment tool and the amount of time to be
able to accurately assess nutrient status.
© 2011 by Taylor and Francis Group, LLC
7
Estimation of Food and Nutrient Intakes of Athletes
TABLE 1.1
Comparison of Dietary Assessment Methods
Method
Description
Advantages
Disadvantages
Applications
Diet Records
Individual writes
down all
beverages and
food consumed
each day for a
speciied period
of time. Portion
sizes are either
measured or
estimated.
Individual
describes in
detail all the
food and
beverages
consumed in the
past 24 hours.
Acceptable
accuracy and
increased
compliance.
Follow-up
interview
further increases
accuracy.
As time period
lengthens,
participant
compliance
decreases.
Usually recorded
for 1–7 days,
including both
weekdays and
weekend days.
Easy to
administer and
little burden on
individual.
Fast to complete.
Used to rank food
or nutrient
groups.
Can be performed
on groups of
people.
Given a
predetermined
list, an
individual states
the frequency of
consumption for
the foods on the
list.
Can be
selfadministered.
Inexpensive and
may represent
usual dietary
intake.
Can provide
quantitative
information.
Dependent upon
individual’s
memory. May
not represent
usual food
intake.
Requires an
experienced
interviewer.
Can be
population
speciic.
Reliant on the
individual’s
memory and
ability to
quantify food
intake over a
speciied period
of time.
Each
questionnaire
requires
validation.
24-Hour
Dietary Recall
Food Frequency
Questionnaires
Used to measure or
rank speciic
nutrients of food
intake.
Can be used with
other methods to
as a cross-check.
Source: Adapted from Magkos, F. and Yannakoulia, M., Methodology of dietary assessment in athletes:
Concepts and pitfalls, Curr. Opin. Clin. Nutr. Metab. Care 6(5), 539–49, 2003.
1.2.4.1 Misreporting
Misreporting is a problematic issue associated with assessing dietary intake and
can present itself as overreporting or underreporting in food recalls, diaries, and
questionnaires.5 Overreporting occurs when an individual claims to consume more
foods, whether they are nutritious or nonnutritious, than he or she actually consumes. Individuals who overreport are commonly those who may not consume
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Nutritional Assessment of Athletes, Second Edition
fruits and vegetables as recommended,6 those who are of low-socioeconomic status,
and those with eating disorders. Of the nutritional components, protein is one of the
most overreported.7
Overreporting, however, is not as problematic as underreporting,5 which occurs
when an individual does not record or report all of the food that was consumed
for that recording period. Individuals and athletes who are overweight are the most
prone to underreporting. However, it is important to note that when assessing a food
recall, diary, or questionnaire, the most prevalent underreported components are
total energy, carbohydrates, and high-fat foods.7
Understanding the concepts of misreporting can provide a better understanding
and awareness of susceptible populations and ultimately provide a more accurate diet
assessment. It should also be recognized that women are 10% more prone to misreporting than men.8 More speciic to athletes, those involved in weight- and bodyfocused sports are more prone to misreport energy intake.9 Inaccuracy in reporting
food intake can cause many problems and lead to false analysis of dietary intake.
Because of this, it is important to determine how to detect and counteract these
issues. The irst step relies on the dietitian’s ability to interview and record recalls.
Previous experience and the willingness to ask detailed questions and lead the conversation in a way that will elicit proper recollection and reporting of food intake
will improve accuracy. The dietitian should also acquire the athlete’s usual intake
instead of just a day’s intake. The usual intake is a combination of several days of
daily intake and consists of both weekdays and weekends. A second step that can be
taken toward counteracting inaccuracy in dietary analysis includes tests involving
determination of urinary biomarkers and the doubly-labeled water technique. These
test methods are used as a means to determine nutrient status of certain nutrients.
Urinary biomarkers tests can determine protein, sodium, and potassium status. The
24-hour urinary excretion of these nutrients is also able to relect the difference
in energy intake resulting from various levels of physical activity, and this is an
important determinant of energy expenditure and therefore energy intake.10 Doublylabeled water is also a means to measure energy expenditure and can be used in
combination with dietary intake data to determine the energy intake compared to
expenditure and determine if over- or underreporting is a problem.11 However, these
methods can be costly and dificult to perform with a large group. The best use of
these assessments may be of use with “special issue” clients and athletes who need
speciic health and dietary attention.
1.2.4.2 Snacking
Snacking is an important aspect in understanding the complete dietary assessment.
The importance of snack food contribution to the overall energy and nutrient intake
of the dietary recall, diary, and questionnaire is vital to the accuracy of such records.
The National Health and Nutrition Examination Survey (NHANES) (2002) illustrates that underreporting of snacking foods and amount of snacking occurs often.
In contrast to the general population, athletes consume about one third of their total
daily energy from snacks.12 The reason for a greater snacking tendency among athletes is an adaption to their high energy expenditure and needs.13 It is important
for athletes who expend great amounts of energy to include snacking in their daily
© 2011 by Taylor and Francis Group, LLC
Estimation of Food and Nutrient Intakes of Athletes
9
routine but be sure to report it in dietary assessment. Be sure athletes are choosing
snacks that are nutritious and that they time intake in accordance with training and
competition schedules. This will lead to improved health and performance. Snacks
should never be used as a meal replacement but rather serve as an addition of food to
the diet. For athletes, the act of snacking may take precedence over other meals, so
it is important to make sure reporting is truthful.14,15
1.2.4.3 Openness in Reporting
To ensure that an accurate nutrient assessment is obtained, one of the most essential
factors to consider is the relationship between the client/athlete and the dietitian. The
more comfortable the athlete is, the greater the response and the more willing he or
she will be in reporting the foods and the amount of foods consumed. The dietitian
must keep in mind the culture, socioeconomic status, religion, and eating behaviors
of the athlete during the assessment. Dietitians must also be aware of any subconscious negative feedback, whether it is a facial expression, comment, or action that
would make the client/athlete uncomfortable and unwilling to respond accurately to
future assessments. With proper technique and instructions, enhanced accuracy will
be ensured.
1.2.4.4 Time Frame for Determination of Nutrient Status
The ability of a food record and 24-hour food recall to precisely and reliably assess
macronutrient and energy status takes more than one recall. The U.S. Committee
on Food Consumption Patterns recommends that at least four 24-hour recalls be
collected during the course of a one-year period.4,16 Diet records collected for a 3to 4-day period are considered an appropriate time frame. However, accuracy is
increased with each additional day but only up to seven extra days. This is because
the longer time that the client/athlete is required to record, the more likely misreporting and nonreporting become.17
When attempting to determine a few major contributing nutrients, the number of
days of analysis varies for each vitamin and mineral. Other considerations include
bioavailability, vitamin and mineral supplements, and foods consumed in conjunction that may affect absorption of one another. The most reliable estimates are
obtained within 10% of the obtained usual intake. Estimates within 20% are also
used, but not as accurate. Determining an individual’s nutrient status can be done
by looking at the nutrient intake and comparing it to the Dietary Reference Intakes
(DRIs). DRIs, according to the Institute of Medicine, are nutrient reference values
based scientiically on provision of good nutrition.
It is important to realize that obtaining accurate nutrient assessment through
dietary assessment may not be plausible for certain nutrients; for example, there are
better ways in which the status of vitamins A and C can be determined. Therefore,
it is necessary for one to be patient when involved in the nutrient assessment process
and to report consistently.
1.2.4.5 Dietary Assessment vs. Clinical Testing
An alternative to assessing nutrient status of a client/athlete is the determination
through blood and urinary biomarkers. Even better yet is their combination. A
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Nutritional Assessment of Athletes, Second Edition
TABLE 1.2
Average Number of Days for Dietary Intake Assessment to Accurately
Determine Nutrient Status in Men and Women
Men
(Number of Days)
Nutrient
Total Energy
Carbohydrate
Fat
Protein
Iron
Calcium
Vitamin A
Vitamin C
Potassium
Sodium
27
37
57
36
68
74
390
249
34
58
Women
(Number of Days)
35
41
71
48
66
88
474
222
48
73
Source: Adapted from Basiotis, P.P., Welsh, S.O., Cronin, F.J., Kelsay, J.L., and Mertz, W., Number of
days of food intake records required to estimate individual and group nutrient intakes with
deined conidence, J. Nutr. 117, 1638–41, 1987.
combined food frequency questionnaire and urinary nitrogen test may be more reliable than a 24-hour recall and a blood biomarker test in determining nutrients, yet
both blood and urinary biomarker tests may be more accurate in assessing nutrients such as β-carotene and folic acid but not protein or α-tocopherol.19 As noticed
here, different nutrients may be better assessed in various ways. If an assessment is
being made for a client/athlete who may need close attention, it would be beneicial
and accurate to perform both recall and biomarker tests. Similarly, because of the
possible misreporting issues concerning dietary recalls, diaries, and questionnaires,
collection of blood, urinary biomarkers, or both, serves as a means to validate or to
require further assessment of an individual.20
1.2.5
EXCHANGE LISTS SYSTEM
The exchange lists system was developed in 1950 by the American Dietetic
Association in conjunction with the American Diabetic Association and the U.S.
Public Health Service. This educational tool was originally created for individuals
with diabetes to assist them with carbohydrate counting and meal planning, so that
they could enjoy consuming a wide variety of foods while balancing their glucose
and insulin levels. The system groups foods into three main categories (some of
which are further divided into subgroups) according to their nutrient and energy content: carbohydrates, meat and meat substitutes, and fats. Any food item from a particular list can be exchanged for another (with the corresponding equivalent portion
size) in the same list because they have similar amounts of calories, carbohydrates,
proteins, and fats.21,22
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Estimation of Food and Nutrient Intakes of Athletes
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Even though this tool was designed for diabetic patients, it could also be useful for the athletic population. Utilization of the food exchanges can provide a fast,
approximate assessment of the amount of calories, carbohydrate, protein, and fat
present in the diet. Therefore, athletes familiar with the use of the exchange lists
could evaluate their own dietary intake, which could possibly translate into more
accurate reporting to their sports dietitians. The use of a Microsoft Excel™ spreadsheet could further simplify the calculation of the amount and distribution of different exchanges throughout the day and their contribution to macronutrient and caloric
intake, as well as the determination of each macronutrient’s contribution to the total
amount of calories consumed, expressed as percentages. These calculations could be
very useful in diabetic athletes as well as their sports dietitians, who may choose to
use this simple method as a irst step in the energy and macronutrient assessment of
these individuals. Moreover, the exchange lists may be of special advantage for those
athletes traveling abroad, not only to estimate their own dietary intake but also to
plan meals according to their sports dietitian’s recommendations.
1.2.6
DIETARY ASSESSMENT ABROAD
It is important to take into account that dietary assessment of individuals can vary not
only due to the method of assessment employed and its accuracy but also due to ethnic
differences. Consider, for example, individuals, especially international-level athletes,
who travel abroad for competition. Other countries may have a different food supply,
availability, forms of food preparation, serving sizes, and serving format, among others; therefore, sports dietitians analyzing athletes’ diets should pay attention to these
discrepancies in order to obtain the most accurate dietary assessments possible.
Moreover, speciic considerations need to be taken into account when assessing the dietary intake of collegiate athletes who come to the United States from
other parts of the world, carrying with them their traditional practices regarding
food consumption. For instance, when conducting the dietary assessment of immigrant groups in Europe, researchers were faced with several challenges, including
the quantiication of speciic portion sizes of traditional foods and dishes (such as
eating from a shared serving dish/pot vs. an individual plate), scarce information on
ethnic dishes and recipes, and composition of culture-speciic foods, among others.23
In order to account for these differences, the method used for dietary assessment
of individuals of different ethnic origins should relect their culture and tradition.
However, literature on dietary habits and dietary assessment methods appropriate for
different ethnic groups in Western society is limited.24
Consequently, there are several things that international networks, such as
the European Micronutrient Recommendations Aligned and the International
Confederation of Dietetic Associations, could do in order to facilitate a more accurate assessment of ethnic groups or individuals traveling to countries with different
cultural traditions regarding food consumption:
• The standardization of food composition tables or software (to translate food
consumption into speciic nutrient intake) and homogenization of assessment methods in Europe25 could ease the comparison between European
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Nutritional Assessment of Athletes, Second Edition
•
•
•
•
countries, and extension of this homogenization across the globe would
further enhance the ability to account for the above-mentioned differences
between people of different ethnicity.
The development of new food-composition tables and computer databases
appropriate for use in various countries and regions (since they are lacking,
are outdated, or are incomplete in many countries) would allow for the correct interpretation of data collected from dietary studies around the world.26
A picture book with country-speciic dishes and common restaurant foods
typical of different nationalities could be used for the quantiication of portion sizes, in order to obtain more accurate assessment of nutrients from
the diet.27
Repeated 24-hour recalls and questionnaires on meal patterns and purchases of foods could be used to assess information regarding food composition and distribution patterns of meals prepared at home, food composition
and selection of foods prepared at restaurants, household portion sizes, and
food patterns at festival days and on special occasions, as well as seasonal
inluences, in order to provide a more accurate diet assessment of different
ethnic groups.24
The creation of culturally sensitive dietary questionnaires for athletes of
different ethnic origins may also contribute to the speciic factors previously mentioned in order to obtain a better nutrient analysis from the diet
assessment of such special populations.28
The creation and implementation of the above-mentioned suggestions would be
beneicial for sports dietitians in the dietary assessment and analysis of athletes who
travel abroad for competition and for international athletes living in the United States.
The availability of culturally sensitive dietary questionnaires, including images of
common foods from different nationalities, would allow sports dietitians to conduct
a more speciic and accurate dietary assessment of ethnically diverse athletes and
those competing abroad. In addition, the availability of complete food-composition
tables, nutrient analysis databases, or software that includes updated information
from household and typical restaurant foods from other countries would allow sports
dietitians to obtain a more speciic and accurate report when interpreting the nutritional status of athletes of different ethnicities.
It is also interesting to note that different U.S. nutrient standards are used around
the world to aid in the determination of nutrient adequacy. For example, a Brazilian
study on the assessment of water and nutrient intake of adolescent athletes used the
DRI and the American College of Sports Medicine (ACSM) guidelines to evaluate the nutritional intake of adolescent athletes.29 Furthermore, the Recommended
Dietary Allowances (RDA) were used for the majority of European surveys to compare micronutrient intake of Europeans25 and to estimate nutrient adequacy for individuals and populations.30
These guidelines serve as a reference for European countries to compare nutrient adequacy from the dietary intake of individuals and populations, although
they should be adapted to the speciic characteristics of European nutrient intake.
However, Europe has not yet adopted standardized tables due to variability in the
© 2011 by Taylor and Francis Group, LLC
Estimation of Food and Nutrient Intakes of Athletes
13
evaluation of nutritional status among European countries and the lack of knowledge
regarding the variability of speciic nutrient intake in the population, as well the
lack of consensus regarding the type of food consumption database that should be
employed to obtain this kind of information.
In addition, there are similarities in the methods of assessment utilized in the
United States compared with other countries. Dietary surveys conducted across
Europe, as well as studies performed in South America, Africa, and Asia, used food
records, food frequency questionnaires, 24-hour recall (single or repeated), dietary
history, and combinations of these dietary assessment methods to register the food
intake of their individual populations.23,26,28,29,31 These similarities could aid in the
comparison of individual dietary intakes across the world. Commonalities and differences among these individuals from diverse countries could be used to establish
worldwide nutrient databases.
1.3
SPECIAL ISSUES WITH ASSESSING FOOD INTAKE IN ATHLETES
For a more complete and comprehensive assessment of an athlete’s diet, special
consideration must be given to issues related to periodization (cycles of training or
eating), luid intake, vegetarian diets, gastrointestinal (GI) issues, supplements, traveling, and weight management. Athletes are often unaware of the importance of
these matters and may not consider these when reporting their diets. The sports
dietitian will need to take additional time with athletes to determine if any of these
issues have an effect on the athlete’s dietary intake.
1.3.1
PERIODIZATION OF TRAINING AND DIETARY PERIODIZATION
Generally speaking people do not consume the same foods and drinks day after day.
Even though a pattern may be followed throughout the week, people may change
it during the weekends. This is why dietitians instruct clients to record at least one
weekend day when gathering multiple-day dietary records. Moreover, food cost,
availability, ethnic background, and family traditions, among other factors, can
inluence the types and amounts of food and beverages people consume throughout
the year, which increases the dificulty of conducting accurate dietary assessments.
Besides these factors, sport dietitians need to take into account periodization patterns speciic to each sport when assessing dietary intake of athletes. They follow
speciic training patterns during the “in” and “off” seasons, as well as during the
pre- and postcompetition periods, which are accompanied by different nutritional
needs that should be considered during their dietary assessment.
In this context it is important to discuss the athlete’s engagement in periodization
of training. This method of training was irst applied in the 1940s due to the discovery by Soviet sport scientists that sports performance could be enhanced by varying the training loads during the year instead of by maintaining a constant training
stress. The implementation of this model of training has been supported by several
research studies32–34 as well as by the ACSM.35
Periodization involves different training cycles, including load cycles, recovery
cycles, peak cycles, and conditioning cycles, that are implemented according to the
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Nutritional Assessment of Athletes, Second Edition
athletes’ sports demands and schedules of competition. 36 The load cycles are considered the building portion of the program and take place during the off-season, in
the precompetitive period. The recovery cycles focus on providing the athlete with
active rest periods that serve as a transition between the building and competitive
phases. Each recovery cycle helps the athlete to be prepared for the following, more
demanding peak cycles. The peak cycles are designed to promote maximal strength
gain, while allowing time to work on motor skills speciic to the sport. The peak
cycles are implemented during, or immediately prior to, the competitive period and
last approximately the same amount of time as the load cycles. After the competitive
season, athletes engage in conditioning cycles, which are periods of active rest that
allow athletes to rest from heavy training while avoiding deconditioning.
The implementation of these cycles allows coaches to separate the annual training
plan into three main periods: preparation (load cycles followed by recovery cycles
and peak cycles), competition (peak cycles), and transition (conditioning cycles and
recovery cycles). Following this pattern an athlete will be trained to achieve peak
performance during the competitive season. Since each of the cycles differs in intensity and type of training, the nutritional demands for each period would also be different. In order to account for the speciic nutritional status of athletes throughout
the year, dietary assessments should be conducted at each of the different training/
competition periods.
Another consideration to be noted with athletes is that different sports require athletes to compete all year long, while others only require them to compete intensely
during one season. Consider, for example, college or professional tennis, which
is played on an all-year-round basis, compared to college or professional football,
which is only played during the fall season. The energy and nutritional requirements
of these two groups of athletes would be different during training, precompetition,
and postcompetition periods and would require sports dietitians to account for these
disparities when conducting diet assessments. Even comparing football, which is
played during the fall, and baseball, which is played during the spring and summer,
will require athletes to have different nutritional plans that are most suitable to the
sport and time of the year in which they are played. Also, individual sports, such
as tennis, compared to team sports, such as football, will place different demands
on the athlete’s energy expenditure and nutritional requirements, which should be
recorded by sports dietitians during the diet assessment process. It is very important
that the sports dietitian, as well as every other member on the athlete’s health professional team, be familiar with the physical demands and schedules of different sports,
such as those listed on Table 1.3.37
In addition to periodization of physical training, dietary periodization needs to
be taken into account when conducting dietary assessments. Dietary periodization refers to the manipulation of energy-yielding nutrients obtained from the diet
that are related to the changes the athlete undergoes during the different periods
of training. These dietary manipulations have an impact on fuel utilization during
exercise, speciic to the period of training and the sport the athlete performs.38 One
such manipulation used by sports dietitians to increase athlete’s muscle fuel storage
and subsequent supply, especially during events lasting over 90 minutes, is carbohydrate loading. Take, for example, a distance runner, who during the peak cycle (right
© 2011 by Taylor and Francis Group, LLC
Sporta
Preseason Trainingb
Competitive Seasonc
Active Restd
Postseason Trainingb
Baseball
Basketball
Cross Country
November–January
August–October
August
February–June
November–March
September–November
August–October
May–July
July–August
Football
Golf
Gymnastics
Ice Hockey
Indoor Track and Field
Outdoor Track and
Field
Soccer
Softball
Swimming
Tennis
June–August
July–August
October–December
August–September
September–November
N/A (most have already competed
during indoor track season)
June–July
November–January
July–September
July–August
September–December
September–May
January–April
October–March
December–February
March–June
3–4 weeks
3–4 weeks
Most compete in indoor/outdoor
track seasons
4–6 weeks
2–3 weeks
3–4 weeks
4–6 weeks
Most compete in outdoor track seasons
3–4 weeks
4–6 weeks
3–4 weeks
3–4 weeks
2–3 weeks
February–May
June–October
April–June
June–July
Men’s Volleyball
Women’s Volleyball
Wrestling
August–September
June–August
September–October
3–4 weeks
3–4 weeks
4–6 weeks
June–August
February–May
June–August
August–December
February–May
October–March
September–November
January–May
October–May
September–December
November–March
February–May
June
June–September
May–July
Most compete in outdoor track seasons
July–August
Estimation of Food and Nutrient Intakes of Athletes
TABLE 1.3
Periodization of Diverse Sports
a
All sports include men and women unless speciied.
The differences in pre- and postseason activities are associated with the training cycle and the type of conditioning that will be performed. The postseason of most athletes
focuses on developing strength, power, lexibility, and agility. The preseason focuses on developing more technical skills and speciic movement and conditioning.
c Competitive seasons vary by age group and skill level. The seasons listed here relect the calendars of most high school and collegiate sports in most states, governing bodies,
and associations.
d Active rest periods vary by age group, skill level, and whether the athlete also competes in other sports. Active rest allows the athlete to recover while engaging in other activities.
Source: Ballew, C. and Killingsworth, R.E., Nutritional Assessment of Athletes, 1st ed., CRC Press, Boca Raton, FL, 2002, p. 27.
b
15
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Nutritional Assessment of Athletes, Second Edition
before competition) may be advised by a sports dietitian to engage in carbohydrate
loading in order to increase muscle glycogen storage and improve performance during the race. This dietary periodization would result in an increase of the athlete’s
carbohydrate consumption compared to the off-season or other periods of training,
where high carbohydrate consumption may not be emphasized.
Both training and dietary periodicities used by athletes should be taken into
account during the dietary assessment process. Since these manipulations are ongoing, sports dietitians should attempt to gather dietary intake data (using any individual or combination of the methods discussed in the previous section) from the
different exercise and dietary periodization phases. Consequently, speciic eating
patterns could be identiied for each of the periodization phases to determine whether
the athlete is able to follow the diet recommendations and to assess whether these
recommendations are effective in keeping the athlete healthy, as well as in helping
him or her meet the energy and nutrient demands of training and competition. Being
unaware of the athlete’s schedule regarding periodization could result in a misinterpretation of the dietary assessment. Following the distance runner example, not
knowing that this athlete is in the peak cycle of training, following a carbohydrateloading diet in preparation for an upcoming race could result in the misinterpretation
that the athlete is consuming inadequate amounts of fats and proteins.
In order to ensure proper dietary assessment planning and gathering of dietary
intake data at each periodization cycle, sports dietitians need to be familiar with the
timing of the training periodization and calendars of the diverse sports (Table 1.3) as
well as with any speciic dietary periodization associated with the different training
cycles or competition periods.
1.3.2
FLUID INTAKE
Sports are very diverse in nature, and the individuality of athletes performing these
athletic events in addition to the variability in training practices results in a great
variability in the luid needs of the athletic population. Fluid intake needs can also
vary between practice and competition, and they can be affected by different environmental conditions as well as by the degree of acclimatization of the athlete.39
Therefore, sports dietitians should be aware of the speciic needs of the athletes they
are working with and take into account these variables to ensure proper luid recommendations. The assessment of an athlete’s luid intake helps monitor whether the
recommendations are adequate. This is especially important since the majority of
athletes do not drink enough to replace their loss of body luids through sweat during
exercise,40 which can have serious consequences in health and athletic performance.
What is more, several athletes appear to avoid drinking, although they recognize that
proper rehydration is likely to enhance their performance.40
However, luid assessment through dietary recalls or food records may not be
very accurate, since athletes commonly underreport luid intake.1 One of the reasons for luid underreporting may be that it is dificult to quantify the amount and
composition of luids consumed during training/practice sessions as well as during competition, since athletes may consume copious amounts of sports drinks with
added carbohydrate and electrolytes, which would have different implications in the
© 2011 by Taylor and Francis Group, LLC
Estimation of Food and Nutrient Intakes of Athletes
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total dietary assessment compared to water. Also, unless athletes are thoroughly
interviewed by a sports dietitian during a 24-dietary recall, for example, they may
not remember when and how much luid they have consumed, resulting in underreporting of luid intake from diet records. In addition, another reason for underreporting of luids consumed throughout the day may be that athletes as well as
nonathletes rely on the thirst mechanism and consequently may not be consciously
thinking about drinking water and other luids. Moreover, luids that are consumed
in between meals are more likely forgotten to be reported in diet records than luids
consumed with meals.7,41
The assessment of hydration status is a critical component to ensure complete
rehydration of athletes engaged in regular and intense training and competition in
hot environments. However, there is controversy in luid balance science regarding
the selection of a proper hydration assessment method.42 There is a lot of variation
in the applicability of the different hydration assessment methods due to methodological limitations; for instance, the presence of needed measurement conditions
(reliability), the simplicity and cost of implementation (simplicity), the sensitivity
for discovering small but signiicant changes in hydration status (accuracy), and
the type of dehydration anticipated42,43 are all valid aspects of study.. In this context, the estimation of an individual’s or a population’s luid needs can be obtained
through dietary recalls, records, or surveys providing qualitative data; however, data
quantiication is dificult using dietary assessment. On the other hand, water balance examination and biochemical assessments provide quantitative data to aid in
the correctness of reported intakes. The combination of plasma osmolality and total
body water (measured by isotope dilution) is the “gold standard” for assessment of
hydration status.43
Other hydration assessment methods include total body water estimated by bioelectrical impedance analysis; plasma markers other than osmolality, such as sodium,
changes in hematocrit and hemoglobin concentrations, or changes in the concentrations of hormones involved in body luids regulation; urine markers, such as speciic
gravity, osmolality, or color; and body mass changes. In addition, other variables
such as salivary measures and physical signs and symptoms of clinical dehydration
can be considered.
The gold-standard methods for assessment of hydration mentioned above are the
most precise, involve substantial methodological control, are expensive, and require
analytical expertise in order to utilize them. Therefore, they are more suitable for
application in sports science or medicine, or for determining reference criteria and
use in research, but they are not practical to employ in the daily monitoring of hydration status of athletes during training or competition. More practical methods to
use in this situation that are suficiently sensitive to identify daily divergences from
euhydration (the normal state of body water content) include measurements of body
mass changes combined with a measure of urine concentration taken from the irst
urination of the morning. These techniques are easy to use, are inexpensive compared to the gold-standard techniques, and can provide accurate distinction between
euhydration and dehydration—thus they can be utilized as an individual source
for assessment.44,45 On the other hand, methods such as plasma markers (except for
osmolality), bioelectrical impedance analysis, saliva measures, and clinical physical
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Nutritional Assessment of Athletes, Second Edition
signs and symptoms of dehydration are frequently confounded or not suficiently
accurate to assess an athlete’s hydration status with reliability.46–49
As mentioned above, simple markers for hydration assessment such as body mass
changes and urine concentration measures are suitable for use with the athletic population. The body mass technique is usually used in the laboratory and ield environment to determine rapid changes of hydration in athletes. These changes are calculated
as the body mass difference between pre- and postexercise. It is best to state the level
of dehydration as a percentage of the pre-exercise body mass instead of as a percentage of total body weight, since the latter varies signiicantly.43 Interpretation of the
results from this method indicates that 1 g of lost mass is equivalent to 1 mL of lost
water. This method focuses in the determination of water loss as a measure of hydration status, but it fails to explain metabolic carbon exchange, which denotes the lone
small error in this assumption.50
Furthermore, in the laboratory setting, this body mass method is frequently used
as a standard against which the resolution of other hydration assessment markers
is compared. Indeed, there is evidence that body mass changes that are accurately
controlled can offer a more sensitive estimation of acute changes in total body water
than repeated measurements by dilution methods.51 The use of this method in endurance athletes during a race, for example, is particularly helpful in deciding whether
the athlete’s symptoms are due to dehydration or overhydration (the latter is usually
associated with symptomatic hyponatremia52), which would impair health and performance. Moreover, changes in body mass may be a satisfactorily stable physiological marker to examine daily luid balance over long periods of time (1–2 weeks),
helping athletes with acute luid changes and undergoing hard exercise to maintain a
stable body mass by compensating for sweat losses estimated by this method.53,54
However, over longer periods, chronic energy imbalance can result in changes
in body fat and lean mass tissues, which would be manifested as changes in body
mass and would consequently be a limitation to this hydration assessment method.
In such case, body mass measurements should be employed in combination with
another hydration assessment method, such as a urine concentration test, to distinguish between tissue and water losses. Urinary markers indicative of dehydration
include reduced urine volume, high urine speciic gravity, high urine osmolality,
and dark urine color. These markers are simple to measure and they provide a reliable assessment technique to distinguish between euhydration and dehydration,44,45
as long as the urine sample used for assessment is obtained from the irst urination
in the morning following an overnight fast.45
Urine samples taken under other conditions may not be as accurate. In fact, they
have a poor correlation with plasma osmolality (one of the gold-standard methods for
hydration assessment), failing to consistently monitor documented changes in body
mass corresponding to acute dehydration and rehydration.55 It seems that there is a
delay in the promotion of endocrine regulation of the reabsorption of renal water and
electrolytes by plasma osmolality changes at the kidney when acute changes in body
water take place.55 It is also probable that composition of the consumed drinks has
an effect on this response. It has been shown that abundant urine production appears
much earlier than the time at which euhydration is reached when drinking large
volumes of hypotonic luids.56 The measurements of urine concentration may also
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Estimation of Food and Nutrient Intakes of Athletes
be altered by diet.57 Nevertheless, analysis of a urine sample obtained from the irst
urination in the morning after an overnight fast reduces confounding inluences and
increases the reliability of this method.45
For practical purposes, sports dietitians should encourage athletes and their
coaches to monitor daily luid balance using the latter two simple methods (irstmorning urine samples and body mass measurements). This can be accomplished
at a relatively low cost and with easy-to-use commercial instruments, such as urine
speciic gravity and conductivity (osmolality equivalent) assessment tools, as well as
urine color charts.44,45,58 Regarding body mass change measures, a kilogram scale or
a medical-grade scale manufactured according to international weighing standards
would be the preferred choice. However, almost any scale can be suitable for athletes
to self-monitor their body mass changes as long as they measure their nude body
mass. Again, these two methods, body mass changes and urine concentration tests,
are simple hydration assessment methods that provide sensitivity for identifying
important differences in luid balance (above 2% of body mass change) for athletes
during training and competition.
There is still a simpler approach recommended for self-monitoring of daily hydration status in athletes. This approach is represented in Figure 1.1. It uses the pneumonic WUT, which combines three of the simplest markers of hydration: weight,
urine, and thirst (WUT).59 By itself none of the three markers provides suficient
evidence of dehydration, but the combination of any two indicates that dehydration is
likely, and dehydration is very likely when all three markers are present. This method
was established in accordance with reliable scientiic principles of hydration assessment.59 However, since the intention of this concept is to provide an easy way to assess
hydration, it only requires a body-weight scale. In case dehydration is suspected and
using WUT and following luid intake recommendations does not result in restoration
of euhydration, then other, more precise assessments should be conducted.
T
Likely
Likely
Very
Likely
Likely
W
U
FIGURE 1.1 Markers of hydration: Weight, urine, and thirst (WUT) athletic hydration
assessment tool. (Adapted from Cheuvront, S.N. and Sawka, M.N., Hydration assessment of
athletes: “WUT” is the answer?, Sports Science Exchange 97 Suppl., 18(2), 11–12, 2005.)
© 2011 by Taylor and Francis Group, LLC
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Nutritional Assessment of Athletes, Second Edition
One of the three assessment components of WUT is weight, which should be measured as nude weight, irst thing in the morning. Body weight losses in excess of 1%
measured on a day-to-day basis may suggest dehydration. This is a day-to-day loss
of 1.54 lbs. (0.7 kg) for an athlete weighing 154 lbs. (70 kg). Athletes should combine
the information from this measurement with the changes in urine or thirst measures
in order to achieve a more certain parameter of dehydration. The second assessment
component of WUT is urine. Indications of dehydration from urine are a diminished
daily urine frequency and darkening of urine color from a sample obtained at the
irst void of the morning. Again, athletes should combine the information from this
measurement with information about thirst and changes in body weight in order to
be more certain regarding the possibility of being dehydrated. The last component
of WUT is thirst. The existence of thirst indicates dehydration and the necessity to
drink. Thus, if athletes experience thirst, they should combine this information with
that from the body weight and urine measures to determine with more certainty if
they are indeed dehydrated.59
Sports dietitians should encourage athletes and their coaches to use these hydration measurement tools in order to monitor and maintain a proper luid balance that
will sustain health and aid in performance. Sports dietitians can explain these assessment techniques to athletes and coaches, giving them speciic tips to help them assess
their hydration status from the discussed measures. For example, they can promote
the use of charts where athletes can record their body weight, thirst, and urine color,
stressing that the loss of 1% of body weight, the presence of persistent thirst, and
dark-colored urine are possible indicators of dehydration.59
Sports dietitians may also want to educate athletes about how to record and analyze these measures. For instance, in order to examine how much luid athletes lost
or gained during a practice session or in a competition event, they need to record
their nude body weight to the nearest pound before and after the exercise. If they
lost an excess of 1% of their body weight, they did not consume enough luids during
exercise; on the other hand, if they gained weight, they consumed an excess amount
of luids. In order to help athletes estimate how much luid they should consume to
reestablish euhydration, sports dietitians could instruct athletes to add the amount of
weight they lost during exercise (in ounces) to the amount of luids they consumed
during exercise (in luid ounces); the value obtained from this addition would be
approximately equal to the amount of luids athletes should consume after exercise
to replace their sweat losses.
1.3.3
VEGETARIAN DIETS AND ASSESSMENT
Vegetarian diets can be healthful and are able to provide adequate nutrition in regard
to the athletic population. A vegetarian diet is one that excludes meat, including fowl
and seafood, and products containing those foods. A lacto-ovo-vegetarian excludes
all meat products but consumes eggs and dairy products. A lacto-vegetarian excludes
meat products and eggs from their diet. A vegan is similar to a lacto-vegetarian; however, vegans exclude all animal products, including meats, eggs, and dairy.60 Athletes,
especially during high physical activity, need to meet their macronutrient needs,
particularly carbohydrates and protein, to replenish glycogen stores, maintain body
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weight, and repair as well as rebuild muscle tissue.61 Protein consumption through the
diet is recommended and encouraged prior to taking additional supplements. Planned
vegetarian diets can meet an athlete’s current protein recommendations through the
diet alone without the use of protein supplements. Although the plant proteins are not
as bioavailable, it is possible for the vegetarian athlete to meet his or her protein needs
through well-planned meals. Vegetarian athletes may need to increase their protein
needs to approximately 1.3–1.8 grams per kilogram of body weight.60
Iron status needs to be addressed when working with vegetarian athletes. Low
iron status can have an effect on performance, muscle function, and work capacity.61
After a thorough nutritional assessment, a dietitian may suggest a blood test to determine iron status. Vegetarian athletes may need to consume an elevated amount of
iron compared to their carnivorous counterparts to meet their RDA. An iron supplement may be beneicial after continued contact with the athlete and monitoring of his
or her iron status. Other nutrients that are found in meat products, such as vitamin
B12, ribolavin, vitamin D, calcium, and zinc, need to be met through other sources.
A sports dietitian can assist vegetarian athletes with high-quality plant protein combinations as well as other sources, such as eggs and dairy, where these nutrients can
be found.60
A concern with vegetarian diets, speciically seen in women athletes, is the avoidance of meat to assist in decreasing caloric intake. If an athlete changes his or her
diet and becomes vegetarian, it is important to monitor the athlete’s energy intake
and body weight as well as body composition. A move toward vegetarian diets has
been a sign of disordered eating, which is one aspect of the female athlete triad.
1.3.4
GASTROINTESTINAL ISSUES AND ASSESSMENT
Celiac sprue disease is a genetic condition when an athlete cannot digest gluten, thus
causing GI issues, and this can lead to other complications such as weight loss. The
small intestine becomes damaged due to the immune response because the gluten
cannot be broken down appropriately. Symptoms of celiac disease include abdominal
pain and bloating, chronic diarrhea, vomiting, constipation, and pale, foul-smelling
stools.62 Without proper care the small intestine eventually will not be able to absorb
nutrients, thus leading to malnutrition. Celiac disease is a highly individualized disease; therefore two athletes will have different tolerances to gluten. Gluten, a protein
that is found in oats, wheat, rye, and barley, can be found in many foods and objects;
athletes will need to be aware of what they are consuming and the products they are
using. Due to its overwhelming presence in foods, an athlete with celiac disease will
need nutritional counseling to assist in food choices as well any changes that can be
made in his or her diet.
Crohn’s disease is a condition of the digestive tract. This disease can be seen in
any area of the GI tract but is usually found in the small intestine, speciically the
ileum. The area that is affected by the disease is inlamed and can cause pain as well
as frequent expulsion of waste, leading to diarrhea. This disease has very similar
characteristics as other bowel diseases, and an athlete will need testing to determine
a speciic diagnosis. Malnutrition can also form due to this disease. It is important
for the athlete to meet with a dietitian to determine possible deiciencies and dietary
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Nutritional Assessment of Athletes, Second Edition
treatment for malnutrition. Again due to the variability of the disease, an athlete with
Crohn’s disease will need to monitor his or her diet with the assistance of a dietitian
to determine the foods that are not well tolerated.
Diverticulosis is a condition where the large intestine forms weak areas that
become pouches. These pouches, called diverticula, become inlamed then progress
into the disease diverticulitis.63An athlete can oscillate between diverticulosis and
diverticulitis throughout the disease. For the most part, people do not feel much, if
any, pain or discomfort with diverticulosis. However, when these pouches become
inlamed, symptoms may arise such as changes in bowel habits, lower abdominal
pain, cramping, and nausea.64 It is suggested that diverticular diseases developed
due to the decreased consumption of iber in the diet. When a stool is caught in the
diverticula, this can cause inlammation, thus causing the condition to progress to
diverticulitis. After a diagnosis of diverticulosis, an athlete should meet with a dietitian to assist in determining the foods that should be consumed during both stages
of the disease.
Irritable bowel syndrome (IBS) is a disorder with symptoms such as abdominal
cramping and pain, bloating, constipation, and diarrhea. Even though this syndrome
can be painful and possibly debilitating for some, it does not have any detrimental
effects in the intestines and does not lead to any serious conditions. Most of the
symptoms can be treated through control of an athlete’s diet, stress management,
and medications. Working with a physician and a dietitian can help an athlete identify possible treatment options as well as different interventions that can be taken to
decrease IBS symptoms.
Diarrhea is deined as loose, watery stool. Acute diarrhea can last less than two
days and does not require medical treatment. However, chronic diarrhea may cause
medical issues and needs to be addressed by a physician. Chronic diarrhea can lead
to possible nutritional complications as well as dehydration. When meeting with a
dietitian, it is imperative to be as open and truthful as possible about bowel movements, which is covered more thoroughly in the “Openness in Reporting” section of
this chapter. Diarrhea is a symptom of many gastrointestinal issues that are listed in
this section.
Constipation is a variable condition as well. For some individuals, not having a
bowel movement each day would be considered constipation. Constipation is deined
as having a bowel movement fewer than three times a week.65 Constipation is a
symptom, not a disease, and can usually be caused by a poor diet. There are many
factors that can lead to constipation, including a lack of iber in the diet, dehydration,
medications, laxative abuse, and changes in a routine.
Lactose intolerance is a common condition where an athlete is not able to tolerate dairy product consumption. Again, this condition is highly variable, and athletes
with this condition may be able to tolerate very different dairy food choices. Lactose
intolerance is due to the gastrointestinal tract not being able to digest the sugar,
lactose, found in dairy products due a lack of the proper enzyme.66 Products such as
milk, cheese, ice cream, and other dairy products may need to be eliminated from
the diet to decrease the symptoms of this condition. Symptoms that are usually seen
with lactose intolerance include diarrhea, abdominal cramping, gas, nausea, and
bloating. Dairy products such as yogurt may be better tolerated due to the inherent
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Estimation of Food and Nutrient Intakes of Athletes
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characteristics of enzymes that can assist in the breakdown of lactose. Meeting with
a dietitian can help an athlete determine the food products he or she can consume.
Products are currently on the market that include the enzyme lactase, thus athletes
with lactose intolerance may be able to consume these products with fewer GI symptoms. Pills and tablets containing the enzyme needed to break down the sugar in
dairy products are also available and can be taken prior to consuming dairy products
to assist in the digestion of these products.
The above descriptions are only a few of the many different gastrointestinal issues
athletes may have or develop. It is important to be aware that everyone has different
symptoms and that diseases affect each individual differently. If athletes have any
gastrointestinal issues or have concerns about possible genetic issues, it is important
to have them visit a physician or a specialist to assist them in gaining knowledge
about the speciic issue.
1.3.5
SUPPLEMENTS
A dietary supplement, as deined by the National Institutes of Health, is a product taken by mouth that contains a “dietary ingredient” intended to supplement the
diet. Such dietary ingredients may include vitamins, minerals, herbs or other botanicals, and amino acids, as well as substances such as enzymes, organ tissues, glands,
and metabolites. Supplements are not currently regulated by the Food and Drug
Administration (FDA) and are still available over the counter, without a prescription.
Unfortunately there are no required tests regarding the safety, eficacy, or purity of
dietary supplements before they are put onto the market. The Dietary Supplement
Health and Education Act (DSHEA) of 1994 speciically removed FDA and other
agency reviews for the sale of these products. However, the FDA reserves the right
to remove a product after it has been proven harmful. The DSHEA places dietary
supplements under the umbrella of “foods” instead of “drugs” and limits the Food
and Drug Administration’s ability to regulate the substances.67 For years, there has
been considerable hype surrounding the use of many of these supplements.
Supplements may be consumed for health purposes or for their performanceenhancement claims. The total amount of money spent on dietary supplements today
is over $20 billion a year.67 Cassileth (2009) reports that about 52% of people consumed one or more dietary supplements on a regular basis in 2009, compared to 46%
of people who consumed supplements on a regular basis in 2006.67 This is owed in
large part to the signiicant promotion by the media. Not surprisingly, athletes are
most likely to use various supplements, especially those that claim to provide a competitive edge.68 It is crucial for the dietitian to work closely with the athlete and be
aware of possible supplement usage for accurate determination of the dietary assessment as well as for health reasons.
Several physical, emotional, and mental stressors are put upon an athlete. This
type of stress on the body can affect health and increase nutritional needs. Especially
for those athletes involved in vigorous training programs, consumption of enough
food may be dificult, as well as the ability to consume enough nutrient-dense foods.
Inability to eat healthfully, in time, can lead to nutrient deiciencies that may affect critical functions of the body and ultimately lead to disease and impaired performance.69
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Nutritional Assessment of Athletes, Second Edition
Vitamin and mineral supplements can be a beneicial addition to an athlete’s daily
regimen. Most often, athletes need to be reminded that the best way to get vitamins
and minerals is from actual food, and a supplement is just that—a supplement to the
diet and not an alternative source. In a well-balanced diet, nutrient needs can usually
be met; however, it is important that appropriate probing about the athlete’s supplement usage occur since there may also be adverse effects, such as interactions with
other nutrients and toxicity from use. When conducting a dietary assessment, any
and all vitamin, mineral, and other supplements should be included to account for
extra nutrient intake. It is important to be aware of the various vitamins and minerals
an athlete is consuming not only for assessment and analysis purposes but also to
understand interactions that may occur with other foods or supplements.
Some of the most important vitamins and minerals for athletes include calcium,
iron, magnesium, potassium, sodium, B vitamins, and vitamins D, C, and E.69
Calcium and iron, in particular, are two minerals for which it is crucial that athletes
have adequate amounts. Calcium is necessary for bone health and protection from
injury as well as muscle contraction. Iron aids in the transport of oxygen throughout
the body and allows oxygen to be taken up into the muscle. Women particularly need
to be aware of their iron status, as menstruation reduces iron levels to an even greater
degree. Iron deiciency causes fatigue, malaise, dificulty breathing, and dizziness.
Iron deiciency for prolonged periods leads to anemia, which causes the heart to have
to work harder to pump oxygen through the body.70 The other vitamins and minerals
noted help keep body luid levels normal and allow other important metabolic functions to take place.69
Protein and amino acid supplements are some of the most popular among athletes. Although they are not a typical food item, protein supplements contain other
nutrients and calories that need to be documented on an athlete’s dietary assessment.
Some athletes may also add fruit and other nutrient supplements to drinks consisting
of a powder base with added vitamins, minerals, and various forms of protein, which
can include whey, soy, or amino acids. During a dietary recall, be sure to inquire
about the use of protein and amino acid supplements and the form in which they are
consumed, as well as any other added nutrients.
Use of supplements can be tricky. It is important to evaluate and make sure supplements do not contain any ingredients banned by agencies, conferences, or leagues.
Unfortunately, for the case of several supplements, not all ingredients included in a
product are listed. Without regulation by the FDA, there is no way to control what
manufacturers include in their product; as such, it is often dificult, if not impossible,
for the buyer to know. There are numerous reports of professional athletes unknowingly consuming banned substances, ultimately failing drug tests, and in many cases
effectively ending their career.68
A couple of the most referenced guides to banned supplements in the United States
stem from the National Collegiate Athletic Association and the World Anti-Doping
Agency. Other countries have very different regulations on supplements and even
banned substances. Each country has compiled its own list of banned substances,
which can be accessed through its national governing bodies.68 Several classes of
supplements and medications are prohibited and include stimulants such as caffeine, anabolic agents, alcohol and beta blockers (only for rile and vehicle racing),
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Estimation of Food and Nutrient Intakes of Athletes
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diuretics and other masking agents, narcotics, cannabinoids, peptide hormones and
analogues, antiestrogens, glucocorticosteroids, and beta-2 antagonists. It is crucial
that the dietitian know about possible supplement use, know which ones may be
more popular for some sports over others, and watch for possible signs, symptoms,
and side effects of prohibited supplement use.
Herbal agents are quickly becoming another popular supplement among athletes.
With the frequency of traveling, athletes are exposed to many different herbal products, especially in China and India.68 Use of these products must be under close
watch because their contents may include over 30 different herbs per supplement.
Oftentimes these herbs may include traces of banned substances or other exotic
ingredients that may cause toxicity or adverse side effects. Like their treatment in
the United States, herbs and other supplements in foreign countries are not regulated.
Ingredients are usually not written in English, and concentrations of each herb may
differ from one batch to the next.68
1.3.6
TRAVELING
1.3.6.1 Jet Lag
Jet lag is a phenomenon caused by changes in the normal circadian rhythm of the
body that affect sleep and wake cycles that occur naturally. Interestingly, there are
similar circadian patterns for daily meal times. These food consumption patterns are
affected just as the sleep cycle is during jet lag. When there is a change in eating patterns, blood low to the gut and consequent inadequate absorption may persist. Some
of the best ways to counter jet lag are behavioral approaches and timing of food
intake. Changing patterns of eating before a long light, such as the Argonne diet,
alter symptoms of jet lag.71 This diet alters days of feeding and fasting on a proteinrich breakfast and carbohydrate-rich evening meal.72 The dietitian must be aware of
travel times to understand any changes in feeding patterns and to be able to advise
the athlete on staying fueled and hydrated throughout the trip.
An important related concern during travel and prolonged lights is the possibility of dehydration. The air circulating inside the airplane cabin is dry, which causes
an increased loss of moisture from respiration. This can be an issue since this may
unknowingly affect the athletes’ hydration, which in turn may have an impact on
performance in outside events in humid and high-temperature climates. Athletes
should be advised to consume more water than normal during the travel period, as
well as a few days before and after the light. Intakes of at least 15–20 mL of luids
per hour of light over and above normal luid consumption are encouraged.71
1.3.6.2 Dining Out and Eating on the Road
Traveling can pose some issues dealing with food, nutrient, and luid consumption of
the athlete. Not having access to regularly consumed foods as well as preparation and
cooking techniques that the athlete is familiar with may be an issue due to differences in
appropriate nutrient intake speciications. Often restaurants use oils, butter, and added
sugars to foods to provide lavor. Not all athletes may be used to consuming these extra
fats and nutrients in their food, and it may cause gastrointestinal complications and be
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Nutritional Assessment of Athletes, Second Edition
problematic for those who are on a restricted diet and watching caloric and speciic
nutrient intake. Restaurants, take-out, and fast-food venues are the main sources of
food consumption for traveling athletes. It can be dificult to control serving size to
get the proper amount of food, and more importantly, preparation and cooking techniques are dificult to control, which can alter the healthfulness of a food. Especially
during recovery, it is important for athletes to consume carbohydrates and protein to
aid in muscle growth and repair. Often, restaurants offer dishes that may not provide
adequate amounts of these nutrients or adequate types (high-fat cut of protein versus a
lean protein). In these cases, it is important for athletes to bring some snacks and food
supplies of their own, such as sports bars, fruits, ready-to-drink protein beverages,
nutrient shakes, and any canned foods such as meats, beans, and soups.71
When dining at a restaurant, choose meats that are grilled or baked and lean
sources. For healthy steaks, choose sirloins. When deciding on soups, dressings, and
sauces, stay away from creamy ones and choose tomato-, broth-, or oil-based instead.
Vegetables are great choices for side dishes, but should be cooked without butter.
Oftentimes the restaurant has nutrition facts on their Internet Web page. This information can be used to ensure a more accurate diet assessment. If there is no information available, be speciic when questioning and performing the dietary recall. Be
sure to ask about preparation techniques and speciics of prepared vegetables and
any sauces or dressings used with the meal. It can be dificult for the athlete to know
about meals and foods made in other locations, which is where the dietitian must try
to extract as much speciic information as possible.
When traveling to different countries, athletes must be aware of diverse eating
patterns. Different eating times, food preparations, types of foods consumed, and
hygiene of food can present various issues for the athlete traveler. Those with a discerning palate may have a hard time adjusting to different tastes. A good consideration for traveling is to investigate the available foods and to also bring along some
food supplies from home (making sure they are in line with travel guidelines). Being
extremely cautious of exotic foods and preparation techniques is crucial to maintaining health. Exotic foods and use of water may cause adverse effects and subsequent
health problems such as gastrointestinal upset and possible viruses. Important tips
to remember, depending on the destination, include drinking only luids from sealed
bottles, avoiding ice in drinks, choosing cooked vegetables instead of raw ones and
salads, peeling all fruits, avoiding all uncooked foods and unpasteurized dairy products, and not buying food from local markets. Again, in this situation it is necessary
for the dietitian to speciically inquire about the foods consumed to obtain an accurate
nutrition assessment.73,74
1.3.7
WEIGHT MANAGEMENT
Speciic body composition or characteristics are associated with different sports that
contribute to the athlete’s chances of success in competition. This is due, in part, to
certain physiological beneits such as effective thermoregulation or a greater powerto-weight ratio associated with speciic body characteristics. Athletes and coaches
in many sports, such as wrestling and gymnastics, are usually convinced about the
beneits of weight or fat loss, based on personal or anecdotal experience, instinct, or
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the false belief in experienced observation of successful athletes. Therefore, athletes
striving to achieve these desired body characteristics are often prone to engage in
unbalanced, irregular, or very restrictive eating patterns, which can increase their risk
of becoming dehydrated or nutrient deicient, or of developing eating disorders.75
The presence of these problems and inadequacies in the diet is then translated
into the dietary assessment of athletes,76 as discussed in Section 1.2 of this chapter.
Therefore, professionals assisting athletes with body-type management should be
knowledgeable and trained in anthropometry.75 In addition, sports dietitians should
be familiar with the sport-speciic nutrition requirements, body composition standards, and athletes’ beliefs toward the standards in order to conduct the dietary
assessment process in the most speciic and effective way possible, so that interpretation of the assessment’s results can help elucidate possible problems in the diet of
athletes that could affect both health and performance.
One case of impaired health and subsequent impaired performance in athletes
results from recognized eating disorders such as bulimia nervosa and anorexia
nervosa. These conditions have speciic symptoms that meet the Diagnostic and
Statistical Manual on Mental Disorder IV diagnostic criteria. Also, another type of
diagnostic criteria that situates athletes at health risk is the Diagnostic and Statistical
Manual IV category, which refers to “EDNOS” (Eating disorder not otherwise speciied),77 meaning that even though some athletes may have a disordered eating pattern, they do not fulill the characteristics to be considered bulimic or anorexic. The
susceptibility and development of eating disorders among athletes may be apparent
in athletes attempting to change body type through diet and/or extreme exercise.76
This underlines the importance of frequent and well-planned diet assessments
in order to detect the presence of eating behaviors to provide early intervention and
nutrition counseling to those athletes who may be at risk of developing eating disorders. Dietary recalls and recognized testing modules like the Eating Attitude Test
and Eating Disorder Inventory are dietary assessment tools that can deinitely contribute to identifying athletes at risk for developing eating disorders that may in turn
impair their health and performance.76
Another aspect of weight management in need of consideration is that standard
measures for body composition used for the general population may not apply to the
athletic population. Such is the case of Body Mass Index (BMI), which is especially
apparent when comparing BMI values from football players to the general population or even other sports. Desirable body sizes for football players for the different
positions in which they play may be considered unhealthy for the nonathletic population. In a study with football collegiate freshmen, the BMI values varied from 23.8
for the quarterback to 33.1 for the offensive lineman.78 In addition, the average BMI
range for players in the National Football League is from 27.2 for the defensive
back to 36.0 for the offensive lineman.79 The differences between the BMI values for
the various football positions and the body size of football players are partially the
reason for which energy needs and body-image perception in collegiate football are
different compared to other sports and the nonathletic population.76
Many athletes have greater Lean Body Mass (LBM) compared with their nonathletic counterparts. In addition, they are routinely involved in rigorous physical
training programs compared to the nonathletes. Therefore, standard calculations for
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body size (such as the BMI) and energy needs (such as Harris Benedict or Miflin-St.
Jeor equations) based on parameters for the regular population are not often useful
for the athletic population. In the case of some football players who weigh 125% or
more of the ideal body weight (based on the standard methods), the resting energy
expenditure should be based on their LBM.76
There seems to be a tendency in the general population toward underreporting
by approximately 20% when assessing dietary intake.80,81 Particularly to the athletic
population, underreporting of dietary intake has been commonly shown in female
endurance runners, gymnasts, divers, and dancers due to dissatisfaction with their
body images.82,83 This could result in a disparity between energy intake and energy
expenditure of athletes, which could in turn have negative health consequences associated with eating disorders, such as bulimia, anorexia nervosa, or EDNOS. However,
“decreased energy availability,” which is a chronic inadequate energy intake with
or without weight loss, has more recently been recognized as the main cause of
amenorrhea and bone mineral loss in female athletes who were otherwise healthy.84
On the other hand, overreporting can also occur in the athletic population, since
athletes may report not only too low but also too high intakes compared to their real
intakes, especially when they know that what they are consuming is unacceptable.85
Consequently, experienced sports dietitians familiar with the speciic nutritional
requirements and anthropometry of the different sports should be able to recognize
these discrepancies.
Dietary assessment of athletes is not an easy task. This is due, in part, to the
expected inaccuracies in using self-reported data, such as in the case of dietary
records kept by athletes. Even considering these inaccuracies in self-reporting, the
7-day food diary seems to be most accurate in the estimation of reported energy and
nutrient intake compared to other food records.86 Separately, an easy-to-use semiquantitative food record was compared to total energy expenditure of nonobese subjects estimated by doubly-labeled water technique, and it was found to provide good
estimates of energy intake.87 However, the comparison of energy obtained from the
diet to the recommended intake is limited by the impact of the speciic sport, type
of training, and individual anthropometrical data, which adds more variability to the
interpretation of dietary assessments.76
Therefore, in order to have a better estimate of the actual energy consumed by
athletes over time, the employment of other methods in addition to dietary assessment can provide more complete and accurate results. For example, biochemical
markers such as unexplained low blood glucose or the existence of urinary ketones
may imply that the athlete has an energy deiciency.88 Observed signs of fatigue,
decline in performance, and in the case of female athletes, irregularity in the menstrual cycle, suggest the possibility of energy deiciency that will need to be further
investigated.84 Anthropometric measures are also helpful, since they can be utilized
to monitor changes in lean and fat mass over time. However, due to the error involved
in the measurement of anthropometric data, and to the unpleasant feeling that some
athletes may experience during this type of assessment, a high level of technical and
counseling expertise is necessary for these measures to be safe and useful.89 Even
though coaches are frequently concerned that tracking body composition in these
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athletes will inluence them to become more focused on their weight,90 failure to do
so may result in continuing and undetected energy deiciency.75
In addition to these methods, there are yet other methods of dietary assessment
available to improve accuracy and reliability. These methods include metabolizable
energy intake balance, room calorimetry, indirect calorimetry, heart-rate monitors,
accelerometers, and doubly-labeled water. The use of some of these methods may be
more pertinent for research purposes due to their high cost and required expertise for
utilization. A study of the direct comparison of estimates of daily energy expenditure
in healthy adults, using energy intake from 7-day self-reported diet records, metabolizable energy intake balance, and energy expenditure measured by doubly-labeled
water and 24-hour room calorimetry showed that self-reported dietary records and
room calorimetry underestimated daily energy expenditure. In addition, while energy
intake balance provided accurate estimates of energy expenditure, energy expenditure measured by doubly-labeled water was a precise and more direct approach.91
The results of this study suggested that metabolizable energy intake can accurately
estimate energy expenditure, but it has to be done with a controlled feeding and
the protocol can be burdensome for the subjects and may even create confounding
results due to the interference it causes in the subjects’ normal daily activities and
eating practices.91
On the other hand, dietary intake records cause less interference but they have
been shown to be inaccurate and to underestimate energy expenditure. The room
calorimeter is the most accurate tool to determine energy expenditure during a
24-hour period; however, the results obtained from this measurement are limited to
the energy expenditure of a subject restricted in activity to a small chamber. Overall,
total energy expenditure measurement using doubly-labeled water is a more direct
approach to determining free-living energy expenditure than metabolizable energy
intake balance or calorimetry methods.91
Another study, conducted with endurance runners to assess their total daily
energy expenditure with the use of heart-rate monitors resulted in a greater than
expected total energy expenditure, which was signiicantly affected by the athletes’
energy expenditure.92 The heart-rate method has been widely used in the athletic
population,93 and it has been considered to be a more convenient method to be used
with athletes when compared to the accelerometers (which were regarded as limited
to ambulatory activities and to be inaccurate at running speeds over 9 km/hour) or
the doubly-labeled water method (regarded as the most accurate method but inconvenient to monitor energy expenditure of shorter durations).92
Actual energy expenditure obtained from several of the above-discussed methods
can be compared with dietary assessment to determine the accuracy in self-reported
food intake of athletes. These energy-expenditure methods, as well as anthropometric measures and laboratory analysis data, can also provide an insight about unsafe
and inappropriate weight-management techniques some athletes may engage in to
meet certain body-type standards. In addition, expertise in the sport-speciic nutritional requirements, body-type characteristics, and athletes’ beliefs toward them, as
well as training in anthropometric techniques, can help sports dietitians determine
possible inaccuracies in the dietary intake and dietary-intake reporting of athletes.
This in turn can allow sports dietitians to elucidate possible problems in the athlete’s
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Nutritional Assessment of Athletes, Second Edition
diet or his or her perceptions toward foods and body-type characteristics that could
affect both health and performance.
1.4
TRANSLATION OF DIETARY ASSESSMENT INTO ANALYSIS
Registered dietitians have a wide availability of computerized nutritional analysis
software, which allows them to obtain individual food composition information as
well as to determine caloric and nutrient intake from nutrition assessment reports.
The computerization process has facilitated the gathering of such data by eliminating the wearisome task of searching for each food item on printed food-composition
tables. However, the process of matching foods and portions recorded during assessment with those found in databases remains a dificult task.
Dietary analysis software programs are periodically updated, and new ones are
often made available in the market. These attempt to include a more varied and
updated array of new foods introduced into the market, and some also include common restaurant foods. Some software may be more appropriate than others depending on the needs of the dietitian and the context in which they will be used. Special
considerations to take into account when choosing software are discussed in this
section, as well as important default assumptions made about databases, analysis of
new and ethnic foods, analysis of luids and hydration status in athletes, and analysis
of nutritional supplements.
1.4.1
INTERNET WEB SITES
The current availability of nutritional analysis tools includes Internet-based options
that are free to the public. These can be used by dietitians as a sole nutrient database reference, as well as in combination with other software when foods from
reports are not found in the currently used software. Although several free online
nutritional-analysis software programs may be available, dietitians should consider
their accuracy, especially when considering the use of free, Internet-based software.
The U.S. Department of Agriculture (USDA) Food Composition Search Tool94 and
MyPyramid.gov94 provide reliable information about caloric and nutritional content
of foods based on scientiic research conducted by the USDA.
The USDA Food Composition Search Tool can be accessed with the following
link: http://www.nal.usda.gov/fnic/foodcomp/search/index.html.94 This Web tool
was created by the Nutrient Data Laboratory (NDL)95 with the responsibility to
develop the USDA’s Nutrient Database for Standard Reference (NDSR), which is the
basis of most food and nutrition databases in the United States, making this source
a reliable option that is available to the public and scientiic community. Nutritional
analysis of a wide scope of foods can be obtained by entering up to ive keywords to
describe single food items, with an option to narrow the search by choosing the food
group to which the speciic food belongs and by choosing the amount of food to be
analyzed. This search tool offers general food items as well as brand-name products
and foods found in restaurant menus. It also offers the option of viewing reports on
foods by single nutrients that are sorted either by food description or in descending
order by nutrient content.
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Moreover, the NDL homepage95 offers accessibility to the Dietary Supplements
Ingredient Database (DSID),96 which was created by NDL researchers in conjunction
with the Ofice of Dietary Supplements, the National Institutes of Health, and other
federal agencies to estimate levels of ingredients in dietary supplement products.
This tool could be especially helpful to analyze the intake of dietary supplements
that might not be included in currently available dietary software. The DSID homepage96 offers several features that dietitians can choose according to the context in
which supplement intake analysis will be made. These include a research summary,
data iles, and a multivitamin/multimineral calculator for adults, with a basic and a
professional version. More information is available for researchers. The use of the
calculator allows for the gathering of estimates for speciic nutrient levels listed on
the Supplement Facts labels of some adult multivitamin/multimineral supplements.
These estimates can aid dietitians in assessing total nutrient intake, since approximately one third of the population in the United States takes vitamin-mineral supplements daily.97
Another reliable Web-based tool for nutritional analysis is MyPyramid.gov,98
which was created by the Center for Nutrition Policy and Promotion branch of the
USDA. This Web site offers several resources that are user-friendly and can be
accessed by the public. One of these resources is MyPyramid Tracker.98 MyPyramid
Tracker is an online tool that can analyze nutritional and physical activity information. It has a Food Calories/Energy Balance feature that calculates energy balance,
taking into account the information provided on foods eaten and physical activity
performed, which is helpful to understand the energy-balance status of the person
being analyzed. Energy-balance history can be saved and viewed in the system up
to a year.
The dietary analysis portion of MyPyramid Tracker allows people to enter food
items individually, using a similar format as mentioned for the NDL nutritional analysis tool, except that with MyPyramid Tracker all items consumed on a day can be
then analyzed altogether, providing caloric and nutritional information of all foods
consumed instead of analyzing a single item at the time. This Web tool offers the
option of creating a list with frequently used foods to facilitate the process of entering foods for a given person after the irst time.98
Once all food items have been entered, the system analyzes food intake based
upon the recommendations of the Dietary Guidelines for Americans, 2005. The
system also uses information entered regarding age, gender, height, and weight of
the person being analyzed. This information is then used to compare the actual
food intake to the intake that would be recommended for the person. Comparisons
are made according to the previously stated person’s characteristics, the type and
amount of physical activity performed, and the selection of weight maintenance or
progressive weight loss chosen for the analyzed person.
Several analysis reports can be obtained from this system. They include nutrient
intakes from foods, comparisons of intakes from basic food groups to the Dietary
Guidelines for Americans, and comparisons between intake and the MyPyramid
recommendations. In addition it is possible to obtain an assessment of intake over
time (up to 1 year) with an average of MyPyramid recommendations by food group
and nutrient intake for the days entered. This report includes graphs of daily intakes
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Nutritional Assessment of Athletes, Second Edition
with trend lines for each MyPyramid food group and individual nutrients to ease
interpretation of results.98
The energy-balance analysis provides information about total caloric intake,
Estimated Energy Requirement (EER), percent of calorie intake from EER, and percent of calories expended from physical activity, and presents a graph of energy balance
for a single day or multiple days (up to a year). This Web tool can be useful to dietetic
students and dietitians who cannot afford or choose not to purchase other nutritional
analysis software. It can be also used as a complementary source that has features, such
as physical activity analysis, that may not be present in other software or databases.
Also, since it is designed for the general population, this tool can be directly used by
anyone interested in knowing about his or her nutritional and physical activity status.
It should be noted that the information provided in the NDL and DSID Web sites
as well as in MyPyramid.gov has gathered data from foods (NDL and MyPyramid.
gov) and nutritional supplements (DSID) available in the United States; therefore
special considerations should be taken when analyzing diets of people consuming
products that are not commonly available in the United States. Information regarding international nutrient-analysis databanks can be found at http://www.nutrientdataconf.org/DatabankDir/IDB_Dir.htm.99 This Web site offers an International
Nutrient Databank Directory99 that was prepared by a committee of the National
Nutrient Databank Conference by compiling an updated international directory of
software applications and their corresponding food composition databases. This
directory can be useful for dietitians to establish the combination of sources that
may best meet their needs and allow them to compare special software and database
characteristics.
1.4.2
SPECIAL CONSIDERATIONS WHEN CHOOSING SOFTWARE
The increasing number of nutritional-analysis software packages available on the
market poses a progressively more dificult task for dietitians and other potential
users to decide which system would best suit their speciic needs and objectives.
These software range in price from free (Internet based) to more than $10,000.100
Price is an important consideration when choosing software. It should be noted that
the price of the software differs in part on the availability of public funding or sponsoring agents. Thus, nonfunded manufactures develop software in a private manner,
which tends to increase the cost of production and therefore the inal cost of the
product. Consequently, the price in itself does not necessarily relect the quality of
the inal product.101 Another factor that affects the software’s price is the number
of users that it has; the more users, the more income developed and thus the lower
the software price. Therefore, since generally there are more clinical than research
users, software applications used by the former tend to be less costly than those used
by the latter.102 Unique features present in more costly software geared to the scientiic population might not be needed for counseling purposes; therefore, lower cost
alternatives that better relect the needs of the user should be considered.101
Although price may limit the decision to buy one type of software over another,
this should not be the main focus when choosing nutritional-analysis software. Even
within their price range, dietitians should aim to choose the software with the highest
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Estimation of Food and Nutrient Intakes of Athletes
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quality of nutrient database as possible. Nutritional-analysis software reviews that
are regularly published in journals such as the Journal of the American Dietetic
Association and Nutrition Today103 center on program features such as screen
presentation, ease of entering foods and amounts, ability to modify the database,
reporting capabilities, hardware requirements, and statistical-analysis functions.
Even though these characteristics are important to consider at the time of choosing
software, the quality of the nutrient database on which all calculations are based
needs to be evaluated; otherwise the program features would be of little help if the
nutrients calculated are of poor quality. Data quality refers to the suitability of the
food values, ensuring that presented values are representative of the composition of
the foods included on the database, and that the food items on the database are those
consumed by the individual or population being analyzed.101
Many software programs provide demonstration packages that can be helpful for
dietitians to test system features, such as data-entry and nutrient-calculation capabilities, before making a decision on which software to buy. However, decisions
regarding the nutrient database component should not be based solely on these demonstrations, since foods and nutrient values included may not represent the complete
database.103 Several questions may arise when trying to determine the quality of the
nutrient database of different systems. Buzzard et al. (1991)103 proposed a series of
speciic questions to be used as guidelines in evaluating databases quality:
1. Does the nutrient database include all the foods and nutrients of interest?
Requirements about particular foods such as fast-food items, speciic
brand-name products, or less commonly consumed foods such as ethnic or
vegetarian foods need to be identiied before choosing a speciic software,
since there is a lot of variation regarding these characteristics among different software packages. Furthermore, there is variation related to food
names, varieties of foods grown and distributed, usual recipes, and fortiication rules and practices among different geographic regions within
the United States and also between the United States and other countries.
Therefore, dietitians should choose a database system that represents foods
available to their research study or dietetic practice population.101
Also the number of food items listed on a database may not relect the total
capability of the software’s system. Some software applications list a relatively small amount of foods; however, they can accommodate differences in
food form, preparation, and amount units through their nutrient-calculation
system, thereby allowing for an equal or more comprehensive number of food
items than systems in which foods are entered separately in the database.
2. Do desirable food items contain complete nutrient analysis?
Nutritional-analysis software packages often present several numbers of
missing values, leading to errors in the accuracy of nutrient calculations.
Misinformation is usually not reported to buyers, and since missing values
are listed as zeros, these could result in misinterpretation of the nutrient content of foods being analyzed. Dietitians should require vendors to provide
them with an estimate of missing values for the nutrients included in the
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Nutritional Assessment of Athletes, Second Edition
database, thus allowing dietitians to check speciic foods for completeness
and currency of the nutrient data.103
Moreover, dietitians can check detailed speciications available from the
Standard Reference104 and Food and Nutrient Database for Dietary Studies
(FNDDS).104 The Standard Reference only lists available values without
providing zeros even when nutrients are known not to be present in a food
(e.g., fat in table sugar), thus some food component ields are empty. On the
other hand, in the FNDDS, all food component ields have a value, using
zeros for absent nutrients or estimated values using imputations. Another
source available to dietitians to check for the nutrient content of speciic
foods with missing values is the International Nutrient Databank Directory
(which is sponsored by the National Nutrient Databank Conference). This
directory is updated every 2–3 years and includes information on available
food components for more than thirty databases.102
3. Do the food descriptions incorporated in the database provide adequate
speciicity to accurately assess the desirable nutrients?
In order to answer this question without using the software, dietitians
should consider the purpose and scope of their practice to determine
whether information regarding special items such as low-sodium or nonfat
versions of food products will be needed, whether they are available on
the database of interest, and whether the software allows for the manual
addition of speciic items (although this would be a labor-intensive, tedious
solution). An even more important factor to consider is the form in which
manufactured foods are entered into the database. Data from manufacturers usually contain only nutrients from the food label or those required
for nutrient claims or for educational purposes published by the company.
Therefore when this source of food composition information is used in the
database, there will be misinformation of certain nutrients for speciic food
items. Dietitians should be aware of this fact and should consult with the
Standard Reference database to obtain a comprehensive nutritional analysis
of speciic food items with misinformation.101 Dietitians can request a listing of the descriptions of the foods included in the database and of their
sources of nutrient content to evaluate the overall suitability of the software
of interest.103
4. What quality control procedures are used to guarantee the accuracy of the
nutrient database?
Software users usually rely on the integrity of software developers to
determine the accuracy of the nutrient database. Therefore quality control
procedures may be required to ensure accuracy.101 Quality assurance procedures are required during the development of nutrient databases. They
include a comparison of calculated algorithms with expected values for
each database entry, cross-checking of all database changes, computerized
edit checks to identify values that fall outside of speciied ranges within
each food group, and repeated calculation of test food records to guarantee
that any differences between database versions are due to intended modiications to the software and not due to error.103
© 2011 by Taylor and Francis Group, LLC
Estimation of Food and Nutrient Intakes of Athletes
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Answering these questions will provide the foundation for a comprehensive
review and evaluation of the nutrient database. However, the inal selection of
the most suitable software package will depend on the additional system features
that best relect the particular needs of the dietitian. Important features to aid in
the selection of software are the system’s cost and the type of output generated
by the system.
The type of output chosen differs based upon the speciic needs of the user. For
example, for an intervention study, the composition of foods consumed over a prolonged period would be the chief information needed, while a menu developer may
ind the composition of foods intended for a meal to be the most valuable information.
In general, dietitians should choose software that summarizes nutritional information analyzed by each meal or menu, or as an average of meals consumed during one
or several days, depending on which analysis would be most helpful to them.101
In some situations, dietitians may need to print materials (for example, for educational purposes), in which case the software chosen should be able to provide simple
and concise outputs. The availability of printed graphs, for instance, would be very
useful to demonstrate adequacy of nutrients to meet speciic aims during counseling
sessions or interventions.101 On the other hand, for educational purposes involving
overall nutrition, displays showing food groups instead of individual components may
be more suitable. For instance, MyPyramid Tracker98 offers the option of comparing the intake of an individual with the MyPyramid recommendations, which could
serve as an evaluation instrument. Yet for research purposes, results may need to be
exported to a spreadsheet format to assist in the creation of summaries, and in the
performance of statistical analysis for comparison between different set of data.101
Choosing software that best its the needs of the dietitian is not an easy task. A
more detailed set of guidelines to further assist professionals in choosing the most
suitable software can be found in Table 1.4.103,105–107 The appropriate selection of
software would enhance the accuracy and utility of the dietary assessment process
as a whole.
1.4.3
DATABASES
Determining the appropriate composition of nutrients in foods is of great importance. Food composition databases can be used to plan and evaluate dietary competence of meals and overall diets. However, accurate assessment of the diet can only
be achieved with an accurate database.
There are other considerations when deciding on which database to use.
Recognition of the target audience, eficiency of the search system for obtaining
nutrient data, the content and format of summary information, and cost are all
important considerations. With increasing use of the Internet, there are a few freely
accessible online databases that are used by clinicians, athletes, the general public,
and researchers. There is also software that can be purchased for more speciic uses.
Costs of this software vary from less than US$100 to as much as US$8,000. The
more expensive systems contain more unique and customized features.108 Lists of
software can be found in the International Databank Directory.
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Nutritional Assessment of Athletes, Second Edition
TABLE 1.4
Guidelines to Choose Dietary Software
Software-computer
compatibility
Type of license needed
Software documentation
Type of database
Fluid consumption
Addition of new foods/
recipes
Type of output produced
File management
• Check RAM, hard disk space, memory coniguration, operating
system, monitor, and printer requirements
• Check whether you need single-user or multiple-user license
• Check documentation to: install and manage software; run all the
software features; troubleshoot; manage iles
• Check whether documentation speciies default assumptions
• Check source of information for nutrients; recency of data; availability
of database upgrades; notiication of database updates; accessibility to
all nutrients of interest
• Check whether foods with missing data are lagged and whether the
totals including these foods are also lagged
• Check whether software allows you to enter water/luid consumption
or whether it contains water content of foods that can be adjusted to
record luid consumption
• Check whether software allows you to add new foods/recipes to the
database, the ease with which to do so, the maximum amount of new
foods/recipes that can be added, and whether the recipe system
includes a retention (cooking gains/losses) algorithm
• Check whether software output will satisfy your needs
• Check whether percent of energy from macronutrients is provided;
whether intakes are broken down by meal; whether intakes are assessed
relative to standards and if so, whether the standards are current and
accurate; whether weight management algorithms are included, and if
so, whether they are suitable for athletes
• Check for ease of ile management use
• Check whether software generates multiple-day averages for
individuals
• Check whether data produced is compatible with statistical software
for research purposes
Sources: Data from Sugerman, S.B., Eissenstat, B., and Srinith, U., Dietary assessment for cardiovascular
disease risk determination and treatment, in Cardiovascular Nutrition. Strategies and Tools for
Disease Management and Prevention, Kris-Etherton, P. and Burns, J.H., Eds., American Dietetic
Association, Chicago, 1998, pp. 39–71; Buzzard, I.M., Price, K.S., and Warren, R.A.,
Considerations for selecting nutrient-calculation software: Evaluation of the nutrient database,
Am. J. Clin. Nutr. 54, 7–9, 1991; Grossbauer S., The number game, Byting In, 7, 3, 1997;
Sugerman, S., What makes a software package worth buying? Byting In, 7, 1, 1996.
Currently, one of the most widely used databases for the United States is the
Nutrient Database for Standard Reference (NDSR), which is maintained by the
USDA. This database is freely available and includes around 7,293 foods and about
140 nutrients for each food.109 All data on food and nutrient composition in the
NDSR are developed from the Agricultural Research Service (ARS) food analysis,
the food industry, scientiic literature, and some are estimated and calculated based
on recipes. It is important to mention that there are missing nutrient values for some
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Estimation of Food and Nutrient Intakes of Athletes
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of the foods in the NDSR database, owing to the fact that some foods have not yet
been estimated.
An additional database upheld by the USDA is the Food and Nutrient Database
for Dietary Studies (FNDDS). This is used primarily to assess dietary intakes for the
National Health and Nutrition Examination Survey. It contains about 7,000 foods and
sixty-two nutrients for each food. Nutrient information in this database is obtained
from the NDSR. In contrast to the NDSR, however, the FNDDS contains all the
missing values on nutrient composition and therefore makes the database complete
for computation of nutrient assessments.
Currently, the Ofice of Dietary Supplements at the National Institutes of Health
is working on producing a nutrient database speciic to dietary supplements. With
such modest information on nutrient composition of supplements available and such
growing use of various supplements, it is necessary to include this information to
obtain an accurate overall nutrient analysis.110 New research on nutrient and nonnutrient components of food is uncovering items that are beneicial to health and aid
in the prevention of disease. Because of this, expanding the database to include these
components is an important goal and will allow greater accuracy when recording
and estimating athletes’ or patients’ nutrient consumption and relative health risks.
Most databases are, however, routinely updated to stay consistent and ensure quality
and accuracy.111 MyPyramid.gov is another freely accessible database with a Web
site that allows for the assessment of dietary intakes based on food groups (fruits,
vegetables, grains, dairy, fats, and protein). Once these intakes are determined, they
are able to be compared to the MyPyramid recommendations and can then be incorporated into analyses for disease risk.98
Although dietary databases are kept up to date and try to incorporate vitamins
and minerals as well as nonnutrient substances, it is dificult to ascertain the actual
intake of the athlete due to the variability of nutrients in similar foods. Variability
accounts for inherent, environmental, processing, and analytical factors. Nutrient
variability needs to be an important consideration when analyzing data. The dietitian must analyze possible differences in food variability and know any major differences between different foods that may have signiicant importance to the athlete
or patient.109
1.4.4
RECIPES
1.4.4.1 New Foods
The food supply is ever changing, and therefore the addition of new foods to the
diet may cause challenges in maintaining a database. Since 2004, over 1,900 new
food products have been manufactured from the top twenty-ive food manufacturers alone. When these new foods are introduced into the market, it is the job of the
database manager to determine if the food should be added and if the product will
be in demand by consumers. Since 2005 and the changes in the dietary guidelines
on consumption of whole-grain carbohydrates, databases have added several wholegrain food products to their systems because of such high demands by the consumer.
There was an increase in the percentage of consumed whole-grain breads (12%),
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Nutritional Assessment of Athletes, Second Edition
whole-grain rice (19%), and whole-grain ready-to-eat cereals (16%).112 Additionally,
databases must also distinguish between the various brands and their different nutrient components to ensure accurate analysis.
Although several measures are being taken to keep databases updated, users often
ind that there are some foods not in a system. When these foods are omitted but are
a main diet staple of the user, it makes it dificult to conduct a proper dietary analysis. The USDA Web site does allow one to inform database manufacturers about the
need for additions. Food labels on products are another way to obtain some nutrient
information about a food product that may not be available on the database. However,
food labels are often very incomplete and do not offer total nutrient composition. If
more information on nutrient composition is warranted, there is usually a phone
number on the product to call for further information.
There are a few software database systems that allow the dietitian to add new
foods and their nutrient content to the current listing of foods. This feature can be
beneicial with athletes since they often consume foods that are not found among
database food choices, such as sports bars, shakes, and energy products.
1.4.4.2 Default Assumptions
Recipes or combination foods constitute another issue for accurately determining
nutrient intake. Although some databases and software (such as FNDDS) contain
combination foods, like lasagna, preparation and ingredients often vary. Similarly,
foods such as fried chicken are found in database systems and the listed ingredients
assume it is made a certain way. If the chicken consumed is fried differently than the
software assumes, there may be signiicant differences in nutrient analysis. If this
is the case, analysis may be erroneous due to the variability of food components.
Therefore, combination foods may be best analyzed by adding the ingredients and
ingredient amounts separately. Although it may take more time, it will ensure a more
precise analysis of nutrient intake.
If eating out, as athletes often do while traveling, many restaurant Web sites
now have nutrient information listed on all of their dishes and are easily accessible. In software, just as addition of new foods to listings is available, addition
of combination foods and recipes is also available. In the case of training tables
for athletes, the chef should be able to provide the nutrient information from
foods to the dietitian and allow for a precise nutrient analysis and addition into a
software database.
1.4.4.3 Ethnic Foods
The International Food Composition Tables Directory113 is a collection maintained
by the United Nations International Network of Food Data Systems. It provides lists
(electronically and hardcopy) of databases from around the world. It can be used to
aid in locating and analyzing data on ethnic and imported foods that are not available in U.S. databases. This is beneicial to athletes during times of travel to other
countries and when consumption of ethnic foods is a factor.109
Recent globalization of the food supply has the ability to alter accurate nutrient
analysis. Even though it may be the same fruit or vegetable, growing conditions and
storage must be considered. Databases have one common nutrient analysis for each
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Estimation of Food and Nutrient Intakes of Athletes
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fruit or vegetable, and only if the nutrient content is signiicantly different will additions be made to the database. This has been the case with various potato varieties
(such as purple and yellow heritage potatoes), which vary in their carotenoid and
lavonoid content from a regular potato.109
1.4.5
FLUIDS AND HYDRATION
Water makes up 50–60% of our body weight. Water is essential for many of our body
functions, including heat regulation, participates in chemical reactions, and is used
as lubrication, as a transport medium, and as a solvent during ionization of electrolytes and acids. Body water is found most abundantly in the skin, organs, muscle, and
blood. Thus, hydration by water as well as other beverages before, during, and after
physical activity is essential to maintain a healthy lifestyle and peak performance.
This section addresses luid replacement and the role of water and sports drinks in
hydration as well as the inluence of hydration on physical performance.
The American College of Sports Medicine’s position stand for exercise and luid
replacement states the following: (1) prehydration is essential and should begin several hours prior to exercise, (2) develop a plan for luid replacement during exercise
that will prevent more than 2% dehydration, (3) luid held at a temperature between
15 and 20°C will be preferred over warmer beverages, (4) consume luids containing
20–30 milliequivalents per liter of sodium, 2–5 milliequivalents per liter of potassium, and 6–8% of carbohydrates to help sustain electrolyte balance and exercise
performance, and (5) consuming beverages with meals postexercise will expedite
rapid and complete recovery due to the stimulation of thirst and luid retention.114
1.4.5.1 Sports Drinks
When sports drinks were developed, they changed the way athletes hydrated before,
during, and after events. Sports drinks are made up of three main components: water,
carbohydrates, and electrolytes.115 Carbohydrates and electrolyte replacement, in
addition to water replacement, is important to assist the body in recovery, especially
after prolonged exercise as well as performing in a hot, humid environment. Table 1.5
lists some popular sports drinks and their relation to other beverages, such as water,
orange juice, and diet and regular soft drinks. As discussed previously, it is important
to understand what an individual is consuming prior to, during, and after exercise to
determine if he or she is adequately hydrating and replenishing luid stores.
The form and concentration of carbohydrates contained in drinks have been studied extensively to determine which would assist in performance and replenish stores.
Some carbohydrates have led to gastrointestinal upset and as such may not be a
good recommendation for athletes. However, since every individual is different, it is
important to try different sports drinks during training to determine which, if any,
work best for the individual. Gisoli and colleagues (1998)117 used different formulas
of carbohydrates to determine if the beverage osmolality would have any effect on
gastric emptying and thus affect water availability. Each beverage contained 6%
carbohydrates but with different formulas. The carbohydrate beverages were not different in comparison to gastric emptying; however, the water that was consumed in
the control group was absorbed faster.117
© 2011 by Taylor and Francis Group, LLC
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TABLE 1.5
Carbohydrate-Electrolytes Beverages versus Water
Carbohydrate Ingredient
Gatorade Thirst Quencher
(Gatorade Company)
Gatorade Endurance Formula
PowerAde (Coca-Cola Company)
Sucrose, glucose, fructose
Sucrose, glucose, fructose
High-fructose corn syrup,
maltodextrin
High-fructose corn syrup
High-fructose corn syrup, sucrose
None
Fructose, sucrose
None
Maltodextrin, glucose, fructose
All Sport (Monarch Beverages)
Coca-Cola
Diet Soft Drinks
Orange Juice
Water
Gatorade Energy Drink
(Gatorade Company)
Carbohydrate
(% concentration)
Grams of
Carbohydrate
Sodium (mg)
6
14
110
25
6
8
14
19
200
55
90
30
9
11
0
11
0
23
21
26
0
26
0
53
55
9.2
0–25
2.7
Low
133
55
Trace
Low
510
Low
70
Source: Modiied from Williams, M.H., Nutrition for Health, Fitness, and Sport, 8th ed., McGraw-Hill, New York, 2007.
© 2011 by Taylor and Francis Group, LLC
Potassium (mg)
Nutritional Assessment of Athletes, Second Edition
Beverage
Estimation of Food and Nutrient Intakes of Athletes
41
1.4.5.2 Water
As discussed above, water is able to be absorbed quicker than the 6% sports drinks,
resulting in more rapid replenishment, which would be vital during exercise under
certain conditions. Ryan and colleagues (1998)118 also found that consuming water
during exercise, even when an individual is hypohydrated, had a slightly higher
absorption than different carbohydrate drinks.118 However, there are many different
aspects that can affect gastric emptying. The main aspects are exercise intensity, the
pH of the stomach, mode of exercise, volume of luid, caloric density, drink temperature, electrolytes, heat stress, and osmolality. Since water plays a vital role within
the body, it is important to replenish luid stores and to stay adequately hydrated.
Therefore, when considering hydration for training and performance, water is a cheap
and easy option, and it should not be dismissed in preference to sports drinks.
1.4.5.3 Other Beverages
As seen in Table 1.5, other beverages have been used to assist in hydration. Soft
drinks are one option that athletes may choose due to their high carbohydrate content. This choice is often a matter of taste preference, however. It should be noted that
many soft drinks contain caffeine, which is considered a diuretic and may negatively
affect hydration status. Likewise alcoholic beverages are inadvisable for the same
reason.119 Fruit juices, on the other hand, not only provide a good source of water
but also may have higher content of carbohydrates. This may be advantageous for
some individuals; however, juice consumption is very individualized and care must
be taken since some individuals may have gastrointestinal upset due to lower pH of
the juices.
1.4.5.4 Fluid Hydration Status
Hydration status may be categorized one of four ways. First, dehydration results
when the body luid volume is decreased. The term hypohydration is also used in
similar situations as dehydration and is deined as the rate of luid intake that is
less than the rate of luid loss. Dehydration or hypohydration has been shown to
impair exercise performance and can lead to detrimental effects on the individual
if not corrected. Voluntary dehydration, which has been used by some athletes to
qualify for a lower weight class, could have a possible detrimental effect on performance. Research clearly shows that voluntary dehydration does not improve
performance and may affect cognitive functioning.120 Involuntary dehydration
occurs most often during prolonged aerobic activities and can have a major effect
on performance and, more importantly, on health. When individuals become
dehydrated, cardiovascular functions and temperature regulation often become
compromised and physical performance may be adversely affected114; as seen in
more severe cases, an athlete may have a reduced sweat rate121 and heat illness
may result.
Second, hyperhydration relects a status where the rate of luid intake is greater
than the rate of luid loss. This can be helpful in regulating body temperature and
cardiovascular functions when the rate of luid intake during performance cannot
keep pace with the rate lost during exercise.122 While there is no evidence to suggest
© 2011 by Taylor and Francis Group, LLC
42
Nutritional Assessment of Athletes, Second Edition
that hyperhydration improves performance per se, hyperhydration prior to some
distance events performed in hot, humid environments may minimize performance
decrements. Therefore, the American College of Sports Medicine recommends that
hyperhydration be used before exercise or performance in heat environments.61 Cold
water or a glucose–electrolyte solution can assist athletes in hyperhydrating.116
Euhydration is deined as the rate of luid intake that is adequate to replace luid
losses. It is important for athletes to be euhydrated or, in certain circumstances,
hyperhydrated prior to exercise or an event. Being properly hydrated helps in minimizing luid loss and performance, and may prevent heat-related illness.116
Rehydration results when an individual consumes luids in an effort to replenish luid lost during an event that has caused the body to be in a dehydrated state.
Rehydrating can also reduce the rise in body temperature and minimize the stress on
the cardiovascular system during longer periods of endurance exercise.116
It is critical for athletes to rehydrate following exercise training or competition
to ensure proper performance during the next day’s training or event. As mentioned
in Section 1.3, rehydration is needed and can be simple using the correct techniques. Being aware of the amount of time available for rehydration is imperative.
It is important to weigh prior to exercise and then immediately after. By comparing
these numbers, rehydration can be determined. For each kilogram lost, a person
should consume 1.5 liters of luid if needing to rehydrate in a short period of time,
approximately 12 hours.123 Plain water with food that contains sodium to assist in the
replacement of electrolytes will be able to adequately rehydrate an athlete who has
an extended amount of time for rehydration.
1.4.6
SUPPLEMENT ANALYSIS
Analysis of supplements will assist in the nutritional diagnosis of an individual. Table 1.6 contains a list of some of the most common supplements in use.
However, due to the wide array of supplements on the market as well as continual
production of new supplements, this list is not meant to be all-encompassing.
Nevertheless, it is important to read the supplement labels as well as view the
recent research and Web sites of the governing bodies to determine if the supplement is not only effective but more importantly both safe and acceptable for use.
As a reminder, because supplements are not regulated by the Food and Drug
Administration, it is imperative to research and review the supplement prior to
recommending it for use.
1.5
CONCLUSIONS
In this chapter the estimation of food and nutrient intake of athletes has been
reviewed, concentrating on three main aspects: (1) methods of assessing food intake,
(2) special issues with assessing food intake in athletes, and (3) translation of dietary
assessment into analysis.
There is a variety of methods of assessing dietary intake, such as diet records,
24-hour dietary recalls, and food frequency questionnaires. When conducting
dietary assessments of individuals, it is important to be aware of certain issues,
© 2011 by Taylor and Francis Group, LLC
43
Estimation of Food and Nutrient Intakes of Athletes
TABLE 1.6
Supplements: Their Safety and Effectiveness
Supplement
Safety (at Recommended Doses)
Effectiveness
Androstenedione
Branched chain amino
acids
Safety concerns about chronic use
Possibly safe
Caffeine
Carnitine
Possibly safe; known to have
adverse effects that could affect
performance
Possibly safe
Not effective
Not effective to delay fatigue; some
studies found related immune
system support
Effective as a stimulant to the
central nervous system
Chromium picolinate
Safety concerns with chronic use
Conjugated linoleic acid
Possibly safe
Creatine
Possibly safe
Dehydroepiandrosterone
(DHEA)
Glucosamine/chondroitin
sulfate
Glutamine
Safety concerns with chronic use
and acute high doses
Possibly safe
Beta-hydroxy-betamethylbutyrate (HMB)
Medium-chain triglycerides
Possibly safe
Multivitamin and mineral
supplements
Protein
Pyruvate
Ribose
Possibly safe
Safety concerns with acute and
chronic use
Safety concerns with doses, in
conjunction with the diet, that
would exceed the upper intake
level (UL)
Possibly safe for individuals
without known or unknown
kidney or liver disease
Possibly safe
Possibly safe
Results from studies are mixed in
terms of effectiveness
Not shown to be effective for
increasing muscle mass as well as
decreasing fat mass
Results from studies are mixed in
terms of effectiveness
Effective in increasing lean body mass
in weightlifters and high-intensity,
short-duration performance
Not effective
Effective in some individuals
Results from studies are mixed in
terms of effectiveness
Results from studies are mixed in
terms of effectiveness
Not effective
Effective with nutrient deiciencies;
daily multivitamin use is
recommended by some to prevent
chronic disease
No difference in comparison to food
protein
Not effective
Not effective
Source: Modiied from Dunford, M., Sports Nutrition: A Practice Manual for Professionals, American
Dietetic Association, Chicago, 2006, p. 131.
paying particular attention to misreporting, snacking, and openness in reporting. A
successful dietary assessment depends on the expertise of the registered dietitian,
who needs to be aware of the client’s perceptions toward food as well as toward the
professional. Special issues that sports dietitians need to be familiar with regarding
© 2011 by Taylor and Francis Group, LLC
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Nutritional Assessment of Athletes, Second Edition
nutritional assessment of the athletic population include periodization, luid intake,
supplements, and traveling. In order to effectively translate dietary assessment into
analysis, sports dietitians should evaluate the population they are working with, as
well as the cost and quality of the extremely wide availability of software and databases in the market. They should also be aware of several factors such as ethnic
foods, luid replacement beverages, and supplements that may not be included in
databases. Therefore, a very detailed dietary assessment needs to be performed in
order to conduct the necessary research that would in turn translate into a more accurate dietary analysis and future recommendations.
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trained female endurance runners, Med. Sci. Sports Exerc. 25, 1398–1404, 1993.
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nutrition issues, and health consequences, J. Sport Sci. 25, 61–71, 2007.
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87. Koebnick, C., Wagner, K., Thielecke, F., Dieter, G., A Höhne, A., Franke, A., Garcia,
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90. Jeffrey, N., Athletes at risk of thinking thin, Australian 21, 19, 2007.
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92. Motonaga, K., Yoshida, S., Yamagami, F., Kawano, T., and Takeda, E., Estimation
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106. Grossbauer, S., The number game, Byting In 7, 3, 1997.
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practice and research, review. J. Am. Diet. Assoc. 107, 2105–13, 2007.
110. Dwyer, J.T., Picciano, M.F., Betz, J.M., Fisher, K.D., Saldanha, L.G., Yetley, E.A.,
Coates, P.M., Radimer, K., Bindewald, B., Sharpless, K.E., Holden, J., Andrews, K.,
Zhao, C., Harnly, J., Wolf, W.R., and Perry, C.R., Progress in development of an integrated dietary supplement ingredient database at the NIH Ofice of Dietary Supplements,
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111. Phillips, K.M., Patterson, K.Y., Rasor, A.S., Exler, J., Haytowitz, D.B., Holden, J.M.,
and Pehrsson, P.R., Quality-control materials in the USDA National Food and Nutrient
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113. International Food Composition, International Network of Food Data Systems Web site,
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114. Sawka, M.N., Burke, L.M., Eichner, E.R., Maughan, R.J., Montain, S.J., and Stachenfeld,
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115. Maughan, R.J., Bethell, L.R., and Leiper, J.B., Effects of ingested luids on exercise
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117. Gisoli, C.V., Summers, R.W., Lambert, G.P., and Xia, T., Effect of beverage osmolality
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120. Montain, S.J., Sawka, M.N., Latzka, W.A., and Valeri, C.R., Thermal and cardiovascular
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122. Lamb, D.R. and Shehata, A., Beneits and limitations to prehydration, Sports Sci
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Association, Chicago, 2006, p. 131.
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of
2 Evaluation
Nutrient Adequacy
of Athletes’ Diets
Nanna L. Meyer and Melinda M. Manore
CONTENTS
2.1 Introduction ..................................................................................................... 51
2.2 Dietary Assessment ......................................................................................... 52
2.3 Dietary Guidelines .......................................................................................... 52
2.4 Dietary Reference Intakes ............................................................................... 54
2.5 Approaches to Assessing Dietary Adequacy ................................................... 55
2.6 Dietary Recommendations for Sport and Exercise ......................................... 58
2.6.1 Energy Intake ...................................................................................... 58
2.6.2 Carbohydrates ..................................................................................... 59
2.6.3 Protein ................................................................................................. 62
2.6.4 Fat ....................................................................................................... 62
2.6.5 Micronutrients..................................................................................... 63
2.6.6 Fluid .................................................................................................... 65
2.7 Future Research and Directions ......................................................................66
2.8 Conclusions .....................................................................................................66
References ................................................................................................................66
2.1
INTRODUCTION
In today’s competitive sports environment, athletes need to be physically and mentally
it to perform at their best. Research clearly shows that nutrition can play an important role in improving exercise performance, decreasing recovery time from strenuous exercise, preventing exercise-associated injuries due to fatigue, providing the fuel
required during times of high-intensity training, and controlling weight.1 Adequate and
proper nutrition is important for active individuals to meet their overall energy, nutrient, and luid needs. Thus, many athletes are interested in learning how to improve
their dietary and luid intakes for health and performance. One of the irst steps in
determining how to best improve an athlete’s diet is to assess his or her food, luid,
and supplement intakes within the context of their weight goals, sport training routine,
and competition schedule. Knowing when an athlete eats in relationship to exercise
training may be as important as knowing what he or she eats. Regular assessment of
51
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Nutritional Assessment of Athletes, Second Edition
an athlete’s diet will help identify potential nutrition problems related to time of year,
changes in training routine, health issues that arise such as injuries or illness, and/or
lifestyle changes. This chapter reviews the methods used to assess an athlete’s diet and
the guidelines used to determine the adequacy of these diets, including the dietary
reference intakes, approaches for assessing dietary adequacy, and speciic macro- and
micronutrient recommendations for active individuals and athletes.
2.2
DIETARY ASSESSMENT
There are a number of traditional dietary assessment methods such as diet histories,
food records, diet recalls, and food frequency questionnaires that can be used to
estimate dietary intake patterns and nutrient intakes of individuals or groups of athletes.2 These diet assessment tools are discussed in detail elsewhere.2–4 However, it
is important to understand the errors associated with each of these methods and how
to use each method to provide the best picture of an athlete’s or active individual’s
typical dietary pattern for each phase of the training program. The more accurate
these dietary assessments can be, the more likely it is the sports dietitian will obtain
the data needed to help the athlete achieve his or her performance, weight, or health
goals. Research shows that the accuracy of self-reported dietary intake data is inluenced by a number of factors such as age, gender, body weight and composition,
restrained eating behaviors, socioeconomic status, and cultural inluences.5 This
reporting bias can lead to misinterpretations of the energy and nutrient adequacy of
an individual’s diet and nutritional status.6 Depending on the instrument used and the
individual assessed, self-reported food intake can be under- or overestimated, which
will result in misinterpretation of an individual’s energy and nutrient intakes.5,7
Based on research comparing doubly-labeled water (DLW) as a measure of energy
expenditure to various dietary assessment methods assessing energy intake, individuals are most likely to underreport energy intake.7 Underreporting of food intake,
and thus energy intake, can occur for a number of reasons, such as underreporting
portion size, forgetting foods, not recording alcohol and high-energy snack foods,
changing eating behaviors to avoid eating foods that are hard to record, or eating
healthier foods during the recording period. Additionally, length of the dietary evaluation period also needs to be given attention because of day-to-day variations in
energy intake due to food availability, training schedules, and time constraints. It is
thus best to evaluate macro- and micronutrient contribution of the diets of athletes
over several days rather than looking at a single day’s intake. It is also best to examine the diet during different phases of the training program, since diet can change
as the exercise training program changes. Thus, it is not only important to use the
appropriate dietary assessment method for the individual or group but to also train
the individual to report food and luid intake as accurately as possible.
2.3
DIETARY GUIDELINES
How do we know we are eating the right foods for good health and performance?
Do athletes have different nutrient needs than sedentary individuals? How
do nutritionists and dietitians know what type of dietary recommendations to
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Evaluation of Nutrient Adequacy of Athletes’ Diets
53
make to athletes and active individuals? Nutritionists use a number of resources
to make dietary recommendations to both groups and individuals. Two national
evidence-based dietary guidelines frequently used are the Dietary Guidelines for
Americans and the Dietary Reference Intakes. Dietary Guidelines for Americans
are introduced next, while the Dietary Reference Intakes are discussed in the following section.
The Dietary Guidelines for Americans (2005) are developed by the U.S. Department
of Agriculture (USDA) and the Department of Health and Human Services (DHHS)
(http://www.cnpp.usda.gov/DGAs2005Guidelines.htm) to guide dietary recommendations for populations and individuals. This evidence-based document, which is
revised every 5 years, is the cornerstone for U.S. nutrition policy and nutrition education activities. To help consumers evaluate their diet and make better eating choices,
the Dietary Guidelines were used to develop MyPyramid and associated nutrition and
diet tools (http://www.cnpp.usda.gov). The 2010 Dietary Guidelines for Americans
are currently under development (http://www.cnpp.usda.gov/dietaryguidelines.htm).
The 2005 Dietary Guidelines for Americans were designed to convey dietary
recommendations and not medical advice, so it is the job of nutrition professionals to help their clients interpret and implement these guidelines into practical eating
behaviors, attitudes, and healthy lifestyle changes. The nine key recommendations of
the 2005 Dietary Guidelines for the general population are listed below:
1. Consume a variety of foods within and among the basic food groups while
staying within energy needs.
2. Control calorie intake to manage body weight.
3. Be physically active every day.
4. Increase daily intake of fruits and vegetables, whole grains, and nonfat or
low-fat milk and milk products.
5. Choose fats wisely for good health.
6. Choose carbohydrates wisely for good health.
7. Choose and prepare foods with little salt.
8. If you drink alcoholic beverages, do so in moderation.
9. Keep food safe to eat.
Similar documents have been developed in other countries. For example,
Canadians use Canada’s Guidelines for Healthy Eating (Health and Welfare Canada
2007) and the Canada’s Food Guide to Healthy Eating. Australia (Dietary Guidelines
for All Australians, 2003) (http://www.nhmrc.gov.au/PUBLICATIONS/synopses/
dietsyn.htm) and New Zealand (Food and Nutrition Guidelines) (http://www.moh.
govt.nz/foodandnutrition) also have similar documents. In Switzerland, the Society
for Nutrition (Schweizerische Gesellschaft für Ernährung) developed the Swiss Food
Guide Pyramid. This document was used to design a food pyramid geared toward
active individuals and athletes (www.sfsn.ch).8
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Nutritional Assessment of Athletes, Second Edition
2.4
DIETARY REFERENCE INTAKES
Over the past 10 years, the Institute of Medicine (IOM) Food and Nutrition Board
(FNB) of the National Academy of Sciences has revised the energy and nutrient
recommendations for Canadian and U.S. populations. These new recommendations relect the growing body of scientiic evidence that chronic diseases may alter
nutrient requirements. These recommendations are termed the Dietary Reference
Intakes (DRIs), which relect a family of reference values. These values are designed
to prevent nutrient deiciency and reduce the risk of chronic diseases for the population in general but also to provide valuable guidelines when working with active
individuals.
The various DRI reference values include the following: the Recommended Dietary
Allowance (RDA), the Adequate Intake (AI), the Estimated Average Requirement
(EAR), the Tolerable Upper Intake Level (UL), and the Acceptable Macronutrient
Distribution Ranges (AMDRs). Each of these values is briely explained below. A
more detailed explanation of the DRIs for micro- and macronutrients, water, and
electrolytes can be found elsewhere.9–14
• Recommended Dietary Allowance (RDA): The RDA is considered the nutrient
intake that meets the requirement of almost all (97–98%) of the healthy individuals in a speciic age and gender group. Based on the scientiic evidence available at the time, the DRI committees calculated RDAs for vitamin A, vitamin
C, vitamin E, phosphorus, magnesium, copper, iron, iodine, molybdenum, selenium, zinc, thiamin, ribolavin, niacin, vitamin B6, folate, and vitamin B12.9–12
• Adequate Intake (AI): When scientiic evidence was not suficient to determine an RDA, an AI value was calculated from experimental or observed
intake levels that appear to sustain a desired indicator of health. AIs can be
used as a goal for intake where no RDAs exist. The DRI committees have
set AIs for vitamin D, vitamin K, luoride, pantothenic acid, biotin, choline,
calcium, chromium, manganese, potassium, sodium, and chloride.9,10,12,13
• Estimated Average Requirement (EAR): In order to determine an RDA,
the nutrient intake value estimated to meet the requirement of half the individuals in a speciic group. This igure is used as a basis for developing
the RDA. For example, the RDA for a particular nutrient is calculated as
follows: RDA = EAR + 2 SDEAR where SDEAR is the standard deviation of
the EAR. If data about the variability in requirements are insuficient to
calculate a standard deviation, a coeficient of variation (CV) for the EAR
of 10% is ordinarily assumed.
• Tolerable Upper Intake Level (UL): The UL is the maximum intake of a
nutrient by an individual that is unlikely to pose a risk of adverse health
effects to most healthy individuals. If intakes of a nutrient are above the
UL for an extended period of time, the risk of adverse effects increases.
The UL typically refers to total nutrient intake from food, fortiied foods,
and supplements. The term “tolerable intake” was chosen to avoid implying
a possible beneicial effect from this level of the nutrient. However, some
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Evaluation of Nutrient Adequacy of Athletes’ Diets
55
ULs were set with limited information and may change in the future as new
information becomes available.
• Acceptable Macronutrient Distribution Ranges (AMDRs): AMDRs have
been established for fat, protein, and carbohydrate. Carbohydrate also has
a minimum recommended amount, and protein has an established RDA
value based on age and gender. Water, total iber, and essential fatty acids
have established AI values.13,14 The total water recommendation includes all
water contained in food, beverages, and drinking water.
2.5
APPROACHES TO ASSESSING DIETARY ADEQUACY
In addition to the aforementioned national guidelines, there are a number of other
resources sports dietitians can use to make dietary, luid, and supplementation recommendations to active individuals and athletes. These speciic recommendations,
frequently in the form of position papers, consensus statements, and sport-speciic
recommendations, synthesize the current science-based information and translate
this into guidelines for athletes.15–22 In Sections 2.5 and 2.6, we integrate these more
speciic dietary recommendations for athletes within the context of the Dietary
Guidelines for Americans and the DRIs.
In order to assess dietary adequacy of athletes training and competing in sports,
it is essential to examine the energy demands of the various activities comprising the
training program. Training and competition vary considerably in many sports. While
training may challenge the athlete in terms of maintaining energy balance and nutrient stores through the preparatory months, during competition many sports focus
solely on racing interspersed with conditioning to keep athletes it. Thus, evaluating
dietary adequacy must take training and competition into account. In addition, most
training plans are organized in phases with varied volume and intensity and progressing from general to sports-speciic training. Coaches typically periodize training programs, which means that training and rest are balanced carefully in order to
maximize the athlete’s training adaptation. Assessment methods should be used that
help differentiate various training phases and recovery periods. This can be done by
a variety of approaches.
To evaluate whether an athlete eats adequately (appropriate quantity, quality,
and timing of energy and nutrient intake), the energy demands of the sport must be
known. To assess energy expenditure in athletes at the least complex level, the sports
dietitian can select physical activity levels (PAL) or physical activity coeficients (PA)
in calculations deriving energy expenditure requirement (EER; DRIs energy) and/
or multiples of resting metabolic rate (RMR). RMR can be measured or assessed.
Thompson and Manore23 have shown that the Cunningham24 equation is best suited
for use in male and female endurance athletes. Other quick approaches include reference tables summarizing energy cost for a given person relative to weight and sport.1
More time consuming, burdensome, and complex are assessment techniques that
involve physical activity records using metabolic equivalents for 24 hours25 or less
(e.g., detailing exercise energy expenditure, EEE) and physical activity protocols.26
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Nutritional Assessment of Athletes, Second Edition
TABLE 2.1
Energy Expenditure in Various Sports Using Doubly-Labeled Water (DLW)
Compared to Energy Intake Estimated by Dietary Recall
Sport
Energy Expenditure
(kcal·d–1)
Energy Intake
(kcal·d–1)
3492 (F)
2990 (F)
8604 (M)
3957 (F)
4373 (F)
7217 (M)
1987 (F/M)
4015 (M)
2318 (F)
2039 (F)
6214 (M)
2214 (F)
4350 (F)
7217 (M)
1745 (F/M)
not assessed
Runners
Runners
Tour de France
Lightweight rowers
Cross-country skiers
Gymnasts
Speed skaters
Reference
27
28
29
30
31
32
33
Note: F = females; M = males.
The irst step, however, when evaluating the energy demand of a particular sport
is to search the research literature. It is possible that studies have been conducted
using DLW (see Table 2.1) or other more valid and reliable techniques than recalls.
In addition, some sports have advanced in technology and offer ways to quantify
total work accomplished. One such example is the sport of cycling in which it is not
uncommon that athletes use power meters integrated into pedals and crank arms.
Martin et al.34 conducted a study in cyclists using a power meter to quantify EEE.
Data from such studies along with a more individualized or team assessment should
be suficient to identify target energy expenditure and macronutrient ranges for a
thorough evaluation of energy and nutrient adequacy in athletes training and competing in a particular sport.
In addition to understanding the annual training and competition plan when evaluating dietary adequacy in athletes, the individual’s body weight and composition
goals must be known. For athletes needing to lose body weight and fat, the sports
dietitian must ensure minimal nutritional risk for energy and for macro- and micronutrients. Nutritional risk for athletes is different than for nonathletes. A diet reduced
in macronutrients, and thus calories, could pose minimal risk to a nonathlete, while
for the athlete energy intake (EI) is simply too low to meet all physiologic functions
beyond what is necessary for exercise. This concept is referred to as energy availability (EA) and is derived from EEE subtracted from EI.18 For female athletes in
particular, reducing EI while continuing with hard training poses a risk due to the
link between low EA and menstrual dysfunction. Menstrual dysfunction can result
in compromised bone mass as part of the female athlete triad.35 Further, low EA can
lead to glycogen depletion, micronutrient deiciencies, and fatigue. Manore et al.36
proposed guidelines for maintaining energy availability in exercising women during
various phases of weight loss, maintenance, growth, and recovery (see Table 2.2).
These values can be used to evaluate a female athlete’s energy intake relative to various phases of training, competition, and growth.
© 2011 by Taylor and Francis Group, LLC
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Evaluation of Nutrient Adequacy of Athletes’ Diets
TABLE 2.2
Recommended Levels of Energy Availability for Female Athletes during
Various Phases of Training, Competition, Growth, and Weight Maintenance
Energy Availability
Weight Loss
(kcal·kgFFM–1·d–1)
Maintenance
(kcal·kgFFM–1·d–1)
Growth/Intense
Training/Racing
(kcal·kgFFM–1·d–1)
30–45
45
>45
Note: FFM, fat-free mass.
Source: Manore, M.M., Kam, L.C., and Loucks, A.B., The female athlete triad: Components, nutrition
issues, and health consequences, J. Sports Sci. 25 Suppl 1, S61–S71, 2007.
With regard to carbohydrate (CHO) consumption, reduced intakes (< 5 g·kg–1·d–1)
in individuals exercising for the purpose of weight control and itness are not problematic. For the athlete, however, CHO adequacy is essential for the maintenance of
glycogen stores and the ability to recover from training on a daily basis.37,38 Depleting
glycogen stores during heavy training may pose both performance and health risks
to the athlete. A minimal CHO intake level of 5 g·kg–1·d–1 is considered necessary to
maintain glycogen stores during intense training.37 Obviously, weight loss and body
composition manipulations should be attempted during off-season and low-intensity
training phases. However, this is not always possible nor is it practical. Therefore
utmost attention should be paid to CHO adequacy. While dietary assessment methods (see Chapter 1) can help evaluate CHO intake, performance indices along with
subjective ratings of fatigue, mood state, and hours of sleep in combination with
interdisciplinary approaches to monitor performance and health in the athlete can
help evaluate overall stress and risk for underrecovery and overtraining39 related to
CHO inadequacy.
Energy restriction can also affect other nutrients such as protein and micronutrients and thereby increase the risk of unwanted side effects such as lean tissue loss
and vitamin/mineral deiciencies, respectively. Protein intake needs to be monitored
during phases of energy restriction, especially if strength and power should not be
compromised. Higher protein intakes may be needed to preserve muscle mass during phases of weight and fat loss,40 and micronutrient intake may be low, especially
if EI falls below 1800 to 2000 kcal per day.
Vitamin and mineral recommendations are not based on activity level; thus, the
DRIs can be used to assess adequacy. Further, many high-level athletes integrate
routine biochemical testing for the purpose of screening and monitoring for health
and performance. Biochemical testing for an evaluation of dietary adequacy in athletes is especially helpful for nutrients involved in oxygen transport (such as iron,
vitamin B12, folic acid) and vitamin D as well as electrolytes under certain conditions
(for example, eating disorders and hyponatremia).
Finally, adequate luid replacement, during and after exercise, can accurately
be assessed using pre- and postexercise weight measures. To evaluate hydration
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Nutritional Assessment of Athletes, Second Edition
status before exercise and to monitor daily luid balance can involve daily weight
measurements, urine volume, urine color, and urine speciic gravity.22
To summarize, dietary adequacy can only be evaluated if an athlete’s sport and
associated energy demands are well understood and assessed. In addition, energy
and nutrient intakes need to be estimated using as much accuracy and precision
as possible without overburdening the athlete. Internet-based software can be integrated not only to assess a person’s diet but also to evaluate energy expenditure.
While the USDA Food Guide Pyramid software (www.MyTracker.gov) provides a
simple approach to evaluating an individual’s diet relative to activity level, sportsperformance software is currently available that can be used to evaluate energy balance and nutrient adequacy in the context of the daily training plan (for an example,
see www.trainingpeaks.com). These software programs are used interdisciplinarily
among coaches and sports dietitians and provide a platform for online interaction
with the athlete regarding training and meal planning. Although not yet sophisticated enough, these programs may offer innovative approaches to evaluating dietary
adequacy in athletes in the future.
Before examining an athlete’s diet, however, the sports dietitian must understand
current recommendations for energy, nutrients, and luids in sports and exercise.
Section 2.6 provides a summary of current guidelines.
2.6
2.6.1
DIETARY RECOMMENDATIONS FOR SPORT AND EXERCISE
ENERGY INTAKE
Energy intake should support the variability of the athlete’s annual training and
competition plan to bring dedicated months and years of training to fruition with
expected performance outcomes. Estimating energy requirements is dificult to
accomplish in the ield, especially in sports that are less well studied. Examining the
literature on DLW, conducted in athletes in free-living conditions, shows that energy
expenditure can be quite high (see Table 2.1). What these studies also show is that
there is a mismatch between energy expenditure and EI in the absence of weight loss,
indicating the inherent bias of dietary assessment methods to underreporting.5,7,41
Unfortunately, only few sports have been studied using DLW; thus, there are many
sports for which it is dificult to estimate total daily energy expenditure (TDEE)
mainly due to the dificulty estimating EEE. The aforementioned approaches (see
Section 2.5) prove useful, but the speciic method used depends on the athlete and
the sport. If a quick reference is needed to establish a baseline for an athlete, the
paper by Economos42 can also be useful. Energy requirements to support daily training for female and male athletes exercising approximately 90 minutes per day or
less was suggested at 45 kcal·kg–1·d–1 and 50 kcal·kg–1·d–1, respectively. This may be
a helpful target for sports dietitians working with athletes. However, these values
do not sufice to quantify more reliably TDEE in athletes, and several of the above
studies (Table 2.1) have shown that energy turnover in certain sports can be high and
easily exceed 50 kcal·kg–1·d–1.
Using EI data from dietary records in combination with stable body weight has
been suggested as a tool to determining energy needs of athletes. Typical EI data
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Evaluation of Nutrient Adequacy of Athletes’ Diets
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assessed by 3- to 7-day dietary records that were reviewed by Burke43 showed that
female distance runners reported eating 2195 kcal·d–1 (43 kcal·kg–1·d–1), while female
strength and power athletes in track and ield documented an EI of 2510 kcal·d–1
(39 kcal·kg–1·d–1). Male endurance athletes reported a mean daily EI of 3320 kcal·d–1
(56 kcal·kg–1·d–1) and strength and power athletes in track and ield sports reported
3893 kcal·d–1 (42 kcal·kg–1·d–1). That these data can accurately relect energy requirement of athletes should not be assumed, however. Several factors need to be considered when using dietary intake data to estimate TDEE in athletes. As mentioned in
Section 2.2, underreporting of dietary intake occurs in individuals and groups.44 In
fact, in the DLW study by Edwards et al.28 an energy discrepancy was found ranging
from 4 to 58% in female runners. Especially in sports that emphasize leanness and
thinness, it should be expected that EI is underreported. Further, ingesting signiicantly less energy than what the athlete’s training load (that is, intensity × volume)
would predict may also result in energy eficiency, where athletes maintain stable
body weights despite eating signiicantly less than their energy expended. Thus,
using EI data from dietary records is a less than optimal method for the prediction
of energy requirement and to establish energy recommendations for athletes training
and competing throughout the year. To increase accuracy and precision in determining an athlete’s energy demand, professionals therefore should use the assessment
techniques discussed previously and elsewhere in this volume, especially focusing
on EEE, as it likely represents the largest variability of TDEE in athletes.
Recommendations to meet high-energy demands in sports depend on many factors, namely the sport itself and the changes in volume and intensity throughout
training and competition. Simple strategies to meet high-energy demands during
intense training are summarized in Table 2.3.
Other factors that should be considered when making recommendations to meet
high-energy demands include environmental conditions (for example, heat, cold,
and altitude), endocrine issues (such as thyroid function and menstrual regularity),
restrictive and disordered eating to achieve and maintain or reduce body weight, and
weight and body composition goals.
2.6.2
CARBOHYDRATES
Carbohydrates provide energy for performance and recovery and exhibit a proteinsparing effect.45 Athletes undergoing prolonged, intense, repetitive training require a
high CHO intake of 7–10 g·kg–1·d–1 and up to 12 g·kg–1·d–1 if subjected to high training
loads. When training at submaximal intensity and for shorter periods of time, athletes should target a CHO intake of 5–7 g·kg–1·d–1.15,19,46 Most elite athletes, training
5–6 hours per day, need a high CHO intake of between 7 and 12 g·kg–1·d–1, which in
absolute terms ranges from 420 to 720 g of CHO per day for a female athlete weighing 60 kg. Particularly for female endurance athletes, such high CHO intakes are
quite dificult to achieve. This was shown by Burke et al.,47 who reported that female
endurance athletes ingest on average 5.5 g·kg–1·d–1, whereas their male counterparts
report a mean CHO intake of 7.5 g·kg–1·d–1. That CHO intakes around 5 g·kg–1·d–1 can
sustain intense training and ensure adequate recovery of muscle glycogen stores is
currently unclear but it appears highly unlikely. In fact, athletes engaging in intense
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TABLE 2.3
Strategies to Increase Energy Intake in Athletes to Meet High-Energy Demands
Area of Focus
Strategies
Frequency of eating
Athletes should be advised to eat three to four meals and two to three snacks
per day. Snacks are predominantly consumed before, during, and after
exercise, between meals, and after dinner.
Athletes should add calories to meals, which can be accomplished by adding
fruit juice, sport drink, or milk as energy-containing luids, by including an
appetizer or dessert, or adding calories from foods that add lavors such as
olive oil, nuts, seeds, cheese, bean spreads, or avocados.
Athletes should become skilled in selecting foods and luids before, during,
and after exercise to (1) optimize performance during and maximize recovery
after exercise and (2) to meet the energy demands of intense training/
competition and environmental extremes. Most athletes consume a signiicant
amount of calories during the actual training or competition period.
Athletes should also learn how to prepare for travel, bringing foods and luids
to accommodate energy and dietary needs on the road or in the air, and to
prepare a travel pack with foods to ease the transition to unfamiliar foods
and jet lag and to get ready for competition.
Athletes should be sensitive to changes in appetite and gastrointestinal issues
while training and competing. Decreased appetite may coincide with intense
training, travel, and race preparation. Structured eating and meal plans can
assist athletes to meet their energy needs during heavy exertion and in
preparation for competition.
Athletes should use strategies to meet energy demands when ill or injured
(increase or decrease EI). Particularly when hospitalized with a traumatic
injury (such as a fractured femur), athletes should refrain from restricting EI,
because this likely interferes with early repair and rehabilitation.
Meal size
Fueling before, during,
and after exercise
Travel nutrition
Appetite and GI issues
Illness and injury
training seem to sustain daily running performance better with a higher CHO intake
at 8.5 g·kg–1·d–1 compared with a lower CHO intake of 5.4 g·kg–1·d–1.38 Carbohydrates
are also important to reduce mental fatigue, and data show that an athlete’s mood
state is maintained more consistently on a higher CHO diet during intensiied training.38 Because endurance athletes are probably at greatest risk for inadequate CHO
intake, it is important to educate them regarding the importance of increasing CHO
intake during intense training periods. That cross-country skiers can manage this
well was shown by the study of Sjödin et al.31 During an intense training period on
snow, female and male Nordic skiers reported eating a high CHO diet consisting of
12 g·kg–1·d–1. This study also measured TDEE using DLW (see Table 2.2) and found
that athletes were able to maintain energy balance and weight despite a high energy
turnover of 80 kcal·kg–1·d–1. This study is a great example showing that female and
male athletes should dare to eat more when EEE is high. Inadequate CHO intakes
during intense training can lead to insuficient muscle glycogen restoration and
delayed recovery, early fatigue during training and competition, and increased risk
for illness and injury.19,46
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Evaluation of Nutrient Adequacy of Athletes’ Diets
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High CHO diets have also been shown to increase intermittent exercise performance,48,49 and several ield studies in nonendurance sports have documented signiicant
glycogen breakdown during training.50–52 However, these athletes do not necessarily eat
a higher CHO diet. Data show that male and female strength and power athletes report
consuming on average 5.5 and 4.7 g·kg–1·d–1 of CHO, respectively, and winter sport
athletes report a CHO intake barely meeting 7 g·kg–1·d–1 during intense training.53
Meeting CHO needs is often accomplished by the additional calories consumed
before, during, and after exercise. Especially the period during exercise offers a great
opportunity to maintain CHO adequacy to support daily training and recovery and to
fuel performance. Brouns et al.54,55 were the irst to document the calories consumed
by Tour de France athletes while exercising. Today, CHO consumption during exercise should be optimized using foods and luids that are easily absorbed and readily
available to fuel working muscle during variable types of activities. Gastric emptying56 and absorption across the intestinal wall57 are probably the most important limiting factors of the muscle’s capacity to oxidize CHO during exercise. Carbohydrate
ingestion at 30–60 g per hour has been shown to increase endurance performance.58
These amounts are typically available in sport drinks (6–8%). Although mixtures
of glucose, sucrose, and fructose are better absorbed in combination due to speciic
transporters,57 at low ingestion rates (< 60 g per hour), the type of sugar does not
appear to matter.59 At higher ingestion rates, a combination of sugars is probably
more effective.57 Carbohydrate ingestion during exercise is especially important if
CHO consumption pre-exercise was insuficient and the athlete is hungry or thirsty.
Carbohydrate intake during exercise should begin early and continue throughout the
session for optimal beneits.19,46
Carbohydrate intake 3–4 hours before exercise enhances liver and muscle glycogen
synthesis and improves subsequent performance.17,19,46 Thus, much emphasis should
be put on the pretraining and pre-event meal, containing between 200 g and 300 g
of CHO, when teaching athletes about proper fueling for training and competition.
Pretraining/event meals must be rich in CHO, low in fat and iber, moderate in protein, adequate in luid, and familiar. Although performance effects are unclear, many
athletes consume a small snack 30–60 minutes before exercise. Due to the inverse
relationship between the timing of CHO intake relative to the beginning of exercise
and the quantity ingested, athletes should be advised to keep their snacks small when
eating shortly before exercise. Finally, endurance athletes may also proit from high
CHO intakes in the days prior to competition through CHO loading. In general, CHO
loading increases muscle glycogen concentration and/or improves performance.19,46
Carbohydrate after exercise is necessary to replenish muscle and liver glycogen
in a timely fashion. Factors that are known to optimize glycogen resynthesis include
the timing60 of CHO intake, amount61 of CHO intake, and the type62 of CHO intake.
It is recommended to ingest CHO within close proximity to exercise and at regular
intervals to maximize glycogen resynthesis rate and optimize recovery, especially
if another workout is planned within 8 hours.15 According to Rodriguez et al.,19,46
1–1.5 g·kg–1 of CHO within the irst 2 hours and at 2-hour intervals for up to 6 hours
are recommended (although less CHO at more frequent intervals is also effective).61
Sports dietitians should adapt recovery strategies to individual athletes to it their
postexercise recovery infrastructure.
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2.6.3
PROTEIN
The RDA of protein is set at 0.8 g·kg–1·d –1 and the AMDR ranges from 10 to 35%
of EI.14 Most of the higher needs for athletes have been established using nitrogen balance studies.63 The protein recommendations for endurance athletes are
higher than the RDA because protein oxidation is accelerated during prolonged
and high-intensity exercise.64 Protein is also needed for strength and to power
athletes in excess of the RDA because additional amino acids are needed to support muscle growth and repair.65 Protein recommendations for athletes are shown
in Table 2.4.
Even though both endurance and strength training reduce protein requirements
due to enhanced eficiency of protein utilization in athletes, protein recommendations remain unchanged. Important, however, is that individuals starting an exercise
program would probably beneit from extra protein as shown in Table 2.3.19,46
Protein intake within short proximity of exercise has the ability to enhance recovery and repair of muscle tissue. Timing of intake, type of protein, and the addition
of other macronutrients such as CHO have all been investigated.21 Data show that
the intake of 10–20 g of intact protein high in essential amino acids (EAA) or as
little as 6 g EAA along with CHO postexercise can positively inluence net protein
balance after endurance66 and resistance exercise.66–68 While most protein shakes
exceed what can be incorporated into muscle tissue, individuals are advised to prefer
food or manufactured recovery products with protein and CHO combinations over
protein powders to support the recovery process postexercise. A thorough dietary
assessment should provide the basis for recommendations given to athletes regarding
daily protein requirements.
2.6.4
FAT
There are currently no speciic fat recommendations or an RDA set for the general
public or the active individual. The AMDR for fat is 20–35% of EI.14 Athletes should
aim to distribute their fat calories among saturated and unsaturated fat based on
the Dietary Guidelines for Americans and consume essential fatty acids as recommended by the DRIs.14 Fat requirements increase in athletes with increased levels of
TABLE 2.4
Protein Recommendations for Endurance and Strength Athletes
Sport/Activity
Endurance
Strength and power
Recommended Amounts
1.2–1.4 g·kg–1·d–1
1.2–1.7 g·kg–1·d–1
Sources: Rodriguez, N.R., DiMarco, N.M., and Langley, S., Position of the American Dietetic
Association, Dietitians of Canada, and the American College of Sports Medicine,
Nutrition and athletic performance, J. Am. Diet Assoc.109(3), 509–27, 2009; Rodriguez,
N.R., Di Marco, N.M., and Langley, S., American College of Sports Medicine Position
Stand, Nutrition and athletic performance, Med. Sci. Sports Exerc. 41(3), 709–31, 2009.
© 2011 by Taylor and Francis Group, LLC
Evaluation of Nutrient Adequacy of Athletes’ Diets
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training volume and intensity. Considering that some endurance athletes expend over
5000 kcal·d–1, increasing fat intake proportionally is often necessary to meet such
high-energy demands. A higher fat intake may also be needed to replenish intramuscular triglycerides (IMTGs) after prolonged exercise.69
2.6.5
MICRONUTRIENTS
Although vitamins and minerals are not a source of energy, they play a vital role in
energy metabolism and overall health. RDAs for vitamins and minerals are deined
to prevent nutrient deiciencies and are not determined based on physical activity levels.9–12 In general, athletes have adequate intakes of vitamins and minerals as long as
EI is appropriate. However, B vitamins, calcium, vitamin D, iron, some antioxidants
(for example, vitamins C and E, beta carotene, and selenium), zinc, and magnesium
can be of concern. Athletes who present with compromised micronutrient status may
be those who restrict energy intake for weight control or performance; eliminate one
or more food groups due to dietary regimens, restrictions, or fear of calories; or consume unbalanced diets characterized by low micronutrient density.19,46
Adequate intakes of B vitamins are essential to support the energy demand of
daily training, recovery and repair of tissues. Data show that restrictions of thiamin,
ribolavin, and vitamin B6 with resulting marginal deiciencies have the potential to
decrease aerobic capacity in trained male cyclists.70 Although no single B vitamin
was responsible for these results, this study at least illustrates that B vitamins are necessary for optimal performance. Thiamin, ribolavin, niacin, and vitamin B6, among
others, are directly involved in energy metabolism, while folic acid and vitamin B12
function to support red blood cell synthesis, tissue repair, and maintenance of the
nervous system. Vegetarian and vegan athletes are at greatest risk for low intakes of
vitamin B12 and ribolavin, and female athletes are also at risk for low intakes of folic
acid and Vitamin B6, in addition to the aforementioned B vitamins.71,72
Adequate calcium intake is important in building optimal bone strength, especially at young age.73 Insuficient calcium and vitamin D intake increases the risk
of low bone mass and stress fractures in athletes.35 Female athletes are at greatest
risk for low bone mass, especially if EA is low and they present with menstrual
dysfunction as part of the female athlete triad.35 Most athletes need to increase their
calcium intake to meet the RDAs, and this can be achieved by incorporating dairy
products, calcium-fortiied fruit juice, and soy products fortiied with calcium sulfate. If athletes are also diagnosed with low vitamin D status, a calcium and vitamin
D supplement may be necessary. Vitamin D deiciency has received a great deal of
attention in the general public in the last few years and data show that athletes are
also at risk.74,75 Athletes living in northern latitudes, who are minimally exposed to
sun year-round and who train predominantly indoors are at greatest risk for vitamin
D insuficiency and deiciency.19,46 In addition, individuals with pigmented skin (for
example, African Americans) are at greater risk for compromised vitamin D status.76
Vitamin D is also involved in skeletal muscle metabolism and immune and nervous
system function,74 and thus vitamin D deiciency in an athlete may affect any or all
of these systems, although only limited data are currently available.
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Nutritional Assessment of Athletes, Second Edition
One of the most common micronutrient deiciencies in athletes is iron deiciency.
Athletes most likely to suffer from low iron status include rapidly growing athletes,
adolescent female athletes, female athletes with heavy menstrual losses, athletes on
energy-restricted or meat-restricted diets, distance runners who may have increased
gastrointestinal bleeding, and those training in environmentally challenging conditions (such as heat, altitude).19,46 While iron deiciency anemia compromises athletic
performance,77 it is unclear whether earlier stages of low iron status affects performance. Most athletes do not present with iron deiciency anemia but suffer from iron
depletion and iron deiciency without anemia. It has been shown that supplementation in previously iron-deicient females improves iron status and has the potential to
enhance aerobic performance parameters such as VO2max.78 Thus, early screening
during preparticipation physicals allows for quick interventions using dietary modiication and possibly low-dose supplementation.
Antioxidant nutrients, including vitamins and minerals such as vitamin C,
vitamin E, beta carotene, and selenium, protect cell membranes from oxidative
damage.79 Chronic exercise is thought to increase oxidative stress because of the
10–15-fold increase in oxygen consumption during exercise. Thus, athletes training
and competing year-round may have an increased need for antioxidant nutrients.
There is, however, little evidence that antioxidant supplementation enhances performance. Athletes should be cautious with high doses of these micronutrients because
they may result in counterproductive effects such as pro-oxidation and hampered
training adaptation.80 Athletes at greatest risk for low antioxidant intakes are those
restricting energy and fat and lacking adequate fruit, vegetable, and whole grain
consumption. Finally, the best antioxidant protection is probably offered by regular
exercise81; data show that even during intermittent altitude training, athletes are not
necessarily at greater risk for oxidative damage,82 and antioxidant supplementation
does not signiicantly alter oxidative stress markers associated with increased energy
expenditure at altitude.83
A few other micronutrients that are typically low in athletes’ diets include zinc
and magnesium, especially in female athletes; vegetarians; and those on energyrestricted diets. Zinc’s functions extend from energy metabolism to growth, muscle
tissue repair, and immune function. Low zinc status is particularly prevalent in those
on energy-restricted diets or vegetarian and vegan diets due to limited zinc content
in plant foods. These diets are also high in iber, potentially further decreasing zinc
absorption.84 Plasma zinc levels poorly relect zinc deiciency85; thus dietary assessments and certain physical symptoms such as loss of appetite, fatigue, and reduced
performance may be better indices to identify mild zinc deiciencies in athletes. It
is important to note that using zinc supplements can interfere with iron and copper
absorption71; hence athletes are best served increasing their consumption of dietary
sources of zinc or cover their zinc needs through a multivitamin/mineral supplement
not exceeding the RDA for zinc.
Magnesium plays a multitude of functions in energy metabolism and regulation
of membrane stability, cardiovascular, neuromuscular, immune, and hormonal functions71; therefore magnesium is a very important micronutrient for athletes. Low
magnesium intakes are prevalent in athletes restricting energy intake most likely
in endurance, weight-class, and aesthetic sports. Magnesium deiciency can lead to
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Evaluation of Nutrient Adequacy of Athletes’ Diets
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impaired endurance performance.71 Exercise-induced muscle cramps in athletes are
often perceived to be due to poor magnesium status. However, athletes should irst
assess hydration status and electrolyte balance before considering magnesium as a
potential factor associated with cramping.
Athletes quickly opt for vitamin and mineral supplements before covering their
micronutrient needs through foods such as fruits, vegetables, and whole grains. It
has to be emphasized with this population that (1) supplementation in the absence of
deiciencies does not increase performance,19,46 (2) too much of certain vitamins and
minerals can have counterproductive effects,80 and (3) dietary supplements may be
contaminated86 or mislabeled,87 increasing the risk for adverse health effects or a positive drug test. Thus a thorough nutritional assessment, including blood parameters, is
still the best foundation on which recommendations should be based for the increased
nutrient intake from food and supplements to meet micronutrient needs in sport.
2.6.6 FLUID
Several documents have been published related to hydration guidelines by organizations such as the American College of Sports Medicine (ACSM), among others.
The following list provides a few highlights from ACSM’s evidence-based Position
Statement on Hydration and Fluid Replacement22; available at www.acsm.org:
1. Exercise can elicit high sweat rates and result in substantial water and electrolyte loss.
2. Sweat rates vary considerably between individuals and different sports.
3. Dehydration (> 2% body weight) can degrade aerobic exercise performance,
especially in the heat.
4. Dehydration is a risk factor for exertional heat illness.
5. Body weight changes can relect sweat loss during exercise and can be used
to estimate individual luid replacement needs for speciic exercise and
environmental conditions.
6. Fluid consumption that exceeds sweat rate is the primary risk factor for
exercise-associated hyponatremia.
Sports dietitians working with athletes must individualize hydration guidelines,
especially targeting luid replacement during and after exercise based on pre- and
postexercise weight measurements. In preparation for exercise, ACSM recommends
ingestion of 5–7 mL·kg–1 of luid 4 hours before exercise and if urine is dark to drink
an additional 3–5 mL·kg–1 2 hours before. During exercise, the athlete is advised to
replace enough luid to avoid excessive dehydration (> 2% in hot weather) and avoid
drinking in excess of sweat rate. To optimize rehydration post exercise, luid intake
must exceed sweat loss. In fact, data by Shirreffs et al.88 have shown that up to 150%
of weight lost due to sweat loss during exercise should be replaced post exercise.
Sport drinks pack CHO and electrolytes that, in combination, beneit luid absorption, and sodium helps luid retention.22,88 Thus sport drinks offer a great avenue
to adequately hydrate and fuel before, during, and after exercise, especially when
exercise occurs at environmental extremes.
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Nutritional Assessment of Athletes, Second Edition
2.7
FUTURE RESEARCH AND DIRECTIONS
Evaluating dietary adequacy in athletes is most likely limited by the assessment
methods currently available to sports dietitians working in the ield. Thus future
research should aim at developing EI and expenditure methods that are more reliable
and valid, eficient, and less burdensome for the athlete. Although sports dietitians
have plenty of sports nutrition recommendations available from position papers and
materials alike, as discussed in this chapter, there are only few benchmark values that
help the professional evaluate quantity, quality, and timing of food intake in athletes
under various conditions. Future research should include more studies in athletes
focusing on macro- and micronutrient needs during speciic phases of the annual
training and competition plan. For example, CHO needs for high-intensity training
phases should be targeted. Protein requirements should be identiied for athletes
needing to maintain lean tissue mass, strength, and power while on energy-reducing
diets to lose body weight and fat. In addition, optimal fat intake should be identiied
for athletes, especially in endurance sports and in athletes on energy-restricted diets.
And inally, micronutrient needs for athletes who expend high amounts of energy but
restricting EI due to weight management plans should also be researched.
2.8
CONCLUSIONS
Good nutrition, appropriately timed, can improve the health and performance of an athlete or active individual. Determining an athlete’s energy needs can be a challenging but
necessary step to ensure that adequate energy and nutrients are consumed to maximize
training potential and performance. The role of the sports dietitian is to keep abreast
with current national and international dietary guidelines and reference intakes for the
general public along with more speciic recommendations aimed at physically active
and athletic individuals in order to accurately evaluate the dietary adequacy of athletes.
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40. Layman, D.K., Evans, E., Baum, J.I., Seyler, J., Erickson, D.J., and Boileau, R.A.,
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41. Hill, R.J. and Davies, P.S., Energy expenditure during 2 wk of an ultra-endurance run
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42. Economos, C.D., Bortz, S.S., and Nelson, M.E., Nutritional practices of elite athletes:
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43. Burke, L.M., Energy needs of athletes, Can. J. Appl. Physiol. 26(Suppl), S202–S219,
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46. Rodriguez, N.R., Di Marco, N.M., and Langley, S., American College of Sports Medicine
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47. Burke, L.M., Cox, G.R., Culmmings, N.K., and Desbrow, B., Guidelines for daily carbohydrate intake: Do athletes achieve them? Sports Med. 31(4), 267–99, 2001.
48. Bangsbo, J., Norregaard, L., and Thorsoe, F., The effect of carbohydrate diet on intermittent exercise performance, Int. J. Sports Med. 13(2), 152–57, 1992.
49. Balsom, P.D., Wood, K., Olsson, P., and Ekblom, B., Carbohydrate intake and multiple sprint sports: With special reference to football (soccer), Int. J. Sports Med. 20(1),
48–52, 1999.
50. Tesch, P., Larsson, L., Eriksson, A., and Karlsson, J., Muscle glycogen depletion and
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53. Meyer, N.L., Female winter sport athletes: Nutrition issues during the preparation for
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54. Brouns, F., Saris, W.H., Stroecken, J., Beckers, E., Thijssen, R., Rehrer, N.J., and ten
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57. Jeukendrup, A.E. and Moseley, L., Multiple transportable carbohydrates enhance gastric
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58. Coggan, A.R. and Coyle, E.F., Carbohydrate ingestion during prolonged exercise:
Effects on metabolism and performance, Exerc. Sport Sci. Rev. 19, 1–40, 1991.
59. Hulston, C.J., Wallis, G.A., and Jeukendrup, A.E., Exogenous CHO oxidation with glucose plus fructose intake during exercise, Med. Sci. Sports Exerc. 41(2), 357–63, 2009.
60. Ivy, J.L., Katz, A.L., Cutler, C.L., Sherman, W.M., and Coyle, E.F., Muscle glycogen
synthesis after exercise: Effect of time of carbohydrate ingestion, J. Appl. Physiol. 64(4),
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61. Jentjens, R. and Jeukendrup, A., Determinants of post-exercise glycogen synthesis during short-term recovery, Sports Med. 33(2), 117–44, 2003.
62. Burke, L.M., Collier, G.R., and Hargreaves, M., Muscle glycogen storage after prolonged exercise: Effect of the glycemic index of carbohydrate feedings, J. Appl. Physiol.
75(2), 1019–23, 1993.
63. Tipton, K.D. and Witard, O.C., Protein requirements and recommendations for athletes:
Relevance of ivory tower arguments for practical recommendations, Clin. Sports Med.
26(1), 17–36. 2007.
64. Babij, P., Matthews, S.M., and Rennie, M.J., Changes in blood ammonia, lactate and
amino acids in relation to workload during bicycle ergometer exercise in man, Eur. J.
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65. Biolo, G., Maggi, S.P., Williams, B.D., Tipton, K.D., and Wolfe, R.R., Increased rates
of muscle protein turnover and amino acid transport after resistance exercise in humans,
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66. Levenhagen, D.K., Carr, C., Carlson, M.G., Maron, D.J., Borel, M.J., and Flakoll, P.J.,
Postexercise protein intake enhances whole-body and leg protein accretion in humans,
Med. Sci. Sports Exerc. 34(5), 828–37, 2002.
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67. Rasmussen, B.B., Tipton, K.D., Miller, S.L., Wolf, S.E., and Wolfe, R.R., An oral essential amino acid-carbohydrate supplement enhances muscle protein anabolism after resistance exercise, J. Appl. Physiol. 88(2), 386–92, 2000.
68. Tipton, K.D., Elliott, T.A., Cree, M.G., Aarsland, A.A., Sanford, A.P., and Wolfe, R.R.,
Stimulation of net muscle protein synthesis by whey protein ingestion before and after
exercise, Am. J. Physiol. Endocrinol. Metab. 292(1), E71–E76, 2007.
69. Van Loon, L.J., Use of intramuscular triacylglycerol as a substrate source during exercise in humans, J. Appl. Physiol. 97(4), 1170–87, 2004.
70. Van der Beek, E.J., van Dokkum, M., Wedel, M., Schrijver, H., and van der Berg, H.,
Thiamin, ribolavin and vitamin B6: Impact of restricted intake on physical performance
in man, J. Amer. College Nutr. 13(6), 629–40, 1994.
71. Lukaski, H.C., Vitamin and mineral status: Effects on physical performance, Nutrition
20(7–8), 632–44, 2004.
72. Woolf, K. and Manore, M.M., B-vitamins and exercise: Does exercise alter requirements? Int. J. Sport Nutr. Exerc. Metab. 16(5), 453–84, 2006.
73. Anderson, J.J.B., Nutrition and bone in physical activity and sport, in Nutrition in
Exercise and Sport, Wolinsky I, Ed., CRC Press, Boca Raton, FL, 1998, pp. 219–44.
74. Willis, K.S., Peterson, N.J., and Larson-Meyer, D.E., Should we be concerned about the
vitamin D status of athletes? Int. J. Sport Nutr. Exerc. Metab. 18(2), 204–24, 2008.
75. Lovell, G., Vitamin D status of females in an elite gymnastics program, Clin. J. Sport
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76. Holick, M.F., Vitamin D deiciency, N. Engl. J. Med. 357(3), 266–81, 2007.
77. Beard, J. and Tobin, B., Iron status and exercise, Am. J. Clin. Nutr. 72, 594S–597S.
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78. Brownlie, T., Utermohlen, V., Hinton, P.S., Giordano, C., and Haas, J.D., Marginal
iron deiciency without anemia impairs aerobic adaptation among previously untrained
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79. Atalay, M., Lappalainen, J., and Sen, C.K., Dietary antioxidants for the athlete, Curr.
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80. Gleeson, M., Nieman, D.C., and Pedersen, B.K., Exercise, nutrition and immune function, J. Sports Sci. 22(1), 115–25, 2004.
81. Powers, S.K., DeRuisseau, K.C., Quindry, J., and Hamilton, K.L., Dietary antioxidants
and exercise, J. Sports Sci. 22(1), 81–94, 2004.
82. Subudhi, A.W., Davis, S.L., Kipp, R.W., and Askew, E.W., Antioxidant status and oxidative stress in elite alpine ski racers, Int. J. Sport Nutr. Exerc. Metab. 11(1), 32–41,
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83. Subudhi, A.W., Jacobs, K.A., Hagobian, T.A., Fattor, J.A., Fulco, C.S., Muza, S.R.,
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75(10), 881–88, 2004.
84. Volpe, S.L., Micronutrient requirements for athletes, Clin. Sports Med. 26(1), 119–30,
2007.
85. Micheletti, A., Rossi, R., and Ruini, S., Zinc status in athletes: Relation to diet and
exercise, Sports Med. 31(8), 577–82, 2001.
86. Green, G.A., Catlin, D.H., and Starcevic, B., Analysis of over-the-counter dietary supplements. Clin. J. Sport Med. 11(4), 254–59, 2001.
87. Gurley, B.J., Gardner, S.F., and Hubbard, M.A., Content versus label claims in ephedracontaining dietary supplements, Am. J. Health Syst. Pharm. 57(10), 963–69, 2000.
88. Shirreffs, S.M., Taylor, A.J., Leiper, J.B., and Maughan, R.J., Post-exercise rehydration
in man: Effects of volume consumed and drink sodium content, Med. Sci. Sports Exerc.
28(10), 1260–71, 1996.
© 2011 by Taylor and Francis Group, LLC
Section II
Anthropometric
Assessment of Athletes
© 2011 by Taylor and Francis Group, LLC
Assessment
3 Physique
of Athletes
Concepts, Methods,
and Applications
Gary J. Slater, Helen T. O’Connor,
and Fiona E. Pelly
CONTENTS
3.1
3.2
3.3
3.4
3.5
3.6
3.7
3.8
3.9
3.10
3.11
Introduction .................................................................................................... 73
Hydrodensitometry ......................................................................................... 74
Total Body Water ............................................................................................ 77
Dual Energy X-Ray Absorptiometry .............................................................. 79
Air Displacement Plethysmography ............................................................... 81
Bioelectrical Impedance ................................................................................. 82
Surface Anthropometry ..................................................................................84
Speciied Landmarks for the Assessment of Skinfolds .................................. 88
Ultrasound .................................................................................................... 102
Three- and Four-Compartment Models........................................................ 103
New Technologies ......................................................................................... 104
3.11.1 Computed Tomography .................................................................... 104
3.11.2 Magnetic Resonance ......................................................................... 105
3.11.3 Three-Dimensional Photonic Scanning............................................ 106
3.12 Practical Recommendations ......................................................................... 107
3.13 Future Research Needs ................................................................................. 108
3.14 Conclusions ................................................................................................... 108
References .............................................................................................................. 109
3.1
INTRODUCTION
A relationship between competitive success and physique traits has been identiied
in an array of sports, including football codes,1 aesthetically judged sports,2 swimming,3 track and ield events,4 and skiing,5 as well as lightweight6 and heavyweight
rowing.7 The speciic physique traits associated with competitive success vary with
the sport. For athletes participating in aesthetically judged sports, maintenance of
low body-fat levels is associated with positive outcomes.2,8,9 A similar relationship
73
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Nutritional Assessment of Athletes, Second Edition
exists in sports where frontal surface area, power-to-weight ratio, and/or thermoregulation are important.10 However, in sports demanding high force production, muscle
mass may be more closely associated with performance outcomes.1,3 Likewise, in
sports such as rowing, other physique traits like a shorter sitting height (relative to
stature) and longer limb lengths are related to competitive success,11 with such information used successfully in talent identiication.12 Because of these relationships, it
has become common practice to monitor physique traits of athletes in response to
growth, training, and dietary interventions.
Despite the association between physique traits and competitive success, the assessment of body composition among athletes, especially female athletes and dancers, has
been questioned due to the possibility of assessments promoting anxiety and disordered
eating.13 This comes despite recognition that evidence supporting a causal relationship
between body-composition assessments and disordered eating has yet to be established.
Furthermore, when undertaken in conjunction with a suitably designed education program, current evidence indicates physique assessments can be undertaken without promoting adverse affective consequences.14 The concurrent education of athletes on the
rationale for assessments makes good sense and should be actively promoted.
An array of techniques are available for the measurement of body composition,
including anthropometric, radiographic (computed tomography [CT], magnetic
resonance imaging [MRI], dual energy x-ray absorptiometry [DXA]), metabolic
(creatinine, 3-methylhistidine), nuclear (total body potassium, total body nitrogen),
and bioelectrical impedance analysis (BIA) techniques. When selecting the most
appropriate technique, a range of factors should be considered, including technical
issues such as the safety, validity, precision, and accuracy of measurement. Practical
issues must also be considered, such as availability, inancial implications, portability, invasiveness, time effectiveness, and technical expertise necessary to conduct
the procedures. Consideration must also be given to the ability of body-composition
assessment methodologies to accommodate the unique physique traits characteristic
of some athletes, including particularly tall, broad, and muscular individuals or those
with extremely low body-fat levels.
This chapter reviews the most common techniques used to assess the physique
traits of athletes, including DXA, air displacement plethysmography (ADP), BIA,
and surface anthropometry. A review of newer techniques with potential application
to athletic populations either directly or via research investigations is also made, as
well as discussion on the factors that should be considered when attempting to minimize measurement error.
3.2
HYDRODENSITOMETRY
Hydrodensitometry, or underwater weighing (UWW), has long been considered
the gold-standard method for assessing body composition. The technique is based
on Archimedes’ principle that body mass in air compared to body mass when
totally submerged in water is directly related to the density of the water displaced.15
Technically, it simply demands the measurement of an individual’s body mass both
in and out of the water with a correction for residual lung volume (RV). The volume
of water displaced can be calculated from the known density of water at any given
© 2011 by Taylor and Francis Group, LLC
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Physique Assessment of Athletes
temperature (1 g of water = 1 cm3 at 39.2°F [4°C]).15 As this does not account for
the RV of air left in respiratory passages and lungs, and gas in the gastrointestinal
tract, a correction for gas volume is necessary. This can either be estimated based on
the subject’s age, height, and mass or measured via an array of dilution techniques,
including oxygen16 and helium dilution.17 The underwater weighing procedure is
usually repeated eight to twelve times until three trials are obtained with results
within 100 g of each other.18 The average of the three trials is used to calculate body
density.19 A more recent study has reported minimal error from four trials with automated data acquisition and in-tank residual volume measurement.20
Failure to account for the RV will underestimate whole-body density, as this
air contributes to the buoyancy effect. Gas in the gastrointestinal tract cannot be
estimated with accuracy and is often disregarded. However, the volume of gas can
be signiicant after ingestion of certain foods and medical conditions.21 The results
obtained from mass in air, mass in water, and RV can be used to calculate body density using the following equation21:
BD =
Wa
−V
− Ww
Wa
Dw
where BD = body density, Wa = weight in air, Ww = weight in water, Dw = known
density of water for the temperature at which Ww was obtained, and V = residual
lung volume.
Body density derived from hydrodensitometry can be used to estimate the relative
fat content of the human body and is based on the principle that water, fat, protein,
and mineral have different but constant densities.21 The density of each body component was derived from calculated volumes developed by Brozek and colleagues22
that were based on autopsy data of just four human cadavers (Table 3.1). Although
cadaver studies are the only true direct method of measuring body composition, they
also have limitations due to the technical dificulty with dissection,21 the unknown
impact of cause of death on body composition,23 and the application of results from
such small samples of geriatrics to a much younger, athletic population.
TABLE 3.1
Density of Four Human Body Components
Body Component
Density (at 37°C)
Fat
0.9007 g.cm–3
Water
Protein
Mineral
0.993 g.cm–3
1.340 g.cm–3
3.000 g.cm–3
Comment
Constant via body site
May vary between individuals
Includes all substances with same density as triglycerides (TG)
May contain solutes of protein and inorganic salts
Value for fully hydrated protein in vitro
Value in vitro
Sources: Adapted from Brozek, J., Grande, F., Anderson, J.T., and Keys, A., Ann. N.Y. Acad. Sci. 110,
113–40, 1963; and Siri, W.E., Nutrition 9(5), 480–91, 1993 (originally published in 1961).
© 2011 by Taylor and Francis Group, LLC
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Nutritional Assessment of Athletes, Second Edition
The relationship between body density and fat shown by Behnke25 in 1942 led to
the derivation of equations for the calculation of percent body fat as follows:
% body fat = (495/body density) – 450 22
% body fat = (457/body density) – 414.2 24
These equations have been used extensively to calculate body fatness in both laboratory studies and in the ield.26 They yield similar results for body densities ranging
from 1.030 to 1.090 g.mL –1.27 However, there are a number of assumptions associated
with the equations that have been largely ignored with their application. Formulas
for estimating fat from density is based on the premise that all adult humans are
identical in composition except for differences in proportion of adipose tissue21,22
(that is, a two-compartment model of fat mass [FM] and fat-free mass [FFM]), and
on assumptions about the consistency in the chemical composition of FFM. For
example, it is assumed that there is a constant ratio of water, protein, and mineral of
73.7%, 19.4%, and 6.8%, respectively.21,24 There is also an assumption that changes
in body mass do not result in any change to the consistency of the FFM. However,
adipose tissue consists of lipid, water, and protein, not fat alone, and changes in body
mass result in changes to all components.24
The fat-mass density assumption is based on the average of 0.9007 ± 0.00068
g.cm–3 for twenty ethyl ether extracted fat samples from the intra-abdominal and subcutaneous tissue of just ive subjects.28 However, it has been suggested that the small
coeficient of variation validates the hydrodensitometric fat-mass density assumption
of 0.9007 g.cm–3.29 Similarly the hydrodensitometric fat-free-mass density assumption
of 1.100 g.cm–3 is based on analysis of just three male cadavers aged 25, 35, and 46
years.22 Biological variation in FFM hydration away from the assumed 73.72% is particularly troublesome given that water has the lowest density but comprises the largest
percentage of any FFM compartment. When total body water is measured directly
via dilution techniques, water comprises 70.4%–75.1% of the FFM.30 Consequently,
hypohydration and hyperhydration, respectively, increase and decrease FFM density
with associated under- and overestimation of percentage body fat via hydrodensitometry. Despite this, the assumed FM and FFM densities are applied irrespective of age,
gender, genetic proile, and training status of individuals.29
Siri recognized that hydrodensitometry did not account for biological variability
between individuals and subsequently assessed the errors associated with the technique.24 He concluded that estimates of absolute fat had an error of 4% and recommended that measurements of different components of the FFM (protein, mineral, and
water) should be treated independently.24 There is now substantial evidence suggesting
that the use of a multicompartment model is essential to quantify differences in FFM.31
Subsequent studies have shown that failure to use other techniques to determine total
body water and bone mineral density can lead to an inaccurate estimation of body
fatness in children,32 the elderly,33 and ethnic populations.34 This is due to variation in
density of FFM with age, gender, ethnicity, level of fatness, and activity level.35–37
While it is often assumed body density derived from hydrodensitometry is a very
robust measure, consideration must still be given to subject presentation. Within an
© 2011 by Taylor and Francis Group, LLC
Physique Assessment of Athletes
77
athletic population, acute variation in hydration status may need to be considered, with
hypohydration shown to reduce estimates of body fat percentage38 and FFM.39 While
the ingestion of 1.2 to 2.4 L of water does not inluence measures of residual volume
or underwater weight, body mass out of the water is increased. Body density is subsequently increased, resulting in a lower estimate of body fat percentage,40 although
this effect may not be evident when smaller volumes of luid (0.5 L) are ingested.38
Although the ingestion of food and luid throughout the day on hydrodensitometry
results has not been investigated, it is reasonable to presume larger volumes could
also inluence hydrodensitometry derived estimates of body composition because of
their inluence on body mass. This is aligned with the original work of Siri, indicating that formulas would become invalid in the presence of abnormal hydration.21,24
Hydrodensitometry has recently declined in its popularity as a method to determine body fatness due to the introduction of simpler, faster techniques (ADP, BIA,
and DXA). There are obvious potential limitations associated with subject anxiety
during measurement, so familiarization is always essential. Although the application of this method is primarily limited to a research setting, it remains an excellent
measure of body density despite some of the assumptions outlined above associated
with the conversion of body density into body composition.
3.3
TOTAL BODY WATER
Measurement of total body water (TBW) is typically reserved for use in research
studies on body composition as it requires dosing with a precisely measured quantity of a tracer (such as deuterium, oxygen-18, or tritium), moderate to sophisticated
laboratory equipment (mass or isotope ratio mass or infrared spectrometry, gas chromatography, nuclear magnetic resonance, or scintillation counting, for example), and
signiicant technical expertise to accurately analyze and interpret the results.41 The
dilution of the tracer in body water can be used to calculate the total volume of
body water. The simplest and most commonly adopted approach for estimation of
body composition via TBW uses a two-compartment model of FM, which is free
of water, as opposed to FFM, which is estimated to contain approximately 73%
water.41 The calculation of FFM using TBW assumes that there is a constant hydration of the FFM compartment, that is, that the ratio of solid to water is the same in
all individuals. Remarkably, early animal work by Pace and Rathburn,42 who irst
recommended the 0.73 FFM hydration constant, has been replicated by a number of
adult human cadaver studies.43,44 This assumption, although reasonable in healthy
individuals, may be altered in athletes who are hypohydrated as a result of luid loss
during training/competition or in clinical populations as a result of abnormal luid
loss or retention due to disease.
Key assumptions of TBW measurement by isotope dilution:41
•
•
•
•
The tracer is not distributed in other body compartments, only in body water.
Equal distribution of the tracer occurs in all anatomical water compartments.
The tracer reaches equilibrium at a rapid rate.
The tracer and body water are not metabolized by the body during the
period of tracer equilibrium.
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Nutritional Assessment of Athletes, Second Edition
Although none of these assumptions are perfect, they are reasonable, and limitations depend on the methodology of dosing, measurement, and population assessed.
Equilibration of the tracer typically takes at least 3–4 h and correction is required for
exchange with nonaqueous hydrogen or oxygen.41 Precision of the method depends
on the analytical approach used and tracer dose but generally mass spectrometric
methods have high precision and accuracy within the range of 1–2%.45,46
There are a number of different approaches to assessment of TBW but the “plateau method” is one of the most frequently used for body-composition assessment,41
although a back extrapolation method is also available.47 In the plateau method,
subjects typically fast overnight (8–12 h) and refrain from exercise (potentially in
athletes for the previous 24 h) to prevent excessive insensible water loss. A baseline
biological sample of blood, plasma, saliva, urine, or breath water vapor is collected
prior to collection of nude body weight (when isotope mass spectrometry is used,
an additional baseline sample should also be taken 24 h prior to dosing to assess
day-to-day isotope variation). After baseline samples are collected, an oral weighed
dose of the isotope is then administered with care taken to rinse the dosing container
with additional plain water (~50 mL) to ensure it is entirely consumed.48 During the
following equilibrium period, the subject should remain nil by mouth. A subsequent
biological sample is typically taken at 3, 4, and 5 h post dose. If urine is being used,
subjects should void and discard a sample before collection of duplicate urine specimens at the above prescribed times. Samples should be stored in airtight containers
to prevent loss of isotope until analysis. Refrigeration or freezing at –20°C is recommended to minimize bacterial growth. Sample enrichment of the two post-dose
samples should agree within two standard deviations.
Precise measurement requires attention to subject preparation, dosing, sample
collection, and isotope analysis. Subjects must present euhydrated and with normal
glycogen stores,41 which can be challenging for some athletes. Speciic dietary guidance for athletic subjects to ensure euhydration and glycogen repletion from at least
12–24 h before dosing is therefore important. The inal meal before dosing should
be consumed 12–15 h prior to the dose to minimize water content in the intestine.
Subjects should also avoid drinking several hours before dosing to avoid overhydration.41 The subjects should also be rested in an environment that prevents excessive
sweating.41 Given these constraints, early morning dosing is most convenient and
reduces the discomfort of fasting. Doses are prescribed relative to body mass of subjects and need to be precisely weighed and transported in a nonpermeable, airtight
container to minimize evaporation.48 A sample of the dose diluted with tap water (so
that the enrichment approximates the concentration in the physiological samples)
should also be measured in the same batch along with the diluting water together
with the samples.49
Deuterium was the irst tracer used for the measurement of TBW. As it is stable,
safe, and relatively inexpensive, deuterium remains the most common choice for
assessment of body composition.41 Analysis using tritium was popular for a time
due to the availability of scintillation counters50 and ease of measurement, but the
disadvantage is exposure to a small radiation dose, and for this reason it is now rarely
used. Oxygen-18 is stable and safe but by far the most expensive isotope for dosing
and can only be accurately measured by mass spectrometry, which further increases
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79
the cost. Use of this method in athletes is reserved for research, typically to assist
with the validation of other body-composition techniques that have practical ield use
application (such as bioelectrical impedance). Those interested in this methodology
are referred to the following resources for an in-depth coverage.41,47–49
3.4
DUAL ENERGY X-RAY ABSORPTIOMETRY
DXA was originally developed for the diagnosis of osteoporosis and remains the
gold-standard tool for this assessment.51 However, DXA technology is also able to
measure soft-tissue body composition, rapidly gaining popularity in recent years as
one of the most widely used and accepted laboratory-based methods for body-composition analysis. DXA not only provides a measure of FM and FFM, it also provides
information on regional body composition (arms, legs, trunk, differences between
left and right side), making DXA technology unique among physique assessment
tools and particularly appealing among athletes when undertaking targeted training
programs or during periods of rehabilitation from injury. Furthermore, whole-body
scans are rapid (~5 min), noninvasive, and associated with very low radiation doses
(~0.5 µSv or approximately 1/500th of annual natural background radiation), making the technology safe for longitudinal monitoring of body composition. Because
of its application in the assessment of bone mineral density, DXA technology is also
becoming increasingly available.
There are three manufacturers of DXA technology: Hologic Inc. (Waltham,
Massachusetts), Lunar Radiation Corp. (Madison, Wisconsin), and Norland Medical
Systems (Fort Atkinson, Wisconsin); all models share in common an x-ray source,
scanning table, detector, and computer interface with complex algorithm software
for the conversion of raw data into estimates of body composition. The systems differ
in analysis software and the geometry of scanning, using either fan, narrow fan, or
pencil beam technology, which ultimately determines scanning time, radiation dose,
and accuracy.52 Because of these differences, longitudinal monitoring of athletes
should be undertaken on the same machine53–55 and using the same technician,56
especially if regional body-composition changes are of interest.
DXA technology is based on the differential attenuation of transmitted photons
at two energy levels by bone, fat, and lean tissue.57 Attenuation of low-energy photons are then expressed as a ratio to attenuation observed for the high-energy photons,
the outcome of which is speciic to different molecular components, including fatty
acids, protein, and bone. In theory, assessment of all three components would require
measurement at three different photon energies. The DXA dual-energy system can
thus only be used to estimate the fractional masses of two components in any one
pixel. That is, in bone-containing pixels, bone mineral and soft tissue can be measured, while in non-bone-containing pixels, fat and bone mineral-free lean mass can
be measured.58 The proportion of fat and bone mineral-free lean in bone containing
pixels is assumed to be the same as the adjacent non-bone-containing pixels,58 with
the software subsequently incorporating individual pixel data into whole-body output.
This assumed ratio of fat to bone mineral-free lean in soft-tissue pixels is applied to
upwards of one third of pixels in a whole-body scan and particularly evident in regions
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of low bone-free pixels such as thorax, arm, or head, resulting in the identiication of
composition changes in these regions as being less reliable.59,60
DXA technology has been validated against the modern day “gold standard” bodycomposition assessment tool, the four-compartment model, which accounts for variation in the water and mineral fractions and the density of the FFM. Although there
is some data suggesting good agreement between DXA-derived measures of body
composition and the four-compartment model in healthy, young males and females,61
others have indicated that DXA underestimates body fat,62 especially among leaner
individuals.30,63 This has been attributed to variation in FFM hydration62 or differences in anterior–posterior tissue thickness.63 However, among athletes where the
primary focus is on monitoring change in body composition, DXA appears to offer
suficient sensitivity to identify small changes in body composition.64,65
The precision of measurement for DXA in sedentary populations has been shown
to be superior to hydrodensitometry and surface anthropometry,66 with a coeficient
of variation of less than 1.0 kg for FM, FFM, and total mass.57,67 Any variability of
results achieved by DXA can be divided into two categories: technical error or biological error. In an effort to enhance precision of measurement, special consideration
should be given to subject positioning,68,69 with subjects resting on the scanner area
in a supine position with special care taken to ensure their entire body its within the
speciied scanning area. Where possible, positioning of the arms and legs should be
standardized, ensuring clear separation from the torso; foam blocks not recognized
by the scanner can be particularly helpful. Clothing should be kept to a minimum,70
with all metal objects removed. While small amounts of food and luid do not appear
to inluence results,71 larger volumes inluence measurement of lean body mass,72 and
thus measurements should be undertaken in a fasted state wherever possible, preferably soon after waking in a euhydrated state.73 Reliability of regional measurements
is inferior to total body results.69,74
Of particular relevance to athletic populations is the deined scanning area available for assessment, typically within the range of 60–65 cm × 193–198 cm, depending on the manufacturer.52 It is therefore dificult to perform whole-body DXA scans
on particularly tall or broad and very muscular athletes, physique traits common to
some sports such as rowing, basketball, volleyball, and rugby union. Thus, taller
individuals are either excluded from investigation, scanned without their head or
feet, or have their knees bent so as to it within the scanned area,75 or data is summed
from two partial scans, the latter appearing to be the method of choice with the
body divided at the neck resulting in the most accurate estimates of bone and soft
tissue composition.76 Until recently, very broad individuals were “mummy wrapped”
in a sheet, bringing the arms forward, so as to it within the scanning area. While
this afforded a whole-body scan to be undertaken, the number of bone-containing
pixels is signiicantly increased and limits the ability to assess body composition at
particular regions of interest, such as the arms and torso. Newer DXA instruments,
like the iDXA from GE Lunar (Madison, Wisconsin), not only have larger scanning
areas (66 cm wide) but also come with software that allows an estimate of wholebody composition from a half-body scan,77 a concept validated previously in obese
individuals.78
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Physique Assessment of Athletes
3.5
81
AIR DISPLACEMENT PLETHYSMOGRAPHY
While ADP has been used to measure human body composition for some time, a
viable system known by the trade name BOD POD (Life Measurement, Concord,
California), has only been available commercially since the mid-1990s with a pediatric version (PEA POD) now also available. This quick, comfortable, automated, noninvasive, and safe technique provides an estimate of percent fat from body density
without being submerged under water and accommodates a range of subject types,79
including very tall and muscular athletes.80 Air displacement plethysmography utilizes basic gas laws to describe the inverse relationship between pressure and volume
in two enclosed chambers, consequently allowing for the calculation of body density
and body composition.
This two-compartment technique involves sitting quietly in an enclosed chamber
while the volume of air displaced by the body is measured. Duplicate measures of
body volume are recommended, with volumes averaged if they differ by ≤ 150 mL,
and a third trial undertaken if they are > 150 mL, with the closest two body volumes
averaged.79 Thereafter, lung functional residual capacity is measured using pulmonary plethysmography or if this is not possible (for example, in the elderly, children,
or those with pulmonary dysfunction), predicted based on age, gender, and height. If
no two measurements meet the acceptance criteria, the entire test procedure (including recalibration) should be repeated.80 Body density is then calculated by dividing
the measured body mass by corrected body volume, with subsequent calculation of
percent body fat using either the Siri24 or Brozek22 equations. As such, the BOD POD
is constrained by the same issues as hydrodensitometry when converting a measure
of body density into body composition.
The measurement of functional residual capacity using pulmonary plethysmography is both reliable and valid.81 However, it can change in response to signiicant
adjustments in body composition and as such should be measured wherever possible
and never used interchangeably with predicted thoracic gas volumes.82 Furthermore,
on an individual basis, body fat can deviate by as much as 3% depending on the use
of measured versus predicted lung volume.83
The BOD POD compares favorably as a substitute for underwater weighing when
a measure of body density is desired,84 although it has been observed to underestimate body fat slightly in males (–1.2 ± 3.1%) and overestimate body fat in females
(1.0 ± 2.5%), independent of age, weight, or height.85 This effect is evident among
athletic populations as well, with BOD POD–derived estimates of body fat consistently lower than those obtained via hydrodensitometry, DXA, and a three-compartment model for male collegiate football athletes.86 Among female athletes, the
BOD POD overestimates body fat when compared against hydrodensitometry but
either compares favorably87 or underestimates body fat when contrasted with DXA.88
These differences between techniques should not be a surprise and are likely a consequence of methodological error of both techniques, including the presumed gold
standard or established techniques.
Although the ability to assess absolute character traits is an important attribute of
a physique assessment technique, equally important is the ability to identify small
but potentially important changes in body composition in response to diet, training,
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or other interventions. Research using the artiicial manipulation of body composition by the addition of 1–2 liters of oil, water, or a combination of both substances to
the BOD POD chamber among normal-weight individuals suggests the technology
has the ability to pick up changes in either component within the range of 2 kg.89,90
When the BOD POD has been used in conjunction with DXA to monitor body-composition changes in response to lifestyle interventions, BOD POD estimates of fat
mass are typically lower, with concomitant higher estimates of FFM.64,91 However,
agreement between techniques was high for identifying the changes in physique
traits in response to lifestyle interventions.64,91,92
As with other physique assessment tools, subject presentation can inluence results,
and thus suitable protocols must be implemented to avoid the impact of these on
the reliability of data. Speciically, uncompressed facial and scalp hair underestimate
body fat due to trapped isothermal air in body hair.93 Similarly, loose-itting clothing worn during assessment inluences body-density measurements, underestimating body fat percentage by upwards of 9%.84,94 Consequently, subjects are advised
to wear standardized tight itting swimsuits consistently84,94,95 in conjunction with
a swim cap and to remove excess facial hair.93 Changes in body temperature and
moisture content may also inluence BOD POD data,96 suggesting that assessments
should be undertaken independent of exercise. This is further supported by the fact
that acute dehydration (within the range often experienced by athletes) inluences
BOD POD results, underestimating both body fat percentage and FFM, although the
effect is within the range of 1% body fat.39
Minimizing the inluence of these variables enhances the ability of the BOD POD
to track small but potentially important changes in body composition. While the
test–retest reliability of the BOD POD is excellent,97 this does not provide insight
into the biological variability evident between test measures. The between-day coeficient of variation for body fat using the BOD POD is within the range of 2.0–5.3%,98
although large discrepancies (up to 12%) between trials have been reported in a
small percentage of individuals,97 for reasons still yet to be determined (but could
include variation in breathing patterns or transient change in pressure within the test
room). In practice, technicians are encouraged to undertake repeat measurements
and if these two tests show a difference in percent body fat greater than 0.5%, then
a third test may be appropriate.83 Although reliability between individual BOD POD
systems is very good,99 athletes should be encouraged to be assessed using the same
machine each time.
3.6
BIOELECTRICAL IMPEDANCE
BIA is a safe and noninvasive method to assess body composition that is based on
the differing electrical conductivity of FM and FFM.100,101 FFM contains water and
electrolytes and is a good electrical conductor, while anhydrous fat mass is not. The
method involves measuring the resistance (R) to low of a low level (800 µA) 50
kilohertz (KHz) current.101 Resistance is proportional to the length (L) of the conductor (in this case, the human body) and inversely proportional to its cross-sectional area (A). A relationship then exists between the impedance quotient (L2 / R)
and the volume of water (total body water), which contains electrolytes that conduct
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83
the electrical current. In practice, height in centimeters is substituted for length.
Therefore, a relationship exists between FFM (approximately 73% water) and height
(cm)2 / R. FM is obtained from FFM by subtracting the value for FFM from total
body mass.101 Two types of resistance exist in the human body. One is resistive (R)
as described earlier, and the other is capacitative or reactance (Xc). “Impedance” is
the term used to describe the two types of resistance. As the electrical properties of
tissue vary depending on nutritional status and hydration, the relationship between
the two can be used to diagnose various disease states.101
Although the relationship between FFM and impedance is readily accepted, there
are several assumptions associated with its use. First, the human body is assumed
to be a cylinder with a uniform L and A.102 However, the human body more closely
resembles several cylinders. The body parts with the smallest FFM (the limbs) have
the greatest inluence on whole-body R. The trunk, which is a shorter, thicker segment, contains 50% of body weight, but contributes a minor amount to the overall
R.102 The second assumption is that the conducting material in the cylinder is consistent throughout. However, this will vary depending on tissue structure, hydration
status, and electrolyte concentration of the tissue.102
Early regression equations to calculate FFM only used height and resistance
without considering many of these assumptions. More recently, other parameters
such as body mass, age, gender, and anthropometric measures have been included
to improve accuracy, resulting in numerous population-speciic equations.101 BIA
appears to give a reasonably accurate assessment of body composition in healthy
individuals provided a validated equation with appropriate age, gender, and ethnicity
compatibility is utilized.
Due to the relevance of body water to conductivity of electrical current, there
is substantial evidence that BIA is not valid for assessment of subjects with abnormal hydration.103 Hydration status is an issue pertinent to athletic populations. A
study by Saunders and colleagues104 found that changes in hydration status in endurance-trained individuals caused large luctuations in percent body fat, with a 1.7%
decrease from euhydration to hypohydration and 3.2% increase from hypohydration
to complete rehydration, and a further 2.2% increase with hyperhydration (3% above
normal body weight). The ingestion of smaller volumes of luid (591 mL) also results
in 1% increase in estimates of percentage body fat, suggesting acute luid (and most
likely food) intake can also increase measurement error,105 prompting recommendations that subjects should remain fasting for at least 8 h prior to assessment.103 Given
this, it would be prudent to undertake assessments in the morning prior to breakfast wherever possible, with subjects encouraged to present in a well-hydrated state;
assessment could be done via the collection of a irst-morning urine sample.
The measurement of difference in electrical properties of various body tissues is not a new concept. The original studies were conducted by Thomasset in
the 1960s using two subcutaneous inserted needles.106 The technique was subsequently reined in the 1970s to four surface electrodes and resulted in commercially available single-frequency analyzers.101 Since that time, there have been
signiicant advances in BIA with options of single frequency, multifrequency, and
segmental BIA.
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Foot-to-foot BIA analyzers are the most readily available for public purchase.107
These inexpensive body fat “scales” are popular among the general public, being
promoted as a simple, portable method of measuring body fatness. However, there
are a number of limitations with foot-to-foot devices as current is only circulated
through the legs and lower part of the trunk with results extrapolated to the whole
body.107 If used within an athletic population, “athlete” mode should be used where
available when monitoring athletes.108
Single-frequency BIA (50 kHz) is most commonly used as a ield technique to
measure body composition. They usually consist of four electrodes placed on the
wrist and hand, plus ankle and foot, although foot-to-foot, and hand-to-hand analyzers are also available. The two source electrodes are placed on the dorsal surface
of the right hand and foot proximal to the metacarpal-phalangeal and metatarsalphalangeal joints respectively. The two voltage electrodes are placed on the midpoint
between the distal prominences of the radius and ulna of the right wrist and between
the medial and lateral malleoli of the right ankle.102 Although this technique is relatively simple, less than optimal accuracy has been observed when compared to other
techniques such as DXA and hydrodensitometry. Possible sources of error have been
attributed to arm positioning, skin temperature, interobserver variability, and electrode placement.103,109 It is apparent that standardized protocols for use (Table 3.2)
are essential to ensure that measurement error is minimized.
Multifrequency BIA consists of measurement of impedance at various frequencies (0, 1, 5, 50, 100, 200, and 500 kHz). At a low single frequency, an electrical current will not fully penetrate the cell membrane, passing through extracellular water,
whereas at high frequencies the current will penetrate the cell membrane.110 By measuring various components across a number of frequencies, a mathematical model
can be derived that can be used to predict TBW and subsequently FFM instead of the
use of standard regression equations. This may be appropriate for individuals where
there is variation in standard hydration status or body composition.111 The results of
various studies comparing multifrequency BIA to single-frequency BIA and other
methods such as DXA have reported mixed results.112,113 Among individuals with
low body-fat levels, BIA tends to overestimate fat mass and percentage fat mass
while underestimating FFM.114
Bioelectrical impedance has become increasingly popular as a tool for assessing the physique traits of athletes given its relative ease of use, portability, and cost
effectiveness. To be conident in the use of this technology to track changes in physique traits, it must be compared against an accepted tool for tracking changes in
body composition. While both single-frequency and multifrequency BIA show good
absolute agreement with DXA during a period of weight loss, large individual variance can occur,115 reinforcing the need to implement assessment practices that limit
measurement noise.
3.7
SURFACE ANTHROPOMETRY
For reasons of timeliness, practicality, and cost effectiveness, the routine monitoring
of body composition among athletic populations is often undertaken using anthropometric traits such as body mass plus subcutaneous skinfold thicknesses and girths at
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TABLE 3.2
Recommendations for Standard Methodology for Bioelectrical
Impedance Analysis
Instrument
Recommendation
Generator
Regular calibration
Battery powered to avoid interfering with current
Ability to identify abnormal skin resistance
Identiies type of signal measured (i.e., resistive or reactance)
Appropriate for subject height (up to 200 cm)
Diameter meets manufacturers recommendations
Meets instrument requirements (> 4 cm2)
Keep electrodes in sealed bag and protect from heat
Analyzer
Cables
Electrodes
Subject
Recommendation
Ethnicity
Height and body mass
Bladder voided
Hydration status
Physical activity
Timing
Note ethnicity and use appropriate equations
Measure at time of assessment; self-reported measures not valid
Void before measurement
Assess upon waking urine sample to determine hydration status
Abstain for 8 h before measurement
Note time of day and replicate for subsequent measurement
Note phase of menstrual cycle in women
Ambient temperature, no skin lesions at site of electrodes
Clean with alcohol
Note side of body and repeat on the same side
Abduction of limbs, arms 30° from trunk and legs separated at 45°
Standardize time before measurements (usually 5–10 min)
Note any abnormalities
Measure in a thermo-neutral environment. No contact with metal
Skin condition
Electrode position
Limb position
Body position
Body shape
Environment
Source: Adapted from Kyle, U.G., Bosaeus, I., De Lorenzo, A.D., Deurenberg, P., Elia, M., Manuel
Gomez, J., Lilienthal Heitmann, B., Kent-Smith, L., Melchior, J.C., Pirlich, M., Scharfetter, H.,
Schols, A.M., and Pichard, C., Clin. Nutr. 23(6), 1430–53, 2004.
speciic anatomical landmarks. Unlike other techniques requiring expensive, laboratory-based equipment, surface anthropometry only requires relatively inexpensive
equipment that is easily portable. However, highly skilled technicians are required
if reliable data are to be collected. Technicians need to be particularly meticulous
with both accurate site location and measurement technique. Measurements just
1–2 cm away from a deined site can produce signiicant differences in results.116,117
Furthermore, if repeat measurements are to be taken over time, it is important that
the same technician collect the data.117
The measurement of skinfolds, or a double layer of skin and subcutaneous tissue,
as an index of whole-body fat would appear to be reasonable. However, what is really
being measured is the thickness of a double fold of skin and compressed subcutaneous adipose tissue (SAT).118 To infer from this the mass or percentage of total body
fat requires a number of assumptions to be made, including
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• Constant compressibility of skinfolds across sites on the body
• The skin thickness at any one site is negligible or a constant fraction of
a skinfold
• Fixed adipose tissue patterning across the body
• A constant fat fraction in adipose tissue
• Fixed proportion of internal to external fat
When assessed via cadaver analysis, few of these assumptions hold true.119 For
example, skinfold compressibility is not constant between sites and as a consequence,
similar thicknesses of adipose tissue may yield different caliper values due to different degrees of tissue compressibility.120 Furthermore, the patterning of adipose tissue
varies markedly between individuals,121 and as such, multiple skinfold sites should
be used, including both upper- and lower-body landmarks.122 Similarly, while it is
estimated that subcutaneous fat comprises one third of total body fat, this can range
from 20% to 70% depending on gender, degree of fatness, and age.27 Despite an obvious violation of these assumptions, a strong relationship does exist between subcutaneous adiposity and whole-body adiposity, and between direct skinfold thickness
measures and whole-body adiposity.119
Estimates of body density, FM, and FFM can then be derived from raw skinfold
data using one of many available regression equations. Altogether, more than 100
equations to predict body fat from skinfolds have been produced.27,118,123,124 However,
these equations are typically based on a single-measurement, between-subject,
cross-sectional comparison of anthropometric parameters and laboratory-based
techniques such as hydrodensitometry,125 increasing the assumptions made. Because
these equations are population speciic, only equations derived from individuals
with similarities in age, gender, body composition, and activity levels should be considered for use. Furthermore, compatibility in technical aspects of data collection,
including anatomical landmarking and anthropometric equipment is also essential.
Consequently, among athletes, skinfold equations derived from athletic populations
such as that of Withers et al.126 are more likely to offer a more accurate estimate of
body composition.127 However, the ability of these equations to track changes in physique traits in response to training and/or dietary interventions has not been widely
assessed.125,128 Preliminary data suggests popular skinfold-based models, including
those derived from athletes, lack the sensitivity to track small but potentially important changes in body composition.129,130 As such, it seems unreasonable to introduce
further error by transforming raw skinfold data into estimates of fat mass or percentage body fat. Thus, despite the advancement in physique assessment techniques and
the notable desire of many athletes wishing to know their “body fat percentage,”
the conclusions of Johnston131 remain true to this date: Practitioners are better off
continuing to using raw anthropometric data than attempting to make estimates of
whole-body composition from available equations.
Although the sum of skinfolds is highly correlated with body fat percentage, FFM
correlates poorly with skinfolds.132 It has been proposed that combining skinfolds
with certain body circumferences leads to a better estimate of FFM.133 In theory,
skinfold-corrected circumferences offer a more direct assessment of muscle mass,
assuming that the skinfold thickness accurately partitions fat and lean components
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Physique Assessment of Athletes
at a speciic site.134 However, the skinfold-corrected girth estimates have been shown
to be less accurate in monitoring changes in muscle mass than predictions using
skinfolds alone.125,135 This imprecision may be explained, at least in part, by the fact
that muscle hypertrophy does not occur uniformly throughout each body region,136
yet the anthropometric fractionation estimate of muscle mass places equal weighting
on each of ive girth measurements.137
A novel approach of assessing lean mass changes in elite athletes using a simple
ield test of basic anthropometric measures has recently been proposed.138 The Lean
Mass Index (LMI) is an empirical measure that tracks within-subject proportional
changes in body mass adjusted for changes in skinfold thickness. As such, the LMI
tracks changes in body mass not associated with changes in skinfolds. Preliminary
data indicates the LMI tracks changes in FFM as well as other more time-consuming
anthropometry-derived measures.139
Aside from the convenience of surface anthropometry for assessing physique traits
of athletes, parameters such as skinfolds are very robust, not readily inluenced by
factors such as hydration status of the athlete.140 However, an interpretation of body
composition using surface anthropometry is typically undertaken in conjunction
with a measure of body mass (Table 3.3), and body mass can be acutely inluenced by
an array of factors, independent of changes in FM or skeletal muscle mass. As such,
body-mass measurements should be made at the same time of day (preferably before
breakfast or training but after voiding the bladder and bowel) and wearing minimal
clothing,141 so as to minimize the inluence of factors other than body composition
that can impact on body mass. Other issues to consider include consistency in scales
used,142 menstrual cycle phase in females,143 and hydration status.
Precise assessment of anthropometric traits—in particular, skinfold thickness—
can be dificult and therefore extreme care in site location and measurement is
required if meaningful results are to be obtained. Prior to assessment, the tester
should develop the appropriate technique, reducing the level of error in repeated measurements, and thus enhancing the ability to detect small but potentially important
TABLE 3.3
Interpretation of Changes in Physique Traits Based on Skinfold and Body
Mass Data
Anthropometric Trait
Interpretation—Physique Trait
Body Mass
Skinfolds
Muscle Mass
Body Fat
Increase
Decrease
Stable
Stable
Increase
Increase
Decrease
Decrease
Stable
Stable
Increase
Decrease
Increase
Decrease
Increase
Decrease
Gain
Loss
Loss
Gain
Potential Gain
Gain
Loss
Potential Loss
No change
No change
Gain
Loss
Gain
Loss
Gain
Loss
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changes. The standard skinfold assessment protocol of the International Society for
the Advancement of Kinanthropometry (ISAK)144 follows:
• The right side of the body is used for unilateral measurements, irrespective
of the preferred side of the subject, unless impractical to use due to injury
or similar cause.
• Prior to measurement, ensure the skinfold caliper is accurately measuring the distance between the centers of its contact faces by using the short
blades of an engineer’s vernier caliper.
• The skinfold site should be carefully located using the correct anatomical landmarks.
• The skinfold is picked up at the marked site. The near edge of the thumb
and index inger are in line with the marked site. The back of the hand
should be facing the measurer. It should be grasped and lifted so that a
double fold of skin plus the underlying subcutaneous adipose tissue is held
between the thumb and index inger of the left hand. The size of the fold
to pick up should be the minimum necessary to ensure that the two skin
surfaces of the fold are parallel.
• The nearest edge of the contact faces of the caliper is applied 1 cm away
from the edge of the thumb and inger. As a guide, the center of the caliper
faces should be placed at a depth of approximately mid-ingernail.
• The caliper is held at 90° to the surface of the skinfold site at all times. The
hand grasping the skin remains holding the fold the whole time the caliper
is in contact with the skin.
• Measurement is recorded two seconds after the full pressure of the caliper
is applied.
• Skinfold sites should be measured in succession, reducing the effects of
skinfold compressibility and measurer bias.
• Duplicate or triplicate measurements should be taken where possible.
Professionals wishing to monitor the physique traits of athletes using surface
anthropometry are strongly encouraged to undertake professional training. ISAK
regularly offers surface anthropometry training courses internationally across a
range of techniques including skinfolds, girths, breadths, and lengths. These courses
are promoted on the oficial ISAK Web site (www.isakonline.com/).
3.8
SPECIFIED LANDMARKS FOR THE
ASSESSMENT OF SKINFOLDS*
In recognition of the need for standardized methods in the assessment of skinfolds
and other surface anthropometry techniques, ISAK has established clearly deined
landmarks from which skinfold sites are identiied. The deinition of these landmarks
*
From Marfell-Jones, M., Olds, T., Stewart, A., and Carter, J.E.L., International Standards for
Anthropometric Assessment, © 2007. Used with permission of the International Society for the
Advancement of Kinanthropometry.
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and associated images to assist in their identiication follow with the permission of
ISAK. Technical issues such as subject positioning for each skinfold measurement
are also addressed.
INTERNATIONAL SOCIETY FOR THE ADVANCEMENT OF KINANTHROPOMETRY
SPECIFIED LANDMARKS FOR THE ASSESSMENT OF SKINFOLDS
Acromiale
Deinition: The point on the superior aspect of the most lateral part of the
acromion border.
Subject position: The subject assumes a relaxed position with the arm hanging
by the side. The shoulder girdle should be in a midposition.
Location: Standing behind and on the right-hand side of the subject, palpate
along the spine of the scapula to the corner of the acromion. This represents
the start of the lateral border, which usually runs anteriorly, slightly superiorly, and medially. Apply the straight edge of a pencil to the lateral and
superior margin of the acromion to conirm the location of the most lateral
part of the border. Mark this most lateral aspect. The acromion has an associated bone thickness. Palpate superiorly to the top margin of the acromion
border in line with the most lateral aspect.
FIGURE 3.1 Acromiale landmark. (From Marfell-Jones, M., Olds, T., Stewart, A., and
Carter, J.E.L., International Standards for Anthropometric Assessment, © 2007. Used with
permission of the International Society for the Advancement of Kinanthropometry.)
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FIGURE 3.2 Radiale landmark. (From Marfell-Jones, M., Olds, T., Stewart, A., and Carter,
J.E.L., International Standards for Anthropometric Assessment, © 2007. Used with permission of the International Society for the Advancement of Kinanthropometry.)
Radiale
Deinition: The point at the proximal and lateral border of the head of the radius.
Subject position: The subject assumes a relaxed position with the arm hanging
by the side and the hand in the midprone position.
Location: Palpate downward into the lateral dimple of the right elbow. It should
be possible to feel the space between the capitulum of the humerus and the
head of the radius. Then move the thumb distally onto the most lateral part
of the proximal radial head. Correct location can be checked by slight rotation of the forearm, which causes the head of the radius to rotate.
Mid-Acromiale–Radiale
Deinition: The midpoint of the straight line joining the acromiale and the
radiale.
Subject position: The subject assumes a relaxed position with the arms hanging by the sides.
Location: Measure the linear distance between the acromiale and radiale
landmarks with the arm relaxed and extended by the side. The best way to
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FIGURE 3.3 Mid-acromiale–radiale landmark. The other marks are the acromiale and
radiale sites. (From Marfell-Jones, M., Olds, T., Stewart, A., and Carter, J.E.L., International
Standards for Anthropometric Assessment, © 2007. Used with permission of the International
Society for the Advancement of Kinanthropometry.)
measure this is with a segmometer or large sliding caliper. It is not acceptable to follow the curvature of the surface of the arm. If a tape must be used,
be sure to hold it so that the perpendicular distance between the two landmarks is measured. Place a small mark at the level of the midpoint between
these two landmarks. Project this mark around to the posterior and anterior
surfaces of the arm as a horizontal line. This is required for locating the
triceps and biceps skinfold sites.
Triceps Skinfold Site
Deinition: The point on the posterior surface of the arm, in the midline, at the
level of the marked mid-acromiale–radiale landmark.
Subject position: The subject assumes a relaxed standing position with the arm
hanging by the side and the hand in the midprone position.
Location: This point is located by projecting the mid-acromiale–radiale site
perpendicularly to the long axis of the arm around to the back of the arm
and intersecting the projected line with a vertical line in the middle of the
arm when viewed from behind.
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FIGURE 3.4 Triceps skinfold site. The horizontal line to the right is the marked midacromiale–radiale site. (From Marfell-Jones, M., Olds, T., Stewart, A., and Carter, J.E.L.,
International Standards for Anthropometric Assessment, © 2007. Used with permission of
the International Society for the Advancement of Kinanthropometry.)
Biceps Skinfold Site
Deinition: The point on the anterior surface of the arm in the midline at the
level of the mid-acromiale–radiale landmark.
Subject position: The subject assumes a relaxed standing position with the arm
hanging by the side and the hand in the midprone position.
Location: This point can be located by projecting the mid-acromiale–radiale
site perpendicularly to the long axis of the arm around to the front of the
arm and intersecting the projected line with a vertical line in the middle of
the arm when viewed from the front.
Subscapulare
Deinition: The undermost tip of the inferior angle of the scapula.
Subject position: The subject assumes a relaxed standing position with the
arms hanging by the sides.
Location: Palpate the inferior angle of the scapula with the left thumb. If
there is dificulty locating the inferior angle of the scapula, have the subject
slowly reach behind the back with the right arm. The inferior angle of the
scapula should then be felt continuously as the hand is again placed by the
side of the body. A inal check of this landmark should be made with the
hand by the side in the relaxed position.
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FIGURE 3.5 Biceps skinfold site. Note the marked mid-acromiale–radiale site to the left.
(From Marfell-Jones, M., Olds, T., Stewart, A., and Carter, J.E.L., International Standards
for Anthropometric Assessment, © 2007. Used with permission of the International Society
for the Advancement of Kinanthropometry.)
FIGURE 3.6 Subscapulare landmark. (From Marfell-Jones, M., Olds, T., Stewart, A., and
Carter, J.E.L., International Standards for Anthropometric Assessment, © 2007. Used with
permission of the International Society for the Advancement of Kinanthropometry.)
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FIGURE 3.7 Subscapular skinfold site. The line (–) to the left and above is the marked subscapulare site. (From Marfell-Jones, M., Olds, T., Stewart, A., and Carter, J.E.L., International
Standards for Anthropometric Assessment, © 2007. Used with permission of the International
Society for the Advancement of Kinanthropometry.)
Subscapular Skinfold Site
Deinition: The site 2 cm along a line running laterally and obliquely downward from the subscapulare landmark at a 45° angle.
Subject position: The subject assumes a relaxed standing position with the
arms hanging by the sides.
Location: Use a tape measure to locate the point 2 cm from the subscapulare
in a line 45° laterally downward.
Iliocristale
Deinition: The point on the iliac crest where a line drawn from the midaxilla (middle of the armpit), on the longitudinal axis of the body, meets
the ilium.
Subject position: The subject assumes a relaxed position with the left arm
hanging by the side and the right arm folded across the chest.
Location: Use your left hand to stabilize the body by providing resistance
on the left side of the pelvis. Find the general location of the top of the
iliac crest with the palm or the ingers of the right hand. Once the general
position has been located, ind the speciic edge of the crest by horizontal
palpation with the tips of the ingers. Once identiied, draw a horizontal line
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FIGURE 3.8 Iliocristale landmark. (From Marfell-Jones, M., Olds, T., Stewart, A., and
Carter, J.E.L., International Standards for Anthropometric Assessment, © 2007. Used with
permission of the International Society for the Advancement of Kinanthropometry.)
at the level of the iliac crest. Draw an imaginary line from the mid-axilla
down the midline of the body. The landmark is at the intersection of the
two lines.
Iliac Crest Skinfold Site
Deinition: The site at the center of the skinfold raised immediately above the
marked iliocristale.
Subject position: The subject assumes a relaxed position with the right arm
folded across the chest.
Location: This skinfold is raised superior to the iliocristale. To do this, place
the left thumb tip on the marked iliocristale site and raise the skinfold
between the thumb and index inger of the left hand. Once the skinfold has
been raised, mark its center with a cross (+). The fold runs slightly downwards anteriorly as determined by the natural fold of the skin.
Iliospinale
Deinition: The most inferior or undermost part of the tip of the anterior superior iliac spine.
Subject position: The subject assumes a relaxed position with the right arm
folded across the chest.
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FIGURE 3.9 Iliac crest skinfold site. The lower line (–) is the marked iliocristale site.
(From Marfell-Jones, M., Olds, T., Stewart, A., and Carter, J.E.L., International Standards
for Anthropometric Assessment, © 2007. Used with permission of the International Society
for the Advancement of Kinanthropometry.)
FIGURE 3.10 Iliospinale landmark. (From Marfell-Jones, M., Olds, T., Stewart, A., and
Carter, J.E.L., International Standards for Anthropometric Assessment, © 2007. Used with
permission of the International Society for the Advancement of Kinanthropometry.)
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Location: Palpate the superior aspect of the ilium and follow it anteriorly until
the anterior superior iliac spine is reached. The landmark is marked at the
lower margin or edge where the bone can just be felt. Dificulty in appraising the landmark can be eased by the subject lifting the heel of the right foot
and rotating the femur outward. Because the sartorius muscle originates at
the iliospinale, this movement of the femur enables palpation of the muscle
and tracing to its origin.
Note: On females, the landmark is usually proportionally lower on the trunk,
due to the latter and broader shape of the female pelvis.
Supraspinale Skinfold Site
Deinition: The point at the intersection of two lines:
1. The line from the marked iliospinale to the anterior axillary border,
and
2. The horizontal line at the level of the marked iliocristale.
Subject position: The subject assumes a relaxed standing position with the
arms hanging by the sides. The right arm may be abducted after the anterior
axillary border has been identiied.
Location: Run a tape from the anterior axillary border to the marked iliospinale,
and draw a short line along the side roughly at the level of the iliocristale. Then
FIGURE 3.11 Supraspinale skinfold site. The dotted line from the marked iliospinale to the
anterior axillary border and the horizontal line at the level of the marked iliocristale is for
illustrative purposes only. (From Marfell-Jones, M., Olds, T., Stewart, A., and Carter, J.E.L.,
International Standards for Anthropometric Assessment, © 2007. Used with permission of
the International Society for the Advancement of Kinanthropometry.)
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run the tape horizontally around from the marked iliocristale to intersect the
irst line.
Abdominal Skinfold Site
Deinition: The point 5 cm horizontally to the right-hand side of the omphalion
(midpoint of the navel).
Subject position: The subject assumes a relaxed standing position with the
arms hanging by the sides.
Location: The site is identiied by a horizontal measure of 5 cm, to the subject’s right, from the omphalion. The skinfold taken at this site is a vertical
fold.
Note: The distance of 5 cm assumes an adult height of approximately 170 cm.
Where height differs markedly from this, the distance should be scaled
for height. For example, if the stature is 120 cm, the distance will be
5 × 120/170 = 3.5 cm.
Medial Calf Skinfold Site
Deinition: The point on the most medial aspect of the calf at the level of the
maximal girth.
FIGURE 3.12 Abdominal skinfold site. (From Marfell-Jones, M., Olds, T., Stewart, A., and
Carter, J.E.L., International Standards for Anthropometric Assessment, © 2007. Used with
permission of the International Society for the Advancement of Kinanthropometry.)
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FIGURE 3.13 Medial calf skinfold site. (From Marfell-Jones, M., Olds, T., Stewart, A., and
Carter, J.E.L., International Standards for Anthropometric Assessment, © 2007. Used with
permission of the International Society for the Advancement of Kinanthropometry.)
Subject position: The subject assumes a relaxed standing position with the
arms hanging by the sides. The subject’s feet should be separated with the
weight evenly distributed.
Location: The level of the maximum girth is determined by trial and error. It
is found by using the middle ingers to manipulate the position of the tape
in a series of up or down measurements. Once the maximal level is located,
the point is marked on the medial aspect of the calf with a small cross (+)
or other suitable mark.
Note: For easier viewing, the photograph shows the medial aspect of the lower
leg. However, the site is located with the subject standing.
Front Thigh Skinfold Site
Deinition: The midpoint of the linear distance between the inguinal point and
the patellare (the midpoint of the posterior, superior border of the patella).
Subject position: The subject assumes a seated position with the torso erect
and the arms hanging by the sides. The knee of the right leg should be bent
at a right angle.
Location: The measurer stands facing the right side of the seated subject on
the lateral side of the thigh. If there is dificulty locating the inguinal fold,
the subject should lex the hip to make a fold. Place a small horizontal
mark at the level of the midpoint between the two landmarks. Now draw a
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FIGURE 3.14 Front thigh skinfold site. (From Marfell-Jones, M., Olds, T., Stewart, A., and
Carter, J.E.L., International Standards for Anthropometric Assessment, © 2007. Used with
permission of the International Society for the Advancement of Kinanthropometry.)
perpendicular line to intersect the horizontal line. This perpendicular line
is located in the midline of the thigh. If a tape is used, be sure to avoid following the curvature of the surface of the skin.
INTERNATIONAL SOCIETY FOR THE ADVANCEMENT OF
KINANTHROPOMETRY SPECIFIED SKINFOLD MEASUREMENTS
Triceps
Deinition: The skinfold measurement taken parallel to the long axis of the
arm at the triceps skinfold site.
Subject position: The subject assumes a relaxed standing position with the
right arm hanging by the side and the hand in the midprone position.
Subscapular
Deinition: The skinfold measurement taken with the fold running obliquely
downward at the subscapular skinfold site.
Subject position: The subject assumes a relaxed standing position with the
arms hanging by the sides.
Method: The line of the skinfold is determined by the natural fold lines of
the skin.
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Biceps
Deinition: The skinfold measurement taken parallel to the long axis of the
arm at the biceps skinfold site.
Subject position: The subject assumes a relaxed standing position with the
right arm hanging by the side and the hand in the midprone position.
Iliac Crest
Deinition: The skinfold measurement taken near horizontally at the iliac crest
skinfold site.
Subject position: The subject assumes a relaxed standing position. The right
arm should be either abducted or placed across the trunk.
Method: The line of the skinfold generally runs slightly downward posterioranterior, as determined by the natural fold lines of the skin.
Supraspinale
Deinition: The skinfold measurement taken with the fold running obliquely
and medially downward at the supraspinale skinfold site.
Subject position: The subject assumes a relaxed standing position with the
arms hanging by the sides.
Method: The fold runs medially downward and anteriorly at about a 45° angle
as determined by the natural fold of the skin.
Abdominal
Deinition: The skinfold measurement taken vertically at the abdominal skinfold site.
Subject position: The subject assumes a relaxed standing position with the
arms hanging by the sides.
Method: It is particularly important at this site that the measurer is sure the
initial grasp is irm and broad since often the underlying musculature is
poorly developed. This may result in an underestimation of the thickness of
the subcutaneous layer of tissue. (Note: Do not place the ingers or caliper
inside the navel.)
Front Thigh
Deinition: The skinfold measurement taken parallel to the long axis of the
thigh at the front thigh skinfold site.
Subject position: The subject assumes a seated position at the front edge of
the box with the torso erect, the arms supporting the hamstrings and the
leg extended.
Method: Because of dificulties with this skinfold, two methods are recommended. Be sure to record on the pro forma the method used as A or B. In
both methods, the leg is extended, and the subject supports the hamstrings.
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Method A: The measurer stands facing the right side of the subject on the
lateral side of the thigh. The skinfold is raised at the marked site, and
the measurement taken.
Method B: Subjects with particularly tight skinfolds are asked to assist by
lifting the underside of the thigh (as in Method A). The recorder (standing on the subject’s left) assists by raising the fold, with both hands, at
about 6 cm either side of the landmark. The measurer then raises the
skinfold at the marked site and takes the measurement.
Medial Calf
Deinition: The skinfold measurement taken vertically at the medial calf skinfold site.
Subject position: The subject assumes a relaxed standing position with the
right foot placed on the box. The right knee is bent at about 90°.
Method: The subject’s right foot is placed on a box with the calf relaxed. The
fold is parallel to the long axis of the leg.
3.9
ULTRASOUND
Ultrasound has been used as an alternative, noninvasive method to surface anthropometry to measure subcutaneous adipose tissue (SAT). Use of ultrasound for measurement of subcutaneous fat was proposed to overcome some of the drawbacks of
subcutaneous skinfolds, particularly error associated with the compressibility and
elasticity of skinfolds,145 accurate measurement in the obese,146 and measurement of
SAT at sites that are dificult for skinfold callipers.147 Ultrasound is capable of measuring subcutaneous fat to a depth of approximately 100 mm or more and emerged
as a body-composition tool in the late 1960s. Although initial research was promising with respect to precision and accuracy compared to skinfolds, over the years
this application has not kept pace with the developments in ultrasound technology.
The recent availability of higher resolution, portable, and more affordable ultrasound
equipment has created renewed interest in this technology for body-composition
assessment in ield settings.
Ultrasound uses high-frequency sound waves introduced to the skin by means of
a probe applied to the skin surface together with ultrasound gel. The sound waves
are relected back to the probe mainly from the deep fascia tissue where they are
converted into an electrical signal. Ultrasound constructs cross-sectional images
from relected sound waves and can measure thicknesses of subcutaneous adipose
tissue and muscle, muscle cross-sectional area, and abdominal depth. Images can be
“frozen” to allow application of electronic calipers to measure areas or depths to the
nearest 1 mm. Ultrasound measurement of subcutaneous adipose tissue avoids the
error associated with skinfold compression from external caliper use. Measures can
also be made in obese subjects where caliper application can be dificult.148
Research using ultrasound for measurement of intra-abdominal adipose tissue
in overweight subjects has reported a strong correlation (r = 0.08) between ultrasound and computed tomography (CT).149 Fanelli et al.150 also reported a signiicant
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correlation (r = –0.58 to –0.70) between body density determined by hydrodensitometry and subcutaneous adipose tissue via ultrasound. A recent study in wrestlers151
demonstrated similar estimates of FFM when subjects were measured by ultrasound
and hydrodensitometry. Another study in a mixed athlete population reported strong
correlations for both women (r = 0.97) and men (r = 0.98) when body fat estimates
measured by ultrasound were compared with DXA.152 Ultrasound may also be useful
for tracking changes in muscle atrophy or restitution as a result of injury or training.153 Despite these recent promising results, limited validation work on ultrasound
renders this method as predominantly a research tool at this stage, but with further
validation this approach may be an alternative to skinfold anthropometry for measurement of subcutaneous adipose tissue and estimation of FFM.
Recent development of more affordable, portable ultrasound devices that require
minimal technical expertise and produce automated, instantaneous results on body
composition have opened up this approach to ield-based athlete assessment.152 The
method is safe and not associated with any health risks. Although more studies are
beginning to appear in the literature, additional validation work is clearly needed. It
remains to be seen if this method will in the long term be more cost effective, practical, and useful than existing skinfold anthropometry.
3.10
THREE- AND FOUR-COMPARTMENT MODELS
A number of well-accepted two-compartment (FM and FFM), body-composition
assessment models are potentially available to monitor body composition, including hydrodensitometry, air displacement plethysmography, and deuterium dilution.
These methods are based on the premise that the body can be separated into two
chemically distinct compartments—that is, FM and FFM.29 However, each of these
methods carries with it some degree of error, most of which lie not in the technical
accuracy of the measurements but in the biological variability of the assumptions
associated with each technique in the generation of body-composition data from raw
measures like body density and total body water. This is especially the case for FFM
estimates. The combination of data from several of these two-compartment models
into a multicompartment model reduces the number of assumptions made and is now
recognized as the current “gold standard” in body-composition assessment.
A commonly used three-compartment model approach adjusts the body density
obtained from hydrodensitometry or air displacement plethysmography154 for FFM
hydration or total body water using isotope dilution, rather than assume a FFM totalbody water content of 73.72%.22 Variation in FFM hydration away from the assumed
constant, as occurs in states of hypohydration and hyperhydration respectively,
increase and decrease FFM density with associated under- and overestimation of
percentage body fat via hydrodensitometry by as much as 10%.32 Furthermore, measurement of FFM hydration is particularly relevant given that it has by far the lowest
density of any of FFM component yet occupies the largest percentage of the FFM.
The introduction of DXA has afforded the creation of a four-compartment model,
controlling for biological variability in both total body water and bone mineral content.
While this model is theoretically more valid than the three-compartment model because
it controls for biological variability in both bone mineral content and total body water,
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work by Withers and associates30 indicates the additional control for interindividual
variation in bone mineral mass achieves little extra accuracy, at least in young, untrained
and trained males and females. This supports the original work of Siri,24 which indicates that the largest source of measurement error is related to FFM hydration.
While this multicompartment approach to body-composition assessment can be
time consuming and expensive, it is now widely recognized as the gold standard in
body-composition assessment, and thus is recommended when undertaking research
where changes in body composition are a key outcome measure. It should also be the
criterion against which other body-composition assessment techniques are validated.
3.11
3.11.1
NEW TECHNOLOGIES
COMPUTED TOMOGRAPHY
CT is a radiological technique irst used for brain imaging in the early 1970s155 and has
been used since around 1979 for the study of body composition.156 CT scanners provide high-resolution cross-sectional images through any region of the body. Clear anatomical boundaries can be delineated between adipose tissue, skeletal muscle, visceral
organs, brain, and bone. Recognition of the value of CT for measurement of regional
adipose tissue followed after the work of Borkan et al.,157 which reported on age-related
differences in adipose tissue distribution. Two other groups subsequently reported on
different approaches to measurement of whole body and regional adipose tissue measurement.158,159 The link between obesity-related comorbidity and visceral adipose tissue160 has driven increased use of CT for measurement of body composition.
CT images for body composition are built up of pixels that have a CT or HU
(Hounsield unit) number. The CT number is a measure of attenuation relative to water
(HU = 0) and air (HU= –1000). CT uses the different attenuation characteristics of
tissues (based on different chemical composition and density) to determine composition. Generally, when measuring the fat content of skeletal muscle, the lower the HU
value, the lower the density and the greater proportion of fat.161 Speciic information
relating to the more radiographic, technical aspects of CT are beyond the scope of
this chapter but those interested would ind the following references useful.156,162,163
Rössner et al. completed one of the earlier CT validation studies for adipose tissue
cross-sectional area via comparison with cadavers.164 High correlation coeficients
were found between CT and planimetry for both total (r = 0.94) and intra-abdominal (r = 0.83) adipose tissue area. A number of subsequent studies in humans and
animals, including comparison using chemical extraction of fat,165 support that CT
is accurate and precise and that repeatability is high.166 In non-athlete populations,
selected CT scan volumes of adipose tissue have been highly correlated with total
FM in men and women.167–169 CT is often used as a reference technique for validation
of other body-composition approaches.161 Technological advances since these studies
were undertaken have improved the resolution of images and extended the measurement to vascular and bone tissue.156
A major impediment to the use of CT for body-composition measurement is radiation exposure (abdominal CT results in an effective dose in the order of 10 mSv but
depends on the scanner and may range from 3 to 14 mSv),170 and this limits its use for
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whole-body or longitudinal studies in humans.156 Use for nonclinical purposes such
as body-composition monitoring in healthy athletes, children, adolescents, and childbearing (or pregnant) women is also contraindicated, and this would still be the case
even with the availability of newer low-dose approaches available in some laboratories.171 The more common need to assess whole-body composition, radiation exposure, and signiicant cost of CT renders this a method that only has application for
speciic regional body-composition research. The introduction of magnetic resonance
imaging (MRI), which eliminates exposure to radiation, is now more typically used
in athletes, although again the cost and relatively limited availability of this method
means it also is predominantly a research tool for body-composition assessment.
3.11.2
MAGNETIC RESONANCE
Measurement of body composition by MRI requires the subject to be placed inside an
imaging device that then creates a magnetic ield approximately 10,000 times stronger than the outside or natural earth force.161 Proton MRI, most commonly used for
clinical and body-composition analysis, is based on the interaction between the nuclei
of hydrogen atoms, which are proliic in all biological tissues. Protons or hydrogen
nuclei behave like small magnets and when exposed to the imaging device, the protons align with the created magnetic ield. A pulsed radiofrequency ield (RF) can be
applied to the subject within the magnet and this causes many of the protons to either
lip or absorb energy. When the RF is removed, the protons gradually release the
absorbed energy and generate a speciic RF signal that can be used to create images
on a computer. Different tissues such as muscle, fat, and bone have differential proton
density and release absorbed energy at different rates. The RF pulse parameters can
be manipulated to exploit the difference in proton density and energy release times
between tissues such as fat and muscle to create high-quality images.161
Application of MRI for body composition was irst done by Foster et al.172 and
Hayes et al.173 who quantiied subcutaneous adipose tissue using MRI. Many studies
since have used MRI to assess skeletal and adipose tissue area and distribution in
clinical and normal populations.174 Many of these studies have used a single crosssectional image but unlike CT, multiple images can be collected using MRI without the health risk of increased radiation dose associated with CT. Technological
improvement has signiicantly reduced the time taken to capture images, and it is
now possible to obtain whole-body MRI data in approximately 30 min.161
Rapid advances in technology have also extended the application of this methodology beyond measurement of body fat and lean tissue. Functional MRI can be
used to track the metabolic activity of organs and tissues and this, in addition to
body-composition measurements, can be used to more deeply explore the underpinning mechanisms associated with disease, especially obesity-related comorbidities.
Diffusion tensor imaging can be used for assessing muscle iber type and proton
(1H-MRS) and phosphorus (31P-MRS) spectroscopy for water-fat imaging. Sodium
MRI and whole-body nuclear MRI systems are also available to quantify total body
lipid and water.156,163 To date, only one validation study exists for nuclear quantitative magnetic resonance (QMR) via comparison to a four-compartment model. This
methodology uses the differences in resonance of organic and inorganic hydrogen
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to fractionate signals from fat, lean tissue, and water. QMR underestimated fat
and overestimated lean mass, and this error increased with increasing adiposity.175
However, the method is simple and rapid and can be completed in less than 3 min,
and further validation work will hopefully bring better understanding and reinement of its accuracy and precision.163
Imaging methods such as MRI and CT are considered to be among the most accurate for in vivo measurement of body composition. High correlation between MRI
and CT for abdominal subcutaneous adipose tissue (0.79), visceral adipose tissue
(0.79), and total adipose tissue (0.99) are observed176 and coeficient of variation is
low (~1.5) for whole body177 and for total abdominal adipose tissue (3%).161,178
As there is no exposure to radiation, it is feasible that MRI has application for
longitudinal monitoring of athletes that can be extended to children and adolescents.
The major limitation with this technology is the size of the person that can be measured (as with CT, persons with a BMI > 40 kg.m–2 do not it inside the scanner),
high cost, and limited availability of scanner time, which is typically heavily saturated with a clinical diagnostic load. Scanning is also contraindicated for individuals
who are claustrophobic or have metal plates, pins, or pacemakers inserted. In athlete
groups, the main contraindication is claustrophobia, large body mass (for example,
U.S. football players) or stature, and existence of internal metal plates or pins. MRI
therefore remains a research-only method for body-composition analysis.163
3.11.3
THREE-DIMENSIONAL PHOTONIC SCANNING
Three-dimensional photonic scanning (3DPS) provides information on the threedimensional size and surface area of the body, and the approach generates data on
regional body volume and dimensions. The application was initially developed for
use in the clothing industry to capture information about body-surface topography,
but soon after it was recognized that the technology has potential application for
medical179 and sports performance ields.180 In brief, subjects being measured for
anthropometric or body-composition assessment wear tight underwear or swimwear
and adopt a standardized position during scanning. Standard anatomical landmarks
using relective markers are needed for measurement of body dimensions. The scanner projects stripes of safe white light onto the body and captures the light distortion
via use of stationery cameras over a period of seconds. The scanners can accommodate individuals up to 2.1 m in height and 1 m in depth. The cluster of photonic
data points are used to reconstruct skin topography using computer algorithms.180–182
The data can be used to calculate total and regional body volumes and surface area,
and can automatically calculate lengths and dimensions. Body volume can be used
to calculate density and body composition.
The method is still relatively new but it is time eficient, noninvasive, and suitable
for serial measurements. It has been used in a large study investigating the relationship between shape and BMI and to examine associations between gender and size
in the U.K. National Sizing Study. This study showed that BMI was signiicantly
associated with hip and bust in women, and chest and waist size in men. Validation
work on this approach for measurement of body composition is limited,179,183 but a
recent study by Wang et al.183 compared 3DPS with hydrodensitometry and tape
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measurements for the assessment of body volume, circumferences, lengths, and percentage body fat. The data generated by the scanner for body volume and lengths
was greater than UWW and tape-derived lengths, respectively, but the values for
percentage body fat were similar. Further validation work is required before the
technique could be conidently used for measurement of body composition in a variety of populations, including athletes.
The 3DPS approach is safe and can be used in children and adults with no known
contraindications. It has application in epidemiology to investigate the association
between shape and health, and within sport, there is a known association between
shape and athletic performance,180 which could be more speciically detailed by this
approach. The technology is currently expensive and not easily portable so the technique is not practical for ield use and is only used for research at this stage. However,
its safety and the potential for individuals to use this more widely in the community
for sizing applications may help this technology to rapidly develop and proliferate,
making measurement more available and affordable for athlete monitoring in the
not-too-distant future. The world’s irst anthropometric survey using 3D scanning
took place at the 2007 Australian Rowing Championships.184
3.12
PRACTICAL RECOMMENDATIONS
A wide range of tools are available to assess the physique traits of athletes. Aside
from talent identiication initiatives and the identiication of a preferred physique
for a given sport and player position, the primary focus is given to the longitudinal
monitoring of physique traits. As such, techniques that are cost and time effective,
portable, reliable, and safe and provide insight into all physique traits, including both
fat and muscle mass, are a priority. Given this, surface anthropometry remains an
effective tool within athletic populations, but it demands highly skilled technicians
if reliable data are to be collected. Recognized training through organizations like
ISAK is strongly recommended for anyone wishing to make use of surface anthropometry to monitor physique traits of athletes. Within Australia, the routine monitoring of body composition among athletes across regional and national institutes of
sport remains with the measurement of skinfolds (± girths) at several anatomically
identiied sites on the body (see Section 3.8, Speciied Landmarks for the Assessment
of Skinfolds).
Irrespective of the test chosen, all physique assessment tools carry with them
some degree of assumptions and measurement error. Having an appreciation of this
measurement error helps to distinguish between measurement error and real changes
in body composition, that is, documented change in physique traits being greater
than reported measurement error. Issues associated with equipment contributing to
measurement error are often beyond the control of technicians, but athlete presentation can also contribute to the error of repeat assessments. As such, factors such
as time of day, hydration status, and gastrointestinal tract contents should be standardized wherever possible; fasted early morning assessments may be the most reliable where practical. Minimizing the error or noise associated with a test enhances
its reliability, making it easier to identify small but potentially important changes.
Reliability of measurement also inluences the frequency of assessment. In general,
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Nutritional Assessment of Athletes, Second Edition
physique assessments should not be undertaken any more regularly than every 4–8
weeks, depending on the individual athlete and his or her body-composition goals.
When collecting data, the physical and emotional well-being of the athlete
should remain a priority. Sensitivity should be shown to cultural beliefs and tradition. Procedures should be explained to those unfamiliar with the testing, with
information provided in advance on what testing is to be undertaken, the reason for
proiling, what measurements are to be taken, and any speciic requirements such
as clothing to be worn. Where appropriate, consideration should be given to gender
comparability between the technician and athlete, with privacy in data collection
and reporting always ensured. With this in mind, consideration should be given to
the establishment of electronic databases that not only provide a secure means of
data collection but also automate reports that provide invaluable historical data as
well as interpretation of existing results against previous assessments. Finally, where
resources permit, the collection of data in duplicate should be considered, enhancing
the reliability of measurement.
3.13
FUTURE RESEARCH NEEDS
Although surface anthropometry does not offer a direct measure of total fat mass or
FFM, its robustness in the ield, convenience, and low cost ensures it remains a popular method of body-composition monitoring among athletes. Newer technologies
like DXA or the combination of technologies in a three- or four-compartment model
offer an opportunity to better interpret surface anthropometry data. Preferably, this
should be developed around interpretation of changes in physique traits over time
rather than a one-off assessment. Such longitudinal investigations also create opportunities to help better understand the association between physique traits and competitive success.
Aligned with this, developing a better understanding of factors inluencing the
noise or error associated with body-composition assessment tools will enable the
development of protocols that afford a much greater resolution of measurement.
Ultimately, this will help to create techniques and protocols that are able to detect
small but potentially meaningful changes in body composition. Once established,
this will also create an opportunity to have better resolution for assessing interventions (such as dietary, training) or unforeseen situations (injury, illness, or detraining,
for example) proposed to inluence body composition, which ultimately will have
application within not only the sports environment but also the wider community.
Our understanding of the application of newer technologies like ultrasound and
3DPS are preliminary. Further exploration of tools such as these will hopefully better our understanding of how these tools can be used into the future.
3.14
CONCLUSIONS
Body composition is just one of an array of “itness traits” that may contribute to the
overall success of an athlete. As such, the association between physique traits and
competitive success should not be overemphasized. However, the regular monitoring
of body composition among athletic populations can offer insight into adaptations
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to training and/or dietary interventions as well as optimization of physique traits for
speciic sports and playing positions. An array of tools is available for the measurement of body composition, the test of choice being inluenced by technical issues like
safety, validity, precision, and accuracy of measurement as well as practical issues
such as availability, cost, portability, invasiveness, time effectiveness, and technical
expertise necessary to conduct the assessment. Among athletic populations, consideration must also be given to the unique physique traits these individuals may possess, including particularly tall, broad, and muscular individuals as well as those with
very low body-fat levels. Considering these factors, the routine monitoring of body
composition of athletes remains with the use of surface anthropometry, although
BIA, DXA, and the BOD POD are becoming more popular as their accessibility
increases. Reinement of protocols such as the standardization of how subjects present for assessment and an improved awareness of the limitations of each technique
will allow more informed protocols to be developed. This will offer greater insight
into acute and longitudinal monitoring of body-composition changes and their importance to competitive success, as well as tailoring interventions that can assist in the
appropriate manipulation of body composition. Despite the array of tools available to
assess body composition, surface anthropometry remains the most practical tool at
present to monitor the body composition of athletes longitudinally. However, given
the ever-increasing interest in the relationship between body composition and competitive sporting success, new, more reined assessment tools with greater reliability
and resolution of measurement are likely to emerge into the future.
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© 2011 by Taylor and Francis Group, LLC
Composition and
4 Body
Gender Differences
in Performance
Peter R.J. Reaburn, Ben J. Dascombe,
and Xanne Janse de Jonge
CONTENTS
4.1
4.2
Introduction .................................................................................................. 121
Gender and Strength ..................................................................................... 123
4.2.1 Gender Differences in Strength Performance .................................. 123
4.2.2 Factors Inluencing Strength Performance ...................................... 123
4.2.2.1 Muscle Characteristics ....................................................... 123
4.2.2.2 Neural Activation ............................................................... 125
4.2.2.3 Hormonal Factors .............................................................. 126
4.2.2.4 Menstrual Cycle ................................................................. 127
4.3 Gender and Anaerobic Performance ............................................................ 127
4.3.1 Gender Differences in Anaerobic Performance ............................... 127
4.3.2 Factors Inluencing Anaerobic Performance .................................... 130
4.3.2.1 Muscle Mass ...................................................................... 130
4.3.2.2 Bioenergetics and Energy Metabolism .............................. 131
4.4 Gender and Endurance Performance ............................................................ 133
4.4.1 Gender Differences in Endurance Performance ............................... 133
4.4.2 Factors Inluencing Endurance Development ................................... 133
4.4.2.1 VO2max ................................................................................ 134
4.4.2.2 Lactate Threshold .............................................................. 137
4.4.2.3 Economy ............................................................................ 138
4.4.2.4 Muscle Mass ...................................................................... 138
4.4.2.5 Blood Volume .................................................................... 139
4.4.2.6 The Role of Estrogen ......................................................... 139
4.5 Summary and Conclusion............................................................................. 139
References .............................................................................................................. 139
4.1
INTRODUCTION
As more and more women started participating in sports over the past 50 years, they
embarked on a “catch-up” race for the world records. World records improved at a
121
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faster rate for females than for males from the 1950s until the late 1980s.1 However,
since the 1990s a stable gap has been observed between male and female elite performances, though it is evident that men typically possess greater levels of strength
and power, and have larger anaerobic and aerobic capacities.2,3
The relatively small number of gender-speciic research studies makes it dificult
to elicit the physiological mechanisms responsible for these performance differences
between genders. The responsible mechanisms are probably related to speciic gender differences such as body composition,3,4 muscle characteristics, 4–7 and hormonal
inluences.2,8–10 It seems likely that much of the reluctance to include females as
subjects in research studies is related to the need to control for hormonal luctuations
due to the menstrual cycles or oral contraceptives. Over the past 10 years, exercise
physiology research on gender differences has increased, but many areas require
further clariication.
Both the body size and body composition are similar in boys and girls during
early childhood. During late childhood, girls begin to accumulate more fat than
boys, while during early adolescence, boys start to develop their fat-free mass at a
higher rate than girls.11 These body-composition differences between the genders
are primarily determined by signiicant hormonal changes that occur during development. Before puberty, small amounts of the gonadotrophic hormones—folliclestimulating hormone (FSH) and luteinizing hormone (LH)—stimulate the growth
of ovaries in girls and testes in boys. However, at puberty, the increased release of
these same hormones from the anterior pituitary gland leads to signiicant increases
in ovary size and estrogen secretion in females and testes size and testosterone secretion in males.12 In females, this increased estrogen secretion leads to a broadening of
the hips, an increased rate of bone growth, and increased fat deposition, especially
in the hip and thigh regions.13 On the other hand, males tend to possess an increased
testosterone production, leading to advanced development of the musculoskeletal
and cardiovascular systems.11
Another important factor to consider is that during the reproductive years, when
most female athletes are competing, their bodies are exposed to rhythmical luctuations in either endogenous (menstrual cycle) or exogenous (oral contraceptives)
female steroid hormones. These variations in estrogen and progesterone not only
have effects on the reproductive system but also cause physiological changes outside
the reproductive system. Receptors for estrogen have been found in multiple tissues,
including the brain, cardiovascular system, kidney, muscle, and many others.14,15
How the secondary effects of estrogen and progesterone, and their interaction, affect
exercise performance in females has recently started to receive more attention in
research. However, this topic is complex and not well understood, thus warranting
further investigation.
This chapter addresses the three main areas of exercise performance—muscle
strength, anaerobic performance, and aerobic performance—in relation to gender and body composition differences. Each section addresses both differences in
body composition and potential effects of male and female steroid hormones on
performance.
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Body Composition and Gender Differences in Performance
4.2
4.2.1
123
GENDER AND STRENGTH
GENDER DIFFERENCES IN STRENGTH PERFORMANCE
Muscle strength is the ability of a muscle to develop maximal contractile force and
is an important factor for performance in most sports. It is widely known that males
possess larger absolute muscle strength than females. In a study with a large number of young men and women, Leyk and others16 reported a difference of approximately 200 N in absolute maximal handgrip strength (540.8 ± 87.1 N for men and
329.4 ± 57.7 N for women). For the lower body, Clark et al.17 reported a similar difference between genders for knee extension (905.0 ± 33.5 N for men and 722.1 ± 33.5
N for women). Further examples of the difference in muscle strength between males
and females are shown in Table 4.1.
A strong relationship between muscle strength and muscle mass has been widely
demonstrated.16,18,19 The different steroid hormone proiles in males and females
result in considerable differences in body composition. The average adult male has a
greater muscle mass than the average female,4 while the average female has a higher
fat percentage than the average male.3,7,20,21 These indings lead to the suggestion that
the strength difference between males and females is largely a result of the difference in muscle mass.
Some studies have demonstrated that this gender difference in muscle strength
disappears when strength is adjusted for lean body mass.22,23 Others, however, have
reported that the difference is reduced when expressed per lean body mass but that
it does not disappear.16,18,19 It also seems that this gender difference in strength may
be dependent on muscle location, as the relative strength of the upper body muscles
remains larger than for the lower body.16 Miller and colleagues19 suggested that this
may be attributed to the lower portion of women’s lean body mass being located in
the upper body.
It is clear that muscle mass plays an important role in explaining the strength
difference between genders. Other factors that may affect muscle strength are muscle architecture and neural activation.19 With regard to gender differences it is also
important to consider hormonal effects, including those of the menstrual cycle, on
muscle strength.
4.2.2
FACTORS INFLUENCING STRENGTH PERFORMANCE
4.2.2.1 Muscle Characteristics
Important aspects of muscle characteristics are the total number of muscle ibers, the
iber type distribution, and the size of the muscle ibers. Some studies have reported
a smaller number of muscle ibers in females than males,24,25 while most have shown
no difference in total iber number between genders.19,26–28 Equivocal results have
been found regarding a potential difference between males and females in iber type
distribution based on the number of muscle ibers.6,7,19,29,30 These conlicting indings
are likely to be related to differences in subject sampling and methodology. Findings
of a thorough study by Staron and others7 on 55 women and 95 men demonstrate
© 2011 by Taylor and Francis Group, LLC
Age (yr)
F
M
F
M
F
M
F
M
F
M
F
M
F
M
F
M
F
M
F
M
F
M
22 ± 1
21 ± 1
21 ± 3
22 ± 5
25 ± 1a
23 ± 1a
26 ± 4
25 ± 4
24 ± 4
27 ± 4
24 ± 4
27 ± 4
24 ± 4
27 ± 4
25 ± 8
27 ± 7
25 ± 1a
23 ± 1a
21 ± 3
21 ± 2
24 ± 1a
26 ± 2a
n
533
1654
20
20
8
8
8
9
8
8
8
8
8
8
35
29
8
8
14
13
11
11
Contraction
Handgrip
Handgrip
Handgrip
Handgrip
Elbow lexion
Elbow lexion
Elbow lexion
Elbow lexion
Dorsilexion
Dorsilexion
Dorsilexion
Dorsilexion
Dorsilexion
Dorsilexion
Knee extension
Knee extension
Knee extension
Knee extension
Knee extension
Knee extension
Knee extension
Knee extension
Strength
329 ± 58 N
541 ± 87 N
354 ± 70 N
504 ± 97 N
40b Nm
70b Nm
43 ± 8 Nm
76 ± 9 Nm
18.2 ± 2.3a N
22.1 ± 2.7a N
66.8 ± 8.5a N
83.7 ± 10.7a N
138.5 ± 12.3a N
195.2 ± 16.3a N
255 ± 51 Nm
339 ± 82 Nm
180 b Nm
260 b Nm
160 b Nm
255 b Nm
722 ± 34a N
905 ± 34a N
Comments
Twitch force (electrical stimulation)
Twitch force (electrical stimulation)
10 Hz force (electrical stimulation)
10 Hz force (electrical stimulation)
50 Hz force (electrical stimulation)
50 Hz force (electrical stimulation)
CSA Quads 55.6 ± 6.9 cm2
CSA Quads 75.5 ± 10 cm2
Fa Type I 31 ± 5%, Fa Type II 69 ± 5%
Fa Type I 27 ± 3%, Fa Type II 73 ± 3%
Reference
Leyk et al., 2007
Leyk et al., 2007
Hunter et al., 2009
Hunter et al., 2009
Miller et al., 1993
Miller et al., 1993
Hunter et al., 2006
Hunter et al., 2006
Russ et al., 2003
Russ et al., 2003
Russ et al., 2003
Russ et al., 2003
Russ et al., 2003
Russ et al., 2003
Wust et al., 2008
Wust et al., 2008
Miller et al., 1993
Miller et al., 1993
Yasuda et al., 2005
Yasuda et al., 2005
Clark et al., 2005
Clark et al., 2005
Note: Data are reported as female/male pairs from the same study, ensuring similar methodology and conditions for gender comparison. Data are reported as mean values ± SD.
Fa = Fiber area.
a = Data are reported as mean value ± SE.
b = Value estimated.
© 2011 by Taylor and Francis Group, LLC
Nutritional Assessment of Athletes, Second Edition
Gender
124
TABLE 4.1
Muscle Strength for Females and Males as Reported in Gender Comparison Studies for Different Muscle Groups
Body Composition and Gender Differences in Performance
125
that there is no real difference in iber type distribution between males and females,
which is supported by Yasuda et al.31
With regards to muscle size, women generally have a smaller total muscle crosssectional area (CSA) than men when matched for training status.7,19,30,32 Staron and
others7 found a mean total CSA of approximately 16 mm2 for the vastus lateralis for
young men and approximately 11 mm2 for young women. Wust et al.32 used magnetic resonance imaging and reported a total CSA mean ± SD for the quadriceps of
75.5 ± 10 cm2 for men and 55.6 ± 6.9 cm2 for women.
Even though there may not be a gender difference is iber type distribution, the
percentage area occupied by the different iber types does appear to exhibit a gender
difference. Women typically have a smaller iber-area percentage for Type II ibers
and a larger iber-area percentage for Type I ibers.7,31 Staron et al.7 found that the
iber area percentage for Type I in the vastus lateralis was signiicantly larger for
females than males (44.0 ± 11.6 for women and 36.2 ± 11.6 for men), while for Type
IIA the percentage was signiicantly smaller for females (33.6 ± 8.7 for women and
41.2 ± 9.4 for men). They found no signiicant difference in iber area percentage for
Type IIB between genders (22.4 ± 10.3 for women and 22.6 ± 11.8 for men).7 Yasuda
and others31 reported smaller but still signiicant differences in Type I iber area percentage (31.4 ± 4.6 for women and 27.2 ± 3.3 for men) and in the combined Type II
iber area percentage (68.6 ± 4.6 for women and 72.8 ± 3.3 for men).
Type I muscle ibers have a slower contraction speed and are more fatigue resistant
than Type II ibers.33 It could therefore be suggested that the higher Type I iber-area
percentage in women may make them more suited to prolonged activity.2 Several
studies have shown that women can maintain submaximal muscle contractions longer than men.17,32,34,35 Besides iber type composition, other potential explanations
for this gender difference in muscle fatigue are neural activation and blood low.32
Hunter et al.36 used superimposed electrical stimulation to demonstrate that there
are no gender differences in voluntary activation, while Wust and colleagues32 found
the same result when eliminating any neural activation problems by using electrical
stimulation only. These indings demonstrate that the gender difference in fatigue
resistance is not related to central activation and is likely to have a peripheral cause.
During repeated contractions the rate of fatigue depends on depletion of energy
stores during contraction and recovery during relaxation. Aerobic recovery, in turn,
will depend on blood low and oxidative capacity of the muscle ibers.32 Wust et al.32
occluded blood low to investigate this further and still found a gender difference in
fatigue, indicating that blood low is not a likely explanation. Others, however, found
that the gender difference in muscle fatigue disappeared when muscle blood low
was occluded,17,37 but these studies did not use electrical stimulation to control for
neural activation. As women typically have a higher iber-area percentage for Type
I ibers than men,7,31 it seems plausible that iber type composition at least partly
explains the gender difference in muscle fatigue.
4.2.2.2 Neural Activation
Miller and colleagues19 reported that the estimated number of motor units and the
number of muscle ibers per motor unit did not differ between genders for both the
vastus lateralis and the biceps brachii. Motor unit activation, calculated from the
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Nutritional Assessment of Athletes, Second Edition
supramaximal twitch superimposed on the maximal voluntary contraction compared to the rest measure, was similar for men and women for both biceps brachii
and vastus lateralis.19 More recent studies have conirmed that there were no signiicant gender differences in voluntary muscle activation.32,36
4.2.2.3 Hormonal Factors
Testosterone has been shown to increase muscle protein synthesis (MPS)38,39 and
muscle mass increases when MPS exceeds muscle protein breakdown.40 After
puberty, testosterone concentrations in males remain approximately ten to ifteen
times larger than in females.31 It therefore is not surprising that males generally have
a larger muscle mass than females. However, research on gender differences in protein metabolism to support this theory is sparse.
Whole-body protein metabolism studies showed no gender difference in leucine rate of appearance (index of whole-body protein breakdown) and nonoxidative leucine disposal (index of MPS) at rest.21 When investigating muscle protein
balance it has been observed that rates of protein synthesis and breakdown were
greater in males than females at rest.41 However, when these rates were normalized for muscle mass, there was no difference between genders.41,42 The methodologies used in these studies combined with small subject numbers and large
between-subject variability may have caused dificulties in detection of small gender differences in muscle protein metabolism. It is evident that further research
in this area is needed, but the limited research to date suggests that basal muscle
protein balance in adults cannot explain the gender difference in muscle mass. It
could be suggested that the muscle mass difference may be largely explained by
changes during puberty or there may be gender differences in response to acute
anabolic stimulation.42
Large luctuations in muscle protein balance occur as a result of acute anabolic
stimulation, such as muscle contraction and nutrient intake. MPS immediately following resistance exercise is decreased.43–45 However, at 1 and 2 hours postexercise,
a signiicant increase in MPS is shown44 and this effect lasts for up to 48 hours.46
An increase in amino acid availability through nutrient intake during this 48 hours
post exercise stimulates a greater MPS.40,43 Research into the dose-response relationship for MPS showed that an intake of 20 g of protein intake maximally stimulated
MPS following resistance exercise.47 The best timing for postexercise nutrient intake
has been open to debate, but a minimum delay appears most beneicial for muscle
adaptations.43 It has been suggested that there is no gender difference in responses
to resistance exercise48 and nutrient intake.43 Most research, however, has been conducted on males only or did not include gender comparisons. Further research on
gender differences in muscle protein synthesis responses to exercise and nutrient
intake is required.
Testosterone clearly has a positive effect on muscle protein synthesis, but much
less is known about the effects of the ovarian hormones on protein synthesis. Most
of the available evidence is based on animal and in vitro studies and supports an
inhibiting effect of estrogen on muscle protein synthesis.49 The effect of progesterone
is inconclusive with progesterone administration in rats, showing both an increase50
and a decrease49 in muscle protein synthesis. Further research, with a focus on in
© 2011 by Taylor and Francis Group, LLC
Body Composition and Gender Differences in Performance
127
vivo studies, is needed to clarify the effect of the ovarian hormones on muscle protein synthesis.
4.2.2.4 Menstrual Cycle
Throughout ovulatory menstrual cycles, women are exposed to continuously changing female steroid hormone proiles. Miller and others51 measured muscle protein
synthesis at rest and after exercise during the menstrual cycle. This irst study of its
kind reported no difference in muscle protein synthesis between the follicular (low
estrogen and progesterone) and luteal (elevated estrogen and progesterone) phase of
the menstrual cycle.51 However, a limitation of this study is its cross-sectional design
(subjects were only tested once in either the follicular or luteal phase). It is evident
that further research in this area is also required.
The research literature is equivocal concerning the effects of the menstrual cycle
hormone luctuations on muscle strength. Several studies have reported changes
in muscle strength throughout the menstrual cycle,52–55 while others found no
change.9,10,56–59 These conlicting indings can largely be attributed to methodological
shortcomings.8 Janse de Jonge and colleagues58 addressed these limitations through
the use of superimposed electrical stimulation to ensure maximal neural activation
and use of strict hormone limits to verify menstrual cycle phase. This study found no
difference in skeletal muscle strength, fatiguability, or electrically evoked contractile characteristics between menstruation (low estrogen and progesterone), the late
follicular estrogen peak, and the luteal phase (elevated estrogen and progesterone).58
More recent studies have also conirmed that hormone luctuations throughout the
menstrual cycle do not affect muscle contractile characteristics.60,61
In conclusion, there are obvious gender differences in muscle strength with males
being stronger than females. This gender difference is clearly related to body composition, as research has shown that it is greatly reduced or even disappears when
strength is expressed relative to lean body mass. Factors that may explain the remaining difference are muscle characteristics, neural activation, and hormonal inluences.
It has been demonstrated that muscle strength does not vary across the menstrual
cycle. Most research indicates that there is no gender difference in total number of
ibers and iber type distribution. For the iber area percentage, however, it was found
that women have a larger Type I area percentage and a smaller Type II area percentage than men. It has been suggested that this difference may partly explain why
women are more fatigue resistant than men. No gender difference has been observed
in neural activation and in whole-body protein metabolism normalized for muscle
mass. Further research on muscle protein synthesis responses to exercise and nutrient intake with a focus on gender comparisons and the menstrual cycle is needed.
4.3
4.3.1
GENDER AND ANAEROBIC PERFORMANCE
GENDER DIFFERENCES IN ANAEROBIC PERFORMANCE
Anaerobic performance corresponds to the ability to produce high levels of power
during periods of very high-intensity exercise (> 100% VO2max) that typically last
anywhere between 10 and 100 seconds.62 Anaerobic energy provision occurs within
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Nutritional Assessment of Athletes, Second Edition
the cytoplasm of the muscle cell through the degradation of creatine phosphate stores
or through anaerobic glycolysis of simple carbohydrates. This, in addition to the
typically high force outputs, suggests that the limiting factors are within the working
muscles or are external factors that affect muscle size and function.
From the existing literature, it is well established through both athletic performance records and scientiic data that anaerobic performance is largely different
between genders.1,63–69 The data illustrated in Figure 4.1 demonstrate the longitudinal
differences in world records and Olympic best times between genders in anaerobic
events. Seiler et al.1 have reported that the anaerobic performance difference between
males and females reached a minimum of 10.3% between 1976–1988 and since then,
has actually increased to 11.5%. The researchers suggested that the increase from
the nadir cannot be explained due to secondary factors such as participation rates
Male
Female
(a)
8.8
8.3
Distance (m)
7.8
7.3
6.8
6.3
5.8
1901
1928
1943
1960
1965
1972
1982
1986
1992
2008
Age (yr)
Male
Female
56
(b)
54
52
Time (s)
50
48
46
44
42
40
1900 1928 1936 1948 1955 1957 1960 1969 1972 1976 1979 1982 1984 1988 1996 2000 2008
Age (yr)
FIGURE 4.1 A gender-comparison in world-record progression and Olympic winning times
in the (a) long jump; (b) 400 m track sprint.
© 2011 by Taylor and Francis Group, LLC
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Body Composition and Gender Differences in Performance
Male
Female
12
(c)
11.5
Time (s)
11
10.5
10
9.5
1932
1935
1952
1961
1968
1983
1991
1996
2004
2008
Age (yr)
Male
100
Female
(d)
90
Time (s)
80
70
60
50
40
1905
1915
1924
1933
1947
1958
1967
1973
1980
1992
2008
Age (yr)
FIGURE 4.1 (continued) A gender-comparison in world-record progression and Olympic
winning times in the (c) 100 m track sprint; and (d) 100 m freestyle swim.
or technological advances or to declines in the training practices of female athletes.
Seiler et al.1 suggests that the expansion of this difference most likely corresponded
to the introduction of a more rigid and sensitive drug testing regime within elite sport
and that the current difference may relect the “natural” physiological difference
between genders. Similarly, several scientiic studies have repeatedly reported that
male participants demonstrate higher anaerobic peak power and capacity than their
female counterparts.1,65–70 These researchers help demonstrate that the observed difference between genders in competition performance also exists in laboratory-based
tests for speciic physiological capacities. Bouchard et al.62 has suggested a range of
factors that have the capacity to inluence anaerobic performance, and these can be
broadly classiied into areas such as muscle mass and function, bioenergetics, heredity, training, and gender. However, it does appear that the strongest inluence on
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Nutritional Assessment of Athletes, Second Edition
anaerobic performance comes from muscle mass and energy metabolism in regards
to the effects of body composition and gender.
4.3.2 FACTORS INFLUENCING ANAEROBIC PERFORMANCE
4.3.2.1 Muscle Mass
A wealth of research is available that strongly demonstrates the relationship between
body size and muscle mass with anaerobic performance. A number of researchers
have presented data reporting that the observed gender difference in anaerobic power
output is completely removed when corrected for total body mass (BM) or lean body
mass (LBM).1,63–70 The anthropometrical differences in body composition between
genders are well established, with females tending to typically possess higher relative
levels of body fat (%BF) and less LBM than males.4,20,21,71 This disparity is most likely
a strong correlate to the differences observed in physiological components between
genders. From the available data it appears that a gender difference is noticeable in
anaerobic performance and capacity and that the typical difference reported in lean
muscle mass is the most likely explanatory physiological mechanism.
With respect to performance in anaerobic events, Stefani68 has demonstrated that
the difference between genders is largely due to the reported difference in lean muscle mass in a range of elite athletic competitions (running, speed skating, jumping,
swimming, and rowing). The researchers reported that the differences in estimated
power output between genders in each selected event (100%, n = 32) and individual
performances in each event (96%, n = 411) were within one standard deviation for
the LBM percentage difference. This inding suggests that the power output and
subsequent performance of male and female athletes are consistent with calculated
differences in their LBM.
While the work of Stefani68 is the only data set that has examined the mechanisms behind the gender difference during performance in anaerobic events, several
other studies have examined this difference in laboratory-based studies. These studies have typically reported that males tend to display higher absolute peak (35–72%)
and mean (~40%) power during anaerobic tasks such as the vertical jump and the
Margaria-Kalamen and Wingate test.65–67,69 Maud and Shultz65 reported that males
possessed a greater (45.6%) vertical jump height than females, though this difference decreased to 13% when corrected for total BM. No difference was observed in
this data set for vertical jump height when both genders were corrected for LBM.
Similarly, this trend was also observed across a maximal 5-s cycle sprint on a windbraked ergometer.65 These data suggest that body composition has a large impact on
performance, in particular during explosive performance tasks.
The impact of muscle mass on longer-term anaerobic power and capacity is also
demonstrated from several studies.1,63–69 A large gender difference has been reported
in peak (45–72%) and mean (48%) anaerobic power across a Wingate test. However,
this difference is substantially reduced when corrected for total BM (15–35%;
20–26%), LBM (2.5–19%; 7.5–17%), and active lower-body muscle mass (ALBMM)
(8.3%; 9.9%), respectively.65,66,69 Interestingly, large differences between genders
were reported for the absolute peak (121%) and mean (66%) power outputs across
© 2011 by Taylor and Francis Group, LLC
Body Composition and Gender Differences in Performance
131
a maximal arm cranking exercise.70 However, these gender differences were also
reduced when corrected for BM (72%; 33%), LBM (55%; 21%), and active upperbody muscle mass (AUBMM) (42%; 9%). Therefore, the data available demonstrate
that correction of anaerobic power for total BM and LBM reduces the gender difference in particular during cycling, whereas a considerably large effect still exists for
upper-body anaerobic exercise. This most likely relects the difference in body composition and development of upper-body musculature that is more typical of males.
Mayhew and Salm66 reported that absolute anaerobic power across the Wingate
test was signiicantly correlated to height, BM, LBM, %BF, and absolute leg extension strength in a large male college cohort. The same correlations were observed
with female anaerobic power, with the exception of %BF. Further, Mayhew and
Salm66 reported that in short explosive anaerobic tasks, LBM, strength, and %BF
accounted for 83% of anaerobic performance in almost all cases. Further, Murphy et
al.67 reported that differences in thigh volume, BM, and LBM explain the majority of
variation in mean (48%; 74%; 79%) and peak (53%; 71%; 76%) power. Interestingly,
Weber et al.70 demonstrated that the correlation between both peak and mean power
outputs across a Wingate test increased in strength when corrected for total BM
(r = 0.95; 0.95) and LBM (r = 0.92; 0.91) when compared to the ALBMM (r = 0.83;
0.86), respectively. Similar relationships were reported for these body-composition
indices and the power output from the upper body across a maximal arm-cranking effort. In support of this inding, Batterham and Birch63 have also reported that
anaerobic performance is independent of volume of active musculature. This observation may suggest that other factors such as neuromuscular functions as well as
differences in bioenergetics and hormonal responses may play a contributing role to
differences observed in physical performance between genders.
4.3.2.2 Bioenergetics and Energy Metabolism
Energy provision during anaerobic performance is dependent upon several key biochemical pathways that occur within the muscle. The suggestion of a gender-based
difference in anaerobic metabolism is dificult to identify, particularly as the majority of data suggests no difference in anaerobic performance when corrected for lean
muscle mass. However, a number of researchers have suggested that the anaerobic
capacity of females is between 70 and 85% of that of men.1,67,72–74
Hill and Smith73 observed a signiicant difference in the energy contribution from
aerobic and anaerobic metabolism during a 30 s Wingate test. The researchers demonstrated that women completed only 50% of the work during the 30 s test, although
when made relative to total body mass the difference between genders was reduced
to 30%. When separated into the contributions of aerobic and anaerobic work, men
produced higher absolute (34% and 55%) and relative to body mass (35% and 7%)
values than women, respectively. However, when made relative to total work, women
contributed a signiicantly higher relative percentage of aerobic work than men (25%
vs. 20%). Moreover, data from Weber and Schneider69 demonstrates that indices of
anaerobic metabolism such as the maximal accumulated oxygen deicit (MAOD)
are signiicantly different between genders (50%), even when corrected for BM
(21%), LBM (12%), and active muscle mass (17%). This suggests that other physiological factors besides body composition are responsible for changes in anaerobic
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Nutritional Assessment of Athletes, Second Edition
metabolism between genders. Weber and Schneider69 reported that this difference
was not the result of an increased ability of males to produce lactic acid or to secrete
catecholamines. It has also been demonstrated that during anaerobic performance,
neither lactate production nor sympatho-adrenergic responses are altered across the
separate menstrual cycle phases.75 Weber and Schneider69 suggested that the differences in muscle iber distribution and associated enzyme activities between genders
may be a contributing factor in this difference.
Equivocal indings have been presented in numerous data sets reporting on the
gender-speciic difference in muscle iber distribution.5–7,30,76,77 It has been reported
that women typically have smaller iber cross-sectional areas, in particular of Type
IIA and IIB/X.5,71,76,77 As such, a larger relative area of the muscle is composed
of Type II ibers in males and this may possibly alter the metabolic capacity of
the muscle.5 Although no difference appears to exist in muscle iber distribution,
the biochemical environment within the muscle appears to show some differences
between genders. Jaworowski et al.5 reported that active men possessed signiicantly higher activities in anaerobic enzymes such as phosphofructokinase (PFK)
(27.6%) and lactate dehydrogenase (LDH) (25.5%) when compared to women. This
supports past research that there is a clear difference in anaerobic enzyme activity
between men and women.6,30,77,78 These data have also reported that other anaerobic
enzymes such as pyruvate kinase, calcium-stimulated ATPase, phosphorylase, and
m-LDH are typically between 15 and 35% higher in men. As such, males tend to
have higher anaerobic capacities than females, which may support the observed differences in performance.
Interestingly, Esbjornsson et al.77 demonstrated that despite this, there was no
direct gender effect observed in muscle metabolites across a Wingate test. The subsequent changes in energy metabolites did not differ between men and women in either
Type I or II ibers following the 30 s sprint. Similarly, the Type II ibers demonstrated
no gender difference in lactate concentration or glycogen reduction following the
Wingate test. However, females demonstrated a signiicantly smaller (42%) reduction
in glycogen and lower lactate concentration (20%) in Type I ibers following the test.
This may be suggestive of a gender-based difference in carbohydrate metabolism
during such high-intensity anaerobic exercise, which may be related to the genderspeciic difference in 17-β-estradiol reported during exercise.79 Therefore, from the
available literature it appears that while there are a few gender differences in energy
metabolism processes activated during anaerobic exercise, these are quite speciic and
do not appear to be of suficient magnitude to individually inluence performance.
In summary, the effect of body composition and gender on anaerobic performance
is relatively apparent from the existing literature. The majority of published data suggests that anaerobic performance is largely related to body mass and, in particular,
lean body mass. A small number of studies suggest that the gender difference in
anaerobic capacity exists regardless of any correction for body mass. As such, men
typically have larger muscle ibers and a superior glycolytic proile within the muscle
for the provision of anaerobic energy supplies, though this appears to have little
inluence on energy provision and reaction product metabolism. These physiological
differences reported between genders are most likely the reason for the large separation between males and females in elite anaerobic performance events.
© 2011 by Taylor and Francis Group, LLC
Body Composition and Gender Differences in Performance
4.4
4.4.1
133
GENDER AND ENDURANCE PERFORMANCE
GENDER DIFFERENCES IN ENDURANCE PERFORMANCE
Despite a suggestion in 1992 that females may one day outrun males in competitive
ultradistance events,80 elite males appear to run approximately 10–15% faster than
elite females across all endurance running race distances from 1500 m to marathon,
with the gender difference narrowing as the race distance increases.81 However, at
distances between 100 km and 1000 km, the difference is even larger, with females
20–30% slower than males.82
The effect of gender on the age-related decline in performance was examined in
a cross-sectional study of swimming performance from the U.S. Masters Swimming
Championships where a greater rate of decline in swim performance was observed
in females than males across all swim events from 50 m to 1500 m.83 In endurance
running events, the decrease in performance is greater in women compared to men,
possibly due to either biological or sociological differences.84 These authors suggested that these gender differences may partly be explained by selection bias. That
is, there are a smaller number of female runners in the older age groups. This suggestion was supported by research examining the running times, age, and gender of
415,000 run performances in the New York Marathon between 1983 and 1999.85 They
observed that female marathon participation showed a signiicantly greater percentage increase in all age groups compared to the males. They also observed that the
number of masters’ participants over the age of 50 years signiicantly increased at a
greater rate than their younger counterparts and that the inishing times for the top
50 male and female inishers over the past two decades showed signiicantly greater
improvement in the masters’ age groups than the younger age groups, especially in
the older female athletes.85
As discussed in detail earlier in this chapter, females possess higher body fat
levels than males, and males possess a greater muscle mass and total body mass.
These gender differences explain performance differences in weight-bearing sports.
However, in swimming events, the increased lotation and smaller body size of
females may increase lotation and reduce drag and resistance compared to males.
Moreover, females have greater peripheral body fat distribution, causing their legs
and arms to loat higher in the water than males86 and increasing the economy of
swimming.87 This may explain the observation that the difference in English Channel
swim records between males (6 h 57 min) and females (7 h 25 min) is only 6.3%, a
lot lower than the 20% gender differences seen in running events of the same duration.82 Therefore, the data available demonstrate that males possess greater endurance potential than females over a range of sports and this would relate back to the
physical and physiological differences reported to exist between genders.
4.4.2
FACTORS INFLUENCING ENDURANCE DEVELOPMENT
For the purposes of this discussion, the model for endurance performance proposed
by Coyle88 will be examined. Coyle88 proposed that performance velocity in endurance events is dependent upon a number of physiological factors, including:
© 2011 by Taylor and Francis Group, LLC
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•
•
•
•
•
•
•
Nutritional Assessment of Athletes, Second Edition
Maximal O2 consumption (VO2max)
Maximal heart rate
Stroke volume
Lactate threshold
Economy of movement
Muscle iber type, morphology, and capillarization
Aerobic enzyme activity
Apart from these above factors, previous research suggests that both muscle mass89 and
blood volume90–92 may affect endurance performance in male and female athletes.
4.4.2.1 VO2max
Until puberty, the VO2max of boys and girls appears to be the same.13 Beyond puberty,
the average female’s VO2max is only 70–75% of that of the average male. In elite adult
athletes from a range of endurance sports, the VO2max of females remains 10–30%
below that of elite male athletes across all ages.93–95 In both young96 and older97,98
endurance athletes, VO2max is a strong predictor of running performance, with stronger correlations observed between endurance performance and VO2max in populations heterogeneous for VO2max.84,99
Coyle88 has identiied VO2max as a major contributor to endurance performance.
According to the modiied Fick equation, VO2max is the product of maximal heart
rate, maximal stroke volume, and maximal arteriovenous oxygen difference.13
Arteriovenous oxygen difference is further inluenced by a variety of factors, including muscle mass, the capacity of the blood to transport and relinquish oxygen (blood
volume, hemoglobin), and the capacity of the working tissues to take up and utilize
oxygen (capillarization, muscle iber type, aerobic enzyme activity).13 Speciically,
within a normal population, women typically possess VO2max scores 15–30% lower
than male counterparts.100 These differences are 30–60% larger when VO2max is
expressed in absolute units (L·min–1)95,101 but is signiicantly reduced to approximately a 20% and 10% difference when expressed relative to body mass (mL.kg–
1·min–1) or fat-free mass (mL·kgLBM–1·min–1), respectively.95,101 These data suggest
that body composition plays a major role in explaining the differences in VO2max and
thus endurance capacities between males and females.
For elite marathon runners, Cheuvront and others82 presented a table (Table 4.2)
that summarized the physiological differences between elite males and females for
the various indices that affect VO2max.
This table reviews the results from a number of studies that measured both the
VO2max and the indices of VO2max in elite male and female marathon runners. The
table suggests 26% (L·min–1), 17% (mL·kg–1·min–1), and 10% (mL·kgLBM–1·min–1)
greater values in male versus female elite marathon runners when VO2max was
expressed in absolute terms, relative to body mass or relative to lean body mass.
Taken together, the research strongly suggests that a female’s lower total and lean
body mass and greater body fat stores are major determinants of gender differences
in endurance performance.
Gender differences in the rate of age-related decline in VO2max are commonly
observed in endurance athletes.93,102 For example, Brown and others93 reported
© 2011 by Taylor and Francis Group, LLC
Males
Females
Diff
% Diff
TBM
(kg)
BF
(%)
LBM
(kg)
HRmax
(b/min)
SVmax
(mL/beat)
Qmax
(L/min)
A-VO2max
(mL/100 mL)
Hb
(g/dL)
VO2max
(L/min)
61.7
54.6
7.1
11.5
6
13
7
53.8
58.0
47.5
10.5
18.1
185
186
1
0.5
157
115
42
26.8
29.1
21.4
7.7
26.5
15
15
0
0
15.0
13.5
1.5
10
4.36
3.22
1.14
26.1
VO2max
VO2max
(mL/kg/min) (mL/kgLBM/min)
70.7
59.0
11.7
16.5
75.2
67.8
7.4
9.8
Note: TBM = Total body mass; BF = Body fat; LBM = Lean body mass; HRmax = Maximum heart rate; SVmax = Maximum stroke volume; Qmax = Maximum cardiac output;
A-VO2max = Maximum arteriovenous oxygen difference; Hb = Hemoglobin.
Source: Cheuvront, S.N., Moffatt, R.J., and DeRuisseau, K.C., Body composition and gender differences in performance, in Nutritional Assessment of Athletes, Driskell,
J.A. and Wolinsky, I., Eds., CRC Press, Boca Raton, FL, 2002, pp. 177–99.
Body Composition and Gender Differences in Performance
TABLE 4.2
Physiological Comparisons between Elite Men and Women Marathon Runners for Indices of VO2max
135
© 2011 by Taylor and Francis Group, LLC
136
Nutritional Assessment of Athletes, Second Edition
declines of 0.65 mL·kg–1·min–1·yr–1 and 0.39 mL·kg–1·min–1·yr–1 in male (17–64 yr)
and female (16–54 yr) high-performance cyclists, respectively. Fitzgerald and others103 used meta-analysis to suggest that VO2max in aging females declines at different rates in sedentary (0.35 mL·kg–1·min–1·yr–1), active (0.44 mL·kg–1·min–1·yr–1),
and endurance-trained (0.62 mL·kg–1·min–1·yr–1) subjects. Wilson and Tanaka104 also
used meta-analysis to suggest age-related declines in VO2max of 0.40, 0.39, and 0.46
mL·kg–1·min–1·yr–1 in sedentary (n = 6,231), active (n = 5,261), and endurance-trained
(n = 1,961) males. Thus, it appears that the VO2max of older endurance-trained males
and females declines with age at a faster rate than similarly aged cohorts.
An expansion of blood volume is a common inding following endurance training.105,106 A 20–25% expansion of blood volume that accompanies endurance training
provides advantages of greater body luid to facilitate enhanced thermoregulatory
ability through sweating, a larger vascular volume for greater cardiac illing and
stroke volume, and thus enhanced cardiovascular stability during both exercise and
changes in posture.105,106 High correlations have been observed between VO2max and
blood volume in both young105 and older male107 and female92 endurance athletes or
aging individuals with high VO2max values.90
Research also suggests that muscle mass differences between the genders can
explain differences in VO2max and endurance performance. This is not surprising
given the long-known relationship between maximum aerobic power and the amount
of total body lean mass.108 A number of studies involving maximal arm cranking109
and walking on a treadmill110 have not shown any gender differences when VO2max is
expressed per unit of appendicular muscle mass. These indings suggest that gender
differences in muscle mass account for gender differences in VO2max.
Apart from the body-composition differences between the genders discussed
above, research has also consistently shown that females have a lower VO2max compared to males as a result of other components of the oxygen transport and utilization
systems.12,13 These include
•
•
•
•
•
•
•
•
Smaller heart size
Smaller left ventricular mass
Lower plasma volume
Lower stroke volume
Lower cardiac output
Lower arteriovenous oxygen difference
Lower hemoglobin concentration
Lower blood oxygen carrying capacity
Research has shown that, at least in younger adult individuals, both males and
females respond to endurance training in the same way. In both genders, VO2max
increases approximately 15–30% depending on endurance training depending on
training frequency, duration, and most importantly, intensity.111,112 Maximum heart
rate does not appear to change as a result of endurance training in either gender.113
However, major increases in maximal cardiac output occur as a result of a signiicant increase in maximal stroke volume that is secondary to increases in both enddiastolic volume and end-systolic volume. These changes are primarily the result of
© 2011 by Taylor and Francis Group, LLC
Body Composition and Gender Differences in Performance
137
a signiicant increase in blood volume and stronger myocardium surrounding the left
ventricle, respectively.114,115
Endurance training also results in similar changes at submaximal endurance exercise intensities in both males and females. In both genders, cardiac output at any
submaximal exercise intensity does not change in either gender. However, endurance
training results in an increased stroke volume and a lowered submaximal heart rate at
the same absolute workload.114 In both genders, there are small but signiicant increases
in arteriovenous oxygen difference at any exercise intensity.116 In both genders the
metabolic and morphological changes that occur with endurance training include
•
•
•
•
Increased maximal muscle blood low117
Increased muscle capillary density118
Increased mitochondrial density119,120
Increased oxidative enzyme activity119,120
Research has shown that signiicant improvements in endurance performance
occur in males and females of all ages, depending on the initial itness level, genetics, and speciic training frequency, intensity, and duration.115,121 In both young and
older adults of both genders, aerobic capacity increases approximately 15–30%.
In both young males and females, this increase in VO2max induced by endurance
training is partly explained by increases in cardiac output as a result of increases in
stroke volume122 and numerous peripheral adaptations discussed earlier. In contrast,
it appears that there may be gender differences in the adaptations to endurance training in older individuals. For older males, it appears a signiicant increase in stroke
volume and thus cardiac output explains the majority of the VO2max increase with
a smaller but signiicant increase in arteriovenous oxygen difference explaining a
minority of the VO2max increase. In contrast, in older females it appears a highly signiicant increase in arteriovenous oxygen difference contributes all of the observed
increase in VO2max.123,124
While VO2max is widely regarded by exercise and sport scientists as the single best
indicator of an individual’s cardiovascular endurance capacity,13 the percentage of
this capacity that an athlete can sustain during aerobic performance has been consistently shown to better predict endurance performance ability.125–127 This level of
intensity is often referred to as the lactate threshold.13
4.4.2.2 Lactate Threshold
Endurance performance is not only determined by an individual’s VO2max.88 Lactate
threshold (LT) has been shown to be a better predictor of endurance performance
in athletes than VO2max. LT is deined as the point at which blood lactate begins to
accumulate substantially above resting concentrations during exercise of increasing
intensity.13 Coyle88 determined that lactate threshold is a major determining factor
in endurance performance. In modeling endurance performance, research has consistently shown that both VO2 at lactate threshold126 and velocity at lactate threshold
are better predictors of endurance running performance than VO2max125,127 in younger
distance runners. A longitudinal study by Wiswell and others128 observed that lactate
threshold as %VO2max did not differ between male and female endurance runners and
© 2011 by Taylor and Francis Group, LLC
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Nutritional Assessment of Athletes, Second Edition
increased signiicantly with age in both groups. Thus, lactate threshold appears to
be similar between similarly trained males and females when expressed relative to
VO2max, suggesting there are no gender differences in lactate threshold.
4.4.2.3 Economy
In modeling endurance performance, Coyle88 identiied economy as a major determining factor in endurance performance. Economy is deined as the oxygen cost
to exercise at a given exercise intensity (velocity or %VO2max) and has been shown
to be a stronger predictor of endurance performance than VO2max in a homogenous
group of endurance athletes.129,130 Moreover, studies that have examined the oxygen
cost of running at the same relative intensity have shown no gender differences in
running economy in young athletes.131 More recently, a study examined mechanical
eficiency in recreationally active males and females matched for %VO2 peak values
at ventilatory threshold and observed similar economy during both arm cranking
and leg cycling.132 Similarly, Evans and others97 tested the hypothesis that declines in
10 km run performance in females were associated with decreases in VO2max, lactate
threshold, and running economy. In thirty-one highly trained female runners aged
23–56 years, they observed that both 10 km performance and age were signiicantly
correlated with VO2max and running velocity and VO2 at lactate threshold. However,
both 10 km performance and age were not correlated with running economy in the
highly trained and competitive female endurance runners.97
In summary, it appears that males and females adapt similarly to similar endurance training loads and have similar relative lactate thresholds and exercise economies. Thus, the available research contrasting males and females of all ages suggests
that endurance performance differences between the genders are primarily the result
of differences in VO2max values. In turn, this gender difference in VO2max appears
largely explained by body composition differences such as the larger muscle mass of
males and the greater percent body fat of females.
4.4.2.4 Muscle Mass
A decreased muscle mass has often been suggested as a contributor to the age-related
decline in VO2max in sedentary aging individuals.89,133 Fleg and Lakatta89 measured
24-hour urinary creatinine excretion (an index of muscle mass) in 184 healthy volunteers aged 22–87 years from the Baltimore Longitudinal Study of Aging. They
observed a signiicant positive correlation between VO2max and creatinine excretion
in both men and women. VO2max showed a strong negative linear relationship with
age in both men and women. When VO2max was normalized for creatinine excretion,
the variance in the VO2max decline attributable to age declined from 60% to 14% in
men and from 50 to 8% in women, suggesting that muscle mass may inluence the
age-related decline in VO2max observed with age in healthy adults.
In summary, it would appear that endurance training into older age may not
reduce the age-related loss of muscle mass observed in a sedentary aging population,
but the quantity and quality of muscle may be enhanced through maintenance of
contractile tissue. Moreover, it appears that the age-related decrease in muscle mass
in particular contributes to the age-related decrease in VO2max and thus endurance
performance in male and female masters athletes.
© 2011 by Taylor and Francis Group, LLC
Body Composition and Gender Differences in Performance
139
4.4.2.5 Blood Volume
Females have a smaller heart volume, lower hemoglobin, and smaller blood volume
than males.115,134 The smaller heart volume leads to a smaller left ventricular mass
in females, which, when combined with a lower blood volume, reduces preload, thus
leading to lower stroke volumes and cardiac output commonly observed in female
athletes and untrained individuals.115,134
4.4.2.6 The Role of Estrogen
Recent research has observed that during endurance exercise females oxidize
more lipid and less carbohydrate and protein than males.135,136 This increased
lipid oxidation is related to higher intramuscular lipid storage and usage as well
as greater adipocyte lipolysis. Moreover, females exhibit lower glucose appearance and disappearance rates than males and some evidence of glycogen sparing during endurance exercise. Circulating estrogens have been implicated as
the hormonal reason for these gender differences in substrate metabolism.136,137
Estrogen appears to upregulate lipoprotein lipase activity during the luteal phase
of the menstrual cycle, the phase of the cycle that has been shown to enhance
endurance performance.137,138
Tarnopolsky79 has suggested that the gender differences in substrate metabolism
are partially due to the higher levels of 17-β-estrodiol in females. This suggestion
is reinforced by research that has shown that 17-β-estrodiol administration in males
leads to lower carbohydrate and protein oxidation and higher fat oxidation during
endurance exercise.79
4.5
SUMMARY AND CONCLUSION
The inluence that gender and body composition have on the several domains of exercise performance comprises several dificult concepts due to the interaction between
the two variables themselves. As such, while considerable differences exist between
genders with regards to physical performance, the causal factors are dificult to strictly
determine. The ultimate goal of understanding the complex mechanisms underlying
variations in exercise performance for both genders is to allow the development of
safe strategies for maximizing exercise performance. Primarily, the characterization of hormonal proiles in distinct menstrual cycle phases, their physiological outcomes, and their effects on exercise performance indicators are of vital importance
to the success of these strategies. The changes in hormonal proiles between genders
appear to have several secondary effects on muscle mass, enzyme activities, and cardiovascular function, among other factors. It is evident from this review that further
research is needed to attempt to identify these causal mechanisms. Clariication on
these issues may allow female athletes to adjust competition and training schedules
to their menstrual cycle in a further effort to maximize performance.
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© 2011 by Taylor and Francis Group, LLC
Section III
Physical Activity Needs
Assessment of Athletes
© 2011 by Taylor and Francis Group, LLC
Methods
5 Laboratory
for Determining Energy
Expenditure of Athletes
Robert G. McMurray
CONTENTS
5.1
5.2
Introduction .................................................................................................. 151
Methods for the Measurement of Metabolic Rate ........................................ 153
5.2.1 Direct Calorimetry ........................................................................... 153
5.2.2 Indirect Calorimetry ......................................................................... 154
5.2.3 Doubly-Labeled Water ...................................................................... 158
5.2.4 Indirect Methods of Estimating Energy Expenditure ...................... 159
5.3 Energy for Work and Sport ........................................................................... 161
5.4 Metabolic Measurements Speciic to Athletes ............................................. 163
5.4.1 Aerobic Power or VO2max .................................................................. 163
5.4.2 Anaerobic Threshold ........................................................................ 166
5.4.3 Economy of Movement ..................................................................... 168
5.5 Resting Energy Expenditure ......................................................................... 169
5.5.1 Measurement of Resting Energy Expenditure .................................. 170
5.5.2 Estimating Resting Energy Expenditure .......................................... 170
5.5.3 Factors Inluencing Resting Energy Expenditure ............................. 171
5.6 Estimating Daily Energy Expenditure.......................................................... 175
5.7 Future Research Concerns ............................................................................ 175
5.8 Conclusions ................................................................................................... 176
References .............................................................................................................. 177
5.1
INTRODUCTION
Determining energy expenditure for athletes can have a positive impact on their
health and their ability to train and compete. Knowing the energy demands of practice can help the athlete maintain a positive energy balance (energy demands vs.
energy intake), which optimizes the ability of the athlete to train and to increase
muscle mass. For example, inadequate energy intake reduces the ability of the athlete to sustain training at high intensities or to exercise for extended periods, and has
the potential to increase his or her risk of injury. Inadequate intake of energy also
151
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reduces the anabolic muscle-building process. From another perspective, measuring
maximal energy capacity can provide the athlete with information regarding the
effects of the training program on metabolic adaptations. Also, knowing at what
exercise intensity the athlete starts to produce signiicant lactic acid can assist the
athlete in identifying the proper intensity at which to train to obtain maximal metabolic beneits. This chapter focuses on the present state of knowledge regarding the
methods of measurement of energy use and provides some insights into how these
measurements can beneit the athlete.
Most athletes think of energy in terms of the requirements for their exercise programs, but energy is also needed to build tissues, digest food, and create enzymes and
hormones. The human body is not very eficient at utilizing the energy it produces,
and about 80–85% of the energy that is produced is ultimately converted to heat.
Thus, metabolism and heat production are typically viewed from the same perspective. For decades, the basic unit of energy for humans in the English system has been
the kilocalorie (kcal). This is the amount of heat required to increase 1 kilogram
(kg) of water one degree Celsius. However, the S.I. unit (le Système international
d’unités) of the kiloJoule (kJ) is becoming more acceptable.1 Conversion between
systems is simple, as 1 kcal is equal to 4.184 kJ. Although these two units are used
in the literature, other units of measure have been used. The kilopond-meter (kpm),
or kilogram-meter (kgm), is a unit of work used frequently on cycle ergometers.2 In
this case the kilopond, or kilogram, is deined as the magnitude of the force exerted
on one kilogram of mass. It is determined by multiplying the kilograms of resistance times the number of revolutions per minute, times the distance traveled per
revolution. Thus, someone pedaling at 60 rpm on a standard cycle ergometer with
a resistance of 2 kg would be working at 720 kgm: 60 rpm × 6 m/revolution × 2 kg.
Kgm can be converted to either kcal or kJ in a two-step process, irst converting to
mL O2 and then to energy units. There are approximately 2 mL of oxygen per kpm
and 5 kcal/liter of oxygen. Using the example above, exercising at 720 kpm would
use approximately 1.42 L O2 /min. At approximately 5 kcal/L O2, energy use would
amount to 7.1 kcal/min or 30 kJ/min. Some researchers have also reported work in
units of watts (W); however, the watt is a unit of power (J/sec) and should not be used
in energy production equations.
Energy derived from the complete combustion of each macronutrient is different.
Fats produce the most energy per gram (9.4 kcal or 39.3 kJ/g), protein produces about
5.65 kcal or 23.7 kJ/g, while carbohydrates yield only 4.3 kcal or 18 kJ/g.3 These values were determined using a bomb calorimeter. The bomb calorimeter is a strong
steel cylinder, resistant to high pressures, with a highly insulated water bath surrounding it.4 The food substance is sealed in the cylinder containing high-pressure
oxygen. The food is electronically ignited and the heat production is computed by
measuring the increase in the water temperature in the water bath, taking into consideration the volume of water encircling the calorimeter. In contrast to the bomb
calorimeter, human metabolism is not as eficient at assimilating and using these
substrates for energy. Thus, for practical purposes the energy production of carbohydrates and proteins is about 4 kcal/g (17 kJ/g), while fats produce approximately
9 kcal/g (37 kJ/g).4
© 2011 by Taylor and Francis Group, LLC
Laboratory Methods for Determining Energy Expenditure of Athletes
5.2
153
METHODS FOR THE MEASUREMENT OF METABOLIC RATE
Our knowledge of the measurement of metabolic rate and energy expenditure during physical activity has changed little since the mid-1990s.5–9 The energy output of
humans is still measured by direct and indirect calorimetry.5–9 The direct calorimetry method measures heat production or air low. Presently, these are the most accurate methods, but most individuals do not have access to the expensive, complicated
facilities and equipment needed to use these methods.5 Indirect methods, which rely
on the measurement of oxygen uptake, are less expensive, smaller, and more portable
than direct methods. Studies have shown good agreement between direct and indirect calorimetry.5,7 However, the advantages of indirect calorimetry are considerable
and the use of indirect calorimetry gained popularity in the early 1900s.9–11 Although
these indirect calorimetry systems are less expensive than direct calorimetry, they
are still outside the limits of cost for most individuals and are usually found in clinics
or laboratories.5 However, as technology advances, costs should decline and systems
will be in more widespread use in itness centers.
5.2.1
DIRECT CALORIMETRY
Direct calorimetry assesses heat production and typically requires a small room with
heavily insulated walls.5,7,9,11 These units are larger versions of the bomb calorimeter,
using the same basic science to measure the metabolic rate. The walls of the unit
contain a series of inned pipes through which water is pumped at a constant rate.
The heat generated by the subject is measured by the difference between the incoming and outgoing water temperatures measured to the 0.01°C, knowing the volume
and rate of the water low. Oxygen is continuously supplied and carbon dioxide is
removed by chemical absorbent. Direct calorimeters come in several sizes and types,
ranging from suit calorimeters, like those used by astronauts, to small chambers and
even larger rooms. In place of a water temperature gradient, the use of incoming and
outgoing air low has been tried and has met with some success for resting measure.5
Since the response time is slow,5 its use in sports is very limited. Using direct calorimetry to measure metabolic rate takes considerable time, as it takes at least 20–30
minutes for the heat loss and heat production to equilibrate.7 Therefore, direct calorimetry appears to work best for measuring resting metabolic rate or energy use during prolonged steady-state activities. The methods will not work for measuring daily
energy expenditure or for most sports or activities because of the conined nature of
the chamber. Another form of direct calorimetry is the isothermal system, which has
a faster response time.5 The isothermal system uses a chamber lined with insulating
materials and a water jacket. In these systems the temperature gradient across the
insulating layer is proportional to the nonevaporative (sweat) heat loss of the person
in the chamber. The response time of these units appears to be moderate (~5 min)
and the measurement error is small5; however, this system would not work for most
sports. In summary, none of the direct calorimetry methods will work to obtain
acute metabolic measures, such as the maximal capacity or anaerobic threshold, that
assist with training programs for athletes.
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INDIRECT CALORIMETRY
The underlying principle of indirect calorimetry is that energy production requires
oxygen.5–9 Thus, if the oxygen uptake is measured, energy production can then be
estimated, and through mathematical conversion, the results can be presented either
in kilocalories or kiloJoules. The equipment to obtain oxygen uptake has been found
to have an error as little as 1% compared to direct calorimetry.10 Indirect calorimetry
appears to be the method of choice for measurements of short-term energy expenditure at rest or during activity.8 The method is based on four assumptions.7 First,
the individual is not in a starvation state. Second, since the individual is not starving, protein makes up only a very small portion of the energy and can therefore be
ignored. Third, the contribution of anaerobic metabolism to the energy production is
quite small. Fourth, when using a combination of carbohydrates, fats, and proteins
as a source of energy, approximately 4.82 kcal (20 kJ) of energy is liberated per liter
of oxygen used.11 For convenience, the 4.82 kcal/L O2 has been rounded to 5 kcal
or 21 kJ per liter of oxygen. In general, in a normally fed individual performing
steady-state exercise, these assumptions are true. However, for short-term (< 5 min)
or anaerobic, high-intensity exercise, these assumptions are not accurate and indirect
calorimetry cannot be used to estimate energy expenditure unless recovery measurements are obtained. Recovery measurements are necessary because the anaerobic
energy will eventually have to be replaced by aerobic means. These recovery measurements can last from 15 to 60 minutes or longer, depending upon the nature of
the activity.
There are actually two general indirect calorimetry methods. One employs a
closed circuit system while the other uses an open circuit system.5 Both appear to be
equally valid; however, the open circuit system has proven to be more advantageous
for activities involving movement.
Closed-circuit spirometry uses a spirometer, an airtight cylinder, illed with 100%
oxygen. The system also contains a carbon dioxide absorbent such as soda lime,
which is used to remove the CO2 exhaled in each breath.3 The person simply breathes
the oxygen from the spirometer. Since oxygen is absorbed by the body and any CO2
produced is removed from the spirometer, the volume of gas in the spirometer is
reduced. The difference between the initial and the inal volumes of oxygen in the
spirometer is the oxygen uptake. The oxygen uptake is then multiplied by 5 kcal/L
of oxygen to obtain energy use. There are some problems inherent with this system.2 First, the system must be airtight so volumes will not change inappropriately.
Second, the temperature of the gas will affect the volume in the spirometer. A 1°C
rise in temperature will cause a 0.34% increase in the volume of air.2 Since expired
air is at a higher temperature than inspired air, failure to correct for this temperature
differential leads to an underestimation of metabolic rate. Third, the CO2 absorbent
must be adequate or the CO2 production simply replaces the oxygen uptake, providing the same absolute volume and reducing the measured oxygen uptake; CO2 is then
recycled and rebreathed. The inadequate CO2 absorbent increases the CO2, drives
up respiration rate, and reduces any exercise performance. Also, at high metabolic
rates, the CO2 absorbent may not be able to keep pace with the respiratory CO2
output, once again reducing exercise performance. Fourth, since the equipment is a
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closed circuit, the apparatus must have the capacity to hold a large volume of oxygen.
For example, during exercise a person may utilize 2–3 liters of oxygen per minute.
Thus, for a 20-min run, the apparatus must be able to contain at least 40–60 liters
of oxygen. Finally, once the subject is on the apparatus, the person cannot come off
the apparatus until the inal measure has been made or room air will enter into the
system and reduce the oxygen uptake. These limitations, plus the bulky size of the
equipment, the need for a large volume of pure oxygen, and the close proximity the
subject needs to be to the equipment, have limited the use of closed-circuit spirometry for exercise studies.
The open-circuit system has proven to be useful in measuring energy both at rest
and during exercise. In this method, the person does not rebreathe his or her air. The
person simply inspires ambient air and expires air through a system of tubes with
one-way valves so that measurements can be made of the total volume of air and the
expired proportions of oxygen and carbon dioxide.7–9 The difference between the
inspired and expired oxygen is the oxygen uptake (VO2).
There are basically three major types of open-circuit systems: (1) a bag system, (2)
a computerized system, and (3) a portable system.11 All three systems start with the
subject breathing through a mask or breathing valve that allows ambient air to enter
and directs the expired air through gas analyzers. All three types contain a meter
to measure total air volume (ventilation meter, turbine, or pneumotach), an oxygen
meter, and a carbon dioxide meter. The bag system collects the volume of expired
air in a large meteorological balloons or a standard rubberized Douglas bag.5,9 The
contents of the bag are measured for the overall air volume and the concentrations of
oxygen and carbon dioxide. These values are then introduced into a formula to compute oxygen uptake. The computerized system takes the output from the three meters
(expired oxygen, expired carbon dioxide, and ventilation) and computes the oxygen
uptake.10 The modern computerized system has the advantage of using instruments
with much faster response time so that oxygen uptake can be captured breath-bybreath. Modern technology and microprocessors have resulted in miniaturizing the
computerized systems to the point that they weigh less than 1 kg and can be worn on
the back or abdomen, thus giving the person freedom of movement. Some of these
portable units contain telemetry systems that allow investigators to obtain breathby-breath information on energy expenditures for many activities with the person’s
movements unimpeded. Since the systems are lightweight, they contribute very little
(1–2%) to the total energy of adults, but the weight of the unit could add 5–10% to
the energy expenditure of a 10–20 kg child.
All of the open circuit systems have the same underlying assumptions as with
other indirect calorimetry systems: The individual is not in a starvation state, protein
makes up only a very small portion of the energy and can therefore be ignored, and
the contribution of anaerobic metabolism to the energy production is quite small.
However, the open circuit systems do not generalize the energy production from
a liter of oxygen (5 kcal/L O2). Instead, the open circuit methods utilize the fact
that energy produced by carbohydrates and fats have different oxygen requirements
(VO2) and carbon dioxide production (VCO2) rates.12 Using open circuit spirometry
to measure energy expenditure requires that the exerciser attains steady state. This
is because the VCO2 and VO2 only represent substrate utilization during steady state.
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In this state the VCO2 is usually less than the VO2, so the relationship, or respiratory
exchange ratio (RER), is always ≤ 1.0. The respiratory exchange ratio (RER), respiratory quotient (RQ), or simply the R value, is the ratio of VCO2 to VO2 uptake.7–9 The
RER does not take protein metabolism for energy into consideration; therefore it is
sometimes referred to as the nonprotein RER.7,9 This method of computing energy
expenditure will not work for individuals in a starvation state in which they are
utilizing considerable protein. The RER for carbohydrate is 1.0, as the oxidation of
a single glucose molecule requires six oxygen molecules and produces six carbon
dioxide molecules, or a ratio of 6:6 (CO2:O2), which equals 1.0. The chemical reaction is C6H12O6 + 6O2 → 6CO2 + 6H2O + energy.3 Conversely, the oxidation of fats
requires more oxygen and produces less CO2. For example, the metabolism of a molecule of palmitic acid, a typical fatty acid used for energy, uses 23 oxygen molecules
and produces 16 CO2 molecules (16/23 = 0.696), summarized by the following chemical equation: C16H32O2 + 23O2 → 16CO2 + 16H2O + energy.3 As the composition of
the substrate used for energy changes from fat to glucose, the RER changes from 0.7
to 1.0. An individual consuming a 50:50 mixture of carbohydrates and fats has an
RER of 0.85. In addition to revealing the source of energy, the RER also relates to
the amount of kilocaloric production per liter of oxygen.12,13 Carbohydrates produce
5.047 kcal/liter of oxygen uptake (21 kJ/L), while fats only produce 4.686 kcal/liter
of oxygen uptake (19.6 kJ/L).
At the onset of exercise or during any high-intensity activity, lactic acid will be
produced from anaerobic metabolism. Lactic acid is buffered by bicarbonate ions
in the blood, causing an increase in CO2 output (H+ + HCO3– → H2O + CO2). The
increased VCO2 will rise above what is expected for aerobic metabolism, causing the
RER to be > 1.0 and abolishing the ability to compute energy expenditure.7–9 This is
the major limitation of indirect calorimetry.
The best method to compute energy expenditure from open circuit spirometry
involves the respiratory exchange ratio, so the oxygen uptake and carbon dioxide
production must be measured.5,7,9 To accomplish this, six factors must be known:
Inspired volume of air (VI) per minute, inspired percent of oxygen (FIO2) and carbon
dioxide (FICO2), the expired air volume (VE) per minute, and the expired percentages of oxygen (FEO2) and carbon dioxide (FECO2). The ventilation, either VI or
VE, is measured directly from a gas meter, pneumotach, or turbine. Knowing either
VI or VE, the other volume can be calculated using the Haldane conversion.9 The
volume of air needs to be corrected, since barometric pressure, temperature, and
relative humidity affect the volume and not the percentage of the gases.9 The correction allows for comparisons of oxygen uptake obtained in the desert or below
sea level with those obtained in the high rain forests or on a cold mountain top.
The standard correction factor is to adjust barometric pressure (PB) to sea level (760
mmHg), temperature to 0°C, and relative humidity to 0%. This factor is known by
the anachronism of STPD: standard temperature, pressure, and dry.9 Failure to apply
the factor can result in a 7–15% error in the overall calculation of energy expenditure
(see Table 5.1). The FIO2 and FICO2 are known (20.93% and 0.03%, respectively),
while the FEO2 and FECO2 are obtained from monitoring expired air using O2 and
CO2 meters. The computational formulas are presented in Table 5.1.
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TABLE 5.1
Calculating Energy Expenditure from Measurements of Oxygen Uptake (VO2)
and Carbon Dioxide Production (VCO2) and Respiratory Exchange Ratio (RER)
VSTPD = [(PB – water vapor pressure)/760] × [273/(273 + Temp of the gas)]
VE = VI × [.794/(1-FEO2 – FECO2)]
VO2 = (VI × FIO2) – (VE × FEO2)
VCO2 = (VE × FECO2) – (VI × FICO2)
RER = VCO2/VO2
RER on chart will give kcal/L oxygen (percent carbohydrates and fats)
kcal/min = (kcal/L O2) × VO2 (L/min)
kJ/min = (kcal/min) × 4.184 kJ/kcal
Note: VI and VE refer to ventilation volumes of inspired (I) and expired (E) air; FIO2 and FEO2 refer to
fractions of inspired (I) and expired (E) oxygen; and FICO2 and FECO2 refer to fractions of inspired
(I) and expired (E) carbon dioxide.
Sources: Consolazio C.F., Johnson R.E., and Pecora L.J., Physiological Measurements of Metabolic
Functions in Man, McGraw-Hill, New York, 1963, pp. 1–98; Krogh, A. and Lindhard, J.,
Biochem. J. 14, 290–363, 1920; McArdle, W.D., Katch, F.I., and Katch, V.L., Exercise
Physiology: Energy, Nutrition and Human Performance, Lippincott Williams & Wilkins,
Philadelphia, 2007; and Zuntz, N. and Schumburg, N.A.E.F., Studien zu Einer Physiologie des
Macsches, A. Hirschwald, Berlin, 1901.
The oxygen uptake values, obtained from the formulas in Table 5.1, are expressed
in units of liters of oxygen per minute (L/min). This is considered the absolute VO2.
The oxygen uptake can also be expressed taking into consideration body mass: milliliters of O2 per kilogram body weight per minute (mL/kg/min). This is considered
to be the relative VO2. The absolute VO2 is used to obtain overall energy expenditure.
Individuals who have large amounts of muscle mass, are tall, or are considered obese
usually have a larger absolute VO2 than normal-sized individuals. When trying to
compare the energy expenditure of individual of differing sizes, relative VO2 may be
the preferred unit of measure. However, larger or taller individuals (including obese
persons) usually have lower relative aerobic power (expressed per kilogram body
mass) because their weight has a greater contribution of bone, connective tissue, and/
or fat than a smaller individual, and these tissues do not contribute to overall oxygen
consumption in the same way that muscle mass does. To overcome these limitations,
some scientists have suggested using the units of mL O2 per kilogram fat-free mass
(mL/kgFFM/min). This is an area in need of further explorations.
In 1936, D.B. Dill14 proposed a system of expressing energy expenditure in increments of resting metabolic rate—thus the origin of the metabolic equivalent or the
MET. The MET has been deined as 3.5 mL/kg/min, or 1 kcal/kg/hr,9,11,15 which
is thought to represent the average resting value for an adult; however, this value
is debatable.16 The MET has become a popular unit of measure in epidemiological
studies of activity or clinical studies in which maximal graded exercise testing is an
integral part. This is because most research has shown that the energy cost of weightbearing activities (for example, walking or running) is fairly similar per kilogram
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Nutritional Assessment of Athletes, Second Edition
weight or per MET.11,14,15 Furthermore, tables have been developed for estimating
energy expenditure of most physical activities, including work, home, transportation,
and sports activities.17 In terms of METs, a normal individual has a maximal capacity of 10–13 MET, while highly trained endurance athletes can have a MET capacity
of 20–24 METs.
5.2.3
DOUBLY-LABELED WATER
Thus far, the methods described for measuring metabolic rate have limitations. They
have the potential for precision, but some methods restrict movements, while others
are limited to gathering information during only minutes or hours of use. None of
the methods relate well to non-steady-state activity or very high-intensity activity in
which CO2 output can become greater than oxygen uptake (anaerobic work). In an
attempt to overcome these problems, a technique using doubly-labeled water has been
developed.5,18–21 Doubly-labeled water is an isotope of water in which both the hydrogen and oxygen are tagged with a tracer, 2H218O. The underlying principles of the
technique are that the hydrogen from the doubly-labeled water is eliminated as part
of the water and the oxygen is eliminated both as part of the water and carbon dioxide
molecule. Since there is equilibrium between the oxygen molecule in the water and
the carbon dioxide, it is possible to measure the carbon dioxide production by measuring the hydrogen and oxygen isotope in the body’s water.21 The energy expenditure
is computed based on total body water, daily CO2 output, and isotope turnover in the
urine. The subject simply consumes a dose of the labeled water. The dose is based
on estimated total body water. The subject then goes about his or her activities for a
period of 5–7 days and collects his or her urine. The isotope turnover in the urine is
measured by high-precision mass spectrometry. The overall error of this method is
about 6–8%; however, considering this is over a week, the error is acceptable.5,21
The doubly-labeled water method is based on six assumptions.19,21 First, the volume of water in which the 2H218O is diluted is constant. This is not quite true because
eating and drinking behavior is episodic rather than constant and some individuals
are losing or gaining weight. However, this difference turns out to be less than a
1–2% error.21 Second, the luxes of water and CO2 are constant. Although this is not
true due to the episodic nature of physical activity, eating, and drinking, once again
the difference appears to be not quantitatively important.21 Third, the body water
compartments act as a single compartment with respect to the equilibration of isotopes. This assumption has proven to be controversial as the hydrogen has been noted
to be more rapidly exchangeable than the oxygen. To avoid the equilibrium issue,
some investigators have used dilution space correction factor rather than total body
water. Fourth, the rate of tracer inlux exactly represents the rate of tracer eflux. The
analytical model has been adjusted for this. Fifth, no CO2 or water enters the body
through the skin or lungs. Because the aim is to measure the dietary water intake
and CO2 production, any additional environmental sources would cause an error.
Cigarette smoking can increase CO2 intake, thus inducing a 3–6% increase in the
estimate of energy expenditure. Although some exchange occurs in a nonsmoking
person, once again the error is quantitatively unimportant.21 Sixth, the food quotient,
obtained from dietary intake, is used to estimate the dietary mix rather than the
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159
respiratory exchange ratio. This is important since the heat production (energy) per
unit of CO2 differs by about 30% when comparing carbohydrates and fats. The use
of the food quotient introduces approximately a 3% error. This assumption does
not account for alcohol intake or if energy intake differs considerably from energy
expenditure. The overall effect of the inaccuracies of these assumptions is to induce
a 2–8% error depending upon dose and duration of the study.18,20
The major problem of the technique is the expense of equipment necessary for
the isotope and total body water analyses and the expense of the dosages of 2H218O.
However, other problems have been reported. Speakman et al.22 found that the error
for estimating VCO2 from doubly-labeled water was not normally distributed and
could result in an error for duplicate samples of 3–47%. In defense, this error could
be reduced considerably by analyzing the samples in sets of ive rather than two.
Roberts et al.23 have reported that the quality of isotope (amounts of 2H2 and 18O) may
differ, resulting in substantial variability, including some physiologically impossible
results. Although these problems exist, 2H218O presently provides our best estimate
of free-living energy expenditure. This method appears to work well for obtaining estimates of overall energy expenditure but will not work to obtain an athlete’s
maximal capacity or anaerobic threshold, both of which are commonly used in the
development of training programs for athletes.
5.2.4
INDIRECT METHODS OF ESTIMATING ENERGY EXPENDITURE
Since metabolic equipment is costly, requires considerable training to use, and is
dificult to use for normal activities of life, indirect methods have been used in an
attempt to estimate energy expenditure (EE). These methods include the use of heart
rate monitors, motion sensors, and even thermal imaging.5
The use of heart rate to estimate energy expenditure has been explored because
it is a relatively inexpensive method that allows the individual to be assessed in a
free-living state.24 Heart rates have the potential to provide information on the pattern of activity as well as a general estimate of energy expenditure. The use of heart
rate monitors to estimate energy expenditure requires planning and calibration, since
individuals vary in both resting and maximal heart rate. Thus, the person must irst
undergo testing so that the resting and maximal heat rates are known, and a heart
rate/energy expenditure relationship developed. This usually requires the use of an
ergometer for exercise and the measurement of oxygen uptake to compute energy
expenditure. The subject then wears a heart rate monitor for a 24-hour period. The
heart rates are downloaded to a computer and then averaged in 1- to 15-minute time
segments. The average energy expenditure during that short time segment is then
estimated by using the previously determined EE/heart-rate relationship and multiplying that by the number of minutes of activity. This procedure is then used repeatedly and totaled until the entire 24-hour EE is obtained.
The major problem with this method is that not all heart rate increases are related
to changes in metabolic rate.24,25 Emotional stress and temperature changes are
known to affect heart rate independent of metabolic rate. Thus, heart rates below 120
are not considered usable to determine energy expenditure.25 In addition, heart rate
only represents metabolic rate when a steady-state of activity has occurred. Thus,
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Nutritional Assessment of Athletes, Second Edition
during anaerobic activities or activities that have a considerable isometric component in which heart rates are elevated above metabolic rate, the use of heart rate can
skew the results. Finally, the heart rate may not be suficiently sensitive to respond
to short-term activities.24,25 Levine5 suggests that the error of estimating metabolic
rate from heart rate during low-intensity exercise is between 3 and 20%. Therefore, it
appears to be impractical to use heart rate to estimate metabolic rate. However, heart
rate can be used to estimate minutes of moderate- to hard-intensity activities.24 More
commonly, heart rates are used by athlete to understand their minute-by-minute
training intensities rather than to estimate energy expenditure.
Motion detectors have also been used to estimate energy expenditure. Motion
detectors can be as simple as a pedometer or as complex as a three-dimensional
or omnidirectional accelerometer.26 Pedometers only measure ambulation and thus
are of limited value when calculating energy expenditure.27 Accelerometers contain a piezoresistive microswitch that responds to motion. The units are small and
usually worn on the hip. Some of these are designed to respond to movement in a
single plane of motion (up–down) while others have the capability to respond in
three dimensions. These units usually require a computer interface. The investigator enters the subject’s age, sex, height, and weight and resets the unit to zero counts
(initializes the unit). The subject then wears the unit for a period of time, sometimes even up to 7 days. The motion counts are then downloaded to a computer.
The accelerometer has a built-in energy expenditure prediction equation based on
sex, age, height, and weight. Energy expenditure is then derived by multiplying the
motion counts by a prediction equation. The accelerometer output can be divided up
into segments as little as 1 sec., giving the ability to compute EE during a speciic
activity as well as overall EE.
In adults, the uniaxial accelerometers appear to slightly overpredict energy
expenditure during those activities that involve ambulation, like level walking or
running.15,28 However, they underpredict the energy cost of activities that involve
arm movement or external work, like stair climbing or hill walking.29,30 In addition,
the units are ineffective for measuring EE for activities that do not involve ambulation, such as swimming, cycling, weightlifting, or any seated activity. Triaxial or
omnidirectional monitors appear to be slightly more accurate, but they still appear
to have the same limitation as the uniaxial models with respect to evaluate intensity of activity, arm work, or nonambulatory activities (such as swimming, weight
lifting, and cycling).26,30 In addition, the formulas to compute energy expenditure
were derived from adult data, which does not directly apply to children.31 Thus,
motion detectors have a limited ability to estimate energy expenditure. They will
not work to obtain maximal capacity or anaerobic threshold used for training programs for athletes.
Estimating energy expenditure from thermal imaging has also been attempted.5
Thermal imaging estimates heat loss from the body to the environment. Early studies showed little promise because of the slow response time, but more modern, highresolution scanning has improved the accuracy during steady-state exercise but not
during acute, short-term (< 10 min) exercise.
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Laboratory Methods for Determining Energy Expenditure of Athletes
5.3
161
ENERGY FOR WORK AND SPORT
The energy expenditure of daily life is greater than the resting energy expenditure
(REE) and is dependent upon lifestyle and occupation. A typical sedentary adult (for
example, an ofice worker) will expend 140% of the REE. A teacher’s lifestyle will
expend 160% of the REE, a nurse’s lifestyle about 170% of REE, while a physical
laborer (brick layer) will expend up to 200% times the REE.4,17,2,32 These calculations
do not include any energy used for an exercise program. This energy expenditure of
exercise training is in addition to the daily need (REE + Lifestyle). For an adult who
exercises about 30–45 min a day, this will amount to 250–450 kcal (1000–1900 kJ),
or only about 10–14% of the total caloric expenditure. However, for the athlete who
exercises 3–5 hours a day, the energy demand of the exercise alone can be greater
than the total energy of REE plus lifestyle. Table 5.2 summarizes the estimated
additional energy needs of individuals training for speciic sports.33 These estimated energy needs should not be taken as absolutes, only as examples of additional
caloric needs. Note that some sports, like recreational basketball, may require only
slightly more than normal amounts of energy, while others, like the Tour de France
cycle race can require an enormous amount of additional energy. The actual energy
demand of the exercise is based on the intensity and duration of the exercise, the
type of activity, and the sex and weight of the exerciser. The weight of the athlete is
why the American football player requires more energy than the endurance cyclists.
The energy demands of activities that are weight bearing will be directly related to
the athlete’s weight, whereas activities that are non–weight bearing, like bicycling,
TABLE 5.2
Estimates of the Energy Requirements for Training of Various Sports
Additional Energy Needs
Sport
Basketball
Crew
Dancers
Gymnasts
Football players
Lacrosse players
Runners (men)
Runners (women)
Swimmers
Tour de France
Triathletes
Wrestlers
Weightlifters
Kilocalories
Megajoules
300
600–5000
1000
1400
2100
700
1000
500
500
4000
1500–2000
200–1000
1400–4600
1.26
2.51–20.92
4.18
5.86
8.79
2.93
4.18
2.09
2.09
16.74
6.28–8.37
0.84–4.18
5.86–19.25
Average Daily Energy Intake
Kilocalories
Megajoules
2200
9.20
2400–7000
10.04–29.29
1500
6.28
1400
5.86
4000–5300
16.74–22.18
3000
12.55
4400
18.41
2400
10.04
2900
12.13
6700
28.03
4095
17.15
Varies with weight
3000–4700
7.17–19.66
Note: In most sports the energy requirements for women are about 15–20% less than for men.
Source: Short, S.H. and Short, W.R., Four-year study of university athletes’ dietary intake, J. Am.
Diet. Assoc. 82, 632–45, 1983.
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TABLE 5.3
A Comparison of the Energy Demands (kcal/min) of Running (a
Weight-Bearing Activity) and Cycling (a Non-Weight-Bearing Activity)
Body Weight
110 lbs (50 Kg)
130 lbs (59 Kg)
150 lbs (68 Kg)
170 lbs (77 Kg)
190 lbs (86 Kg)
Running
~ 6 mph (9.6 km/h)
kcal/min
9.7
11.4
13.1
14.9
16.6
Cycling
~ 9 mph (14.5 km/h)
kcal/min
5.0
5.9
6.8
7.7
8.6
Sources: Swain, D.P., The inluence of body mass in endurance bicycling, Med. Sci. Sports
Exerc. 26, 58–63, 1994; Swain, D.P. and Leutholtz, B.C., Metabolic Calculations
Simpliied, Williams & Wilkins, Baltimore, MD, 1997, p. 14.
require less increments of energy as the individual’s weight increases (Table 5.3).34
Thus, an overweight or obese athlete who wants to increase energy expenditure is
better off walking than riding a bicycle. Interestingly, this overweight athlete actually utilizes signiicantly more energy to walk at a given speed than a nonobese
athlete, but riding a bicycle at the same speed the overweight athlete uses just slightly
more energy that a lean athlete.
Energy expenditure during activity is usually measured by open circuit spirometry. As previously mentioned, at this point in time, a miniaturized, computerized
system appears to work best. Some of these systems are stationary and will only
work with activities in which the participant is within 5–6 ft of the measurement
device. Such systems have been used to measure energy cost of walking and running
on treadmills, cycling on cycle ergometers, swimming using a swimming ergometer, rowing using a rowing ergometer, stair stepping using an escalator-type or step
ergometer, elliptical trainers, or arm ergometer. The treadmill allows the subject to
walk or run at speciic speeds while maintaining a stationary location. Although the
treadmill simulates ambulation, it is not quite the same as normal walking or running as the person’s legs are propelled backward off the treadmill rather than the leg
propelling the body forward. Also, there is a difference in air resistance between
treadmill and normal ambulation that may decrease the energy cost of ambulation on
treadmill.35,36 The same is true for cycle ergometers, as they eliminate air resistance;
however, the ergometer also eliminates the friction of the tires on the riding surface.
With swimming and rowing ergometers, the problem is that they eliminate water
resistance (drag forces, frontal resistance, and skin or surface friction).37 Water resistance is considerable; therefore, the use of swimming ergometers may underestimate
the true energy expenditure of swimming. To overcome some of the drag issues,
swimming lumes have been developed. The lume is like the “endless pools” in that
the water is forced past the swimmer and the swimmer swims against that force or
current to stay in place.
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The bag technique of open circuit spirometry has been used to measure oxygen
uptake during ergometry work as well as during actual cycling, swimming, rope
skipping, or household chores.5,6 Since the expired air bag is connected to the subject by a breathing tube, this technique requires the researcher to move with the
subject yet not impede any of the subject’s movements. The subject usually wears a
mouthpiece and has to support the breathing tube during the collection period. The
weight of the breathing tubing, breathing valve, and mouthpiece can be uncomfortable for the subject or cause additional effort to support the apparatus and maintain
the mouthpiece in the mouth. The air collections bags are typically bulky and hard
to control during exercise. They are not totally impermeable to gas exchange and if
used for longer than 10–15 minutes, gases may diffuse and the results can be unreliable. Therefore, bag measurements are usually taken over periods of time lasting less
than 10 minutes and the contents measured as quickly as possible at the end of the
collection period. The bag method can be used successfully but takes preparation,
training, and good timing to obtain accurate data.5,9,11
The use of miniaturized portable systems has revolutionized our ability to obtain
energy expenditure data during activities.6 These new systems are small enough to be
worn during activity, providing little impairment of motion. The systems have been
used to measure energy expenditure of household chores, basketball, inline skating,
cycling, tennis, and kayaking, to name a few.31 Some of these systems include a fairly
large memory or telemetry, which allows the investigator to obtain hours of real-time
data without being tethered to the subject.
Although these systems have proven to be accurate, there are some minor problems. As mentioned previously, the additional weight of the apparatus can increase
the energy cost of the activities. It is also important that the systems be securely
attached to the subject. If not, the system can impede motion, which will modify
the energy cost. Most of these systems require that the subject wear a mask to measure expired gases, rather than the cumbersome breathing valve and mouthpiece. An
improperly itting mask can result in air leaks that can modify both the measured
volume of air and the fractions of expired gases. Experience has also shown that the
systems may lose their ability to function via telemetry if they are near an electric
ield such as a video display. Proper consideration and planning can eliminate these
problems and allow the investigator to obtain accurate data.
5.4
5.4.1
METABOLIC MEASUREMENTS SPECIFIC TO ATHLETES
AEROBIC POWER OR VO2MAX
Two metabolic measures that athletes are generally interested in are the maximal
metabolic rate, referred to as their VO2max, and their lactate threshold. VO2max is the
maximal amount of oxygen that can be consumed and is considered by many to
be the most valid indicator of aerobic itness. A high VO2max is particularly important for endurance athletes. For example, a 2-hour, 20-minute marathon run is performed at about 11.5 mph (18.5 kpm). To maintain that speed on a level surface,
an oxygen uptake (VO2) of about 65 mL/kg/min is required.38 From Table 5.4, the
normal VO2max for a sedentary adult is around 30–4 mL/kg/min; thus, the normal
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TABLE 5.4
Aerobic Power or VO2max (mL/kg/min) for Different Athlete Groups
Presented by Sex
Sport
Females
Males
Basketball players
Cross-country skiers
Cyclists
Distance runners
Gymnasts
Ice hockey players
Kayakers
Rock climbers
Rowers
Sailors
Soccer players
Surfers
Swimmers
Sedentary adults
Speed skaters
Sprinters (< 400 m)
Tennis players
Triathletes
U.S. football players
Weight lifters
Wrestlers
38–52
55–65
53–70
48–71
36–49
35–55
50–57
50–55
46–55
50–64
43–56
52–60
58–60
30–48
46–55
No Data
44–61
47–58
No Data
No Data
No Data
38–53
58–85
56–80
55–81
45–55
50–61
40–50
No Data
55–65
45–55
55–68
50–80
54–68
35–49
56–81
47–71
50–70
55–72
32–56
36–61
54–65
Sources: Obtained from our laboratory and from McArdle, W.D., Katch, F.I., and Katch, V.L., Exercise
Physiology: Energy, Nutrition and Human Performance, Lippincott Williams & Wilkins,
Philadelphia, 2007; Wilmore, J.H. and Costill, D.L., Training for Sport and Activity: The
Physiological Basis of the Conditioning Process, Wm. C. Brown Publishers, Dubuque, 1988;
Draper, N. and Hodgson, C., Adventure Sport Physiology, Wiley-Blackwell, Chichester, U.K.,
2008; Mendez-Vallanueva, A. and Bishop, D., Physiological aspects of surfboard riding performance, Sports Med. 35, 55–70, 2005; Pluim, B.M., Stall, J.B., Marks, B.L., Miller, S., and
Miley, D., Health beneits of tennis, Br. J. Sports Med. 41, 760–68, 2007; and MacDougall, D.J.,
Wenger, H.A., and Green, H.J., Physiological Testing of the High-Performance Athlete, Human
Kinetics Books, Champaign, IL, 1991.
adult could not run at that speed because the required metabolic rate could not be
attained (among other reasons).11,40–44 Although there is a genetic component to
VO2max,39 hard training can result in as much as 30% improvement, but normally the
improvements are about 10–15%.11,40 The VO2max of different types of athletes can
be found in Table 5.4. They were obtained from a variety of sources and measurements obtained at the University of North Carolina. The values reported in Table 5.4
simply represent a wide range of responses and should not be considered for success
in athletics. One reason for the wide range of values is body size. For example, if one
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Laboratory Methods for Determining Energy Expenditure of Athletes
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examines the VO2max of the U.S. football player, there are values that are lower than
for some sedentary adults, yet we know these athletes can sustain more exercise than
a sedentary adult.45 A normal adult male is about 75 kg and 1.78 meters tall, while
most football linemen weigh about 130 kg and are about 1.98 meters tall. Because of
the larger muscle mass of the football player, he will usually have a higher absolute
VO2max (L/min) than the smaller, sedentary person. From Table 5.4, and knowing the
mass in the above example, an estimate of 2.1 L/min and 4.2 L/min can be calculated
for the normal adult and the football player, respectively.45 Consequently, the football
player has a higher overall metabolic rate, but when expressed per kilogram body
mass, the rate is lower. Thus, care should be taken when interpreting the VO2max,
and attention should be paid to the units in which it is expressed. Clearly, endurance
athletes need high VO2max, but success in many athletic endeavors does not hinge on
aerobic power.
Maximal oxygen uptake is usually measured by a progressive, incremental exercise test on an ergometer.44,46–48 The test is also referred to as a graded exercise test
(GXT).46,47 The test starts out with a warm-up and then progresses in a stepwise-fashion
from a low workload (for example, speed, resistance, or rpm) to the maximal workload
that can be sustained by the individual. Each workload (step) typically lasts from 1 to 3
minutes, with an optimal duration of 10–15 minutes for the whole test. The test termination is usually subjective and considerable motivation is needed to have the individual
attain true maximal capacity. However, there are some criteria validating that the person
attained VO2max: failure to keep up with the exercise protocol, plateau or a slight decline
in VO2 with increasing workload, reaching maximal heart rate and failure to rise with
increasing workload, and RER ≥ 1.10, or lactate levels of 8 mmol/L or greater.49
Maximal aerobic power can also be estimated from submaximal exercise testing.47,48,50 These tests usually have the person exercise on a calibrated ergometer and
complete two to four stages of a maximal test or continue until their heart rates reach
~160 beats per minute. The heart rates or oxygen uptakes are measured the inal
minute of each stage. The assumption is that there is a predictable, linear relationship
between steady-state heart rate and steady-state VO2, so using that heart rate or VO2
data, maximal capacity is then predicted using a graph or an equation.
The heart rate and VO2 (or workload) data are usually plotted against each other,
with heart rate on the x axis and VO2 (or workload) on the y axis. An example is presented in Figure 5.1. A straight line of “best it” is drawn and then extended out to the
individual’s predicted maximal heart rate. (The maximal heart rate is predicted from
220 – age.) A line is then extended to the y axis to obtain the VO2 at that maximal
heart rate, with that VO2 value representing the VO2max. Alternatively, the relationship
between the heart rates and oxygen uptakes can be calculated mathematically (computing slope and intercept of the line) and VO2max can be determined from that equation.
These tests vary in accuracy, with correlations of 0.6 to 0.85 (moderate to strong)
between measured VO2max and submaximal predictions.48 The beneits of this testing
are: (1) the results do not rely on the person pushing himself or herself to maximal
limits, (2) they take less stafing, (3) they are safer with less physical risk, (4) require
less time to run and interpret, and (5) many can be completed using a cycle ergometer or treadmill and a heart rate monitor, making them less expensive.48 On the
other hand, there are limitations especially for trained endurance athletes. Factors
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Nutritional Assessment of Athletes, Second Edition
Predicted HRmax = 192
5
Predicted VO2max = 5.0 L/min
VO2 (L/min)
4
Stage
3
Stage 3
2
Stage
Stage 1
1
Res
0
0
20
40
60
80
100
120
140
160
180
200
Heart Rate (bt/min)
FIGURE 5.1 Predicting VO2max from heart rate and oxygen uptake for an individual who
completes four stages of an exercise test with heart rate and VO2 measured. The individual
has a resting heart rate of 60 beats/minute and a predicted maximal heart rate of 192 beats/
minute (on a cycle ergometer 300 kpm = 0.9 L/min VO2; thereafter, each increment of 300
kpm = 0.6 L/min VO2.
like dehydration, prior exercise, and environmental conditions (temperature and
humidity) and length of test can inluence the heart rate and therefore the accuracy
of the results.48 Athletes typically take longer than nonathletes to achieve the work
rates normally needed to produce results. The longer the test, the greater chance that
the athlete will elevate his or her core temperature, which will drive up heart rate
over and above what would normally occur for a given work rate. The higher heart
rate will result in an underprediction of maximal capacity. Most of the standard
submaximal tests rely on heart rate and the prediction of age-appropriate maximal
heart rate (HRmax); typically HRmax = 220 – age.47,48 However, many trained athletes
have lower than predicted maximal heart rates. Thus using the 220 – age prediction equation could result in an overprediction of maximal capacity. In addition the
anaerobic threshold cannot be determined from this form of testing as it can from
the true VO2max test. Thus, as noted above, the accuracy of the predicted value is not
that good. Submaximal tests can be used for athletes as a test–retest to determine if
the exercise training program is progressing as expected. However, a simpler way to
check progress is to have the athlete complete a standard exercise test and simply look
at performance or heart rate. For example, a runner could do a time trial for a speciic
distance and then simply compare times. A swimmer could do a standardized set of
interval training (sets of 100 to 200 m) and look at average times or heart rates. This
would accomplish as much as the submaximal test. In summary, there appears to be
limited value in using speciic submaximal tests for athletic populations.
5.4.2
ANAEROBIC THRESHOLD
The anaerobic threshold is another metabolic measure that has several applications
for athletes.44 There are several terms commonly used: the anaerobic threshold (AT),
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Laboratory Methods for Determining Energy Expenditure of Athletes
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the lactate threshold, or the onset of blood lactate (OBLA).44 Regardless of the terminology, the anaerobic threshold is the level of exertion at which there is a considerable increase in the use of anaerobic energy systems, causing the production of
lactic acid.44,46 Lactic acid (referred to as lactate) is associated with fatigue, and the
higher the lactate levels the shorter duration an athlete can exercise. For example, at
a lactate level of 2 mmol/L, an athlete can usually exercise for more than an hour.
At 5 mmol/L, the athlete may only be able to exercise for 20–30 minutes, and at 8
mmol/L the athlete may only last 2–5 min.11,40,50 The application of this is that when
two athletes with the same VO2max are running at the same pace, the one producing
less lactate will be able to sustain the run for a longer period of time with less fatigue.
Also, the athlete with the higher AT will be able to run faster without the detrimental
effects of lactate. This is why the AT of most marathon runners is typically > 80% of
VO2max, whereas the threshold of sprinters is typically in the 55–65% VO2max range.50
This is clearly an advantage for most endurance athletes.
The anaerobic threshold can provide an estimate of endurance potential when
expressed as a percentage of VO2max. Athletes with a high proportion of fast-twitch
ibers have the potential to produce considerable lactic acid at lower intensities of
exercise. So if a coach is trying to determine if an athlete would make a better sprinter
than a long-distance runner, one way would be to measure the athlete’s VO2max and
AT. If the AT is at a low proportion of VO2max (~60%) and the VO2max is not very high
(50–55 mL/kg/min), then the athlete might be better at sprint events. If the AT is low
and the athlete has a high VO2max (> 55 mL/kg/min) then the athlete could be better
at middle distance events or may have the potential through training to be a good
endurance athlete. If the athlete has a fairly high VO2max and the AT is a high percentage of that maximal capacity, then the athlete could be better at endurance events. Of
course this method is not foolproof. Finally, at some point the endurance athlete can
reach his or her aerobic potential and VO2max cannot be changed signiicantly with
training. However, training can increase the anaerobic threshold.40,50 If the threshold
increases as a proportion of VO2max, then the athlete can exercise at a higher intensity
with less buildup of fatigue-related lactate. Finally, the anaerobic threshold can be
used by coaches and athletes during training to optimize the exercise intensity for
maximal training results.40,44,50
The anaerobic threshold can be measured during an incremental VO2max test.44,46
Usually the stages last about 3 minutes and increments in workload are smaller than
for a normal VO2max test. Oxygen uptake and heart rates are obtained the last minute of each stage and blood lactate is sampled at the end of each stage. For runners,
cyclists, cross-country skiers, skaters, or rowers, a sport-speciic stationary ergometer can be used for the test. The test can also occur in a ield setting, in which the
athlete exercises at speciic incremental speeds in 5-minute stages and blood lactate
levels are measured between stages. This approach has been commonly used with
swimmers.
Two common lactic acid demarcations have been used to determine the threshold:
a lactate level of 2 mmol/L or 4 mmol/L.44 For athletes, the 4 mmol/L threshold
appears to have more relevance.40,44,50 The concept is to ind the exercise intensity
at which the threshold level of lactate is reached. The exercise intensity could be
related to speed (for swimmers and runners), heart rate (for any training athlete), or a
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Nutritional Assessment of Athletes, Second Edition
proportion of VO2max. Training below the threshold optimizes the aerobic energy system and maximizes the duration of the training session. Training above the threshold
improves the athlete’s speed, power, and ability to buffer the fatigue-related acids but
reduces the duration of the training session.
Measuring the anaerobic threshold using lactate requires blood samples and a
machine to analyze the compound. Although small portable machines for measuring lactate are available, some individuals do not like to have blood sampled. To
avoid the blood sampling and still obtain an estimate of the AT, some scientists have
suggested the use of the relationship between ventilation and metabolic rate.46 The
theory is that in an aerobic state there is a consistent relationship between ventilation
and metabolic rate (VE/VO2). However, when lactate is produced and buffered, the
hydrogen ions and additional CO2 cause an increase in ventilation, over and above
what is required for metabolism. Thus, this substantial increase in ventilation is a
“surrogate” for the anaerobic threshold. For example, the VE/VO2 ratio is normally
about 25 L air/1 L VO2, but for some athletes it can be as low as 15/1. So the scientist simply computes the VE/VO2 ratio for each stage of the VO2max test and where
an abrupt increase in the ratio occurs, that is the AT. Since some of the lactate is
buffered and may not inluence the ventilation, some researchers have suggested that
both the VE/VO2 and VE/VCO2 ratios need to be taken into consideration.46 With
this method there must be a rise in the VE/VO2 without an increase in the VE/VCO2.
This method is controversial and probably represents only an estimate of the AT in
normal, healthy individuals. Regardless of the methodology, the anaerobic threshold
is a very useful metabolic measure for aerobic athletes.
5.4.3
ECONOMY OF MOVEMENT
As the distance of a competitive event increases, another metabolic measure comes
into play: economy of movement. Economy is basically the energy expenditure
per unit speed.9 Better economy of movement relates to sustaining endurance performance and delaying fatigue. Measurements of economy are typically used for
sports like marathon and ultramarathon running, long-distance cycling, rowing, and
paddling or swimming—events that drain the muscle and liver glycogen supplies.
Fatigue in short events lasting 5 minutes or less is not related to depletion of muscle
glycogen; however, in prolonged events glycogen depletion is central to fatigue.11,40
So a sprinter can “waste” some energy to attain the goal, whereas a long-distance
cyclist must be as eficient as possible with metabolic resources to attain his or her
goal. Consistent with this, a study of elite long-distance (> 10 km) and middle-distance (800 m) runners found that the long-distance runners used 5–11% less oxygen
at a given speed.51,52 For long-distance swimmers (≥ 1500 m), technique has a very
important role. Measuring economy as the swimmer trains can be an indicator of
improvement in technique. The concept can also be applied to rower and paddlers.
Fortunately, measuring economy is not dificult. The athlete simply exercises at
several speeds, attains a steady state at each speed, and the metabolic rate (VO2) is
measured. The ratio of VO2 to speed is calculated. Since there is no “perfect ratio,”
the characteristic is individually applied and measured several times during a train-
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ing season to substantiate that training is producing the desired results.53 Speciically,
economy has improved when energy cost per unit speed has decreased.
A number of individual characteristics can inluence economy. Fiber composition is one of those characteristics.53 Three types of muscle ibers dominate skeletal
muscle: slow-twitch oxidative (Type I), fast-twitch glycolytic-oxidative (Type IIa),
and fast-twitch glycolytic (Type IIb). Slow-twitch ibers are the most mechanically
eficient and the most aerobically energy eficient but do not produce large power
outputs.54 They can use both fats and glycogen for energy production.11,40,50 Fasttwitch glycolytic ibers produce the most power but are the least aerobically eficient
and rely on glycogen as their primary source of energy. The fast-twitch oxidativeglycolytic ibers are a mix of the two extremes and end up to be the most “trainable”
of the ibers, taking on the characteristics of training regimen (sprint or endurance).
These differences in muscle characteristics are why successful long-distance athletes typically have more slow-twitch ibers, while successful sprinters have a high
proportion of fast-twitch ibers. The iber type distribution is also the reason that
most sprinters cannot run long distances, and long-distance athletes are not successful at sprints.40,50 Of course there are exceptions!
Another factor contributing to economy is the physical characteristics of the athlete. Body size appears to be important for swimming, running, or cycling. Taller
individuals have longer arms and legs, which appears to be an advantage. Shorter
individuals require higher stroke frequencies at the same speed than a taller individual, and typically increased frequencies cause greater energy expenditure and
less economy. The combination of size and muscle iber type distribution may be
contributing to the fact the women are more eficient at slower speed running but
less eficient at high speeds.55 However, body composition (greater fat content) and
biomechanical factors (leg alignment) are also contributing factors to sex differences
in economy.54,55
Finally, equipment can have an impact on economy. In long-distance running, the
weight of the shoes can have an impact on energy use. In swimming, the advent of
the “laser” swimsuit (Speedo) reduces drag forces, improves economy, but is now
against international rules. There are several examples in cycling as well, including bike and helmet designs that reduce drag forces and toe-clips that increase eficient use of energy throughout the pedal revolution.56 Thus physical characteristics,
technique, physiology, biomechanics, and equipment all contribute to economy of
movement.
5.5
RESTING ENERGY EXPENDITURE
The resting energy expenditure (REE) accounts for about two thirds of the daily
energy expenditure and is therefore important when analyzing an athlete’s energy
balance. Resting energy expenditure is sometimes confused with the basal energy
expenditure (BEE, or sometimes referred to as the BMR). The basal energy expenditure is the minimal amount of energy necessary to sustain life—the energy needed
to keep the heart beating, respiration going, and maintain cell metabolism, nerve
transmission, body temperature, and so forth. The BMR requires that the person
have no additional physiologic or psychologic stimulation, such as digestion, excess
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temperature regulation, psychological tension, or any form of physical activity or
movement.56,57 It is usually measured with the person resting supine after at least 8
hours of sleep, and at least 12 hours after the last meal or exercise.6,57 On the other
hand the resting energy expenditure (REE), or resting metabolic rate (RMR), is the
energy expenditure required to maintain normal body functions at rest.8,11 The REE
is typically measured in the morning after a normal night’s sleep, with the individual
lying down or sitting in a thermo-neutral environment, after a 12-hour fast, and not
having exercised for 12 hours. Since the two states are relatively close in deinition,
and since the difference between the BMR and the REE is less than 10%, the terms
are often used interchangeably.9,11 In fact, Schutz and Jéquier suggest that if the REE
is measured in a postabsorptive condition, it is the same as BMR.8 However, they are
really two differing states. True BMR is dificult to precisely measure and requires
more controls than the REE and as a result, the REE is usually obtained. Both the
BMR and the REE are usually expressed in kilocalories per hour (kcal/h) or kiloJoules per hour (kJ/h). The rate varies as much as ±20% from individual to individual.8,11 Although REE provides basic information on resting energy expenditure,
it does not provide information that could inluence an athlete’s training program. It
might provide insights into the nutritional balance of the athlete when the athlete’s
performance is declining for no apparent reason.
5.5.1
MEASUREMENT OF RESTING ENERGY EXPENDITURE
Any of the methods of calorimetry can be used to measure REE. However, the REE
is usually obtained from two 5- to 7-minute continuous measures of VO2 and VCO2.
In some cases a single 15-minute collection period is used, with the irst 5 minutes of
measurement discarded and last 10 minutes of measurement averaged to obtain the
REE.6,58 The subject usually reclines in a supine position for approximately 30–45
minutes in a quiet, thermo-neutral environment, sometimes covered with a light blanket. The mask or mouthpiece is put into place so that the subject is breathing through
the apparatus during this initial rest period. This reduces any anxiety caused by the
equipment. The subject is told to remain fairly still but not to sleep. At the end of the
initial rest period the measurements are made. The methods for measuring BMR need
to be more restrictive to reduce subject awareness and anxiety and usually involve gas
measurements obtained with the subject inside a transparent hood or using a room
calorimeter.8,58 In addition the BMR measures are usually obtained over a 20- to
45-minute period rather than the two 5- to 7-minute measurements.7,58
5.5.2
ESTIMATING RESTING ENERGY EXPENDITURE
Resting energy expenditure can be directly measured. The measurement takes
considerable equipment, time, and knowledge; thus methods have been derived to
estimate REE based on indirect measures of weight, height, and age. The simplest
method is based on gender. Adult males will use 1.0 kcal/kg/h or 4.186 kJ / kg/h,
while females will use 0.9 kcal/kg/h or 3.77 kJ/kg/h.4,6,8,59 The person’s body mass
(kilograms) is multiplied by the appropriate gender factor to obtain kcal/h. A variation on this simple method is to multiply the weight in pounds times 10. These
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TABLE 5.5
The World Health Organization Equations for Estimating Daily Resting
Energy (kcal/day) Expenditure Based on Age, Gender, and Body Mass
Equation
Age Range
(yr)
Males
Females
0–3
3–10
10–18
18–30
30–60
> 60
(60.9 × kg) – 54
(22.7 × kg) + 495
(17.5 × kg) + 651
(15.3 × kg) + 679
(11.6 × kg) + 879
(13.5 × kg) + 487
(61.0 × kg) – 51
(22.5 × kg) + 499
(12.2 × kg) + 746
(14.7 × kg) + 496
(8.7 × kg) + 829
(10.5 × kg) + 596
Note: kg = body mass in kilograms
Source: World Health Organization, Energy and Protein Requirements, Report of the Joint FAO/WHO/
UNU Expert Consultation, Technical Report Series #724, WHO, Geneva, 1985, p. 206.
methods are crude and do not take into consideration age, size, muscle, or fat mass;
therefore, they should only be used to estimate REE. Since REE declines with age,
the World Health Organization (WHO) improved upon these simple prediction
equations by developing six age-within-gender prediction equations.59 The WHO
equations correlate from 0.60 to 0.97 with reported direct measurements of REE
(Table 5.5). Table 5.6 summarizes and compares the results obtained by using the
four different analytical methods to estimate REE. As evident from Table 5.6, there
is over a 15% difference between methods of estimation, and there is no simple way
to determine which formula is most accurate for which person. Generally, equations based on gender, age, weight, and height may be more accurate, usually within
10–15% of direct measures.4 These formulas, however, do not take into consideration
extremes in muscle or fat mass. Thus, for the athlete who has larger muscle mass and
less fat mass than a normal individual, the best means for obtaining REE appears to
be some method of direct measurement.
5.5.3
FACTORS INFLUENCING RESTING ENERGY EXPENDITURE
It is important to note that not all calories ingested are usable. The processes of
digestion and absorption, as well as assimilation of substrate in the liver (proteins, glycogen), after feeding require energy. These processes are about 65–95%
eficient, dependent upon the type of food.3,8,58 Therefore, at rest 5–30% of the
calories are given off in the form of heat.8,60 These heat calories are referred to
as dietary-induced thermogenesis or speciic dynamic action (SDA). The dietaryinduced thermogenesis varies by substrate. Carbohydrates increase REE about
4–5%, while fats only increase REE by about 2%.3,8 Conversely, protein increases
REE by 20–30% and ethanol is about 22%.3,8 A typical mixed meal would increase
REE by about 5–10%. Dietary-induced thermogenesis usually peaks about an
hour after eating and, if the meal is high in protein, the thermogenesis can last
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Nutritional Assessment of Athletes, Second Edition
TABLE 5.6
Examples of Computations Comparing Methods of Estimating
Energy Requirements
Male: 20 years old
Height = 5′10″ (1.78 m)
Weight = 163 pounds (72 kg)
Female: 20 years old
Height 5′5″ (1.65 m)
Weight = 136 pounds (62 kg)
1. REE = 10 × wtlbs
10 × 163 = 1630 kcal/d
REE = 10 × wtlbs
10 × 132 = 1360 kcal/d
2. REE = 1.0 kcal/kg/h
1 × 72 × 24 = 1728 kcal/d
REE = 0.9 kcal/kg/h
0.9 × 62 × 24 = 1339 kcal/d
3. WHO Equations Based on Age and Gender
(15.3 × kg) + 679
(14.7 × kg) + 496
15.3 × 72 + 679 = 1781 kcal/d
14.7 × 62 + 496 = 1407 kcal/d
4. Equations Based on Gender, Weight (wt = kg), Height (ht = cm), and Age (a = yr)
66.5 + (13.8 × wt) + (5 × ht) – (6.8 × a)
655 + (9.6 × wt) + (1.7 × ht) – (4.7 × a)
66.5 + (13.8 × 72) + (5 × 179) – (6.8 × 20)
655 + (9.6 × 62) + (1.7 × 165) – (4.7 × 20)
66.5 + 994 + 895 – 136 = 1819.5 kcal/d
655 + 595 + 281 – 94 = 1437 kcal/d
Comparison of the Results of the Four Methods
Method
Male Example
1
1630 kcal/d
2
1728 kcal/d
3
1781 kcal/d
4
1820 kcal/d
Female Example
1360 kcal/d
1339 kcal/d
1407 kcal/d
1437 kcal/d
for a considerable amount of time, 3 to 5 hours.8 The thermogenesis seems to be
more dependent upon the feeding pattern than the total caloric intake, as feeding
four meals produces a larger increase in thermogenesis than feeding one meal of
the same caloric content.60 However, gorging signiicantly elevates the thermogenesis,61,62 but the effect may not be as signiicant for obese individuals.63 This
is thought to be in some way related to their body fat.63 Endurance training, on
the other hand, may also lower the dietary-induced thermogenesis compared to
untrained subjects.64–67 The reduced thermogenesis could help conserve energy
during periods of intense physical training. Other factors that may inluence
dietary-induced thermogenesis include genetics, caffeine, nicotine, and diseases
like diabetes mellitus that effect insulin.8,59
The resting energy expenditure is directly inluenced by the amount of metabolically active tissue, or lean body mass.8 The National Research Council reports that
lean body mass accounts for about 80% of the variance in measuring REE.68 Failure
to account for lean body mass can produce erroneous results. For example, publications have reported that the 24-hour energy expenditure of highly active subjects
was greater than sedentary controls.69 However, when the expenditure was reported
based on lean body mass, the groups were found to be similar.
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Although the lean body mass has a major inluence on REE, the size of the individual will modify that relationship. Size is concerned with the height for a given
weight.68 Nutritionists deine size using body mass index, a weight–height ratio
(wtkg/htm2), whereas physiologists use the body surface area to mass ratio (AD/kg).
Regardless of the units, the taller, thinner person will have a higher REE than the
shorter, heavier person of the same weight. This difference is related to the fact that
the taller, thinner person has more surface area through which heat is lost. Thus, the
tall, lean person must produce more heat to maintain thermo-balance.
Age and gender are also signiicant factors affecting REE (Figure 5.2).70 The
total resting energy expenditure of children is less than adults, generally < 75 kcal/h
(314 kJ/h) vs. > 90 kcal/h (377 kJ/h).68 However, when expressed per unit of body
weight, the expenditure of children is more than double that of an adult: 100 kcal/kg
(418 kJ/kg) vs. 30–37 kcal/kg (126–155 kJ/kg).68 The greater REE is related to growth
and activity patterns.71 Once growth has stopped, the REE declines about 2% per
year, relating to only about 100–150 calories in 50 years.68,70,72 Interestingly, lean body
mass declines at a rate of about 2–3% per decade.68 Thus, if the decline in lean body
mass could be avoided, the age-related reduction in REE probably would not occur.
Figure 5.2 illustrates that there is little difference in the REE of boys and girls
until about the age of 10 years. At approximately this time, pubescence starts and
the body composition of the genders begins to differentiate. The boys continue to
gain muscle mass, while the girls develop a greater proportion of body fat. This
difference amounts to about a 10% greater REE in adult males. Thus, in general,
210
200
RMR (kJ/m2/h)
19
180
170
Males
160
150
Females
140
130
5 10 15 20 25 30 35 40 45 50 55 60 65 70 75 80
Age (yr)
FIGURE 5.2 Relationship of age and gender to basal metabolic rate. The data is corrected
for body surface area. (From Altman, P.L. and Dittmer, D.S., Metabolism, Federation of
American Societies for Experimental Biology, Bethesda, MD, 1968.)
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Nutritional Assessment of Athletes, Second Edition
women expend about 0.9 kcal/kg body weight/hour. In contrast, men expend about
1 kcal / kg/h. This difference may not be a true gender difference but related to the
greater body fat of females, or, conversely, to the greater muscle mass of males.
This is veriied by the fact that when metabolic rate is expressed per unit of fat-free
mass (lean body weight), the comparative resting metabolic rates between men and
women are very similar.16,70,73
Other factors like climate,3,11,74 pattern of food intake,6,61,75 and hormones3,8,11,72
affect REE. Finally, exercise training may have an effect on REE (Figure 5.3). The
effect of training on REE is controversial. Some studies have suggested that highly
trained athletes have a greater REE per unit lean body mass than sedentary controls,64,70,76,77 while others disagree.66,67,78,79 The disagreement may be related to differing methodologies that have not controlled for a carryover effect of the previous
exercise, which can persist up to 12–13 hours after prolonged strenuous exercise of
3–5 hours, the thermic effect of subsequent food intake, or the use of cross-sectional
samples. Cross-sectional evidence suggests that highly active males and world1.25
Kcal/KgFFW/h
1.20
1.15
1.10
1.05
1.00
Sedentary
Trained
Training Status
FIGURE 5.3 Effect of exercise training on the basal metabolic rate. The data presented
with respect to lean body mass is a compilation of a number of studies The open diamond
(◊) represents the mean response for all studies in that group. (Data from Poehlman, E.T. et
al., Am. J. Clin. Nutr. 47, 793–98, 1988; Davis, J.R. et al., Eur. J. Appl. Physiol. 50, 319–29,
1983; Poehlman, E.T. et al., Metabol. 41, 915–19, 1992; Tremblay, A. et al., Int. J. Obes. 10,
511–17, 1986; Wilmore, J.H. et al., Am. J. Clin. Nutr. 68, 66–71, 1998; Dolezal, B.A. and
Potteiger, J.A., J. Appl. Physiol. 85, 695–700, 1998; Poehlman, E.T. et al., Brit. J. Clin. Pract.
41, 684–88, 1987.)
© 2011 by Taylor and Francis Group, LLC
Laboratory Methods for Determining Energy Expenditure of Athletes
175
class endurance athletes have a higher REE per unit lean body mass compared to
moderately trained individuals.80 At the other end of the spectrum, exercise training programs in sedentary individuals cause an elevation in RMR.77,81 Thus, there is
accumulating longitudinal data to support an increased RMR with aerobic training.
Also, the trained individuals usually have more lean body mass at a given weight,
thus increasing absolute REE.
5.6
ESTIMATING DAILY ENERGY EXPENDITURE
The total, daily energy expenditure can be estimated by summing the REE, the daily
activity factor, and the exercise program. For example, consider a 20-year-old woman
who weighs 132 pounds (60 kg), works as a receptionist, and takes a 45-minute aerobics class 5 days a week. Her REE would be 1296 kcal per day (60 kg × 0.9 kcal/
kg/h × 24 h). Her daily activity would be an additional 390 kcal (REE × 30%).
The aerobic program would expend about 275 kcals (6.1 kcal / min × 45 min).
Thus, on the days she exercises, her total energy expenditure amounts to 1961 kcal
(1296 + 390 + 275) or 8.2 mJ/day, while on her nonexercising days she expends
1686 kcal (1296 + 390) or 7.0 mJ/day. By estimating the energy requirements for the
day, the coach or a nutritionist can then combine this information with caloric intake
to obtain caloric balance. A negative caloric balance (output greater than intake) of
3 days or longer can have an impact on the athlete’s ability to train or perform, especially for endurance athletes. Conversely, a positive balance (intake slightly greater
than output) allows the athlete to optimize his or her training and, in the long run,
perhaps competitive performance.
5.7
FUTURE RESEARCH CONCERNS
Advancements in the measurement of energy expenditure allow us to obtain realtime data on energy expenditure during many different sports and activities for
which we presently have only estimates. Researchers, scientists, and coaches now
need to follow up and make these measurements for a variety of sports. However,
these miniature metabolic systems are expensive and the risk for damage to this
equipment or of injury is high for sports in which there is contact. So the use
of these metabolic systems in many athletic situations is tenuous. In addition,
having athletes wear the equipment during competition is not possible in many
cases. So the best that can probably be accomplished is to measure the energy
expenditure during practice and simulated situations. We have tried this for the
sport of fencing.82 The fencer’s mask was modiied to accommodate a breathing
mask from a miniaturized metabolic system, the system was moved from the
front of the body to the lower back, and the back of the fencer was eliminated as
a target for scoring. These modiications allowed for most foil, épée, and saber
“touches” (scores) and also minimized risk to the equipment. Since fencing is
ballistic in nature and metabolic rate could not be measured for a typical 10–15
second “touch” and the equipment slightly changes the fencer’s normal competitive movements, we could only simulate a competitive bout and had to extend the
© 2011 by Taylor and Francis Group, LLC
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Nutritional Assessment of Athletes, Second Edition
“sparring” for several minutes to obtain energy data. Attempts like this need to
occur with other sports.
Another major issue is the measurement of anaerobic energy. Most sports are not
performed at a constant rate or speed, so measurements of energy that rely on oxygen uptake are not directly applicable. As mentioned with the fencing example, most
points are scored within 10–15 seconds of the start and this time frame is even faster
for saber events. Most team sports, such as soccer, ield hockey, or American football, have times when the athletes are sprinting for short period of time interspersed
with rest or periods of light exercise. At present we do not have a means of accurately
estimating the energy costs of these types of activities. Oxygen uptake will not work
because these types of activities do not directly rely on oxygen. Measuring oxygen
uptake and the exercise and recovery is one way to estimate the energy cost, but
oxygen uptake during recovery is not only dependent upon the anaerobic demands of
the exercise but also on any elevation in core temperature. Hence, during activities
like fencing, where the athlete is wearing a uniform that reduces heat loss and consequently heats up, total energy cost of the sport would be overestimated. Heart rate
may not relate to metabolic rate, so what is needed is a means of measuring anaerobic
energy expenditure. A promising approach would be to use accelerometry in conjunction with prior titrating of energy expenditure (oxygen uptake) and accelerometer
counts. This approach needs to be reined for speciic athletes and speciic sports.
One inal issue in need of resolution is the effect of exercise training on resting
metabolic rate. Such studies should be longitudinal in nature and should begin using
unconditioned individuals and progress through the entire competitive season. The
problem with this approach is that high-performing athletes usually do not become
“unconditioned.” One approach may be to use athletes who are injured and cannot
exercise for quite some time and follow their responses as they become conditioned.
Resting metabolic rate studies also need to be completed on strength training athletes. Regardless of the group of athletes, measurements of metabolic rate need to be
adjusted for fat-free mass (lean body mass) or changes in lean body mass that are a
result of the training or detraining.
5.8
CONCLUSIONS
Knowing energy demands of an athlete and the metabolic responses to speciic sports
can provide an advantage to an athlete by improving nutritional balance and his or
her ability to optimize exercise training and performance. However, the measurement of energy expenditure is a complex process that can be completed by several
methods. Early studies employed direct calorimetry in which the person was placed
in a closed chamber and the person’s heat production was directly measured. Since
direct calorimetry conines the movement of the subject, there is limited application
to athletes and physical activities. These limitations have led to the development
of indirect calorimetry methods. These methods are based on the fact that the production of heat requires the use of oxygen and the production of carbon dioxide.
Therefore, measuring the oxygen uptake and carbon dioxide production allows for
the computation of energy use. Indirect calorimetry has evolved to the point where
systems are suficiently small so that subjects can exercise unimpeded, and metabolic
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Laboratory Methods for Determining Energy Expenditure of Athletes
177
measurements can occur. Indirect calorimetry has a limited capacity to obtain data
and has therefore been used mostly for measurements during short periods of time
(such as minutes, hours). However, indirect calorimetry can provide the athlete with
measures of both maximal capacity and anaerobic threshold—two characteristics
that can be used as markers for training and that indicate the training regimen is
working. Since indirect methods are not appropriate to obtain a measure of energy
expenditure over a period of days, a double-isotope method using 2H218O has been
developed. This method is most applicable when measuring overall (total) energy
expenditure over days; however, it will not work to measure the speciic energy cost
of a given activity. Thus, it appears that indirect calorimetry is best for measuring
speciic activities, while the doubly-labeled water is best to estimate overall, daily
energy use.
The resting energy expenditure (REE) can be deined as the minimal amount of
energy necessary to sustain the human organism in a conscious, resting state. The
REE makes up about two thirds of daily energy expenditure for a normal adult. In
general, the REE is dependent upon the amount of metabolically active tissue, lean
body mass. However, other factors such as age, gender, body size, climate, caloric
intake, hormones, and exercise training will modify the REE. Resting energy expenditure can be measured by a variety of means ranging from room calorimeters that
use direct calorimetry to simply measuring oxygen uptake, which is indirect calorimetry. Measuring VO2 using a mask, hood, or even a whole room is the simplest
means for obtaining an estimate of the energy expenditure. On the other hand, the
measurement of energy expenditure during activity can be either quite simple or very
complex depending upon the movements of the activity. Presently the best methods
are through the use of portable, indirect calorimetry units. However, the measurement of energy expenditure from oxygen uptake requires that the activity can be
completed in an aerobic state, which means that the activity is of a low-to-moderate
intensity. At present, we have a limited capability to measure energy cost of very
high-intensity exercise, which results in the production of considerable lactic acid.
Ultimately, to compute the individual daily energy expenditure, three factors
must be summed: (1) the REE for the 24-hour period, (2) the energy expenditure
based on lifestyle (work/school), and (3) the energy expenditure from any exercise
program. For a sedentary adult, the irst two factors (REE and lifestyle) coalesce
to cause the vast majority of energy consumption. However, for some athletes their
training programs can result in energy demands greater than the REE and lifestyle
combined. For these athletes, knowledge of their energy needs can be vital for success in their sport.
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© 2011 by Taylor and Francis Group, LLC
Assessment
6 Field
of Physical Activity
and Energy Expenditure
among Athletes
Nuala M. Byrne, Sarah P. Shultz,
and Andrew P. Hills
CONTENTS
6.1
6.2
6.3
Introduction .................................................................................................. 183
Deinitions..................................................................................................... 185
Methods of Assessing Physical Activity and Energy Expenditure .............. 187
6.3.1 Objective Measures........................................................................... 187
6.3.1.1 The Doubly-Labeled Water (DLW) Technique ................. 187
6.3.1.2 Heart Rate Monitoring ....................................................... 190
6.3.1.3 Pedometers ......................................................................... 191
6.3.1.4 Accelerometers................................................................... 193
6.3.1.5 Combined Approaches and New Devices.......................... 198
6.3.2 Subjective Approaches...................................................................... 199
6.3.2.1 Direct Observation .............................................................200
6.3.2.2 Physical Activity Records or Diaries ................................. 201
6.3.2.3 Physical Activity Questionnaires ....................................... 201
6.3.2.4 Self-Report Physical Activity Questionnaires ...................203
6.4 Conclusions ...................................................................................................204
References ..............................................................................................................205
6.1
INTRODUCTION
A large number of physical activity measures are currently utilized in the ield setting
to proile activity in terms of amount and type of movement performed, and many
of these tools are also employed to predict energy expenditure. Physical activity is
a multi-faceted construct, and although there are numerous techniques for assessment there is no “gold standard” measurement method.1 In contrast, energy expenditure, which is a biological variable relecting the sum of internal heat produced by
external work, can be measured using well-accepted gold-standard methods. It is
183
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Nutritional Assessment of Athletes, Second Edition
important to remember that physical activity is a behavior that results in an elevation
of energy expenditure above resting levels, and although these terms are often used
interchangeably, they are inherently different and can be measured differently.2 The
techniques available to researchers, coaches, and athletes to measure physical activity and energy expenditure are vast, but the applicability of the different measurement tools will depend on the aspect of physical activity or energy expenditure that
needs to be measured.
Historically, coaches have relied on personal experience to prescribe training programs to achieve optimal athletic performance; the trend now is to adopt a scientiic
approach to the development and monitoring of training programs.3 Enabling the
more scientiic approach in recent years has been access to the signiicant increase
in commercially available devices to monitor and assess physical activity. The
increased number of devices now available can be attributed to multiple factors,
including the translation of laboratory-based approaches to the ield, largely due to
signiicant advances in technology and the production of lightweight portable devices.
Consequently, the objective measurement of physical activity and quantiication of
energy expenditure in athletic and free-living contexts, across all age groups, is now
possible using a wide range of measures. In choosing among the methods available,
there commonly is a tradeoff between cost, participant burden, and the ability to
assess speciic features of the physical activity with ease of measurement, number of
participants to be assessed, and time frame over which the assessment is to be made
also considered.2,4,5 Given the strengths and limitations inherent in each of the methodologies available, there is value in using combined approaches in many situations.
For example, objective measurement of daily total energy expenditure (TEE) and
activity energy expenditure (AEE) of athletes using the doubly-labeled water (DLW)
technique can be combined with heart rate (HR) monitoring and accelerometry, or
global positioning systems (GPS) in some situations, to assess the number of bouts of
activity and the duration and intensity of each bout. Furthermore, use of self-report
instruments such as activity diaries provides valuable contextual information and
subjective ratings of perceived exertion for the speciic types or sessions of physical
activity undertaken. Subjective diaries can also provide information regarding the
psychological state of the athlete during and after training sessions or competitions.
To effectively manage the demands of athletic performance in training and competition requires a coupling between energy intake and expenditure to maintain a
stable body weight. This necessitates a sound working knowledge of both food and
energy, including the energy cost of physical activity. The assessment of physical
activity and energy expenditure presents numerous challenges, including the affordability of techniques to the researcher or practitioner and the data collection burden
on the athlete. As physical activity is a complex and multidimensional behavior,
precise quantiication is particularly challenging under free-living conditions.6
Numerous factors should be considered in the selection of assessment methods,
including the age of participants, sample size, participant burden, method/delivery
mode, assessment time frame, the type of physical activity information required,
data management, measurement error, cost of the instrument, and others.4,5,7,8 It
is important to appreciate that no single technique is able to quantify all aspects
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Field Assessment of Physical Activity and Energy Expenditure among Athletes 185
of physical activity under free-living conditions; therefore, multiple measurement
approaches are often used.
This chapter provides deinitions of the major terms of importance followed by an
overview of selected objective and subjective approaches used in athletic populations
to assess physical activity and energy expenditure.
6.2
DEFINITIONS
The assessment of physical activity and energy expenditure has been affected by
the inconsistent use of terms; therefore it is critical to provide an overview of key
terminology. Physical activity is a global term and traditionally deined as bodily
movement resulting from contraction of skeletal muscle leading to a substantial
increase in energy expenditure above resting levels. In turn, physical activity can
be categorized according to context or setting, for example, leisure-time or recreational physical activity, including sport, transportation, and occupational activity
(Figure 6.1). In contrast, exercise is commonly deined as planned, structured, and
repetitive movement with the intention of promoting or maintaining one or more
components of physical itness.9 The measurement of physical activity and exercise
can therefore be complex given the variety of conditions in which an athlete lives,
trains, and competes. Dimensions of physical activity and exercise include intensity,
duration, frequency, and mode or type, for example, walking, running, swimming,
or cycling. The duration of the activity or exercise refers to the time spent in the
task, and frequency refers to how often one exercises, trains, or competes. Readers
are referred to the paper by Howley,10 which provides a good overview of the various terms associated with physical activity and exercise, and provides guidelines for
consistent interpretation of exercise intensity and volume.
PHYSICAL ACTIVITY
Leisure-time physical activity including sport
Occupational or work-related activity
Transportation activity
Activity in the home
Sedentary activity
FIGURE 6.1 Components of total physical activity.
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It is important to recognize that an outcome of participation in physical activity or exercise is the expenditure of energy that is commonly quantiied in terms of
intensity of effort. Intensity can be referenced in a number of different ways.10 For
resistance weight training the training intensity is described as the relative weight
lifted (%1-Repetition Maximum), and in aerobic exercise this is typically according
to the elevation of HR in beats per minute. In other words, training intensity is the
energy expended over and above the body’s basal metabolic requirements, and we
can deine physical activity broadly as activity energy expenditure (AEE) or more
speciically as exercise energy expenditure (ExEE). AEE and ExEE can be expressed
relative to resting values where 1 MET (metabolic equivalent) at rest has been considered to equate to 3.5 mL/O2/kg/min–1 or 1 kcal/kg/hr. It is important to note that the
conversion of METs to kcal can be erroneous when using these standard conversion
factors.11–15 However, we have shown that a correction factor based on measured or
predicted resting metabolic rate (RMR) can reduce this error in some activities.12
Gross energy expenditure is quantiied according to oxygen consumption and referenced in kcal/min or kJ/min to be more relevant to the individual, relative to body
weight. In many athletic events and particularly in team sports, an overall assessment
of the intensity of the event or game can be dificult given the often intermittent and
variable pace and differences across playing positions. Figure 6.2 subdivides TEE
into component parts and relects the commonly used ield assessment techniques to
quantify these components.
Energy Expenditure Components
Activity
Energy
Expenditure
(AEE)
Exercise Energy Expenditure
(ExEE) *
Non-Exercise Activity
Thermogenesis (NEAT)
Thermic Effect of Feeding (TEF)
Total Energy
Expenditure
(TEE)
Resting Metabolic Rate (RMR)
*60–70% of TEE
Objective or Derived Methods
Heart Rate Monitoring
Accelerometry
GPS
Heart Rate Monitoring
Accelerometry
Or by subtraction:
NEAT = TEE – (ExEE+TEF+RMR)
Indirect Calorimetry
Or by calculation: ~10% of TEE
DoublyLabeled
Water
(DLW)
Indirect Calorimetry
FIGURE 6.2 Assessment of TEE and techniques commonly used to quantify the separate
components. It is important to note that each of the components listed in the diagram can also
be measured directly using a whole-body calorimeter. However, the restrictive nature of the
measure (participants are conined to a small room for the length of the measurement) means
that free-living measurements are not possible. *ExEE and thus AEE are the most variable
components; therefore, the proportions of TEE that RMR, TEF, and AEE represent differ
between individuals.
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Field Assessment of Physical Activity and Energy Expenditure among Athletes 187
6.3
6.3.1
METHODS OF ASSESSING PHYSICAL
ACTIVITY AND ENERGY EXPENDITURE
OBJECTIVE MEASURES
Typically, more objective methods of assessing physical activity involve the systematic measurement of physiological and/or biomechanical parameters and the subsequent use of this information in proiling the amount and nature of the activity as
well as in the determination of AEE.
6.3.1.1 The Doubly-Labeled Water (DLW) Technique
The DLW technique is the gold-standard or criterion measure to assess TEE.16–18
The major advantage of the DLW technique is that it is noninvasive and imposes
minimal participant burden, which enables the assessment of TEE in athletes under
normal living and training conditions over a 7- to 14-day period (depending on the
analysis approach and age of the athlete). Another signiicant advantage of the technique is its accuracy and precision; however, the DLW technique provides a gross
measure of energy expenditure and is not able to provide information on the nature
or types of activity an individual has been engaged in.7 A further disadvantage is
that although the sample collection can be undertaken in the ield with little equipment or imposition to the participant, the sample analysis requires laboratory-based
assessment using specialized equipment. Therefore the technique is prohibitive for
large-scale, population-based assessments of energy expenditure. However, because
of its gold-standard status, the DLW technique is commonly used to validate other
techniques that are employed to quantify free-living energy expenditure, including
physical activity questionnaires.5,19–21
The DLW technique requires the collection of daily urine samples over 10–14
days, the measurement of RMR via indirect calorimetry (or prediction using equations), and specialist laboratory equipment and personnel for analysis.16 The two stable
isotopes, deuterium (2H) and oxygen-18 (18O) are administered orally via a drink of
water, and the elimination of the isotopes from the body is tracked by analyzing daily
urine samples.22–24 The difference between the elimination rates of the two isotopes
is equivalent to the rate of carbon dioxide production, which can then be converted
to average daily energy expenditure.25 The DLW technique provides an indication of
daily energy expenditure across the measurement time frame. For a detailed overview of the DLW technique for the assessment of TEE, readers are referred to a
recent publication by the International Atomic Energy Agency (IAEA).16
If RMR is accounted for, AEE can be calculated by assuming a constant for the
thermic effect of feeding (TEF) (10% TEE):
AEE (kcal/d) = 0.9 × TEE (kcal/d) – RMR (kcal/d)
AEE is therefore all the energy expended above resting and food ingestion–related
energy costs. The ratio of TEE to RMR is a common measure of physical activity
level (PAL); however, there is some query about the relevance of PAL if it is not
independent of body weight.26 Similarly, AEE is inluenced by body weight (energy
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expenditure is generally higher for the larger person moving at a given speed) and
by the economy or eficiency with which a movement is performed.4 Furthermore,
because AEE is an average value for the 7–14 days over which the DLW method is
utilized, it provides no information on the type, intensity, or duration of physical
activity that comprised the AEE. To overcome both the body size and eficiency
differences and enable AEE values to be compared between individuals, Weinsier et
al.27 devised an index, the activity-related time equivalent (ARTEEE), of the amount
of time a person spends at a level of energy expenditure equivalent to a reference task
(such as walking at 5 kph) or set of activities (such as standing, walking, or running
circuit). The index is calculated using the equation
ARTEEE index (min/d) = (TEE [kcal/d] × 0.9 – RMR [kcal/d]) /
(reference activity EE [kcal/min] – REE [kcal/min])
Despite the validity of this index, because it is based on the DLW technique, the
authors recognize its usefulness will be limited to studies of small groups.4 However,
there is the possibility of using a similar approach to “calibrating” accelerometer
data, discussed later in the chapter.
The maximum performance in endurance activities depends on the availability
and convertibility of energy.28 It is recognized that there must exist a ceiling, or
upper limit, to the TEE and that this ceiling in humans may be set by maximal
daily energy intake.29 In addition to maximal rates of food intake and digestion,
Hammond and Diamond30 identify maximal sustainable energy expenditure is limited by rates of O2 uptake and distribution, metabolite removal, and energy utilization by end organs. The most likely limiting factor is end-organ use, the work levels
that can be maintained by our musculature. It was estimated from factorial analyses
by Brody31 that heavy labor could increase the TEE to approximately four times the
metabolic rate (BMR). These values were conirmed with DLW studies showing that
while the upper limit to sustainable TEE in the general population is 2.2–2.5 times
BMR, well-trained athletes who consume large quantities of food while training and
competing can maintain energy balance while still expending 4–5 times BMR.32
Higher levels of daily energy expenditure are possible; however, these are not sustainable and the participant will be in negative energy balance and possibly even in a
negative nitrogen balance. The consequence is a loss of weight, a higher proportion
of which over time will be lean body mass.33 It has been speculated that it is dificult
to ingest and digest enough food during prolonged exercise in excess of 4780 kcal/
day.34,35 However, Eden and Abernathy36 reported that a male ultraendurance runner
covering 1005 km over 9 days (111.7 km/d) consumed 5975 kcal/d. Similarly, Gabel
et al.37 reported the average daily energy intake of two elite male cyclists covering
3280 km in 10 days (Pony Express route) was 7122 kcal/d.
It is important to acknowledge that in addition to the exercise intensity, the
energy expenditure in exercise is related to body size and the type of exercise
being performed. The DLW technique has provided an opportunity to investigate
energy expenditure during multi-day endurance events such as cycle tours and running events, as well as in hostile environments (treks in Antarctica or climbing
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Field Assessment of Physical Activity and Energy Expenditure among Athletes 189
Mt. Everest, for example) and in military exercises. Westerterp et al.38 measured
DLW using a 6- to 7-day protocol, three times in four elite cyclists (69.2 ± 5.9 kg)
during the 22-day Tour de France and found average daily TEE to be 7000–8600
kcal/day, which equates to 3.6–5.3 times the RMR (that is, a PAL range of 3.6–5.3).38
Over the 3826 km race, participants were reasonably weight stable; weight decreased
on average 1.4 kg. In another study, Rehrer et al.39 used DLW to measure the TEE
in ive cyclists who completed the 6-day, 10-stage, 883 km Tour of Southland. The
average TEE was 6550 kcal/day, but as this cohort were on average 14.6 kg heavier
(and thus had a higher RMR) than the cyclists measured by Westerterp et al.,38 the
average PAL was lower at 2.39. DLW has also been used in ultraendurance running
events. A 2-week DLW study was undertaken in weeks 2–4 of a 14,964 km run
around the coast of Australia; the 63 kg male completed the distance in a record
195 days, running on average 76.74 km per day.40 During the study period, body
weight decreased by 1.5 kg and over the 195-day run, body weight loss was only
1.0 kg suggesting there was neither a signiicant nor a persistent energy deicit. In
this participant, TEE was 6321 kcal/d, and using an estimated RMR, PAL was 3.96.
Fudge et al.41 used a 7-day DLW protocol in nine elite Kenyan endurance runners
(56.0 ± 3.4 kg) during a precompetition training phase. Weight loss was not statistically signiicant (0.3 ± 0.8 kg) and TEE was ~3500 kcal/d, with an average PAL of
2.3. Hoyt et al.42 used DLW to measure 23 Marines (79.8 ± 1.3 kg) during 11 days
of severe cold-weather mountain training; the average TEE was 4924 kcal/d with
a PAL of 2.8 ± 0.2. Reportedly during the irst 4 days of the exercise, the Marines
were physically active for 17.93 ± 0.22 hours/day and during this time TEE was 7131
kcal/d with a PAL of 4.0 ± 0.2. However, during the 11 days there was a loss of body
weight of –2.48 ± 0.25 kg. Similar TEE values have been reported in other military
cohorts,43,44 and weight loss is common. Thus, although the energy expenditure is
lower than seen in studies of athletes, energy intake is not well matched. Finally,
in possibly the most extreme test of human energy expenditure, a DLW study was
undertaken of two men (89.9 kg and 69.0 kg) who pulled sledges initially weighing
222 kg for ~10 hours/day over 95 days in temperatures ranging from –10ºC to –55ºC,
covering a distance of 2300 km across Antarctica.45 The reported TEE in the irst
50 days (multiple DLW doses were administered) was 8485 kcal/d and 6955 kcal/d
for the heavier and lighter man, respectively. Because energy intake was on average
5090 kcal/d, both men lost more than 25% of body weight. The highest TEE values
were 10,660 kcal/d and 11,640 kcal/d for the two men; these were recorded between
the 20th and 30th days of the expedition, during which time the sledges were pulled
for 12 hours/day up hills of 50 m to > 3000 m in altitude. The PAL values reached
6–7, although these were not able to be sustained due to the rapid weight loss.33 These
are the highest values reported in the literature using DLW; however, these are lower
than the 14,980 kcal/day (8 times BMR) predicted by Davies and Thompson46 for
ultraendurance running.
These DLW studies provide us with objective gold-standard data and a “reality check” as to what the highest levels of sustainable and short-term (in terms of
days to months) levels of daily energy expenditure that are physiologically possible
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in athletes. Any measurement tool that provides values beyond 4–5 PAL in weight
stability, or 6–7 PAL in any situation, is most certainly erroneous.
6.3.1.2 Heart Rate Monitoring
6.3.1.2.1 Measuring Energy Expenditure
The use of heart rate (HR) monitoring to estimate energy expenditure is based on
the assumption that there is a linear relationship between HR and oxygen consumption (VO2).47 Although there is considerable between-individual variability in the
slope of the HR-VO2 relationship relecting differences in movement eficiency, age,
and itness, the linear relationship holds well within an individual across a range
of submaximal aerobic exercise tasks.48–50 Consequently, when an individual or
group regression line has been determined, HR can be used to estimate an individual’s oxygen consumption and in turn energy expenditure in free-living conditions.
Since the late 1970s, the development of portable HR monitor devices has broadened the potential usefulness of this relatively low-cost technique for quantifying
daily energy expenditure in real-world situations.51 HR monitors now with increased
memory storage and downloading facilities provide the means for recording average
HR data per 5 seconds or per minute for over a week continuously.52 The advantage
of HR monitoring at the individual level is the ability to calibrate the monitor to each
individual. Individualized HR-VO2 regression equations provide greater accuracy as
they account for individual differences in health and itness. An individualized calibration equation can be developed if the athlete completes a submaximal treadmill
or ergometer test that reaches 80–85% of an individual’s age-predicted maximum.53
A wide range of HR data ensures that the calibration is accurate for various intensities of physical activity.
However, there are important limitations of the method. First, the HR-VO2 relationship does differ between tasks, particularly for predominantly upper-body versus
lower-body activities.54 Consequently, the use of a single regression line derived from
one movement proile (for example, running) will not be accurate for activities with
very different biomechanics (for example, cycling, swimming, rowing).55 Another
limitation of this approach when used to measure TEE or AEE over a day or days
is that despite there being a close relationship between HR and energy expenditure
during exercise, there is little relationship between the two parameters during rest
and periods of light activity.7,56,57 To overcome this problem, Spurr et al.58 developed
the lex heart rate (lex-HR) method that utilizes an individually predetermined HR
to discriminate between resting and exercise HR. The lex-HR method was validated in adults against whole-body calorimetry56,58,59 and against DLW60 with good
agreement for group comparisons. Livingstone et al.61 used DLW as the criterion
and showed that lex-HR was a low-interference technique for accurately predicting group estimates of habitual TEE in healthy, free-living children. The lex-HR
method has been applied to verify the minutes spent in activities of different intensities by Ekelund et al.62 and to assess TEE and patterns of physical activity in adolescents. Similarly, Grund et al.63 used the approach to verify the effect of gender on
different components of total daily energy expenditure (TDEE) in free-living prepubertal children. The accuracy of the method depends on the appropriateness of an
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Field Assessment of Physical Activity and Energy Expenditure among Athletes 191
individually predetermined HR that can be used to discriminate between resting and
exercise HR. Li et al.54 suggest that the relationship between energy expenditure and
HR differs between individuals and within individuals on different occasions and
that it is therefore necessary to develop individual calibration curves immediately
before the HR recording period. Other studies have conirmed this suggestion64–66
and established that the lex-HR method of estimating EE is reliable at the population level but not necessarily stable for individuals over time. While the best value of
the lex-HR may be participant-speciic, it may also depend on the mode of activity
used to determine the VO2–HR relationship.67 A further limitation is that HR may
be affected by a range of factors other than physical activity, including temperature,
humidity, dehydration, emotion, and itness, and provides no contextual information
on the physical activity being performed.7,8 Overall the general consensus is that
while the HR method provides satisfactory estimates of average energy expenditure
for a group, it is not necessarily accurate for individual participants.
6.3.1.2.2 Monitoring Training Load
The real value of the HR method is in determining the intensity of discrete bouts of
exercise and the estimation of the energy expended in continuous or steady-state aerobic exercise. The American College of Sports Medicine68 recommends that the use
of HR to describe exercise intensity be expressed using %HR Reserve and/or %HRmax.
Exercise intensity can then be classiied into six categories from very light to maximal. Using the classiication process, it is possible to equate the HR category with
its associated %VO2max or %VO2Reserve or metabolic equivalent without actually needing to measure VO2. However, it is well recognized that greater accuracy is ensured
when the VO2–HR relationship is measured for each individual.52
In short, despite being a physiological marker for physical activity, HR can be
inluenced by a wide range of factors potentially unrelated to the activity being monitored. Therefore, HR can provide an estimate or general picture of physical activity7 but particularly when used for longer time frames outside a training or exercise
competition situation, energy expenditure estimates are improved if HR monitors are
used in conjunction with other devices.
Heart rate is also used to monitor training loads and as a physiological marker of
overtraining.69 In particular, HR can be used to assess the autonomic nervous system
following a training stimulus via monitoring heart rate variability (HRV)70–72 and
heart rate recovery (HRR).71,73 Lamberts et al.73 studied the HRR after exercise and
cycling performance in fourteen well-trained cyclists undertaking a 4-week highintensity training (HIT) phase. It was found that endurance performance (40 km time
trial) improved more in the cyclists who demonstrated a decrease in HRR toward the
end of the HIT period, indicative that a decrease in HRR could be a marker of an
inability to cope with the training load and the accumulation of fatigue.
6.3.1.3 Pedometers
Pedometers have become popular for health professionals to encourage sedentary
adults to adopt a more physically active lifestyle by providing a “steps per day” goal.
While the concept of the pedometer is accredited to Leonardo da Vinci, a number
of versions of the device were developed in the seventeenth century to count steps
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TABLE 6.1
Average Steps per Day Associated with Activity Level
Activity Level
Sedentary lifestyle
Low active
Somewhat active
Active
Highly active
Steps per Day
< 5000
5000–7499
7500–9999
10,000–12,500
> 12,500
for the purpose of measuring plots of land.74 More recently, pedometers became
the focus of attention after Japanese researchers recommended a daily step count
of 10,000 steps as a threshold for health beneit and cardiovascular disease prevention.75,76 Hatano75 equated walking 10,000 steps per day with 300 kcal energy expenditure, a daily amount identiied in the College Alumnus Health Study as optimal
to reduce the risks of an initial heart attack.77 However, the rationale for the 10,000
steps has been challenged as a viable recommendation for all people.78,79 Based on
the equivalence of approximately 1250–1550 steps being taken per kilometer,80 30
minutes of brisk walking per day translates to approximately 3000–4000 steps.
Using a range of study indings, Tudor-Locke and Bassett81 have devised Table 6.1 to
categorize activity levels relative to different accumulative step counts.
It is beyond the scope of this chapter to compare the relative merits of the different operating mechanisms of pedometers, but the reader is referred to a number
of other publications for these explanations.74,82–87 A well-recognized problem with
the accuracy of pedometers is that step counts are inaccurate for speeds slower than
60 m.min–1, which could be a problem when using the devices in elderly or inirm
populations.88–90 Furthermore, pedometers worn by different people often register a
different step count for the same number of actual steps taken. One reason suggested
for this inding is that the impact of foot strike is not uniform for right and left legs,
so the pedometer readings can vary depending on where the monitor is worn.91,92
Another factor inluencing accuracy is waist girth; for centrally obese persons the
monitor may rotate when worn on the waistband.82
Even if the steps are measured accurately by the monitor, the interpretation
of the step count needs to be clariied. It is common for step counts to be used
to determine distance traveled by a simple multiplication of the number of steps
taken by the average stride length. The accuracy of this calculation depends not
only on the determination of stride length but also on the pace of walking. Stride
lengthens with increases in speed.93,94 Therefore, walking faster than normal may
cause an underestimation of the total distance walked whereas slower walking will
cause an overestimation in distance unless there are commensurate relative changes
in stride length and step frequency as speed changes; this is not always the case.
Furthermore, if stride length is related to height, differences in height will also
have an impact on the number of steps taken per unit distance. Most devices do
not account for individual differences in height and particularly leg length and its
impact on step counts. We have found in a sample of 205 adults heterogeneous in
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Field Assessment of Physical Activity and Energy Expenditure among Athletes 193
height (1.70 ± 0.09 m; range: 1.50–1.92 m) that leg length was negatively associated
with the number of steps taken to cover 2 km at a self-selected walking speed, with
30% of the variance in steps taken explained by leg length. However, even after
adjusting step count for leg length, self-selected walking speed remains a moderately strong inluence on the number of steps taken to travel 2 km (unpublished
data). The implications are that steps should not be used as a proxy for distance
traveled without undertaking an individual calibration of the pedometer to know
how many steps are taken for a given distance; calibrating at a range of speeds may
also be warranted.
Pedometers can be problematic particularly for youths and the inquisitive participants who continuously look at the readout and can enthusiastically change typical
movements to enhance the increasing step count. Pedometers are often taped shut for
this reason, and the irst few days of recording are often discarded. The advantage of
pedometers is that they are relatively inexpensive, are easy to use, and have output
data that can be meaningful to the end user as well as to the researcher. Given that
walking is the most common physical activity in both light- and moderate-intensity
categories, having a good measure of distance and speed is important.95 Additionally,
it is important that if pedometers are to be used in an intervention or as a tool to
monitor changes in daily physical activity, that the sensitivity of the tool to measure
change is high. In a small sample (N = 9) of obese sedentary adults, Tudor-Locke
and Myers96 reported that pedometers were able to track modest increases in walking
volume, whereas physical activity diaries were not sensitive to the change in ambulation associated with a walking-based intervention. An unfortunate consequence of
the popularity of pedometers has been the distribution of many substandard models
by companies within breakfast cereal packs, attached to fashion magazines, or made
available through general practice clinics. Without individual calibration at regular
intervals, these instruments have little more than gimmick value.
6.3.1.4 Accelerometers
Accelerometers measure the rate or intensity of body movement in terms of acceleration, and this enables a proile of the intensity of movement over time. Most devices
incorporate piezoelectric sensors that detect acceleration in one to three orthogonal
planes (vertical, anteroposterior, and mediolateral). These sensors respond to both
frequency and intensity of movement, and in this way are superior to pedometers
and actometers that are attenuated by impact or tilt and only count body movement
if a certain threshold is passed.97 The method is based on the fact that speed is the
change in position with respect to time, and acceleration is the change in speed with
respect to time. Acceleration is usually measured in gravitational acceleration units
(g; 1 g = 9.8 m · s–2). When acceleration is zero, the speed is not changing; however,
there may still be movement taking place, but it is just happening at a constant speed.
Acceleration is proportional to the net external force involved and therefore is more
directly relective of the energy costs associated with the movement. Consequently,
measuring physical activity using acceleration is preferred to using speed. The
reader is referred to the following papers that provide good reviews of the technical
aspects of the methodology and these devices: Chen and Bassett,98 Bouten et al.,97
and Plasqui and Westerterp.99
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The irst generation of accelerometers consisted of a single accelerometer placed
on the waist, due to the proximity with the center of body mass, or on the ankle or
wrist to proile movement of the limbs. The most commonly used models of this kind
of device include Caltrac, Tritrac-R3D, RT3, Actigraph (formerly known as Computer
Science and Applications [CSA] and Manufacturing Technology Inc. [MTI]), Actical,
and Actiwatch. Chen and Bassett98 provided the technical details of three of the commonly used devices; information is reproduced in Table 6.2. Bouten et al.97 have summarized the frequency and amplitude range required to accurately measure human
movement. It was proposed that for accelerometers placed at waist level, a frequency
band between 0.3 and 3.5 Hz and an amplitude range of –6 g to +6 g should sufice
to capture daily physical activities. Within these ranges, accelerations during lowintensity activities, such as sedentary activities or walking, as well as high-intensity
activities or exercise, such as running and jumping, can be measured. Low- and highpass ilters can be used to eliminate those frequencies that are unlikely to arise from
human movement, such as high frequencies due to transportation.99 As can be seen
from Table 6.2, not all models meet the criteria proposed by Bouten et al.,97 and so
arguably may undermine the reliability and precision of the device, and then adversely
affect the accuracy of the resulting energy expenditure measurements.
Advantages of these instruments include their relatively small size and capacity
to record data continuously for days or even weeks.7,98 Unlike pedometers, there is
no obvious feedback provided to the participant wearing the monitor. As accelerometers provide no meaningful readout on the monitor itself, there is less likely to be
overestimates of physical activity measures in the same way as is seen in pedometers. Compared to the uniaxial sensors, triaxial devices theoretically provide a more
comprehensive assessment of body movements. Further, it has been reported in studies of adults and children that higher precision is achieved using triaxial devices for
the estimation of energy expenditure when compared to uniaxial devices.100 One of
TABLE 6.2
Technical Details of Several Commonly Used Accelerometry-Based Physical
Activity Monitors
Manufacturer
Battery type
Battery life
Epoch
Number of axes
Sampling frequency
Frequency response
Intermonitor CV
ICC
Actigraph
(MTI/CSA)
RT3
MTI
Coin cell
160 days
1 s–10 min
Uniaxial
10 Hz
0.25–2.5 Hz
4–5%
0.8
StayHealthy
1 AAA
30 days
1 s or 1 min
Triaxial
Unpublished
Unpublished
4–26%
0.73–0.87
Actical
Mini Mitter
Coin cell
180 days
15 s–15 min
Uniaxial
32 Hz
0.5–3 Hz
4–19%
0.62
Source: Chen, K.Y. and Bassett, D.R., Jr., Med. Sci. Sports Exerc. 37, S490–500, 2005.
© 2011 by Taylor and Francis Group, LLC
Field Assessment of Physical Activity and Energy Expenditure among Athletes 195
the methodological issues is that while there is a good linear relationship between
accelerometer counts and energy expenditure during walking, there have been some
concerns in studies of running activities. Early work by Haymes and Byrnes101 demonstrated that the Caltrac accelerometer was a valid indicator of physical activity
during walking but did not adequately discriminate between running speeds of
8–12.8 kph. A decade later, Brage et al.102 assessed the reliability and validity of
the CSA (model 7164) accelerometer (MTI) in a wide range of walking and running
speeds in the laboratory and ield settings. It was noted that the CSA output rose
linearly (R2 = 0.92) with increasing speed until 9 kph but remained at ~10,000 counts
· min–1 during running; the consequence is an underestimation of oxygen uptake at
speed > 9 kph. Brage et al.102 proposed that the lack of linearity between the uniaxial
CSA output and speed when running was presumably due to relatively constant vertical acceleration in running. In Figure 6.3 (unpublished data), we show comparable
results using the Actigraph (GT1M); the slope of the relationship reduces at 8 kph.
Rowlands103 compared uniaxial (ActiGraph) and triaxial (RT3) devices and conirmed an increasing underestimation of activity by the uniaxial monitor as speed
increased. It was proposed that this underestimation was related to frequency-dependent iltering and assessment of acceleration in the vertical plane only. In contrast,
the triaxial output was strongly related to speed, relecting the predominance of
horizontal acceleration at higher speeds. Rowlands103 concluded that high-intensity
activity is underestimated by the uniaxial device even after correction for frequencydependent iltering, whereas the triaxial device was not limited in the same way.
However, there has been some criticism of studies that seek to compare the superiority of triaxial monitors over uniaxial for the purpose of estimating energy expenditure. In these studies, not only are there differences in the number of axes but also
the model of device, and hence the monitor technology differs. To overcome this
10,000
9,000
Counts per minute
8,000
7,000
6,000
5,000
4,000
3,000
2,000
1,000
0
0
1
2
3
4
5
6
7
8
9
10
11
12
13
Speed (kph)
FIGURE 6.3 Average counts per minute of an individual walking (3–6 kph) and running
(7–13 kph) using the Actigraph (GTlM).
© 2011 by Taylor and Francis Group, LLC
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Nutritional Assessment of Athletes, Second Edition
limitation, Howe et al.104 has recently used a single device that is capable of measuring and reporting movement in all three axes separately and simultaneously (RT3)
to determine whether using three planes of acceleration signals is superior to using
only the vertical plane of the same unit for predicting AEE during locomotion and
activities of daily living. Compared with vertical-only counts, using the integration
of the three axes did not signiicantly improve the relationship between counts and
AEE. However, it is important to note that compared with indirect calorimetry, RT3
overestimated AEE for treadmill activity by 9% and underestimated activities of
daily living (ADL) by 34%. The RT3 underestimated activity with greater upper
body movements by 24–64%. Compared to DLW over 15 days and using the proprietary algorithms, Maddison et al.105 found the RT3 underestimated AEE by 15% on
average. The authors suggest that while the RT3 may provide a relatively accurate
assessment of free-living AEE at the group level, it generally underestimated the
activity-related energy expenditure compared to DLW. These studies demonstrate
that is not suficient only to consider the number of axes used; the technology inherent in the device or the data processing may be the source of error. When using
multiple regression to devise an AEE prediction equation from participant characteristics and activity counts, many studies do not mention partial correlations for activity counts or the increase in R2 caused by the activity counts. Plasqui et al.106 note
that age, body mass, and height collectively explained 64%, while the triaxial accelerometer (Tracmor) added only an additional 19% of the variation in TEE. In some
studies it is possible that most of the variance is explained by participant descriptors
and the accelerometry data may have only marginal additional value. Few studies
have provided data to show the ability of the accelerometer to predict individual
AEE rather than AEE on a group level only; standard errors or limits of agreement
should be presented. Plasqui and Westerterp99 outline an important range of issues
for consideration when comparing the validity of different accelerometers.
Even without converting the accelerometer counts to energy expenditure, the raw
data from the accelerometer can be used to quantify time spent by an individual in
activities of different intensities. As shown in Figure 6.4A, the output can be related
to standard thresholds for light, moderate, and vigorous intensity movement.107–111
However, uniform cutoff points may not be truly representative of the same exercise
intensity across individuals. As shown in Figure 6.4B, individuals walking at the
same speed (4.8 kph) had an average output (vector magnitude) over 6 minutes of
1778 counts per minute. However, the variance around the group mean indicates a
high interindividual variation with a range of 71–129% of the mean value.
Shortcomings of the system are the low sensitivity to sedentary activities and the
inability to register static exercise.97 Because accelerometery is insensitive to physical activity that does not involve a transfer of the center of mass at a rate relative to
the energy expended (for example, weight lifting, walking up a grade, walking while
carrying a load), this will result in errors in energy expenditure measurement.111,112 It
has been demonstrated that both inter- and intramonitor variability exists with monitors; therefore, it is recommended that every laboratory perform trials to identify
outlying monitors and satisfy itself that the intermonitor variability is acceptable
before use.113,114 Further, as outlined above, accelerometers should be calibrated to
each individual user.
© 2011 by Taylor and Francis Group, LLC
Field Assessment of Physical Activity and Energy Expenditure among Athletes 197
Vector Magnitude
(counts/min)
6,000
5,000
Vigorous
4,000
3,000
2,000
Moderate
1,000
Light/
sedentary
0
0
4000
2000
6000
8000
10000
Time (minutes)
(a)
Vector Magnitude at 4.8 kph (cts/min)
2500
2000
1500
1000
500
0
1
2
3
4
5
Participant
(b)
6
7
8
FIGURE 6.4 (a) Raw RT3 accelerometer counts categorized according to activity thresholds; (b) interindividual variability in accelerometer counts when walking at the same speed
(4 kph); horizontal line represents the group average.
Accelerometers may also be used as a measure of inactivity. We have previously
shown in a sedentary group of men with schizophrenia that accelerometry was a poor
measure of activity energy expenditure when compared with the criterion measure of
DLW.115 The correlation between the accelerometry output (VM) and AEE was not
signiicant. However, a signiicant negative relationship was found between inactivity
(deined as a VM less than 20 counts/min) and AEE (r = –0.83, p = 0.001), with minutes
spent sedentary explaining over three quarters of the variance in AEE. Therefore, in
very sedentary groups the accelerometer data may be a valid measure of inactivity and
therefore could be used for research or clinical purposes to quantify the contribution of
sedentary behavior to weight gain or medical conditions associated with inactivity, such
as cardiovascular disease and diabetes. Further, the effectiveness of interventions to
reduce sedentary behavior could also be objectively monitored with accelerometers.
To improve the categorization of movement in recent years, multiple accelerometers have been worn on different body parts (trunk, chest, wrists, legs, and feet)
© 2011 by Taylor and Francis Group, LLC
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Nutritional Assessment of Athletes, Second Edition
and whole-body energy expenditure determined from the composite of movements.
Recently, devices other than standard accelerometers have been developed, such
as the ActiReg116 and the Intelligent Device for Energy Expenditure and Activity
(IDEEA),117,118 that use multiple sensors to assess both body posture and body movement, which are then translated into energy expenditure. These new technologies
have been evaluated in a range of studies with mixed results.
The ActiReg has two body position sensors (tilt switches) and two motion sensors.
The state of the tilt switches and motion sensors is checked every 1 second. The sensors discriminate between the four body positions (sit, stand, bent forward, or lie),
and between the four states of no motion, motion on either chest or thigh sensor, or
both. This gives a matrix of 24 = 16 possible combinations with ActiReg codes from
0 to 15. These codes are linked with an activity factor, from which energy expenditure can be determined. In the irst published study using the ActiReg, the calculated TEE did not signiicantly differ from DLW-measured TEE on a group level
in adults, but the individual variation in the difference between both methods was
large. Furthermore, the ActiReg underestimated TEE to a greater extent at higher
levels of energy expenditure.116 More recently the device has been used to assess
energy expenditure in clinical populations.119–121 The IDEEA device showed good
results under laboratory conditions but require multiple sensors to be attached to the
body and have a relatively large data acquisition unit, thereby diminishing wearing
comfort. So far, they have not been proven to be superior in the estimation of EE to
simpler accelerometers, and further research is required to determine their effectiveness as a measure of daily life AEE.99
Rather than using multiple devices that may increase cost, increase the possibility of missing data, and raise the participant and researcher/coach burden, recent
studies have focused on the identiication of activity types based on the acceleration
features measured with a single accelerometer.122,123 Bonomi et al.124,125 measured
activities of daily living with a single accelerometer during daily life in a population
of healthy adults, and utilized a decision tree to identify the different activity types
performed. The decision tree evaluated attributes of the acceleration signal. Using
DLW as the criterion measure, the identiication of types of physical activity, such as
lying, sitting or standing, active standing, walking, running, and cycling, performed
during the day combined with a simple methodology to deine activity type intensity
improved the estimation of TEE, AEE, and PAL compared with activity counts.
The ongoing technological advancements in accelerometer design and data processing approaches are likely to see this methodology become a tool of choice for
assessing both physical activity and energy expenditure in the future.
6.3.1.5 Combined Approaches and New Devices
The idea that HR monitoring and accelerometry be used simultaneously to assess
energy expenditure has been suggested by several researchers.100,126–128 The major
underlying rationale for using both techniques simultaneously is that the accelerometer is used as a backup measure to verify that elevations in HR are indicative
of physical activity.100 HR monitoring and accelerometry both encompass several
very different limitations. The heart rate–energy expenditure relationship is affected
by age, sex, training state, stroke volume, hemoglobin concentration of the blood
© 2011 by Taylor and Francis Group, LLC
Field Assessment of Physical Activity and Energy Expenditure among Athletes 199
and its O2 saturation, mental stress, ambient temperature, hydration, and quantity of
muscle mass involved in the activity. The limitations of the accelerometry devices
are biomechanical in nature and include issues with graded and load-bearing activity. Accelerometers lack both the ability to account for changes in the grade of the
exercise surface and any changes in load carried by the user.126 Since the limitations
of each technique are unrelated, the combination should theoretically yield a more
precise estimate of energy expenditure than either used alone.126,127 Another reason
for combining the techniques would be to employ HR monitoring for the assessment
of physical activity energy expenditure and use accelerometry to assess total daily
movement and calculate activity patterns that make up the AEE. The heart rate–VO2
relationship is consistently linear only during dynamic muscle exercise of moderate
to high intensity,129 thereby supporting the use of HR monitoring for the quantiication of physical activity energy expenditure (PAEE) and not the lower-intensity
activity that occurs in daily living. In contrast, accelerometry is very limited in
assessing AEE yet appears to accurately quantify low levels of activity or sedentary
behavior.128 A range of devices combining HR and movement monitoring capabilities are now on the market (Actiwatch/Actiheart/Actiband; ActiTrainer).
Other devices are being developed that extend beyond the combination of heart
rate and movement monitoring. The SenseWear Armband (www.bodymedia.com) is
a multiple sensor device collecting data from a skin temperature sensor, near-body
temperature sensor, heat lux sensor, galvanic skin response sensor, and a biaxial
accelerometer. These signals are combined to assess the type and intensity of an
activity. Together with information about gender, age, height, and weight, energy
expenditure is estimated using activity-speciic, proprietary algorithms. According
to the manufacturer, the device is clinically valid in subjects between 7 and 65 years
of age who are engaged in resting, ambulatory, stationary biking, motoring, and
weight-lifting activities. These tools are largely marked to the weight-management
rather than athletic market.
For the athlete, various companies are developing tools for monitoring exercise,
not all of which have been independently evaluated. Three of the more prominent
companies are Polar (www.polar.i), Suunto (www.suunto.com), and Garmin (www.
garmin.com). There is a growing range of products that, in addition to heart rate
monitoring, enable data collection of numerous mechanical variables: distance,
speed, altitude, cycling power output, running pace, and cadence, as well as other
compass features, altimeter features, GPS features, and cycling and running features. It is beyond the scope of this chapter to review each of these new technologies.
However, it is evident from the range of new tools currently available and under
development that there will be a wide array of possible assessment tools available in
the future. More research is of course required to evaluate the relative merits of each
of these new technologies.
6.3.2
SUBJECTIVE APPROACHES
Subjective approaches include direct observation, activity diaries, and physical activity questionnaires and interviews. A major shortcoming of subjective methods is that
the accuracy of information collected is inluenced by a range of factors, including
© 2011 by Taylor and Francis Group, LLC
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Nutritional Assessment of Athletes, Second Edition
the ability of the athlete to recall information retrospectively and the perception of
the participant regarding the nature of the responses required or expected. Borresen
and Lambert3 compared what athletes reported doing in training and what was actually completed. Twenty-four percent of the participants overestimated the duration of
training they were doing, and 17% underestimated their training duration. Because
this margin of error in self-reported data may signiicantly affect the prescription
of training, it has been suggested that the error be accounted for or, where possible,
physiological measurements be used to corroborate self-reported data.130 The use of
data collected by questionnaires to quantify exercise load is also limited by inadequate reliability and validity compared with laboratory measures; for example, the
reliability decreases as the time between the activity and recall increases, because
this is dependent on human memory.131
Interview-administered approaches are generally superior to self-report questionnaires and the validity of such approaches may be severely compromised in younger
athletes who typically have more problems in recalling physical activity. Direct
observation was one of the earliest methods of physical activity assessment used
and while it is often categorized as an objective approach, unlike other objective
tools (such as timing lights to measure speed, ilming for video analysis), it relies
predominantly on the coach’s perceptions of the athlete’s level of effort or quality of
training or performance. Perceptions by coaches and athletes of the same training
have been studied by Foster et al.,132 who showed signiicant differences between the
training that the coaches prescribed and the training the athletes actually completed.
Therefore, the extent to which training can be quantiied based on direct observations has been questioned.3 Further, because this method requires the presence of
an observer at every training session, which may be impractical or impossible, the
amount of data able to be collected in order to monitor and evaluate training accurately may be inadequate.130
The validity of data at the individual level collected using subjective measurement
approaches is commonly not as strong as using a more objective approach such as
accelerometry or the doubly-labeled water technique across a 7- to 14-day period.
However, the validity of data at the group level may be higher and the low cost of
most subjective methods creates an advantage for large, population-based studies.7,133
In addition to the low relative cost, a major advantage of subjective approaches is the
ability to derive information about speciic physical activity behaviors.8 A brief overview is provided of a number of the subjective approaches to assess physical activity.
6.3.2.1 Direct Observation
Direct observation generally encompasses a signiicant element of subjectivity in
scoring activity participation and the subsequent interpretation of data. The presence
of an observer can cause the participant to react differently, and this may result in
an activity being over- or underestimated. Similar changes to behavior can be seen
when equipment—for example, a video camera—is used to record activity. However,
such differences are likely to diminish over time and therefore be normalized for the
period of observation.
Familiarization periods can be used to allow participants time to adapt to the presence of an observer and subsequently diminish the error from participant reactivity.
© 2011 by Taylor and Francis Group, LLC
Field Assessment of Physical Activity and Energy Expenditure among Athletes 201
Observer bias is also a concern when using direct observation and can be inluenced
by the participant’s gender, the purpose of the study, or the behaviors of surrounding
peers.133,134 The approach is not suited for use in free-living activities due to the burden on the observer; however, a major advantage of direct observation is its suitability
for small numbers of participants over short periods of time, assuming the availability
of trained observers.8 The method has also provided important contextual information—for example, regarding activity level and distance covered during match conditions—which may not be obtainable with other physical activity measurements.135
6.3.2.2 Physical Activity Records or Diaries
Physical activity records, or diaries, can provide detailed accounts of activity types
and patterns through descriptions of activity type (such as walking, watching television), purpose (for example, exercise, occupation, housework), duration (minutes or
hours, for example), intensity (light, moderate, vigorous), and body position (reclining, sitting, standing, moving, and so forth).2 Considerable detail may be recorded in
relatively short time intervals, typically every 15 minutes. This information can be
collated to determine time engaged in various activities and/or translated into predictions of energy expenditure using metabolic equivalent (MET) values for each task
and intensity level.2 Typically, this requires the use of the compendium of physical
activities and a coding scheme that is based on a ive-digit code that describes physical activities by major headings (occupation, transportation, and so on) and matches
the speciic activities within each major heading with a corresponding intensity (displayed as METs). The compendium of physical activities was created in 1989 and
updated in 2000. It is often used in physical activity records because of its easy
translation across studies.11 However, the amount of detail necessary to complete the
records over small amounts of time can create a high administrative burden for both
the participant and the investigator.2 Because of this burden, it has been suggested
that the physical activity records primarily be used to monitor high risks of energy
imbalance (such as obesity, metabolic syndrome) or when detailed physical activity
information is needed in relation to health conditions.2
A disadvantage of activity diaries is that individuals are required to record physical activities in blocks of time (ideally to account for each 15 minutes) across multiple 24-hour periods. Diaries have been used in different populations but have a high
participant burden.
6.3.2.3 Physical Activity Questionnaires
Physical activity questionnaires are the most commonly used physical activity
assessment tool.132 There are three main types of questionnaires: global, recall, and
quantitative. A global questionnaire is a brief survey that is easy to complete in
relatively short periods of time but does not provide explicit detail of the physical
activity. It is useful when a group is being generally categorized, such as “active” or
“inactive.” Recalls are longer and more detailed accounts of physical activity and
are typically considered a separate assessment tool. Quantitative questionnaires are
long and detailed, providing information about the frequency and duration of speciic activities over extended periods of time (such as year, lifetime). Although a
heavier burden on the participant, the quantitative questionnaire is good for assessing
© 2011 by Taylor and Francis Group, LLC
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Nutritional Assessment of Athletes, Second Edition
lifestyle factors or physical activities that are associated with disease or chronic
health.2 Physical activity questionnaires vary in terms of amount of detail provided,
length of time assessed, and the extent of supervision during the completion of the
questionnaire.131 The most common questionnaires are the Baecke, Tecumseh, or
Minnesota Leisure Time Physical Activity Questionnaire, or variations thereof. A
systematic review of physical activity questionnaires identiied four physical activity
questionnaires that had the basic research design components necessary to estimate
activity energy expenditure, which included the Tecumseh and Minnesota Leisure
Time Physical Activity Questionnaire (alone and in combination), as well as the
Questionnaire d’Activité Physique Saint-Etienne.20 The Tecumseh questionnaire
involves individual interviews pertaining to the estimated hours per week spent in
sport, home repair, sleeping, eating, quiet leisure time, and all remaining activities.136 The Minnesota Leisure Time Physical Activity Questionnaire assesses daily
physical activity completed during leisure time and household activities for a period
of 12 months.137 Both studies, as well as the Baecke questionnaire and others, have
been validated using doubly-labeled water as the criterion measure for assessing
physical activity in various populations. The correlation to doubly-labeled water is
low, speciically at the individual level, with group levels reaching only moderate
correlations to the criterion measure.20,133 Additionally, longer tests can confuse or
bore the participant, resulting in low validity and test–retest variability.138,139 Simpler
tests, such as the Baecke and Godin questionnaires, have test–retest correlations as
high as 0.81 and have had better success, relative to a Caltrac motion assessment of
concurrent validity.131
Physical activity recalls are a type of physical activity questionnaire and include
approximately 7–20 items to identify details about physical activity.2 The recall is
completed over at least a 24-hour period, with 7-day recalls typically used to assess
physical activity.20 Because of the length of time that is necessary for a person to
recall, physical activity recalls are more valid when administered as an interview
(either by telephone or in person). Similar to the physical activity records, information provided by a physical activity recall can identify exercise intensity levels
through METs. However, recalls tend to overestimate vigorous physical activity
while simultaneously underestimating the amount of time spent completing habitual
activities of daily living.2 In spite of this error, physical activity recalls have been
used to determine if a person is meeting activity guidelines.2
Self-report questionnaires represent the most commonly employed methods of
physical activity assessment and such instruments are suitable for individuals over
approximately 10 years of age (assuming a standard level of comprehension and literacy). Parent, teacher, and/or health professional proxy report approaches are required
when working with younger children or older adults, respectively. Although numerous self-report measures are available, they vary substantially. A particular strength
of questionnaires is their ability to capture the type, duration, and frequency of daily
physical activities, which is not possible using the DLW technique or sums of HR
over extended periods of time. However, there is a need to devise and validate appropriate questionnaires for the purpose of both evaluating physical activity and predicting total and activity energy expenditures. Questionnaires are most valuable when
used simultaneously with objective energy expenditure measurement approaches.
© 2011 by Taylor and Francis Group, LLC
Field Assessment of Physical Activity and Energy Expenditure among Athletes 203
Population-based surveys are commonly self-report instruments completed by
respondents or based on telephone responses to questions. Some of the strengths of
population surveys include the large numbers, the potential to access representative
samples, and the consistency of questions over time when the surveys are repeated.
However, weaknesses include the reliance on self-reported data, restriction to collect
only data on certain types of physical activity behavior and energy expenditure, and
a lack of coverage for some population subgroups. Given these shortcomings, the
validity of the data and conidence in the results may be questioned.
6.3.2.4 Self-Report Physical Activity Questionnaires
Questionnaires are commonly used to evaluate the frequency and duration of speciic
physical activities. The method is relatively economical and can therefore be used to
assess large numbers of participants. Table 6.3 provides an overview of the strengths and
limitations of this methodology with speciic reference to individual questionnaires.
The validity of some self-report physical activity data and energy expenditure
values derived from this data has been questioned. For example, some groups may
overreport the volume of physical activity they engage in. The accuracy of one’s
ability to recall physical activity also varies according to age, gender, body size,
level of education, and household income. It is also unclear which aspects of misreporting may be most problematic: the duration, intensity, frequency, or type of
activity. Any miscalculation of the total volume or intensity of physical activity may
have different implications in the determination of, for example, the dose–response
relationship between physical activity and health. It is highly desirable to include
objective measures with self-report instruments to minimize intentional or unintentional misreporting of physical activity. If a combined approach is not possible in
TABLE 6.3
Strengths and Weaknesses of Self-Report Questionnaires
Strengths
• Able to measure large numbers of participants
at low cost
• Theoretically, the recall process does not alter
behavior
• Variety of dimensions of physical activity can
be assessed
• Extrapolation to energy expenditure estimates
can be made
• Suitable for a wide variety of populations as
only a pen and paper are required
• Measurement tool can be adapted to suit the
population
• It is possible to compare results from different
locations when the same instrument is used
(e.g., International Physical Activity
Questionnaire—IPAQ)
© 2011 by Taylor and Francis Group, LLC
Limitations
• Recall limitations for some populations (for
example, children and the aged); therefore,
cognitive demand needs to be considered
• Semantics used may be a problem in some
settings; for example, terms may be ambiguous
to some (such as “physical activity,” “moderate
intensity,” “energy expenditure”)
• Dependent upon response rates and ability of
participants to follow instructions
• Completeness of questions answered
• Activity choices listed in questionnaire may not
be relevant for some certain populations
• Minimum amount of detectable change may not
be well deined; sensitivity
204
Nutritional Assessment of Athletes, Second Edition
the whole cohort, it is recommended that both measurement approaches be used in
a representative subsample.
In many settings, data from physical activity questionnaires have been used to
quantify energy expenditure. The metabolic equivalent (MET) has been widely used
to provide a common descriptor of intensity of physical activity in multiples of RMR.
One MET equates with the oxygen consumption (VO2) required at rest, assumed
to be 3.5 mL/O2/min/kg body weight. The MET is also deined as the ratio of work
metabolic rate to a standard RMR of 1.0 kcal (4.184 kJ)/kg/h. Comprehensive lists
of energy expenditure estimations for numerous physical activities have been developed and published in a compendium.11 Typically, an estimation of daily energy
expenditure can be gained by converting time spent in physical activity to energy
equivalents using the compendium.
The precision of this factorial method140–142 in quantifying human energy expenditure is inluenced by two main factors. First, physical activity estimates are only
as good as the information recorded, and therefore the accuracy of an individual’s
recall of the physical activities completed is a major inluencing factor. Secondly,
energy expenditure estimates will be inluenced by the accuracy of the assigned
MET level and the underlying premise of the factorial system; that is, how consistent
is the assumed resting value of 3.5 mL/O2/min/kg body weight across individuals of
different sizes and shapes?
It is important to highlight that the compendium was not developed to determine
the precise energy cost of physical activity within people.11,143 Rather, the approach
was developed to classify activity and standardize the MET intensities in population
health research. The MET system has been widely used by researchers, clinicians,
and practitioners to identify and prescribe physical activities. There is increasing evidence that estimates of activity energy expenditure using the factorial system may
be inaccurate across individuals of different body mass and body fat categories. In a
heterogeneous sample of 769 adults (18–74 years of age, 35–186 kg) who were weight
stable and healthy, albeit obese in some cases, the 1 MET value of 3.5 mL/kg/min
overestimated the actual resting VO2 value on average by 35% and the 1 MET of
1 kcal/kg/hr overestimated resting energy expenditure by 20%.12
6.4
CONCLUSIONS
Accurate measurement of physical activity and quantiication of energy expenditure can be challenging with the vast array of approaches available. All methods
have inherent strengths and weaknesses, and it is therefore important that one understands these strengths and limitations and makes a selection based on the appropriateness of an instrument or instruments to meet his or her speciic needs. Subjective
approaches, including diaries and recall, have the potential to provide rich descriptive data but are heavily reliant on the memory of the individual and may be prone to
overreporting some activities and underreporting others, such as incidental physical
activity. More objective methods such as accelerometers fail to adequately assess
some modalities of activity such as cycling and swimming, or are impractical in a
sporting context.
© 2011 by Taylor and Francis Group, LLC
Field Assessment of Physical Activity and Energy Expenditure among Athletes 205
With the availability of more sophisticated technology, we are certain to see
further growth in the range of tools to assess physical activity levels and energy
expenditure. To do justice to this growing ield we need to be sure of the reliability
and accuracy of the tools used to collect the data we are intending to measure and
to know how to interpret any change or difference we may see. When there is the
opportunity to measure physical activity with research quality tools, a multimethod
approach enables a more complete picture to be gained. It is important that physical
activity as well as inactivity is monitored; that exercise intensity as well as total dose
are considered; that reliability of instruments are checked regularly to account for
signal decay; and, where possible, that instruments are calibrated to the individual.
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© 2011 by Taylor and Francis Group, LLC
Aspects of
7 Molecular
Physical Performance and
Nutritional Assessment
Yousef I. Hassan and Janos Zempleni
CONTENTS
7.1
7.2
Introduction .................................................................................................. 213
Physical Performance Genes ........................................................................ 214
7.2.1 Cardiorespiratory and Endurance Genes.......................................... 214
7.2.2 Muscle Growth and Repair Genes .................................................... 215
7.2.3 Pain Relief Genes ............................................................................. 216
7.2.4 Fracture Repair Genes ...................................................................... 217
7.3 Molecular and Epigenetic Changes during Exercise .................................... 218
7.4 Implications for Nutritional Assessment ...................................................... 220
7.5 Gene Transfer and Potential Applications in the Field of Sports Nutrition .... 221
7.6 Gene “Doping” and Its Detection ................................................................. 222
7.7 Conclusions ...................................................................................................224
Acknowledgment ...................................................................................................224
References ..............................................................................................................224
7.1
INTRODUCTION
From the dawn of history, athletes paved the road for humanity to enhance human
physical performance. Through improved and rigorous training methods, controlled
surroundings, and precisely measured food intakes, they have attained the highest
possible levels of human achievability. Traits are affected by genes as well as by
environmental factors. Variations in any trait/phenotype (athleticism among them)
are expressed as the result of genotype by environmental interactions (G × E).
Historically, most of the performance-enhancing methods targeted environmental
factors, since controlling the genetic variability was not an option within the reach
at that time.
Recently with the completion of human genome sequencing projects and the
full sequencing of entire genomes of other model organisms, such as baker’s yeast
(Saccharomyces cerevisiae), fruit ly (Drosophila melanogaster), zebra ish (Danio
rerio), and roundworm (Caenorhabditis elegans), and the initiation of sequencing
projects for additional organisms such as bovine and swine genomes (Bos taurus
213
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or the domestic cow), an unprecedented abundance of information about different
genomes became publicly available. Our understanding of genes, their products, and
their functions has been enhanced dramatically in the past two decades. Comparative
genetics, bioinformatics, and sequence alignment methods have been successfully
used to annotate genes and discover their novel functions. Conditions affecting transcript abundance coded by these genes can be easily analyzed presently using stateof-the-art, real-time polymerase chain reaction (RT-PCR) machines and changes
taking place at certain genomic loci or even the entire genome can be tracked with
chromatin immunoprecipitation (ChIP) or ChIP to Chip methods, respectively.
These advancements in our understanding of genomes and proteomes went hand
in hand with similar research methods trying to ind empirical uses of this acquired
knowledge through biotechnological methods in almost all branches of life sciences
spanning physiology, medicine, nutrition, and sports. For the irst time in history we
are facing ethical dilemmas of our increased ability to control and enhance human
performance. Improvements in gene therapy techniques and the successful horizontal gene transfer (from person to another within the same generation) as compared
to vertical passage of genes from generation to generation, started adding new challenges to our comprehension and defying our traditional concept of sportsmanship
and fair competition. This chapter discusses and introduces the readers to some of
these current issues.
7.2
PHYSICAL PERFORMANCE GENES
Evidence has recently linked genetic variation to athletic ability. Early observations
of genetic variations and DNA polymorphisms and their association with elite athlete status and training responses are being conirmed every day. A literature search
reveals that almost all of desired physical performance characteristics are inluenced
somehow by the genetic component. More than eighty different genetic markers
(located within autosomal genes, Y chromosomes, and mitochondrial DNA) are
linked to elite athlete status and might explain the variations among individuals in
their response to training.1,2
7.2.1
CARDIORESPIRATORY AND ENDURANCE GENES
Endurance sports (such as swimming, running, and rowing) require athletes to perform low- to medium-intensity work over a long period of time. These types of sports
differ from the explosive form of energy and muscle strength needed in power sports
(such as shot puts, weight lifting). Training methods target enhancing and developing eficient energy production systems needed by these athletes to keep the demand
during competitions and events. The athlete’s heart (modulated heart size) is among
the observed adaptations to such training conditions. Yet this trait shows considerable variation among athletes and trainees. Recently, Karlowatz et al.3 reported that
this adaptation correlates with genetic polymorphisms in insulin-like growth factor 1
(IGF1). The analysis of IGF1 gene, IGF1 receptor (IGF-R), myostatin (MSTN), and
mutation screening of the MSTN gene in 110 elite athletes engaged in endurance training and their relation to left ventricular mass (LVM) revealed that polymorphisms
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in the IGF1 and the IGF1-R gene, such as G to A substitution at position 3174, has
signiicant relation to left ventricular hypertrophy (LVH) in male athletes. The team
also conirmed the effect of one additional unnoticed polymorphism (allele deletion
shifting AAA to AA) targeting the irst intron of the MSTN gene, which increases
the myostatic effect.
In the past decade, much of the attention to polymorphisms and endurance training associations was drawn to the angiotensin-converting enzyme (ACE), which is
part of the renin-angiotensin system (RAS). ACE plays a key role in circulatory
homeostasis by degrading vasodilator kinins and generating angiotensin II, a growth
factor. Intron 16 of the human ACE gene has been linked to endurance training
response by two polymorphisms.4 One is an insertion (I allele) and the other is a
deletion (D allele) of a 287 base pair (bp) fragment. The deletion polymorphism is
associated with lower serum and tissue ACE activity while the I allele is associated
with endurance performance and found with more than usual frequency in elite
athletes.4–20
In a study conducted by Karjalainen et al.,21 the LVM was measured in eighty
young elite endurance athletes (age 25 ± 4 years) screening the angiotensinogen (AGT),
angiotensin-converting enzyme (ACE), and angiotensin II type 1 receptor (AT1) genes
for the M235T, insertion/deletion (I/D), and A1166C polymorphisms, respectively.
The study concluded that the M235T polymorphism affecting angiotensinogen gene
was signiicantly associated with the variability in LVH induced by endurance training and athletes carrying homozygous T alleles developed the largest hearts. Both
ACE and AT1 polymorphisms showed little association with LVH variability.
Recently, the peroxisome proliferator-activated receptor-alpha (PPAR-α) gene
was suggested to also be involved in LVH. Originally, this receptor regulates genes
involved in fatty acid oxidation in heart and skeletal muscles. One polymorphism
in this receptor targeting intron 7 (with a G to C change) is associated with left
ventricular growth in response to exercise. Endurance-oriented athletes, power-oriented athletes, and athletes with mixed endurance/power activity were tested for this
polymorphism.22 An increasing linear trend of C allele was found with increasing
anaerobic component of physical performance. The GG homozygotes were more
prevalent within the endurance-oriented athletes. The second interesting observation that was found in this study is the connection between PPAR-α gene variant and
iber type composition. Muscle biopsies from m. vastus lateralis that were analyzed
revealed that GG homozygotes have signiicantly higher percentages of slow-twitch
ibers than CC homozygotes.
The above results show the importance of polymorphisms affecting different signaling pathways (receptors and growth factors) on variant degrees of physiological
hypertrophy of athletes. Some of these polymorphisms do confer an advantageous
effect, most likely mediated via improved muscle eficiency with secondary beneits
in terms of conservation of nonfat mass.
7.2.2
MUSCLE GROWTH AND REPAIR GENES
Muscle growth and strength is an essential trait in sports and usually constitutes
the irst target for any training program. The desired rate of achieved growth and
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strength differs from one sport to another and depends on the targeted muscles.
Muscle development and growth under training is affected largely by certain genes.
Most studies associate the ACTN3 genotype with this trait and knockout studies carried out in mice gave conclusive evidence for such association.23–49 The actin-binding
protein α-actinin-3 (ACTN3) is expressed only in fast-twitching ibers (Type 2) in
skeletal muscles and evidence is provided that an early termination condon within
the coding region of this protein leads to a R577X phenotype. This phenotype is
prevalent in at least 18%, 25%, and less than 1% of healthy white, Asian, and African
Bantu individuals, respectively.50 The presence of untruncated ACTN3 protein generates forceful contractions at high velocity compared to the absence phenotypes.
The presence of this protein is more frequently found in elite power athletes.48 A
study conducted on 107 elite athletes (males and females) specializing in sprint/
power events showed signiicantly higher frequencies of 577R allele than the control
individuals. As mentioned earlier, studies with the mice knockout model conirmed
these observations.31 The absence of α-actinin-3 resulted in a reduced force generation, reduced fast-twitched iber diameter, increased activity of multiple enzymes
in the aerobic metabolic pathway, and enhanced recovery from fatigue, suggesting
that the null phenotype in mice and humans is more suited for endurance sports
compared to strength performance. The developed model in these aforementioned
studies suggests also a role for myogenin (muscle regulatory factor) as a positive
regulator for muscle growth compared to α-actinin-3, which acts as a negative regulator. A genetic test for the presence/absence of 577R alleles is currently available
commercially to test teenagers and junior athletes in order to help them in deciding
which sport would best suit them and support their maximum achievability.
Other genetic variants and polymorphisms within muscle growth and strength
regulators (positives and negatives) are also known. Polymorphisms that affect IGF1, ibroblast growth factor (FGF), hepatocyte growth factor (HGF), mechano growth
factor (MGF), and myostatin are also known to affect muscle growth and regeneration after exercise, and readers are directed to more detailed reviews to explore the
functions of these factors.1,3,51–59
7.2.3 PAIN RELIEF GENES
Pain is frequently associated with rigorous training that results in damages to skeletal muscles manifested in delayed muscle pain. Clarkson et al.46 proposed that variations in ACTN3 and MLCK genes might explain the large variability in the response
to muscle-damaging exercise. Speciic single nucleotide polymorphisms (such as
C49T and C37885A) in myosin light chain kinase (MLCK) showed a greater loss
in muscle strength and a greater increase in blood creatine kinase (CK) and myoglobin (Mb) in response to eccentric exercise. Their results indicate that variations in
gene coding for these speciic myoibrillar proteins inluence phenotypic responses
to muscle damage, hence the accompanied pain.
Pro-inlammatory cytokines such as interleukin-1, IL-6, and IL-17 are also known
to be involved not only in inlammation but also in the induction and probably the
perpetuation of pain.60,61 These cytokines exert their biological effects on C-reactive
protein (CRP) by signaling through their receptors on hepatic cells and activating
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different kinases and phosphatases, leading to translocation of various transcription
factors to CRP gene promoter and production of CRP protein, which is considered
the triggering compound of most chronic diseases and the associated pain.62
More polymorphisms and genetic factors related to pain sensitivity are being
identiied.63 Subjects with single nucleotide polymorphisms in GTP cyclohydrolase
(GCH1) and mu opioid receptor (OPRM1) genes are known for their higher pain
sensitivity and lower pain thresholds.64 Studies also reveal that extracellular adenosine 5′-triphosphate (ATP) and its P2 purinergic receptor located on cell surface are
involved in neuropathic pain. Polymorphisms that cause changes of this receptor
function lead to an increased pain sensitivity induced by the cold stimuli.65 Finally,
the relationship between functional polymorphisms in dopaminergic genes and sensitivity to pain in healthy subjects was established. The variable number of tandem
repeat (VNTR) polymorphisms of three dopamine-related genes were investigated
(a 30-bp repeat in the promoter region of the monoamine oxidase-A gene [MAO-A],
a 40-bp repeat in the 3′-untranslated region of the dopamine transporter gene [DAT1], and a 48-bp repeat in the exon 3 of the dopamine receptor 4 gene [DRD4]). The
results indicated a signiicant association between cold pain tolerance and DAT-1
and MAO-A polymorphisms, suggesting that low dopaminergic activity is associated
with high pain sensitivity.66
7.2.4
FRACTURE REPAIR GENES
Stress fractures (such as affecting mid-tibia, diaphyseal femur) constitute challenging problems in the upper-tier athletes. The demand for continuous training with
very little room for prolonged rest periods makes the susceptibility for such injuries
higher among this population.67–71 Bone tissue development and repair is a complicated process under the control of different types of proteins and enzymes (such
as IGF, mineralization proteins, regulatory factors). The repair process requires
the activation and coordination of several pathways leading to the transformation
of mesenchymal precursor cells to osteoblasts. Recently, a transcription regulator, CBP/p300-Interacting-Transactivator-with-ED-rich-tail-2 (CITED2), which
suppresses genes involved in angiogenesis, osteogenesis, and extracellular matrix
(ECM) remodeling, was identiied.72 In fractured mandible, CITED2 expression
was inversely related to the expression of matrix metallo-proteinases (MMP -2,
MMP-3, MMP-9, MMP-13) and the overexpression of CITED2 in osteoblasts
inhibited the activity of these metallo-proteinases. This suggests that CITED2 has
a critical function as an upstream regulator of fracture healing and that the suppression of CITED2 early after fracture may allow for an optimal initiation of the
healing response.72
In a similar study, the role of Akt protein kinase was scrutinized. Mukherjee and
Rotwein73 demonstrated that dominant-negative Akt cells prevented osteoblast differentiation in a similar manner to IGF binding protein IGFBP5, a protein crucial
for normal skeletal development and bone remodeling. An adenovirus encoding an
inducible-active Akt was able to overcome the blockade of differentiation caused by
IGFBP5 and restored normal osteogenesis. The team concluded that an intact IGFinduced PI3-kinase-Akt signaling cascade is essential for osteoblast differentiation
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Nutritional Assessment of Athletes, Second Edition
and maturation, bone development, and growth, and suggested that manipulation of
this pathway could facilitate bone remodeling and fracture repair in athletes.73
After reviewing genes related to the athletic performance and setting examples
of some desired traits spanning strength, endurance, pain relief, and fracture repair,
we agree that the sport genetics ield is still in its early stage and more detailed gene
maps will appear in the future with much higher resolution of the genetic elements.
The list of related genes will expand and more polymorphisms will be identiied.
This will enhance our understanding of the athletic potential and shift athlete selection process toward an educated decision as compared to a semirandomized one.
7.3
MOLECULAR AND EPIGENETIC CHANGES DURING EXERCISE
It is well known that exercise enhances coordination, stress resistance, and stress
coping capabilities; however, the details and locations of the short-term memory
effects formed after exercise on the central genetic dogma are still ambiguous
despite speculations and assumptions actively being made. Recently, a novel mechanism was suggested connecting epigenetic changes and gene transcription activities
taking place at dentate gyrus neurons in response to training, forming the base for
performance and stress response enhancement of exercise.74 The study attributed the
performance enhancement of exercise to increased hisotne H3 phosphorylation and
increased c-Fos protein induction.
Histones are basic proteins that associate with DNA in a cell nucleus.75 They are
rich in basic amino acids (around 20% of their amino acids compositions are arginines and lysines).76 Electrostatic interactions between the positive charges of these
amino acids and the negative charges of phosphate groups in the DNA backbone
mediate packaging of DNA into chromatin.77 Two copies of each of the four core
histones (H2A, H2B, H3, and H4) form an octamer. DNA (around 147 base pairs) is
wrapped around this octamer to produce a nucleosomal core particle.78 The second
level of organizing chromatin comes with what is known as a linker region where
20–60 bp of DNA link one nucleosome to another. Each linker region is occupied
by a single molecule of histone H1, giving a “beads on a string” appearance.79 This
11-nm histone iber is then further packed into an irregular 30-nm chromatin iber
structure that is coiled into even more complex structures to eventually assemble
the chromosome (Figure 7.1). Binding of histones to DNA does not depend on a
particular nucleotide sequences in the DNA but does depend critically on the amino
acid sequence of the histone.80 Histones are some of the most conserved proteins in
eukaryotes. Calf histone H4 differs from pea H4 by only two amino acid residues.81
Binding of transcription factors to gene promoters may be inhibited if the promoter
is blocked by a nucleosome, and is usually associated with sliding nucleosomes
along the DNA molecule, exposing the gene’s promoter so that the transcription factors can access that region.82,83 Transcription of protein-coding genes is carried out
by RNA polymerase II (RNAP II).77 In order for the polymerase to travel along the
DNA, a complex of proteins removes the nucleosomes in front of RNAP II and then
replaces them after RNAP II has transcribed the sequence. This removal of histones
in front of RNA polymerases and putting them back after transcription is completed
is known as a chromatin-remodeling event.83,84 Two major types of chromatin exist
© 2011 by Taylor and Francis Group, LLC
Molecular Aspects of Physical Performance and Nutritional Assessment
300 nm Coiled chromatin
fiber
Coiled coil
(700 nm)
219
Metaphase
chromatid
(1400 nm)
30 nm Chromatin
fiber
11 nm Histone
fiber
DNA double strand (2 nm)
FIGURE 7.1 Chromatin structure.
in the cell nucleus: heterochromatin and euchromatin.85,86 Heterochromatin is the
chromatin that is condensed during the interphase whereas euchromatin is actively
transcribed.87 Around 75–80% of the histone amino acids are incorporated in the
core and only the N-terminal tails of histones protrude from the nucleosomal surface.
Through modiications of the side chains of different amino acids on the N-terminus
(exposed side of the nucleosomes) of histones, the chromatin structure can be controlled and part of the DNA sequences can be actively expressed or silenced.75,76,88
As stated above, chromatin remodeling is mediated through various chemical modiications of amino acid residues in histones; these modiications include covalent
attachment of acetyl groups (CH3CO –) to lysines, phosphate groups to serines and
threonines, methyl groups to lysines and arginines, biotin to lysine groups, ubiquitinylation and sumoylation of lysine residues, and poly-ADP-ribosylation of glutamic
or aspartic acid residues.81,89–98 Chemical modiications occur on these tails, especially for H3 and H4 histones (Figure 7.2).86,99 The most important feature of these
modiications is that they are reversible. For example, acetyl groups are added by
enzymes called histone acetyltransferases (HATs) and removed by histone deacetylases (HDACs).100,101 Acetylation of histone tails occurs in regions of chromatin that
become active in gene transcription.102,103 Adding acetyl groups neutralizes the positive charges on lysines, thus reducing the strength of the association between the
negatively charged DNA and the positively charged histones. Likewise, methylation,
which also neutralizes the charge on lysines (and arginines), can either stimulate
or inhibit gene transcription in that region.88,104,105 Methylation of lysine-4 in H3 is
associated with active genes while methylation of lysine-9 in H3 is associated with
inactive genes.106–108 It is now clear that histones are a dynamic component of chromatin and not simply inert DNA-packing material. All these modiications are part
of what is known as the histone code.85,89,109,110
Collins et al.74 took a close look at how well-exercised lab rats perform better
under stressful environments than their control (rested) counterparts. The team
showed that epigenetic mechanisms in the brain played a major role in this adaptation. Rats were initially divided into two groups: The irst experimental group was
trained on an exercise wheel for 4 weeks, while the second group did not undergo
any training or exercise regimen (control group). Both groups were then subjected to
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Nutritional Assessment of Athletes, Second Edition
Ac
M M
Ac
M
M
Ac
Ac
K79
K115
K122
Ac
Ac
M
Ac
MM
M
Ac
Ac
Ac
M
K59 K77
K79
K91
R92
M
P M Ac Ac
Ac
Ac
M
SGRGKGGKGLGKGGAKRHRKVLR
5
10
15
20
B
B
GERA
H3
ARTKQTARKSTGGKAPRKQLATKAARKSAPATGGVKKP
5
10
15
20
25
30
35
P
P
B
BP
B
P
Ac
H4
GFGG
FIGURE 7.2 Modiication sites in histones H3 and H4. Ac = Acetate; B = biotin; M = methyl;
P = phosphate; U = ubiquitin.
two types of stresses: novel environment exposure and forced swimming. After tests
were conducted, dentate gyrus tissues were collected and examined for histone H3
phospho-acetylation and c-Fos induction. During the novel environment exposure
test, the unexercised group was more nervous, exploring their surroundings during
the whole testing period, whereas the trained group was more relaxed and inished
exploring the testing stage within 15 minutes of start time.
In the forced swimming experiment, the rats were placed in a container of water
for 15 minutes and observed. This was repeated again 24 hours later for 5 minutes.
Both exercised and control groups showed similar behavior in the initial test, but
later in the repeat, the exercised rats showed better mobility, coordinated behavior,
and less struggling as compared to control rats. It was concluded from these results
that the exercised group was better able to cope and create memories of the irst
stressful event, enabling them to react better when exposed to the same stressful
event the second time. When brains of these rats were harvested and examined using
immunohistochemical techniques, the research team found signiicant increases in
histone H3 phospho-acetylation and induction of c-Fos in the brains of the exercised
rats. Others have reported similar observations that conirm this model connecting
behavioral observations, epigenetic changes, enhanced stress response, and memory
formation.111–113
7.4
IMPLICATIONS FOR NUTRITIONAL ASSESSMENT
It has been known for decades that the nutrition requirements of athletes differ substantially from the rest of the human population. In order to repair muscles and
excrete metabolic by-products, there are increased demands for energy, proteins,
amino acids, and several metabolic cofactors such as vitamins and minerals. What
is considered suficient for an active person with 2000-calorie intake daily would
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221
deinitely be considered an inadequate intake for an Olympic swimmer who needs a
6000-calorie daily intake.
Despite the early knowledge of these higher demands of athletes, it was only recently
elucidated that a connection exists between physical activity, genetic polymorphisms,
and the elevated needs in those individuals. Murakami et al.114 were the irst to connect
genetic polymorphisms affecting the vitamin D receptor to low resistance training.
These researchers reported that some SNP (single-nucleotide polymorphisms: changes
in the genomic DNA sequence affecting only one single nucleotide) patterns show better improvement of parameters associated with the effects of low resistance training. In
another study that was conducted on adolescent soccer players in Brazil, Diogenes et
al. demonstrated that FokI polymorphism in vitamin D receptor (VDR) genes affected
bone mass in those players and suggested that the FokI effect on bone mineralization
occurs during bone maturation, possibly at the initial pubertal stages. This observation
was conirmed by measuring total body bone mineral content (TBMC), total body
bone mineral density (TBMD), insulin-like growth factor-I (IGF-1), testosterone, intact
parathyroid hormone, and inally the activity of bone alkaline phosphatase found in the
plasma.115 Certain polymorphisms not only have been reported to affect the athletic
ability, but in fact some of these polymorphisms, such as the one that is found in intron
8 (ApaI) and exon 9 (TaqI) of vitamin D receptors, have long been known for their
reverse health effect and association with increased risks of chronic disease development such as colorectal116 and renal117 cancers.
What is true for vitamin D is also true for several other vitamins and cofactors in
increasing the risk of cancers and other diseases. These risks are documented and
the relations between folate, vitamin B6, and vitamin B12 with breast cancers.118,119
as well as that between ribolavin, vitamin B6, and vitamin B12 with the risk of new
colorectal adenomas,120 are well established.
7.5
GENE TRANSFER AND POTENTIAL APPLICATIONS
IN THE FIELD OF SPORTS NUTRITION
Molecular biology is one of the most rapidly growing scientiic disciplines. This
ield is concerned with studying molecular structures and events underlying biological processes and understanding the relationship between genes and the cellular characteristics determined by these genes. The human genome contains around
50,000 to 100,000 genes, and each gene is responsible for the synthesis of a speciic
cellular protein/enzyme. Multiple forms of each protein might exist due to phenomena of mRNA alternative splicing and/or post-translational modiication of proteins
(included but not limited to glycosylation, phosphorylation).
Exercise physiologists pay close attention to cellular processes and the signals that
trigger them, such as signals that regulate protein synthesis by turning on or turning
off speciic genes. Understanding the relationship between exercise and such factors
is of invaluable practical importance. The recent technical revolution in the ield of
molecular biology offers opportunities to make use of scientiic information for the
improvement of human performance. For example, training results in modiications
in the amounts and types of proteins synthesized in the exercised muscles. Indeed, it
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is well known that regular strength training results in increased muscle size due to an
increase in contractile proteins. Pointing out the exact molecular targets of such phenomenon might lead to more eficient training programs. In the following paragraphs,
some of the technical issues related to the use of our accumulated knowledge of
genomics and proteomics in the ield of enhancing human athleticism are addressed.
In sports, there is an extended list of reasons why individuals might want to test
their genomes/gene combinations. Among these reasons is the search for certain
risk factors (weakness or increased susceptibility to injuries) or just the eagerness to
conirm a potential athletic ability.
Recent advancements in biotechnological and molecular tools have resulted in
the availability of commercial kits to test the presence/absence of certain genes and
variants. Genes reported earlier in this chapter and involved in endurance, muscle
growth, fracture repair, and pain tolerance are among the alluring targets for such
detection kits. In fact, companies are in a fast race to produce and validate easy-touse kits that could be easily used with little instrumentation to serve the sportsperson. The irst commercially developed kit on the market targeted the ACTN3 gene
involved in regulating the fast-twitch muscle iber function. With simple steps of collecting a biological sample (usually saliva) and a polymerase chain reaction (PCR)
assisted ampliication of the targeted coding region, the available allelic combination could be deciphered. Athletes with two disrupted copies (homozygous) of the
ACTN3 gene might be oriented to endurance sports rather than sports that require
explosive power.24
Gene testing is expected to expand in the future. These methods do not always
give a reliable prediction, but individuals seeking to choose their own sport participation might ind such testing very helpful. Sport coaches testing young team
members to select professional careers, physicians predicting risks of illness and
advising for preventative measures, and insurance companies seeking to estimate
career-threatening injuries based partly on genetic information will heavily rely on
these kits in the near future.
In this regard, it should be mentioned that other personal and social factors also
contribute to the motivation of individuals to embrace certain types of sports. In
reality these factors are as important as the athletic ability detected by genetic tests.
In fact, genetic tests may turn problematic and start challenging our ethical code of
conduct if these tests are used to form the only base for including/eliminating individuals from certain activities.
7.6
GENE “DOPING” AND ITS DETECTION
In many sports, such as track and ield, it takes at least 8–10 years of hard training
and intensive collaboration between coaches, nutritionists, and physicians to create
high-caliber champions starting from talented trainees. With the “winner takes all”
attitudes prevailing in sports, the ine line between success and failure, between
fame and the attractions connected to it compared to going home with only silver/
bronze medals, makes it very alluring to use any performance-enhancing method
available on the market at the time of competition without paying much attention to
the ethical consequences related to such use.1,2
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The recent advances of gene therapy methods could be effectively used to enhance
athletic performance. The dificulty in distinguishing transgenic proteins from wildtype partners makes these approaches more attractive. Generally, any method that
depends on the horizontal transfer of genes in order to enhance performance is designated as “gene doping.” According to the World Anti-Doping Agency, gene doping
is deined as “the non-therapeutic use of genes, genetic elements and/or cells that
have the capacity to enhance athletic performance.”1 Gene doping not only undermines principles of fair play in sports, but most importantly it involves major health
risks to athletes who partake in gene doping and it forms a real threat to the world of
sports in human populations.121–124
From a technical point of view, there are two approaches for using genetic
engineering in enhancing performance. The irst approach depends on expressing and purifying engineered proteins/enzymes in preferred hosts such as E. coli,
Saccharomyces cerevisiae, and human cells. The puriied and tested proteins will
be then injected for their effects. This approach has some disadvantages such as
triggering strong immune reactions leading to inlammation, low expression levels
achieved with this method, and inally the need to repeat the injection every time the
accompanied effect is desired.1,125 The second approach depends on introducing viral
particles carrying transgenic proteins/enzymes to integrate within the infected cell’s
genome. These vectors can be inducible/noninducible depending on their nature,
and they carry some additional regulatory genetic elements. Expression of inducible
vectors can be under the control of certain chemicals (such as antibiotics like tetracycline or doxycycline) to start locally producing the transgenic protein/enzyme.
These chemicals can help in regulating the timing and duration of gene expression.
Tissue-speciic promoters could be integrated within the vector backbone so the gene
expression takes place only in speciic tissues. The second approach eliminates any
possible allergenic reactions toward the engineered protein/enzyme.1,126,127
The gene therapy that was originally designed to overcome serious human diseases is now a major challenge facing our deinition of fair competition in today’s
sport. In less than 30 years of development, gene therapy is the predominant topic
that covers sports ethics and sportsmanship. In addition to the ethical side of this
issue, the danger of spreading viral particles carrying vectors encoding proteins or
performance enhancers in humans is not appealing at all.128
Since the early realization of the threat of gene doping in sports, scientists from
different disciplines have been concerned with potential misuses of gene therapy
technologies and have invested extensive efforts to develop robust methods for genedoping detection. Different technologies are being optimized for the detection of
gene doping. Generally speaking, factors such as detection target, type of sample
required for analysis, and the response of the body at both cellular and systemic levels should be considered when evaluating strategies for gene-doping detection. The
current available knowledge of many ields such as gene technology, immunology,
transcriptomics, proteomics, biochemistry, and physiology is being utilized in order
to establish reliable detection methods. So far, only protein biomarkers are proving
to be successful as indirect indicators of gene doping.129,130 In principal, transgenic
proteins once introduced into the cell may alter the proteomic content of that cell and
affect the metabolic pathways within that cell. In addition, they might produce some
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characteristic immune responses (as they are initially carried by viruses). Tracking
changes in the proteome, metabolic pathways, and/or immunological responses
might prove to be the only way to discover gene doping.129,131
7.7
CONCLUSIONS
Every individual comes with a genetic map that dictates some of his or her future
potentials in every aspect of life. Genes might mark the sidelines of life’s highway,
but certainly the genes do not have the power to choose which lane we take. Factors
such as nutrition, training programs, family support, education, motivation, culture,
and social background complement the genetic map to deine us as human beings.
Having certain genes that give us the advantage over others in sport and physical
performance is desirable, but this gift should be nourished with training and eagerness to excel in order to achieve our maximum potentials.
While gene therapy and its possible misuse in sports doping is still in its infancy,
the time will come soon when it will form a major challenge for sportsmanship. The
commercialization of every aspect of our lives is an alluring and driving force for
sport personnel to win gold medals, break world records, and hence sign big contracts for advertising companies. Resources should be invested in developing analytical methods for tracking changes in cellular pathways to increase our chances
of detecting gene doping and protect human populations from uncontrolled and
misused gene technology.
Fair competition principles and ethical practices should be included in the education of people working in sports. Setting examples of successful fairly competing
champions, in addition to pointing out misconducts and their severe consequences,
should be part of this process.
ACKNOWLEDGMENT
The authors would like to thank Ruba Zeinou (Atomic Energy Commission of Syria,
Damascus) for her help during the review phase of this chapter.
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© 2011 by Taylor and Francis Group, LLC
Section IV
Biochemical Assessment
of Athletes
© 2011 by Taylor and Francis Group, LLC
of Lipid
8 Assessment
Status of Athletes
Richard B. Kreider, Jonathan M. Oliver,
and Amy F. Bragg
CONTENTS
8.1
8.2
Introduction .................................................................................................. 235
General Lipid Metabolism ............................................................................ 236
8.2.1 Dietary Lipids ................................................................................... 236
8.2.2 Digestion and Absorption ................................................................. 237
8.2.3 Lipid Transport ................................................................................. 238
8.2.4 Endogenous Production ....................................................................240
8.2.5 Reverse Cholesterol Transport ..........................................................240
8.3 Athlete Screening .........................................................................................240
8.3.1 Types of Lipid Disorders .................................................................. 241
8.3.2 Lipid Markers and Norms................................................................. 242
8.3.3 Screening Process .............................................................................244
8.3.4 Other Methods of Determination .....................................................246
8.4 Lowering Blood Lipids .................................................................................246
8.5 Implications for Athletes .............................................................................. 249
8.6 Future Research Directions .......................................................................... 249
8.7 Conclusions ................................................................................................... 250
References .............................................................................................................. 250
8.1
INTRODUCTION
The incidence of obesity and metabolic syndrome in the United States has reached
an epidemic level and has increased in prevalence even among our nation’s youth.1
In addition, athletes in some sports like American football and basketball are larger
than ever and would be considered obese by conventional body mass index (BMI)
and/or percent body fat criteria.2 A recent study examining the prevalence of markers
of metabolic syndrome in 70 Division I, II, and III American football players found
a disturbing incidence of athletes with abdominal adiposity, high percent body fat,
and low high-density lipoproteins (HDL).3 In addition, they had high blood pressure,
fasting blood glucose, fasting cholesterol, and serum triglycerides.3 In terms of blood
lipids, the researchers found that 46% of the athletes had total cholesterol to HDL
ratios greater than 5.0, 17% of the athletes had total cholesterol above 200 mg/dL, and
235
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24% of the athletes had low-density lipoproteins greater than 130 mg/dL. Further,
21% of the athletes had elevated C-reactive protein values (an indicator of inlammation) while 49% were found to have clinically diagnosed metabolic syndrome. The
presence of several of these risk factors signiicantly correlated to abdominal obesity
and body fat percentage. The researchers recommended that all athletes who had
an abdominal circumference of greater than 100 cm (40 inches) be screened for risk
factors associated with metabolic syndrome. While many presume that athletes are
lean, it, and have low blood lipids, given the incidence of hyperlipidemia and dyslipidemia in the population, this assumption may be misguided. Consequently, the
sports medicine professional must understand the proper methods of assessing and
managing lipid status of athletes. This chapter presents an overview of general lipid
metabolism, lipid screening processes, and ways to manage athletes found to have
high blood lipids.
8.2
GENERAL LIPID METABOLISM
Studies of dietary intake of athletes have shown their macronutrient composition to
be similar to those of the standard U.S. population, differing only in the amount of
calories consumed.4 Therefore, for practitioners involved directly in the performance
of athletes, it is necessary to understand the components of their diet to make clear
suggestions and educate them on their dietary needs. The purpose of this section is
to highlight the importance of lipids by providing an explanation of lipid metabolism, both exogenous and endogenous, as well as to provide guidelines for assessing
lipid proiles in athletes for the determination of future health risk.
Lipids consist of triglycerides, phospholipids, and cholesterol, and serve as a
major biological component of cells as well as a fuel source for energy for many
human processes. The majority of dietary lipids come in the form of triglycerides,
while dietary cholesterol contributes to a much smaller degree.5,6 The metabolism of
lipids involves several processes to enable their use for biological components and
energy, including digestion and absorption, transport of dietary lipids, endogenous
lipid production, and reverse cholesterol transport.
8.2.1
DIETARY LIPIDS
Dietary fats consist of triglycerides, phospholipids, and cholesterol. They are classiied by the chemical structure based on the number of fatty acids and carbons they
contain. Medium-chain fatty acids are considered shorter than 10 carbons in length,
while long-chain fatty acids are 10–12 carbons or longer in length. Fatty acids can be
further classiied by their chemical structure into four categories (saturated, monounsaturated, polyunsaturated, and transaturated fats). Saturated fatty acids contain
the maximum number of hydrogens attached to each carbon in the chain. Saturated
fats are usually solid at room temperature and come almost exclusively from animal
sources. Overconsumption of this type of fat has been reported to be a risk for cardiovascular disease.
Monounsaturated and polyunsaturated fats are missing at least one pair of hydrogen atoms attached to a carbon and have a double bond in its place. Monounsaturated
© 2011 by Taylor and Francis Group, LLC
Assessment of Lipid Status of Athletes
237
fats only have one double bond, while polyunsaturated fats have more than one double bond. When the double bonds of monounsaturated or polyunsaturated fatty acids
exist on opposite sides, these fatty acids are referred to as trans fatty acids. This is
usually the result of hydrogenation, the artiicial adding of hydrogen bonds, which
is used to increase shelf life of many products. Monounsaturated fats can be found
in oils such as olive, canola, and peanut. In addition, salmon, mackerel, halibut,
trout, and shellish are also high in monounsaturated fats. Polyunsaturated fats can
be found in foods such as ish oils; seafood; polyunsaturated margarines; vegetable
oils such as saflower, sunlower, corn, or soy oils; nuts such as walnuts and brazil
nuts; and seeds. Unsaturated fatty acids also contain a special subgroup known as
essential fatty acids, due to the body’s inability to make these fatty acids in the body.
Therefore, these fatty acids must be obtained in the diet and include omega-3 and
omega-6 unsaturated fatty acids. “Omega-3” and “omega-6” describe where the double bonds exist in the fatty acid, counting from the terminal end of the fatty acid.7,8 A
number of health beneits of a diet high in unsaturated fats and essential fatty acids
have been reported. Consequently, it is generally recommended that total fat intake
be limited to 30% or less of total energy intake, with the majority of dietary fats
consumed in the form of unsaturated fats.
8.2.2 DIGESTION AND ABSORPTION
The process of digestion of dietary lipids begins in the stomach. Lingual lipase,
increased by neural stimulation and by the intake of dietary fat, is secreted by the
salivary glands.6,9 As lingual lipase combines with foodstuff in the mouth and moves
into the stomach, the sheer stress caused by passage of food through sphincters and
the contractions of the stomach create an emulsion, allowing lingual lipase to come
in contact with the ingested lipids.6 The acidic pH of the stomach is ideal for the lingual lipase to facilitate the enzyme’s ability to break down the lipid contents. Once
the stomach has mixed all its contents, the partially digested lipid emulsion moves
into the small intestine where the majority of digestion of lipids occurs.
Upon ingestion of a lipid-rich meal, the gallbladder contracts in response to cholecystokinin (CCK) secreted from the small intestine. The contents of the gallbladder,
which include bile acids and lecithin produced in the liver, is secreted into the small
intestine, where with the newly formed emulsion creates a favorable pH for lipid
digestion.6,10,11 While bile acids contain no enzymes to break down lipids, the process
of emulsiication is essential in lipid digestion. The bile salts contained within the
bile acid work as a detergent with contractions of the small intestine to break up the
lipid emulsion. Enzymes secreted by the small intestine also work to further break
down the lipids. CCK stimulates the release of pancreatic lipase, phospholipase A-2,
and cholesterol esterase. Pancreatic lipase breaks down triglycerides into free fatty
acids, diglycerides, and monoglycerides. Phospholipase A-2 works on phospholipids resulting in the production of a monoglyceride and lysophospholipid. The inal
enzyme in the process is cholesterol esterase, which metabolizes cholesterol into free
cholesterol and a monoglyceride.6 After this breakdown has occurred, the fatty acids
are absorbed by the intestinal mucosal cells.
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At this point in the process, approximately 98% of the ingested triglycerides, along
with 15–40 g of endogenous lipids, have been absorbed6 and are ready for transport.
The small intestine is very eficient in its absorption of triglycerides, resulting in very
little triglyceride in fecal excrement. However, only about 30% of dietary cholesterol
has been absorbed at this point.12 Cholesterol in the form of bile appears to be better
absorbed than its dietary counterpart. This is partly due to the higher secretion rate of
biliary cholesterol, which is two times the amount of dietary cholesterol, as well as the
physical composition of cholesterol in bile. Dietary cholesterol entering into the small
intestine requires emulsiication by the bile salts and lecithin into the micellar state,
whereas biliary cholesterol enters the intestine in the micellar state.12 This could contribute to the less-than-optimal absorption of dietary cholesterol. Endogenous cholesterol production accounts for this deicit and increases when dietary consumption is
low and decreases when dietary cholesterol is high.12
8.2.3
LIPID TRANSPORT
Small- and medium-chain triglycerides (10 to 12 carbons in length) can enter
directly into the blood for transport after absorption by intestinal cells. This is due
to their reduced hydrophobic nature compared to that of longer-chain fatty acids.
Larger-chain fatty acids (greater than 12 carbons in length) are more hydrophobic
and require further packaging. The ability of these lipids to be transported in plasma
depends on their incorporation into lipoproteins. Lipoproteins contain lipids and
transport proteins termed apoproteins (apo). Lipids and their apoprotein counterparts are termed apolipoproteins. Apolipoproteins are classiied by their size, lipid
content, apoprotein content, and subfraction of major lipoprotein class. Apoproteins
are listed in Table 8.1 with their associated lipoprotein and their major functions.
TABLE 8.1
Types of Apolipoproteins, Associated Lipoproteins, and Major Functions
Apolipoprotein
Associated Lipoproteins
Major Functions
A-I
Chylomicron, HDL
A-II
B-48
HDL
Chylomicron, HDL
B-100
VLDL, IDL, LDL
C-I
Chylomicron, VLDL, HDL
C-II
C-III
apo E
apo(a)
Chylomicron, VLDL, HDL
Chylomicron, VLDL, HDL
Chylomicron, VLDL, HDL
Lp(a)
Cholesterol acceptor from peripheral cells through
ABCA1; cofactor for LCAT; facilitates lipid uptake
Displaces apo A-I; facilitates lipid uptake
Assembly and secretion of chylomicrons from small
intestine; structural component
Assembly and secretion of VLDL from liver; LDL
receptor
Inhibits hepatic uptake of chylomicron and VLDL
remnants
Cofactor for LPL
Inhibits LPL
Facilitates lipid uptake through LDL receptor
Most likely inhibits ibrinolysis
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Assessment of Lipid Status of Athletes
The four major classes of lipoproteins are chylomicrons, very-low-density lipoproteins (VLDL), low-density lipoproteins (LDL), and high-density lipoproteins (HDL).
Low-density lipoproteins are often classiied further by their density into intermediate-density lipoproteins (IDL) and at the lower end of the density spectrum, LDL.13
Once absorbed in the intestinal mucosal cells, longer-chain fatty acids are packaged into chylomicrons to facilitate transport. Apo B-48 is essential in the transport
of exogenous lipids in chylomicrons from the intestine. Upon secretion from the
mucosal cells of the intestine, the chylomicrons enter the lymphatic system where
several changes occur, including the addition of several apoproteins that allow the
lipoprotein to be metabolized upon entering the bloodstream. The most important
apoprotein addition is that of apo CII. Apo CII serves as a cofactor for lipoprotein
lipase (LPL), which is synthesized in adipose and muscle cells.14 LPL catalyzes the
hydrolysis of the triglyceride from the chylomicron, allowing the fatty acid to be
taken up by adjacent tissues (mostly muscle and adipose) to be stored or used as
energy.15 What remain after the hydrolysis are small particles of the chylomicron,
which include cholesterol, phosphospholipids, apolipoproteins, and very little triglyceride. These remaining particles can then be integrated into HDL, which occurs
with the majority of apo A and some apo C, with the remaining being catabolized by
the liver.13,14,16–18 Figure 8.1 diagrams the process of lipid transport and endogenous
production and transport.
Peripheral Tissue
Small Intestine
VLDL
LPL
FFA
Liver
HL
LPL
LPL-R
LPL
IDL
Chylomicron
FFA
FFA
LPL
LRP
Chylomicron
Remnant
Apo A & C
to HDL
FIGURE 8.1 Lipid transport and endogenous lipid production. Once absorbed in intestine,
large-chain fatty acids are secreted in chylomicrons which enter the lymphatic system where
apolipoproteins are added to aid in transport. When the chylomicrons enter the blood, LPL
catalyzes the hydrolysis releasing the fatty acid (FFA) to the peripheral tissues, while the apo
A & C are integrated into HDL while the remaining chylomicron remnant is taken up and
disposed of by the liver. Lipids produced by the liver are released into circulation in VLDL.
LPL hydrolyzes the triglyceride in VLDL releasing the FFA to the peripheral tissues. This
reduces the VLDL to IDL which is again hydrolyzed by LPL and HL (hepatic lipase) releasing the remaining FFA to peripheral tissues allowing the inal LDL product to be taken up by
the liver to be made available for other processes. (Adapted from Davis, P.G. and Wagganer,
J.D., in Lipid Metabolism and Health, Moffatt, R.J. and Stamford, B., Eds., CRC Press, Boca
Raton, FL, 2006, pp. 47–60.)
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ENDOGENOUS PRODUCTION
Although the liver prefers the use of dietary lipids and those stored in adipose tissue, it also has the ability to produce lipids, which becomes important during the
fasting state. Lipids produced by the liver (endogenous pathway) are released in
VLDL, which utilizes a number of apoproteins. Of importance are apo B-100, a
longer version of apo B-48, and apo CII, which serves again as the cofactor for LPL.
In the case of endogenous lipids, LPL hydrolyzes the majority of the triglyceride
contained within VLDL. Once hydrolyzed they become less dense and are converted
to IDL and further into LDL. The remaining LDL particle is taken up by liver and
adrenal cells to be made available for membrane structures and steroid hormone
synthesis.13,14,16–18
8.2.5
REVERSE CHOLESTEROL TRANSPORT
The body has yet another mechanism that provides a cardioprotective beneit in the
removal of cholesterol from peripheral tissues and vascular lesions. This mechanism
utilizes HDL, which works in conjunction with adenosine triphosphate-binding cassette-A-I (ABCA-I) transporter. Briely stated, the small apo A-I of HDL is formed
in the lymph and delivered into the circulation where it interacts with peripheral
tissues and other areas in the arterial walls that contain free cholesterol. Apo A-I
removes free cholesterol with assistance from ABCA-I. The free cholesterol then
incorporates into the apo A-I HDL. As more cholesterol is incorporated, it becomes
a strong cofactor for lecithin-cholesterol acyltransferase (LCAT). This allows further
packaging of the cholesterol within the HDL, which through interaction with LCAT
becomes HDL2. The Sr-B1 receptor on the liver recognizes the mature HDL and
allows for crossing into the liver, resulting in its excretion in bile.18
8.3
ATHLETE SCREENING
Many studies have evaluated the lipid proiles of athletes. Most studies indicate that
athletes have lipid proiles that are associated with a lower incidence of cardiovascular disease (CVD).19 The most beneicial effects seen in most of these studies has
been the increased levels of HDL, particularly in endurance athletes.19 A reduction
of triglycerides and an increase in HDL appear to be long-term effects of exercise
training.20 However, athletes are not immune to lipid disorders, including dyslipidemia, and should therefore be screened appropriately. This is increasingly true
among college athletes; few studies have studied this age group, as little data exists
as to the prevalence among this age group. In a recent study of collegiate athletes,
10% reported having cholesterol levels greater than the current recommendation
levels, while 24% of males and 30% females had HDL levels lower than recommended values.21 The majority of studies on athletes have focused on the beneicial
effects experienced by endurance athletes; however, while strength and power athletes experience some protective beneits of training, their proiles differ overall.
This has been shown to be true in athletes with a higher BMI,22 such as football
linemen, and those participating in little endurance training, such as power lifters
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and throwers.23,24 Currently, a different means of analyzing lipid proiles of athletes
compared to their sedentary counterparts does not exist. For this reason, the standard for the normal population is discussed, with emphasis placed on where athletes
may differ.
8.3.1
TYPES OF LIPID DISORDERS
There are several types of dyslipidemia disorders that practitioners should be aware
of if they are involved in screening of hyperlipidemia. The Fredrickson classiication
system has been developed and adopted by the World Health Organization to characterize different types of hyperlipoproteinemia disorders.25
Hyperlipoproteinemia Type I is a rare condition associated with deiciencies in
the enzyme lipoprotein lipase (LPL) or its cofactor apolipoprotein CII. The
LPL enzyme is found primarily in endothelial cells and serves to hydrolyze
lipids found in chylomicrons and VLDL into free fatty acids and glycerol.
Individuals with Type I hyperlipoproteinemia typically have high cholesterol, marked elevations in chylomicron levels, and triglyceride levels ranging from 1,000 to 10,000 mg/dL. It is usually treated with diet control and
is not associated with elevations in risk to cardiovascular diseases.
Hyperlipoproteinemia Type II is the most common dyslipidemia and is further
classiied as Type IIa or Type IIb hyperlipoproteinemia.
Type IIa hyperproteinemia is also known as polygenic hypercholesterolemia
of familial hypercholesterolemia. This is a genetic-related disorder associated with LDL receptor deiciency. Individuals with Type IIa hyperlipoproteinemia present with elevated cholesterol, LDL, and VLDL.
Individuals with Type IIa hyperproteinemia also may have tendon xanthomas (deposition of yellowish cholesterol-rich material in tendons) and/
or xanthelasma (deposition of yellowish cholesterol-rich material on eyelids). It is usually treated with bile acid sequestrants, statins, and niacin
therapy.
Type IIb hyperproteinemia (also known as combined hyperlipidemia)
is similar to Type IIa hyperproteinemia with the exception that this
form of dyslipidemia is also associated with elevated triglyceride levels. Individuals with Type IIb hyperproteinemia typically have elevated cholesterol, LDL, and triglycerides typically due to an inability
to metabolize and/or clear fats in the liver. It also may be associated
with low HDL cholesterol. They also have an increased incidence of
metabolic syndrome. Patients with Type IIb hyperlipoproteinemia are
typically treated with diet therapy, ibrate medications (which work on
perixisome proliferator-activated receptors to decrease free fatty acid
production), and statin drugs (which can reduce LDL levels by promoting LDL uptake in the liver by increasing LDL-receptor expression).
Both of these forms of dyslipidemias are associated with an increased
incidence of cardiovascular disease.
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Type III hyperlipoproteinemia is also known as broad beta disease or dysbetalipoproteinemia. Type III hyperlipoproteinemia is a rare, genetically related
dyslipidemia that affects about 0.02% of the population. Individuals with
Type III hyperlipoproteinemia have the ApoE E2/E2 genotype. It is associated with elevations in cholesterol, triglycerides, chylomicrons, intermediate density lipoproteins (IDL), and risk of cardiovascular disease. Treatment
typically involves diet therapy, ibrates, and statins.
Type IV hyperlipoproteinemia is a dyslipidemia disorder affecting about 16%
of the population according to the NCEP-ATPIII criteria, where hypertriglyceridemia is greater than 200 mg/dL. Individuals with Type IV hyperlipoproteinemia have elevated VLDL production and a reduced capacity to
eliminate VLDL. This dyslipidemia is characterized with elevations in triglycerides (200–1,000 mg/dL) and VLDL. However, total cholesterol levels
are typically within normal ranges. Treatment options include diet therapy,
ibrates, niacin, and statins.
Type V hyperlipoproteinemia is a rare condition that is commonly known as
endogenous hypertriglyceremia. It is similar to Type I but is associated with
high VLDL in addition to elevated cholesterol, chylomicrons, and triglycerides usually greater than1000 mg/dL. Individuals who have Type V hyperlipoproteinemia typically have an increased production of VLDL, decreased
LPL, glucose, glucose intolerance, and hyperuricemia. Treatment typically
includes diet, niacin, and/or ibrate therapy.
8.3.2
LIPID MARKERS AND NORMS
The primary purpose for cholesterol screening is the determination of risk of development of CVD. The National Cholesterol Education Program (NCEP) recommends
a fasting lipoprotein proile (total cholesterol, LDL cholesterol, HDL cholesterol, and
triglycerides) for all adults aged 20 years and older every 5 years. In addition to a
fasting lipoprotein proile, the NCEP also recommends an assessment of accompanying risk factors, which include cigarette smoking, hypertension (blood pressure ≥
140/90 mm Hg or on an antihypertensive medication), family history of premature
cardiovascular disease, and age (men ≥ 45; women ≥ 55).26 Table 8.2 outlines the current guidelines provided by the NCEP for identiication of risk. Figure 8.2 provides
the appropriate testing timetable with current recommendations.
Although cholesterol screening provides an assessment of CVD, the role of triglycerides in lipid abnormalities cannot be overlooked. Cross-sectional studies have
shown that mean triglyceride levels have increased, particularly in the United States.
Although HDL attenuates some of the risk associated with high triglycerides and the
development of CVD, a full lipid proile and clinical assessment is needed to determine full risk. As recent data have shown, CVD risk is still apparent when patients
present with low LDL.27
It is important to note several factors play a role in lipids and lipoproteins. Age,
weight loss, the use of anabolic steroids, and lifestyle choices such as smoking and
alcohol consumption all contribute to the levels of circulating lipids. Cholesterol levels have been shown to increase with age, with a greater increase in men.28 During
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TABLE 8.2
NCEP Classification of LDL Cholesterol, HDL
Cholesterol, Total Cholesterol, and Triglycerides
LDL Cholesterol (mg/dL)
< 100
100–129
130–159
160–189
≥ 190
Optimal
Near or above optimal
Borderline high
High
Very high
HDL Cholesterol (mg/dL)
< 40
Low
≥ 60
High
Total Cholesterol (mg/dL)
< 200
Desirable
200–239
Borderline high
≥ 240
High
Triglycerides (mg/dL)
< 150
150–199
200–499
≥ 500
Normal
Borderline high
High
Very high
Source: Panel E, Executive summary of the third report of the
National Cholesterol Education Program (NCEP) expert
panel on detection, evaluation, and treatment of high
blood cholesterol in adults (adult treatment panel III),
JAMA, 285, 2486–97, 2001.
• Fasting lipoprotein profile (total cholesterol, LDL cholesterol, HDL cholesterol, and triglycerides)
– If non-fasting, only total cholesterol and HDL are usable. A second fasting profile should
be obtained if total cholesterol > 200 mg/dL or HDL < 40 mg/dL. If values are abnormal,
a second profile should be obtained.
• Screening recommended for all adults aged 20 years or older every 5 years
• Other major risk factors
– Smoking
– High blood pressure (≥ 140/90 mm/Hg)
– Low HDL (< 40 mg/dL)
– Family history of cardiovascular disease
– Age (men ≥ 45, women ≥ 55)
• Treatment decision should involve athlete and practitioner including dietary and
pharmacological interventions.
FIGURE 8.2 Appropriate timetable for lipoprotein proile testing.
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Nutritional Assessment of Athletes, Second Edition
dieting and weight loss, the activity of LPL is altered, which can result in changes in
the blood lipid proiles, and thus a lipoprotein proile should be conducted when the
athlete is not trying to lose weight or restricting calories.29 Anabolic steroid use can
affect screening by altering lipoprotein fractions and increasing triglyceride levels.30
Smoking, a risk factor acknowledged by the NCEP, has been shown to decrease
HDL, while alcohol consumption has been shown to increase triglyceride levels.31
8.3.3
SCREENING PROCESS
In their most recent report, the NCEP established guidelines for the identiication and
treatment of persons with high cholestero1.26 Based on these recommendations, athletes should be screened appropriately following these guidelines, since any beneits
seen from training will be elucidated in the identiication and evaluation process.19
Athletes who may be particularly susceptible are those with waist circumferences
greater than 40 inches and/or a body fat percentage greater than 25%.3
The initial step set forth by the NCEP is the assessment of the person’s risk.
Risk assessment, as previously stated, should include a fasting lipid proile, which
includes categorization based on LDL, HDL, and total cholesterol values listed in
Table 8.2. A fasting blood lipid proile (8–12 hours fasting) is recommended, as
the concentration of blood lipids in blood can range from 5% to 10% daily. This
variation can be attributed to several factors, including dietary intake, exercise, and
alcohol consumption, to name a few. The blood is usually drawn from the antecubital
space. Serum is typically used for determination of lipid proiles, and this requires an
amount of blood that is greater than can be obtained from a inger stick.
For estimating cholesterol and triglyceride concentrations, enzymatic procedures
are most commonly employed in the clinical setting. The enzymes required for these
assay procedures may be prepared by the researcher, but most are commercially
available, which makes them the most widely used clinically. Determination of cholesterol involves three enzymes: cholesterol esterase, cholesterol oxidase, and peroxidase. Cholesterol esterase hydrolyzes the cholesterol esters to free cholesterol and
fatty acids. Cholesterol oxidase then oxidizes the free cholesterol. The inal step is a
quinoneimine dye, which is produced when hydrogen peroxide oxidizes p-hydroxybenzenesulfonate and 4-aminoantipyrine in the presence of the peroxidase.32–34
Cholesterol can then be indirectly quantiied using spectrophotometry. HDL can
be measured by precipitating non-HDL cholesterol with heparin and measuring the
total cholesterol remaining. Currently, in clinical setting the most common procedure used to determine LDL is using the Friedewald calculation. This calculation
utilizes total cholesterol and HDL to estimate LDL. This practice, however, suffers
from several limitations.35,36 Other more accurate methods for determination of HDL
and LDL have been developed using their density and/or charge. These methods
employ the use of ultracentrifugation and electrophoresis.36,37
Triglyceride determination involves a different set of four enzymes: lipoprotein
lipase, glycerol kinase, glycerol phosphate kinase, and peroxidase. Lipoprotein
lipase serves to hydrolyze the triglycerides into fatty acids and glycerol. Glycerol
from the irst step can then be phosphorylated to glycerol-1-phosphate and
adenosine-5-diphosphate. Glycerol phosphate kinase can then oxidize the glycerol-
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1-phosphate to dihydroxyacetone phosphate and hydrogen peroxide. Again, a quinoneimine dye is formed when hydrogen peroxide reacts with 4-amino-antipyrine and
5-dichloro-2-hydroxybenzene sulfonate. Triglyceride concentration can be indirectly
quantiied using spectrophotometry.32–34
In addition to a fasting lipid proile, the presence of clinical coronary heart disease
(CHD) should be determined. The next step in risk assessment is determining the
presence of the other major risks: cigarette smoking, hypertension (blood pressure ≥
140/90 mm Hg or on an antihypertensive medication), family history of premature
cardiovascular disease, and age (men ≥ 45; women ≥ 55).26
After determination of risk, clinicians can then divide the athlete into one of three
categories based on the presence of CHD and other risk factors, with the appropriate
goal for LDL. If the athlete has the presence of CHD and any risk factors, his or her
goal LDL is < 100 mg/dL. If he or she has more than two risk factors and no presence
of CHD, then the goal LDL is < 130 mg/dL. The lowest risk, those with 0–1 risk factors, should have an LDL proile of < 160 mg/dL. When more than two risk factors
are present, the clinician should do a 10-year risk assessment carried out using the
Framingham scoring to determine if intensive treatment is necessary.19,26
Table 8.3 outlines the goal LDL levels for the three groups based on risk assessment and the corresponding point at which to begin therapeutic lifestyle changes
(TLC), as deined by NCEP, or drug therapy. Athletes are a special population and
thus require added attention at this point; any therapy, whether it be TLC or drug
related, must also focus on ensuring the athlete can still participate in his or her
sport.19 TLC, as recommended by the NCEP, includes reducing intakes of saturated
fats to < 7% of total calories and cholesterol intake to < 200 mg/day, increasing
physical activity, implementing weight reduction, inclusion of plant stanols/sterols
in the diet, and increasing iber intake.26 Drug treatment is recommended after
TABLE 8.3
LDL Cholesterol Goals and Guidelines to Begin Therapeutic Life Changes
and Drug Therapy
Risk Category
CHD or CHD risk equivalents
(10 yr risk > 20%)
2+ risk factors
(10 yr risk ≤ 20%)
0–1 risk factor
LDL Goal
(mg/dL)
LDL to Start
Therapeutic
Lifestyle Changes
(mg/dL)
< 100
≥ 100
< 130
≥ 130
< 160
≥ 160
LDL Level to Consider
Drug Therapy
(mg/dL)
≥ 130
(100–129, drug optional)
≥ 130, 10 yr risk 10–20%
≥ 160, 10 yr risk < 10%
≥ 190
(160–189, drug optional)
Source: Panel E, Executive summary of the third report of the National Cholesterol Education Program
(NCEP) expert panel on detection, evaluation, and treatment of high blood cholesterol in adults
(adult treatment panel III), JAMA, 285, 2486–97, 2001.
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Nutritional Assessment of Athletes, Second Edition
three months of TLC if goal LDL levels are not met and should be evaluated and
administered by a registered physician.19
8.3.4
OTHER METHODS OF DETERMINATION
More recent advances in the study of lipids and risk factors associated with the development of CVD have led to the discovery of other methods for the determination
of risk. The NCEP currently only recommends the above guidelines in determining CVD risk, even though other methods discussed have shown to be a stronger
predictor of the development of CVD. The reasoning for acknowledgment of only
the NCEP guidelines is multifaceted. Some of the methods discussed have been
shown to have no greater signiicant diagnostic value than the standard lipid proile.38
For methods with greater signiicant value, the question remains as to how long a
reeducation of physicians and patients alike would take and to what beneit these
measurements could improve determination of CVD risk in those already at risk.39,40
Additionally, the tests required with some of these methods are not part of the standard lipid proile. Insurance carriers currently believe these to be experimental and
thus the burden of cost would fall to the patient.40 Therefore, the methods described
only provide insight into the new ways of analyzing risk factors associated with the
development of CVD.
Two ratios have been shown to be strong predictors of the development of CVD,
the LDL-C/HDL-C ratio and the apo B/apo A-I ratio. The LDL-C/HDL-C ratio has
been identiied as associated with risk of development of CVD in several large-scale
studies.40–42 However, the majority of these studies were conducted on middle-aged
men, and this should be taken into account when assessing athletes. The level of apo
B and the ratio of lipoproteins apo B/apo A-I have recently proved to be the most
accurate predictors of CVD.43,44 The apo B is a structural protein responsible for
VLDL transport of lipids from the intestine and the liver to tissues, while apo A-I
is used in reverse cholesterol transport carrying particles to the liver for excretion.43
The relationship of these two lipoproteins therefore provides a direct ratio of atherogenic to nonatherogenic.
C-reactive protein (CRP), an inlammatory marker, has shown to be strongly associated with the development of CVD. Studies have shown that CRP levels increase
with age and are higher in the obese and smokers. Due to these factors, there has
been a strong association between CRP and the development of CVD.45 However,
more recent studies have shown that CRP levels provide no greater diagnostic value
than the standard lipid proile recommended by the NCEP.38
8.4
LOWERING BLOOD LIPIDS
The NCEP has recommended using LDL levels in combination with assessing risk
factors of CHD as a criterion in determining treatment options for patients with
dyslipidemia. The greater the risk proile, the lower the LDL level needs to be to
initiate treatment options. For individuals with moderately elevated LDL levels and
a low risk-factor proile, lifestyle alterations involving increasing physical activity,
losing weight, and consuming a low-fat and low-cholesterol diet are typically the
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Assessment of Lipid Status of Athletes
irst treatment course.46 Table 8.4 has dietary recommendations provided by NCEP
as well as others for a healthy lifestyle. Those with more risk factors may require
additional dietary and/or pharmacological interventions.
Sustained endurance or aerobic-based exercise (walking, running, cycling, swimming, etc.) have been reported to lower total cholesterol and LDL cholesterol while
increasing HDL cholesterol.47 In addition, increasing the amount of endurance exercise appears to have a dose-related beneit, particularly in individuals who have lower
BMIs.47 Individuals who primarily engage in high-intensity intermittent exercise or
power-based physical activity (such as resistance training, American football, baseball, and softball) may not observe as much beneit of exercise training on blood lipid
proiles unless they include some aerobic-based exercise in their training.47 This is
particularly true for larger athletes who have a high percent body fat or higher BMIs.3
Weight loss that may occur as a result of exercise training and/or caloric restriction
has also been shown to have positive beneits on blood lipid proiles.48,49
The second general guideline to help individuals lower blood lipids is to consume
a low-fat and low-cholesterol diet. Animal sources of food (such as meats, poultry,
shellish, eggs, butter, cheese, whole or 2% milk) are relatively high in fat, saturated fats, and cholesterol. The American Heart Association (AHA) recommends
that individuals consume 25–35% of their total daily caloric intake in the form of
fat. In addition, the AHA recommends that saturated fat intake should be less than
7% of fat intake, transfat intake should be less than 1% of total daily caloric intake,
and cholesterol intake should be less than 300 mg/day.46 Moreover, individuals who
are prescribed lipid-lowering medications should consume less than 200 mg/day of
dietary cholesterol.
TABLE 8.4
Dietary Guidelines to Lower Blood Lipids and Composition
of NCEP TLC Diet
Saturated fat
Polyunsaturated fat
Monounsaturated fat
Total fat
Carbohydrate
Fiber
Protein
Dietary cholesterol
Soluble iber
Plant sterols/stanols
Omega-3-containing ish
Less than 7% per day
Up to 10% total calories
Up to 20% total calories
25–35% total calories
50–60% total calories
20–30 grams/day
15% total calories
Less than 200 mg/day
5–10 grams/day
3 grams/day
2 × per week
Source: Panel E, Executive summary of the third report of the National Cholesterol
Education Program (NCEP) expert panel on detection, evaluation, and
treatment of high blood cholesterol in adults (adult treatment panel III),
JAMA, 285, 2486–97, 2001.
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Additional dietary and/or pharmacological interventions may be needed for individuals at high risk of CHD with elevated LDL levels.46 There are several nutritional
strategies that may help in the management of dyslipidemia. For example, nicotinic
acid (niacin) supplementation (up to 2 grams/day) has been reported to lower LDL,
triglycerides, and lipoprotein-a cholesterol by 15–35% while increasing HDL cholesterol by as much as 25%.48,49 Although ingesting large amounts of niacin can cause
lushing of blood to the skin, skin rashes, gastrointestinal distress, increases in uric
acid levels, elevations in blood glucose, and liver dysfunction, longer-acting or slowreleasing forms of niacin seem to have less of these side effects. Individuals interested
in taking niacin to help manage blood lipids should do so only after consulting with
their physician. In addition, most people have to start with lower doses or consume
niacin with food to lessen side effects. Nevertheless, nicotinic acid therapy appears
to be an effective nutritional intervention to help manage blood lipids in addition to
exercise, weight loss, and diet management.
Plant sterols and stanols (also known as phytosterols and phytostanols) are naturally occurring compounds found in plants. Phytosterols and phytostanols have been
reported to inhibit cholesterol absorption in the intestine.46 A number of studies
have indicated that adding 2–3 g of plant stanol esters (expressed as free stanols)
decreases total cholesterol, LDL, and triglycerides by 5–10%.46,50–54 Phytosterols and
phytostanols have been added to margarines and other functional foods in an attempt
to help increase dietary availability of these lipid lowering compounds. A recent
study reported a dose-related effect of increasing dietary intake of phytosterols.55
Therefore, another nutritional strategy that individuals with high blood lipids can
employ is to consume these types of functional foods in their diet.
Omega-3 fats are considered essential fatty acids and are classiied as a polyunsaturated form of fat.2 There are three forms of omega-3 fats: alpha linoleic acid,
eicosapentanoic acid, and docosahexaenoic acid. Research has shown that increasing
dietary availability of omega-3 fatty acids can reduce LDL and triglycerides.46,52,56–58
The best sources of omega-3s are from fatty ish such as mackerel, lake trout, herring, sardines, albacore tuna, and salmon.2 Also, the oils of tofu, other forms of soybeans, canola, walnut, and laxseed all contain alpha linoleic acid.2 For this reason,
the AHA recommends consuming omega-3 containing ish two times a week. Fish
oil supplements also contain omega-3s, but obtaining omega-3 fatty acids from the
foods listed above is preferable to ingesting a ish oil supplement.2
Pharmacological interventions for lowering blood lipids include use of statins,
ibrates, and ezetimibe.46 Statin medications (for example, atorvastatin and rosuvastatin) have been considered as a irst-line pharmaceutical approach for the treatment
of dyslipidemia.46,59 Statins inhibit HMG-CoA reductase, resulting in a reduction
in cholesterol synthesis. Clinical trials have indicated that statins can reduce LDL
cholesterol by 20–60% and triglycerides by as much as 45%.46 The most signiicant
potential side effect for athletes is that statins have been reported to elevate creatine
kinase (CK) up to ten times normal levels, resulting in myositis and in rare incidents
promote rhabdomyolysis, leading to fatal renal damage. Fibrates (bezaibrate, fenoibrate, gemiibrozil, and ciproibrate, for example) have also been reported to lower
triglycerides, increase HDL levels, and have variable effects on LDL cholesterol.46
Finally, ezetimibe is a drug that has recently been found to inhibit dietary and biliary
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absorption of cholesterol in the intestine by interfering with cholesterol transport.
For example, a recent study reported that ezetimibe reduced LDL by 18% while
favorably inluencing HDL, triglycerides, and apolipoprotein B.60 Combination therapies of nutritional and pharmacological interventions have also been shown to be
an effective means of managing dyslipidemia when exercise, weight loss, and dietary
interventions fail to promote the types of clinical changes desired.
8.5
IMPLICATIONS FOR ATHLETES
There are a number of implications for athletes that the sports medicine professional
needs to consider. First, one should not assume that just because athletes are engaged
in intense training that they do not have dyslipidemia. Athletes who are larger, maintain higher BMIs and percent body fat, do not regularly perform endurance exercise,
and/or have a signiicant family history should undergo screening, as a high percentage of athletes who have these characteristics have been found to have higher blood
lipids. Once an athlete is found to have high cholesterol, LDL, and/or triglycerides, he
or she should meet with a sports dietitian and strength and conditioning staff to discuss alterations in diet and/or training that may help lower blood lipids. For athletes
with only moderately elevated LDL levels and a lower number of CHD risk factors,
increased aerobic exercise, loss of body fat, and reduced consumption of high-fat
and high-cholesterol-containing foods should be the initial therapeutic intervention.
In addition, greater dietary intake of phytosterols and omega-3 fatty acids may help
manage blood lipid levels. For those with more signiicant dyslipidemia, nicotinic
acid supplementation and/or pharmacological approaches may need to be prescribed
by the athlete’s physician. Since athletes engaged in intense training may experience
marked increases in CK levels, the sports medicine professional should monitor athletes taking statin drugs, particularly when they exercise in hot and humid environments. The reason for this is that one of the side effects of taking statin medications
is myositis and rhabdomyolysis. Athletes engaged in intense training may therefore
be at greater risk of these complications, particularly if they have sickle cell trait and/
or sickle cell anemia. Finally, since many athletes are susceptible to weight gain once
they retire from athletics, they may be at greater risk to observe elevations in blood
lipids as they get older. Athletes should be properly educated as they complete their
careers on ways to maintain an active lifestyle and consume a healthy diet in order
to prevent the adverse health outcomes associated with obesity.
8.6
FUTURE RESEARCH DIRECTIONS
Additional research should evaluate the prevalence of dyslipidemia in different types
of athletes; the impact of lifestyle, gender, nutrition, and pharmaceutical interventions in athletes who have dyslipidemia; and the ways to reduce the risk of athletes
gaining weight and experiencing elevations in blood lipids and risk to CHD after
they retire. In addition, athletes should be properly educated on ways of adjusting
their physical activity and diet patterns once they retire from organized athletics so
they do not experience adverse health outcomes as they get older.
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8.7
Nutritional Assessment of Athletes, Second Edition
CONCLUSIONS
Athletes are not immune to having dyslipidemia. Athletes who maintain higher BMI
and body fat, do not participate in regular endurance exercise, or have a signiicant
family history may be at greater risk and should therefore be screened by health-care
professionals. Athletes found to have high blood lipids should increase the amount
of endurance exercise they regularly perform and reduce fat and cholesterol intake
in their diet. If these strategies are not effective, they should consult with their team
physician and sports nutritionist to determine if additional nutritional and/or pharmacological interventions are necessary. Finally, athletes should be properly educated upon retiring from athletics on ways to minimize risk of dyslipidemia and
CHD as they get older.
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23. Hurley, B.F., Seals, D.R., Hagberg, J.M., C. G.A., Ostrove, S.M., Holloszy, J.O., Wiest,
W.G., Goldberg, A.P., High-density-lipoprotein cholesterol in bodybuilders v power lifters: Negative effects of androgen use, JAMA 252, 504–13, 1984.
24. Lee, H., Park, J.E., Choi, I., and Cho, K.H., Enhanced functional and structural properties of high-density lipoproteins from runners and wrestlers compared to throwers and
lifters, BMB Rep. 42, 605–10, 2009.
25. Fredrickson, D.S. and Lees R.S., Editorial: A system for phenotyping hyperlipoproteinemia, Circulation 31, 321–27, 1965.
26. Panel E, Executive summary of the third report of the National Cholesterol Education
Program (NCEP) expert panel on detection, evaluation, and treatment of high blood
cholesterol in adults (Adult Treatment Panel III), JAMA 285, 2486–97, 2001.
27. Kannel, W.B. and Vasan, R.S., Triglycerides as vascular risk factors: New epidemiologic
insights. Curr. Opin. Cardiol. 24, 345–50, 2009.
28. Connor, S., Connor, W., Sexton, G., Calvin, L., and Bacon, S., The effects of age, body
weight and family relationships on plasma lipoproteins and lipids in men, women and
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Llobera, M., Changes in lipoprotein lipase modulate tissue energy supply during stress,
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30. Bahrke, M.S. and Yesalis, C.E., Abuse of anabolic androgenic steroids and related substances in sport and exercise, Curr. Opin. Pharmacol. 4, 614–20, 2004.
31. Hata, Y. and Nakajima, K., Life-style and serum lipids and lipoproteins, J. Atheroscler.
Thromb. 7, 177–97, 2000.
32. Allain, C.C., Poon, L.S., Chan, C.S.G., Richmond, W., and Fu, P.C., Enzymatic determination of total serum cholesterol, Clin. Chem. 20, 470–75, 1974
33. Bucolo, G. and David, H., Quantitative determination of serum triglycerides by the use
of enzymes, Clin. Chem. 19, 1973.
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plasma. Clin. Chem. 20, 1964.
35. Friedewald, W.T., Levy, R.I., and Redrickson, D.S., Estimation of the concentration of
low-density lipoprotein cholesterol in plasma, without use of the preparative ultracentrifuge, Clin. Chem. 18, 499, 1972.
36. Nauck, M., Warnick, G.R., and Rifai, N., Methods for measurement of LDL-cholesterol:
A critical assessment of direct measurement by homogeneous assays versus calculation,
Clin. Chem. 48, 236–54, 2002.
37. Warnick, G.R., Nauck, M., and Rifai, N., Evolution of methods for measurement of
HDL-cholesterol: From ultracentrifugation to homogeneous assays, Clin. Chem. 47,
1579–96, 2001.
38. Wilson, P.W.F., Nam, B.-H., Pencina, M., D’Agostino, R.B., Sr, Benjamin, E.J., and
O’Donnell, C.J., C-reactive protein and risk of cardiovascular disease in men and women
from the Framingham Heart Study, Arch. Intern. Med. 165, 2473–78, 2005.
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39. Faergeman, O., Apolipoproteins and guidelines for prevention of cardiovascular disease,
J. Intern. Med. 259, 434–36, 2006.
40. Fernandez, M.L. and Webb, D., The LDL to HDL cholesterol ratio as a valuable tool to
evaluate coronary heart disease risk, J. Am. Coll. Nutr. 27, 1–5, 2008.
41. Manninen, V., Tenkanen, L., Koskinen, P., Huttunen, J.K., Manttari, M., Heinonen,
O.P., and Frick, M.H., Joint effects of serum triglyceride and LDL cholesterol and HDL
cholesterol concentrations on coronary heart disease risk in the Helsinki Heart Study:
Implications for treatment, Circulation 85, 37–45, 1992.
42. Kannel, W.B., Risk stratiication of dyslipidemia: Insights from the Framingham study,
Curr. Med. Chem. Cardiovas. Hematol. Agents 3, 187–93, 2005.
43. Marcovina, S. and Packard, C.J., Measurement and meaning of apolipoprotein AI and
apolipoprotein B plasma levels, J. Intern. Med. 259, 437–46, 2006.
44. Meisinger, C., Loewel, H., Mraz, W., and Koenig, W., Prognostic value of apolipoprotein
B and A-I in the prediction of myocardial infarction in middle-aged men and women:
Results from the MONICA/KORA Augsburg cohort study, Eur. Heart J. 26, 271–78,
2005.
45. de Farranti, S. and Rifai, N., C-reactive protein and cardiovascular disease: A review of
risk prediction and interventions, Clin. Chim. Acta. 328, 1–15, 2002.
46. Thompson, G.R., Management of dyslipidaemia, Heart 90, 949–55, 2004.
47. Williams, P.T., Incident hypercholesterolemia in relation to changes in vigorous physical activity, Med. Sci. Sports Exerc., 41, 74–80, 2009.
48. Hausenloy, D.J. and Yellon, D.M., Targeting residual cardiovascular risk: Raising highdensity lipoprotein cholesterol levels, Postgrad. Med. J. 84, 590–98, 2008.
49. Cziraky, M.J., Management of dyslipidemia in patients with metabolic syndrome, J. Am.
Pharm. Assoc. 44, 478–88, 2004; quiz 89–90.
50. O’Neill, F.H., Sanders, T.A., and Thompson, G.R., Comparison of eficacy of plant
stanol ester and sterol ester: Short-term and longer-term studies, Am. J. Cardiol. 96,
29D–36D, 2005.
51. O’Neill, F.H., Brynes, A., Mandeno, R., Rendell, N., Taylor, G., Seed, M., Thompson,
G.R., Comparison of the effects of dietary plant sterol and stanol esters on lipid metabolism, Nutr. Metab. Cardiovasc. Dis. 14, 133–42, 2004.
52. McGowan, M.P. and Proulx, S., Nutritional supplements and serum lipids: Does anything work? Curr. Atheroscler. Rep. 11, 470–76, 2009.
53. Ferdowsian, H.R. and Barnard, N.D., Effects of plant-based diets on plasma lipids, Am.
J. Cardiol. 104, 947–56, 2009.
54. Wu, T., Fu, J., Yang, Y., Zhang, L., and Han, J., The effects of phytosterols/stanols on
blood lipid proiles: A systematic review with meta-analysis, Asia Pac. J. Clin. Nutr. 18,
179–86, 2009.
55. Demonty, I., Ras, R.T., van der Knaap, H.C., Duchateau, G.S., Meijer, L., Zock, P.L.,
Geleijnse, J.M., and Trautwein, E.A., Continuous dose-response relationship of the
LDL-cholesterol-lowering effect of phytosterol intake, J. Nutr. 139, 271–84, 2009.
56. Lewis, S.J., Prevention and treatment of atherosclerosis: A practitioner’s guide for 2008,
Am. J. Med. 122, S38–S50, 2009.
57. Reiner, Z., Combined therapy in the treatment of dyslipidemia, Fundam. Clin.
Pharmacol. 2009, Aug 14.
58. Riediger, N.D., Othman, R.A., Suh, M., and Moghadasian, M.H., A systemic review of
the roles of n-3 fatty acids in health and disease, J. Am. Diet Assoc. 109, 668–79, 2009.
59. Betteridge, D.J., Dodson, P.M., Durrington, P.N., Hughes, E.A., Laker, M.F., Nicholls,
D.P., Rees, J.A., Seymour, C.A., Thompson, G.R., et al., Management of hyperlipidaemia: Guidelines of the British Hyperlipidaemia Association, Postgrad. Med. J. 69,
359–69, 1993.
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60. Knopp, R.H., Dujovne, C.A., Le Beaut, A., Lipka, L.J., Suresh, R., and Veltri, E.P.,
Evaluation of the eficacy, safety, and tolerability of ezetimibe in primary hypercholesterolaemia: A pooled analysis from two controlled phase III clinical studies, Int. J. Clin.
Pract. 57, 363–68, 2003.
61. Davis, P.G. and Wagganer, J.D., Lipid and lipoprotein metabolism, in Lipid Metabolism
and Health, Moffatt, R.J. and Stamford, B., Eds., CRC Press, Boca Raton, FL, 2006, pp.
47–60.
© 2011 by Taylor and Francis Group, LLC
of Protein
9 Assessment
Status of Athletes
Benjamin F. Miller and Matthew M. Robinson
CONTENTS
9.1
Introduction .................................................................................................. 256
9.1.1 Importance of Protein for Athletic Performance.............................. 256
9.1.2 Proteins versus Amino Acids ........................................................... 256
9.1.3 Protein Quality ................................................................................. 257
9.1.4 Adaptation to Exercise: Signals, Transcription, and Translation ..... 259
9.2 Protein Metabolism ......................................................................................260
9.2.1 Protein Turnover ...............................................................................260
9.2.1.1 Protein Synthesis................................................................260
9.2.1.2 Protein Breakdown ............................................................ 261
9.2.1.3 Net Balance ........................................................................ 261
9.2.2 Fates of Amino Acids Other than Protein Synthesis ........................ 263
9.2.3 Skeletal Muscle Protein Turnover .....................................................264
9.2.4 Turnover of Protein in Other Tissues................................................264
9.3 Importance of Energy Balance .....................................................................264
9.4 Determinations of Protein Status .................................................................266
9.4.1 Laboratory Determinations of Protein Status...................................266
9.4.1.1 Whole Body Protein Turnover ...........................................266
9.4.1.2 Skeletal Muscle Protein Turnover ...................................... 269
9.4.2 Clinical Evaluation of Protein Status ............................................... 275
9.4.2.1 Dietary Records ................................................................. 275
9.4.2.2 Body Mass and Body Composition ................................... 275
9.5 Protein Turnover and Exercise...................................................................... 276
9.5.1 Protein Turnover and Resistance Exercise ....................................... 276
9.5.2 Protein Turnover and Endurance Exercise ....................................... 276
9.5.3 Timing of Protein Intake .................................................................. 277
9.6 Protein Requirements ................................................................................... 278
9.7 Special Considerations.................................................................................. 279
9.7.1 Sex Differences ................................................................................. 279
9.7.2 Aging ................................................................................................ 279
9.8 Future Directions ..........................................................................................280
9.9 Conclusions ................................................................................................... 281
References .............................................................................................................. 281
255
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9.1
9.1.1
Nutritional Assessment of Athletes, Second Edition
INTRODUCTION
IMPORTANCE OF PROTEIN FOR ATHLETIC PERFORMANCE
Although not considered a major source of energy, dietary protein (or more accurately amino acid) intake is important for exercise adaptation. The body functions
on a simple scheme of sensing a stress and responding to minimize the disturbance
caused by that stress if it is encountered again. As far as exercise and performance
are concerned, the stress is designed to make the body better able to run, jump,
throw, etc. The way the body—or more accurately, the individual cells—adapt to
the stress is to increase the making of proteins that provide the metabolic and structural support needed to adapt to the stress. Simultaneously, proteins that might not
be needed are broken down because they are energetically expensive to maintain.
The turnover of proteins, which is dictated by gene expression in response to stress,
determines the phenotype of the athlete. Important to this chapter is that the making
of proteins requires amino acid building blocks and energy, which are consumed in
the diet.1 In a broad sense, then, we need dietary amino acids to help make the proteins that the cell requires to adapt to an exercise stimulus.
9.1.2
PROTEINS VERSUS AMINO ACIDS
Proteins are contained within and surround every cell of the body in a wide variety of
forms, including enzymes, hormones, transporters, extracellular matrixes, contractile proteins, etc. In its simplest form, a protein is series of amino acids connected by
peptide bonds into a polypeptide chain. Amino acids are organic compounds containing a carboxyl-carbon group attached to a nitrogen-containing group. All amino
acids share the form R-CH-NH2-COOH in which the R designates the functional
group, varying from a proton for glycine to double-ring structures of tryptophan.
The functional R group is attached to the α-carbon in a left-handed orientation in
proteins, and thus amino acids in the body are L-α-amino acids. There are over
300 amino acids; however, 23 are genetically encoded and used to build proteins in
eukaryotic cells.2 Twenty common amino acids are used for building new proteins
in humans and animals, and eight of these cannot be synthesized and must be consumed through dietary sources. The other twelve amino acids are synthesized within
the body or are only required in the diet to support the growth of children, as is the
case of histidine and arginine. Amino acids that must be supplied in the diet are
considered essential amino acids (EAA) compared to the nonessential amino acids
(NEAA), although it should be noted that all twenty of the amino acids are essential
for life. Other nomenclature attempts to clarify this fact by identifying amino acids
as nutritionally indispensable or nutritionally dispensable. Additionally, two amino
acids (cysteine and tyrosine) are synthesized from other EAA precursors and are
considered conditionally dispensable because depletion may occur if the precursor
becomes deicient. Amino acids are consumed from dietary sources as proteins and
free amino acids. Long polypeptide chains are digested into short sequences or individual amino acids and are transported through the gut into general circulation.
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9.1.3
PROTEIN QUALITY
The quality of a protein is its ability to meet metabolic requirements. Traditionally,
protein quality was represented by the ability of a protein source to maximize
growth rates, commonly in rats but also in humans. This view, however, focused
on amino acids being used for protein synthesis and neglected other roles of amino
acids such as nutrient signaling or neurotransmitter production. The quality of a protein is characterized by the amino acid content and availability in the protein source.
Classifying a protein based on its quality is useful for nutritional recommendations;
however, empirically determining quality is dificult and has been revised over many
years. A simple method for calculating protein quality is to compare the amino acid
pattern against a reference protein source that is known to promote growth, such as
egg or milk proteins. Although simple, the method does not consider the ability of
the amino acids to be absorbed and used in the body (bioavailability) or the amino
acid requirements of the organism. In order to address these issues, protein quality can be determined by the ability of a protein source to promote growth rates,
commonly using rats.3 The amount of protein fed to the rat is divided by the weight
gained to calculate a protein eficiency ratio (PER). A greater amount of weight
gained for a given weight of food will produce a higher PER. Although the PER
provides an indication of protein quality, the differences in growth rates between
strains and different metabolic characteristics from humans limit the reliability and
applicability of the data for human health recommendations.
In 1991, a joint committee of the World Health Organization and the Food and
Agriculture Organization (WHO/FAO) recommended an amino acid scoring calculation to evaluate protein quality.4 The score represents the ability of a protein
source to provide individual amino acids compared to the amino acid requirements
of a human reference population, and corrects that score for the digestibility of the
protein source. It assumes that amino acids must be provided in suficient quantities to meet metabolic demands, and that a limitation of any one amino acid would
impair processes, such as protein synthesis. Since EAA cannot be synthesized
endogenously, the individual EAA that is consumed in insuficient quantity to meet
metabolic demands is considered the limiting amino acid. The required intake of the
limiting amino acids is based on amino acid balance studies using preschool children
as a reference population, and the amino acid score of a protein is calculated as
amino acid score =
mg of amino acid in 1 gm testt protein
mg of amino acid in reference protein
The digestibility of the protein is calculated from the ingested nitrogen content
compared to the fecal nitrogen content, corrected for required nitrogen loss determine on a protein-free diet. Thus, the digestibility of a protein is
digestibility(%) =
© 2011 by Taylor and Francis Group, LLC
I − ( F − Fr )
× 100
I
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Nutritional Assessment of Athletes, Second Edition
where I is the intake of nitrogen, F is fecal nitrogen content, and Fr is required fecal nitrogen content determined on protein-free diet. The digestibility is used to adjust the amino
acid score to calculate the protein digestibility-corrected amino acid score (PDCAAS):
PDCAAS(%) = digestibility × amino acid score
The PDCAAS attempts to classify protein sources based on their amino acid content
and bioavailability.
A low-quality protein limits protein utilization and must be consumed in higher
quantity or in combination with high-quality proteins to meet protein requirements.
In contrast, a high-quality protein can more readily meet protein demands and can
be consumed in lower quantities. Additionally, protein quality is decreased if amino
acids have limited bioavailability due to limited digestibility, absorption, or incorporation into new proteins. Factors that contribute to limited bioavailability can be
intrinsic to the protein source, develop with disease or aging, or be introduced during
the manufacturing processes. For example, heating a protein source in the presence
of reduced sugars can cause a Maillard reaction that creates cross-linkages between
amino acid residues and decreases protein quality.5
The PDCAAS classiies protein sources based on their protein quality; however,
the WHO/FAO and others suggest that the PDCAAS is based on assumptions that
limit interpretation and should be revised.4,6,7 Criticism of the PDCAAS score suggests that using preschool children as a reference population may not be representative of all populations and their amino acid needs.6 In particular, older people appear
to be less sensitive to circulating amino acids,8 thus their dietary requirements
are elevated due to changes in sensitivity and not necessarily metabolic demand.9
Additionally, the protein digestibility is calculated from fecal values; however, fecal
values are the results of net contributions of the entire digestive tract. It was suggested that the amino acid absorption that is relevant for protein requirements occurs
within the ileum, and additional amino acid consumption by bacteria within the
colon will overestimate the true nitrogen digestibility.6 Another limitation of the
PDCAAS is that protein quality can never be greater than 100% compared to the
reference population because amino acid scores greater than 1.0 are truncated and
digestibility cannot exceed 100%.7 Thus, protein sources are compared against the
limiting amino acid regardless of the other EAA. Two protein sources with the same
limiting amino acid content and digestibility will have the same PDCAAS but could
vary in EAA content. The PDCAAS is limited because it does not consider that
different protein sources could be complementary to each other by providing EAA
that are deicient in one of the sources.6 Energy balance is also not considered when
determining overall protein quality but appears to be very important when evaluating protein metabolism.7,10 Age, gender, physiological status, and disease states are
also not considered and can impact on the ability of protein intake to meet protein
demands. In summary, the PDCAAS provides a standardized measure of protein
quality; however, its limitations must be recognized and addressed.
A quantitative measure of protein quality is beneicial for classifying protein
sources and to ensure adequate protein intake for people on strict diets. For athletes
and those on a restricted diet, consuming a high-quality protein may be beneicial
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because it limits excess caloric intake that comes with added protein. Different protein
sources can also inluence training adaptations even though the same quantity of protein is consumed.11,12 Therefore, a high-quality protein, such as those from egg or milk
sources, may be beneicial to cutting weight while maintaining lean body mass.
9.1.4
ADAPTATION TO EXERCISE: SIGNALS, TRANSCRIPTION, AND TRANSLATION
Exercise is a strong signal to induce changes in protein content, including those more
pronounced like muscle hypertrophy or those subtler like altered mitochondrial proteins. Regardless of their different types or functions, the production of proteins
from individual amino acids is a highly coordinated and multifaceted process. As
described above, the general process is sensing stress signals to induce adaptations
to minimize future perturbations. A single exercise stimulus contains a multitude of
diverse signals, including energetic stress, nutrient deiciency, mechanical loading,
and circulating hormones. The nucleus integrates multiple signals and responds by
encoding mRNA transcripts from the appropriate DNA sequences, a process termed
transcription. The mRNA transcript contains the coding template for the amino
acid sequence of the protein. Translation is the process by which RNA polymerase
enzyme complexes read the mRNA transcript and attach amino acids together in
the proper order. Following translation, the new polypeptide strand must be properly
folded into its inal structure to allow proper function. The endoplasmic reticulum is
a major site for protein folding of the cell and contains the necessary environment
and machinery to process nascent polypeptide chains.13
It is necessary to recognize that not every signal will lead to the expression of
a fully functional protein. Multiple independent regulation steps within signaling,
transcription, and translation pathways coordinate protein synthesis. A signal can
also have diverse responses to coordinate a single goal. The regulation steps may
be speciic, such as turning on a speciic transcription factor for a family of gene, or
more general, such as limiting the overall protein synthesis machinery of the cell.
Short-term signals are often mediated by changing the phosphorylation state of
a protein that subsequently alters the activity or function of a protein. For example,
eukaryotic elongation factor-2 (eEF2) is a regulatory protein that decreases protein
synthesis when phosphorylated. Increased phosphorylation of eEF2 was shown following a single minute of exercise and remained elevated through 90 minutes of
endurance exercise.14 Speciic mRNA transcripts also increase following exercise,
but the time course appears to be longer than phosphorylation events with some
transcripts increased immediately postexercise and peaking between 2 and 8 hours
postexercise.15–17
The time course and signaling characteristics between initial stimulus (such as
exercise) and eventual synthesis of proteins is important when attempting to maximize adaptations to exercise. Initial increases in translational activity appear to
mediate acute adaptations to exercise and are followed by increased transcriptional
activity to create more mRNA.18 The increase in mRNA provides additional transcripts that can be subsequently translated into new proteins. The combination of
rapid translational events and delayed transcriptional events causes the resultant
increase in protein content. Recommendations to maximize recovery from exercise
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Activation
Nutritional Assessment of Athletes, Second Edition
mRNA content
mRNA translation
Phosphorylation
Minutes
Hours
Days
Time Post Exercise
FIGURE 9.1 Exercise activates protein synthesis through rapid changes in phosphorylation
states of regulatory proteins that allow increased translation of existing mRNA transcripts.
Increased transcription activity will increase mRNA content over longer time periods. The
shaded region represents the optimal timing for maximal stimulation of protein synthesis
during initial recovery period.
are based on these time-course characteristics. For example, when the duration for
elevated mRNA transcript is compared against the increased activity of protein synthesis machinery, then we can identify a time period when maximal adaptations
most likely occurs (Figure 9.1). This concept is very important when discussing the
timing of nutrient intake around exercise to maximize recovery.
9.2
9.2.1
PROTEIN METABOLISM
PROTEIN TURNOVER
The total protein content in a cell, tissue, or organism is the net contribution of the
synthesis of new proteins and the breakdown of existing proteins. The combination of
these two processes (protein turnover) is necessary for maintaining cell processes by
replacing older proteins with newer proteins. The renewal of proteins promotes cell
function by allowing older proteins that may have diminished function to be replaced
by new proteins that have improved function. The overall content of proteins may not
change, but the quality and function of the proteins are improved. The rate at which a
protein is synthesized and degraded is referred to as its half-life (t1/2) and often determined by its physiological task. Proteins that are involved in regulatory roles, such as
transcription factors or hormones, can have higher turnover rates (t1/2 < 30 min) than
contractile proteins such as myosin heavy chain (t1/2 ~ 54 days).19 Either accumulation
or loss of the protein occurs when the contribution of synthesis and breakdown are
not in equilibrium. These two processes will be discussed separately.
9.2.1.1 Protein Synthesis
Protein synthesis is the translation of mRNA transcripts to combine individual
amino acids (speciically amino-acyl tRNA) into polypeptide chains. These nascent
peptides are then folded into their proper structure by chaperone proteins and are
transported to their appropriate destination such as the plasma membrane for transmembrane receptors, released into the cytosol for intracellular signaling proteins, or
secreted as in the case of peptide hormones. Interestingly, the machinery required
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Assessment of Protein Status of Athletes
261
for protein translation is made of proteins (for example, ribosomes and chaperones);
thus cells must maintain basal rates of protein synthesis to maintain the proteins
necessary for translation.
9.2.1.2 Protein Breakdown
Protein breakdown is the removal of existing proteins and yields either short chains of
amino acids or individual amino acids. These can then be used by the cell as needed,
including for translation of new proteins, oxidation for adenosine-5′-phosphate (ATP)
production, or export and transport to other cells. Protein breakdown occurs through
a host of enzymatic processes. Peptide chains are cleaved by proteases into short
peptide chains, which are then digested into individual amino acids by endoproteases. These proteases can be free within the cell or contained within intracellular
organelles that serve as major sites for protein degradation, such as the lysosome and
proteosome. The proteosome pathway uses short amino acid sequences (called ubiquitin) and a series of enzymatic reactions to target proteins for degradation within the
proteosome. Polyubiquitination of proteins can occur and accelerate proteolysis.
Although nutritional research and recommendations often focus on protein synthesis pathways, protein breakdown is a necessary and important process for maintaining
cell function and the health of the organism. As indicated above, protein breakdown
contributes to protein turnover and promotes cellular function by replacing older proteins with newly synthesized proteins. Additionally, protein breakdown can provide
amino acids to the pool of intracellular amino acids. This is especially important
when considering essential amino acids (EAA), which cannot be synthesized and
enter the intracellular amino acid pool through either dietary sources or release from
protein breakdown. If dietary EAA are insuficient to meet the needs of protein synthesis, then existing proteins can be degraded and supply the necessary amino acids.
This concept indicates that skeletal muscle can serve as a reservoir to store and release
amino acids depending on their availability and metabolic demands.20
9.2.1.3 Net Balance
The net balance of proteins is the total contribution of protein synthesis and breakdown and is commonly expressed as
Net Balance = Protein Synthesis − Protein Breakdown
If the synthesis and breakdown of proteins are occurring at equal rates, then the
net balance will be zero and no gain or loss of protein occurs (Figure 9.2). It is possible for both synthesis and breakdown to be elevated and cause an increased protein
turnover without net gain or loss. If protein synthesis exceeds protein breakdown,
then net protein balance will be positive and indicate an accumulation of proteins.
Conversely, if protein breakdown exceeds protein synthesis, then the net balance
will be negative and indicate a loss of proteins. When considering net balance, it is
necessary to understand the context in which the parameter is being evaluated. For
example, if whole-body protein synthesis and breakdown are being evaluated, then
net balance relects the entire change in the protein pool of the body. It is possible
to evaluate speciic limbs and tissues in order to determine local changes to net
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Synthesis
Breakdown
Net Balance
Low Turnover
Net Balance
High Turnover
Positive
Balance
Negative
Balance
FIGURE 9.2 Schematic contribution of protein synthesis and breakdown to net balance and
turnover.
balance that may not be detected with whole body measures. For example, wholebody protein turnover did not change following a resistance exercise session in
young men.21 However, a limb-speciic model showed increased protein synthesis in
the legs of young men, with a larger increase of protein breakdown that resulted in a
net negative protein balance.22 These studies support that protein metabolism can be
evaluated generally (whole-body protein balance) or locally (protein balance within
the leg), and that different conclusions may be drawn based on the study design.
Methodological advances have allowed protein synthesis rates to be determined for
individual muscle proteins.23 Future advances may allow protein breakdown rates to
be determined and allow determination of net balance of individual proteins. Thus,
net balance provides insight into the overall contribution of protein synthesis and
breakdown and allows a more complete evaluation of protein metabolism than either
individual process.
Net balance can be somewhat limiting in the absence of information about synthesis and breakdown. As discussed above, synthesis and breakdown can vary without
changing net balance. Further, net balance does not consider that a high rate of protein turnover allows rapid ampliication of protein content following changes in the
rate of protein synthesis or breakdown, or a combination of both. One such example
is found with the transcription factor hypoxia inducible factor-1α (HIF-1α), which
degrades rapidly after it is synthesized and maintains a constant protein content.
However, hypoxia produces a signal to stabilize HIF-1α and causes a rapid accumulation of protein to promote the transcriptions of genes and subsequent adaptation.24
Thus, the net balance of a protein does not reveal information about synthesis or
degradation kinetics or their regulation.
Protein synthesis appears to respond to stimuli and inluence net balance to a
greater extent than breakdown. For example, Paddon-Jones et al. used leg-speciic
measures and showed that 28 days of bed rest caused muscle atrophy with decreased
protein synthesis but no change to protein breakdown.25 Furthermore, older adults
have decreased rates of muscle protein synthesis but no difference in protein breakdown as compared to younger people during resting conditions.26 These indings do
not diminish the importance of degradation pathways but suggest that changes to net
protein balance are driven primarily by changes to rates of protein synthesis.
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9.2.2 FATES OF AMINO ACIDS OTHER THAN PROTEIN SYNTHESIS
Amino acids are commonly considered in reference to protein synthesis; however,
they can serve as precursors for others processes, including gluconeogenesis, synthesis of neurotransmitters, intermediates in the Kreb’s cycle, and ATP production
(Figure 9.3). Before individual amino acids can be used for such pathways, the amino
group is removed by transamination. Transamination is reversible enzymatic reaction catalyzed by speciic aminotransferases that transfer the amino group from an
L-α-amino acid to an α-keto acid. Removing the amino group converts an α-amino
acid to its α-keto acid form. Transamination does not degrade an amino acid but
converts an L-α-amino acid to an α-keto acid and uses the nitrogen group to convert
another α-keto acid to an L-α-amino acid. The process can be reversed to produce
the twelve nonessential amino acids from their α-keto acid, which are found as intermediates within glycolysis and the Kreb’s cycle.
The α-keto acids can be incorporated into the Kreb’s cycle to expand the pool of
intermediates (a term called catapleurosis) and can be used as substrates for eventual
production of ATP by oxidative phosphorylation. For example, L-glutamate can be
transaminated to form α-ketoglutarate and used to produce NADH in the Kreb’s
cycle by the α-ketogutarate dehydrogenase complex. The α-keto acid products can
also be used as gluconeogenic precursors, such as L-alanine being transaminated to
pyruvate for eventual formation of glucose.
Amino acids can be also be catabolized by amino acid oxidase enzymes to produce NADH, a process termed oxidative deamination. Glutamate is a common
amino group acceptor from transamination and is therefore a primary amino acid
Diet
Protein Breakdown
Protein Synthesis
Intracellular Amino Acid
Oxidative Deamination
Excreted
FIGURE 9.3 Intracellular fates of amino acids.
© 2011 by Taylor and Francis Group, LLC
α-Keto Acid
Other fates
-DNA and RNA base
synthesis
-Neurotransmitter production
-etc.
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used for oxidative deamination in mammalian tissue. The liver contains many amino
acid oxidases and is a major site for oxidative deamination. However, other tissues
can oxidize amino acids, which must be considered when evaluating the fate of
amino acids. For example, skeletal muscle can use leucine but not phenylalanine as
an energy source. Thus, the fate of leucine uptake into skeletal muscle cells includes
protein synthesis and oxidation, whereas phenylalanine will be used only for protein
synthesis. The metabolism characteristics of amino acids must be considered when
evaluating protein turnover methodology.
9.2.3
SKELETAL MUSCLE PROTEIN TURNOVER
Skeletal muscle protein turnover is especially important when considering athletic
performance because of its size, its important role in locomotion, and its role in
energy balance. Small changes in turnover relative to a given mass of tissue will be
ampliied by the sheer size of tissue to large absolute rates. This concept is important
in regards to energy balance because skeletal muscle is a highly metabolic tissue
in terms of absolute rates. Other tissues, such as liver, have higher relative rates of
energy consumption and protein turnover, but the large size of skeletal muscle is a
greater absolute contributor to whole-body protein turnover and metabolic rate.27
Since amino acids do not have a speciic storage site such as adipose tissue for fatty
acids, synthesizing amino acids into skeletal muscle proteins may be the only way to
“store” amino acids during times of excess (such as feeding) to be used in times of
need (such as fasting). Therefore, investigations of protein turnover and nutritional
requirements often focus on skeletal muscle because of its size and dynamic nature,
and its importance in the determination of exercise performance or health.
9.2.4
TURNOVER OF PROTEIN IN OTHER TISSUES
All tissues synthesize and degrade proteins continually, and some tissues have very
high rates of protein turnover. Loss of skin, hair, blood, sweat, and cells lining the
intestinal tract are continual sources of protein loss from the body that need to be
replenished. Depending on the involved processes, the rates of protein turnover can
be very high relative to the tissue size. The liver is a major source of secreted proteins such as hormones and lipoproteins and has high rates of protein turnover. In
fact, the liver accounts for ~20% of whole-body oxygen consumption although it is
only ~2% of the body’s mass.27 Contrasted against skeletal muscle that is ~42% of
the body’s mass and consumes ~20% of total oxygen consumed, it is apparent that
smaller tissues can be highly metabolic.27 Skeletal muscle receives much focus when
considering protein requirements and turnover, but that focus should not detract from
the importance and contribution of other tissues to protein metabolism.
9.3
IMPORTANCE OF ENERGY BALANCE
Protein synthesis is the greatest energy-consuming process of the cell, and under resting conditions protein turnover contributes to about ~20% energy requirements.27,28
Protein synthesis requires the hydrolysis of four high-energy phosphates per peptide
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bond: two ATP for charging the aminoacyl tRNA molecule and two guanosine-5′triphosphates (GTPs) for entry and translocation on active sites of the ribosome complex. Additionally, the formation of the ribosome complex requires GTP hydrolysis
to form peptide bonds between amino acids of the lengthening protein. In addition
to peptide bond formation, protein synthesis requires RNA synthesis and transport
of amino acids across membranes into the cell, all of which are ATP-consuming processes. Thus, the energetic calculation of protein synthesis needs to evaluate these
processes as well. A single protein can be made of hundreds of peptide bonds; thus
protein synthesis requires a continual supply of energy. As an example, hemoglobin
contains 574 amino acids and requires ~2300 high-energy phosphates to form all of
its peptide bonds. Since red blood cells contain many hemoglobin molecules and are
being continually replaced, one can imagine that much energy is required to maintain hemoglobin protein levels, let alone the other proteins found within a red blood
cell. Even synthesis of a smaller protein such as pro-insulin, the precursor to secreted
insulin, with 119 peptide bonds has large energy requirements (~476 ATP).
Protein breakdown is also an ATP-consuming process, although to a lesser extent
than protein synthesis. The ubiquitin–proteosome pathway consumes approximately
four ATP per degraded protein.29 The combined energetic costs of protein breakdown and synthesis using protein turnover and metabolic rate have been estimated
at 1.04 kcal for each gram of protein,28 with 1–2% of all proteins within the body
replaced daily. Conditions with elevated protein turnover will increase protein intake
requirements along with energy costs. For example, burn victims have a hypermetabolic state characterized by increased resting energy expenditure and higher rates
of protein synthesis. About 25% of the increase in energy expenditure is due to the
energy requirements of increased protein synthesis.30
Energy balance is the difference between energy consumed and energy expended
and has a critical contribution to protein metabolism. The synthesis and breakdown
of proteins are ATP-consuming processes, and it has been recognized since the irst
part of the twentieth century that protein balance is strongly inluenced by energy
balance.31 In 1954 Calloway and Spector performed an important review of available
nitrogen balance data and concluded that at a ixed adequate protein intake, energy
level is the deciding factor in nitrogen balance.32 Their paper also established minimal protein or energy intakes at which increasing one or the other has no inluence
on nitrogen balance. Two additional studies from Calloway’s laboratory demonstrated
that nitrogen balance is better maintained when a caloric deicit is induced from physical activity rather than diet,10 and that exercise training actually increases the ability
to maintain nitrogen balance at a given energy balance and protein intake.33 Finally,
Chiang and Huang showed that increasing levels of positive energy balance (+15% and
+30%) caused greater nitrogen retention when provided a given amount of protein.34 It
is now evident that energy-sensing pathways can regulate protein turnover, in particular through regulating protein synthesis. For example, one negative regulator of protein
synthesis is AMP-activated protein kinase (AMPK). AMPK responds to low-energy
states by activating energy producing pathways and impairing energy-consuming pathways including protein synthesis.35 Additionally, the mammalian target of rapamycin
(mTOR) complex is a primary regulator of protein synthesis and directly responds to
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decreased cellular energy status by decreasing protein synthesis.36 In summary, energy
balance is an important regulating factor for protein turnover.
Energy and protein levels supplied by a Western diet are typically in excess of
requirements; therefore energy intake is commonly suficient to supply protein turnover needs. There are examples of negative energy balance that could be detrimental
for protein balance such as with aging, dietary restrictions for weight loss, total parenteral nutrition, or exercise without increased energy intake. These conditions may
cause an undesired loss of muscle mass through decreased energy availability. The
recognition that protein turnover is energetically costly is not novel but is commonly
overlooked when evaluating protein requirements.1
9.4
DETERMINATIONS OF PROTEIN STATUS
There are various methods to assess protein status of an individual. Some methods evaluate the organism as a whole (for example, nitrogen balance) and others evaluate tissues
or even individual proteins (such as fractional synthesis rates using stable isotope tracers). Each method has beneits, limitations, and assumptions that should be considered
when interpreting the results. A brief discussion of common methods for evaluating
protein metabolism is included; however, additional resources provide more in-depth
discussions of the derivations, applications, and assumptions of each method.37
9.4.1
LABORATORY DETERMINATIONS OF PROTEIN STATUS
9.4.1.1 Whole Body Protein Turnover
9.4.1.1.1 Nitrogen Balance
Amino acids are the primary carrier of nitrogen in the body, so when we are considering amino acid and protein metabolism, we are ultimately considering nitrogen
metabolism. Nitrogen balance compares the amount of nitrogen consumed versus
the amount lost and gives an indication if protein is being retained or excreted on a
net basis. If the amounts of nitrogen consumed (Nin) and excreted (Nout) are known,
then nitrogen balance (N balance) is expressed as
N balance = N in − N out
Nitrogen content is converted to protein content by the relationship that 6.25
grams of protein contain 1 gram of nitrogen (multiply grams of N by 6.25 to determine grams of protein). Nin is controlled by dietary intake since nitrogen is consumed
only as proteins or amino acids. Diet records can be analyzed to estimate nitrogen
consumption; however, the records or analysis programs may not be fully accurate.
Precise determination of nitrogen intake often requires prepared diets with known
amounts of nitrogen content. Additionally, oral or intravenous delivery of amino acid
solutions improves control of Nin.
Nout is much more dificult to quantify than Nin. Fundamentally, Nout represents the loss of nitrogen from the body. However, nitrogen is lost from the body
in many forms, including urine, feces, hair, blood, sweat, and cells from the skin
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and gastrointestinal tract. Thus a precise determination of Nout requires that each
of these sources of nitrogen loss be collected and quantiied. Fortunately, previous
studies have taken labor-intensive measures (such as loss during tooth brushing) and
attempted to fully quantify nitrogen loss.38 The results indicate that nitrogen loss
from sources other than urine and feces are minimal (~500 mg/day) and can be
accounted for with a mathematical correction factor. Urine and feces are the major
routes of nitrogen loss and can be analyzed for nitrogen content, although urine is
the most commonly measured source of excreted nitrogen. Using urinary nitrogen
content and standard correction factors to account for nonurine losses, daily nitrogen
balance can be expressed as
N balance = N in − (N urine + 5 mg/kg + 2000 mg)
with miscellaneous nitrogen losses accounted by 5 mg per kg body weight and fecal
loss at 2000 mg per day.
The nitrogen balance technique allows insight into the overall net contribution of
protein synthesis and breakdown in the body. Nitrogen balance is a relatively simple
and noninvasive method for evaluating whole-body protein status over longer periods such as days to weeks39 and is useful as an overall evaluation of protein gain or
loss. Although less precise than other methods, nitrogen balance can be used with
other measurements to provide a more complete evaluation of protein balance.40,41
9.4.1.1.2 Isotopes in Metabolic Research
The use of stable isotopes in metabolic research has allowed a greater insight into
the kinetics behind observable changes. It is apparent that the absolute quantity of a
substance (such as muscle protein content) is the sum total of synthesis and degradation pathways and that the movement of substrates through these pathways, termed
lux, yields more information than just changes in total quantity. Isotopes are used
to determine the kinetics (rate of movement) of metabolic pathways. Isotopes are
atomic elements that contain the same number of protons but vary in the number
of neutrons and subsequently their atomic mass. These isotopes can be stable or
experience radioactive decay. For example, carbon exists primarily with twelve neutrons and is referred to as 12C but can also exist as stable (13C) and radioactive (14C)
isotopes. Radioactive isotopes were traditionally used in metabolic research due to
their analytical sensitivity; however, technological advances in mass spectrometry
(the primary analytical tool for stable isotopes) have brought stable isotopes to the
forefront of isotope research. Amino acids contain carbon, nitrogen, and hydrogen
atoms that can be isotopically labeled. Isotopic tracers nomenclature identiies the
atom that is labeled and its position within the molecule. For example, a leucine
molecule that is labeled with a single 13C as the irst carbon is 1-13C-leucine. Multiple
isotopes can be identiied such as [6,6]-2H2-glucose, which has two deuterium atoms
on the sixth carbon of glucose, or ring-13C6-phenylalanine containing 13C for all six
carbons in the ring structure of phenylalanine. Molecules that contain isotopes are
considered to be enriched tracers and are treated the same as the nonenriched molecules they resemble. Tissue samples (for example, blood or muscle biopsy samples)
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are analyzed for tracer content by determining the ratio of tracer to tracee, called the
enrichment of the sample.
The concept of isotope tracer research can be represented by dilution of a dye into
a bathtub with a constant level of water. The dye represents the infusion of a tracer
and the tub of water represents the tracee content of the entire body. Water lows
into the tub via the faucet and drains out at an unknown rate. If a known amount of
dye is dropped into the tub, the dye will be diluted due to the rate of water lowing
through the tub. Using the rate of infusion of dye into the tub, we can then calculate
the low rate of the water through the tub. This concept of tracer dilution is central
for isotope methodology.
Amino acid tracers that are either orally consumed or intravenously infused have
the same fates as other amino acids, namely, to be incorporated into proteins, oxidized as energy substrates, or excreted from the body. If the body is considered a
single pool of amino acids, then amino acids enter from either exogenous (dietary
and infusion) or endogenous sources (protein degradation and amino acid synthesis).
Since essential amino acids (EAA) are not synthesized endogenously, then the entry
of an EAA into the body pool is restricted to consumption or infusion and release
from protein breakdown (Figure 9.4). Since tracers exist in very small quantities
within the body, the amino acids released from proteolysis will be mostly unlabeled
and will dilute the amount of labeled tracer that was infused. Thus in the fasted state,
the dilution of the labeled tracer is used to determine the rate of appearance of amino
acids from protein breakdown.
Amino acids that leave the pool can either be oxidized as an energy substrate
or be used by nonoxidative pathways, which is primarily protein synthesis. If an
amino acid tracer with a carbon isotope is consumed or infused, then the carbon will
be removed during oxidation and exhaled in the breath as labeled carbon dioxide.
Breath samples are collected and analyzed for labeled carbon dioxide to determine
the amount of amino acid oxidation. The total rate of disappearance is known from
Essential Amino Acid
Tracer Infusion
Protein Breakdown
Ra
Whole Body Free
Amino Acids
Rd
Non-oxidative disposal
(Protein synthesis)
Oxidation
FIGURE 9.4 Single pool model. Under fasted conditions with an essential amino acid
tracer, the source of amino acids for tracer dilution is protein breakdown. The low of amino
acids entering the pool (Ra) equals the low leaving (Rd).
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blood samples and the rate of oxidation is known from breath samples. The primary
nonoxidative fate of amino acids in skeletal muscle is protein synthesis and is represented as nonoxidative disposal. The value is calculated from the difference between
the total rate of disappearance and oxidation.
In practice, 1-13C-leucine is intravenously infused in fasted individuals with venous
blood and breath samples obtained periodically (usually hourly). 1-13C-leucine is
commonly used as the tracer of choice for whole-body protein turnover characteristics because it yields 13CO2 when oxidized and its major nonoxidative fate is protein
synthesis. It is also an EAA, so in the fasted state the appearance of leucine can only
come from protein breakdown. The dilution of the infused tracer by unlabeled leucine represents protein breakdown and is calculated as
Ra =
F
EKIC
where F is the infusion rate of the tracer and EKIC is the isotopic enrichment of
α-ketoisocaproate (KIC). KIC is the α-keto acid produced from leucine transamination. Since transamination occurs intracellularly and then KIC is released into
circulation, circulating KIC represents the intracellular content of leucine. The Rox
of leucine is calculated by measuring the 13CO2 content in breath samples and KIC
enrichment in blood:
Rox =
13
CO 2
EKIC
Since the whole-body protein model assumes a steady state in which the rates of
amino acid disappearance (Rd) and appearance (Ra) are in equilibrium
Rd = Ra
NOLD + Rox = Ra
NOLD = Ra − Rox
where nonoxidative leucine disposal (NOLD) represents whole-body protein synthesis.
9.4.1.2
Skeletal Muscle Protein Turnover
9.4.1.2.1 3-Methyl-Histidine
Modiications to amino acids occurring after protein translation are used to evaluate characteristics of protein turnover in skeletal muscle. Common posttranslational modiications include hydroxylation and methylation of amino acid residues
within proteins. Because tRNAs do not exist for these modiied amino acids,42
protein breakdown releases the modiied amino acids and they are not recycled
into other proteins. Following protein breakdown, the modiied amino acids are
released into circulation and are eventually excreted. Thus, the presence of these
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posttranslational modiied amino acids in blood or urine is representative of protein breakdown.
One such modiication is methylation of histidine to from 3-methyl-histidine.
Skeletal muscle actin and myosin proteins contain much of the 3-methyl-histidine
(3-MH) content in the body, and therefore the appearance of 3-methyl-histidine in
urine can be used to evaluate skeletal muscle protein breakdown, speciically myoibrillar protein breakdown.43 However, the content in urine is from proteolysis of the
entire body, inluenced mostly by skeletal muscle (~75%) but also other sources such
as rapidly turning over gut and skin proteins.44 Localized sampling techniques such
as arterial-venous (A-V) differences and microdialysis can limit the contribution
of 3-MH from nonskeletal muscle and evaluate proteolysis over more speciic tissues.45,46 A-V differences between the 3-methyl-histidine concentration in the blood
supplying the muscle (arterial) and blood draining the muscle (venous) determine the
protein breakdown of the tissue bed. Increased proteolysis will release more 3-MH
into venous blood and increase the A-V difference. A-V differences provide more
localized values but are still inluenced by all the tissues that release 3-MH into the
sampled vein. Microdialysis procedures allow a further degree of localization. The
technique involves inserting a small tube (called a probe) through the tissue of interest. A section of the probe within the tissue contains a semipermeable membrane
that allows molecules to pass into the lumen of the probe and be collected. If the
probe is inserted into skeletal muscle, then that speciic tissue is the primary source
of 3-methyl-histidine. In summary, posttranslational modiications to amino acids
can provide insight into protein breakdown, but the source of the compound and the
site of sampling need to be considered.
9.4.1.2.2 Fractional Synthesis Rate
A widely used method uses stable isotopic tracers to determine the fractional synthesis rate (FSR) of proteins. The FSR indicates the fraction of the protein pool that is
synthesized over a given time, usually represented at %/hour. By deinition, proteins
with a higher FSR are being synthesized at a faster rate. It is important to note that
FSR represents a fraction of the protein pool being synthesized. In order to obtain
absolute synthesis rates, the FSR is multiplied by the pool size of the protein. Thus,
a small protein pool with a high FSR rate may have a lower absolute synthesis rate
than a large protein pool with a lower FSR.
Measuring FSR is based off a precursor–product relationship in which amino
acids are the precursor building blocks to form protein products. Amino acid isotopic tracers are infused into circulation and are incorporated into the intracellular
amino acid pool that is used to synthesize new proteins. Tissue biopsy samples are
then analyzed for tracer content and FSR is calculated as
FSR =
Et 2 − Et1
E p (t2 − t1 )
where Et2 and Et1 are the isotopic enrichments of the protein product at two time
points, Ep is the enrichment of the precursor, and t2 and t1 are the times for tissue
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sampling. FSR is the change in product enrichment divided by the average precursor enrichment during the sample time period. Speciicity of FSR is limited by the
ability to sample a tissue or isolate a speciic protein. For example, a muscle biopsy
sample that does not undergo further separation techniques will yield mixed muscle
FSR.47 Additional steps can separate various protein subfractions such as myoibrillar, sarcoplasmic, and mitochondrial proteins to determine the FSR of each group of
proteins.48 Even further analytical steps can determine the FSR of individual proteins
and have identiied that different proteins within subfractions have varied synthesis
rates.23 The concept of subfractions is further discussed in Section 9.4.1.2.5.
Continuous infusions of stable isotopes are commonly used over a period of hours
(4–10) to allow suficient tracer incorporation into the protein product during an isotopic steady state such that Ep is constant. However, a single large looding dose of
isotope can be used to shorten the time period necessary (30 to 90 minutes) to allow
suficient label incorporation. Both methods rely on the precursor–product relationship in which the true precursor for protein synthesis must be known. Although
amino acids are commonly considered the building blocks for proteins, the inal
form that is incorporated into polypeptide strands is charged aminoacyl-tRNA.
Thus, the true precursor for protein synthesis is tRNA, which is very dificult to
measure in small muscle samples such as human biopsies.49 The looding dose technique avoids this problem because all amino acid pools are looded with tracer such
that sampling any of the pools (such as blood) represents the isotopic enrichment of
the true precursor. The constant infusion technique requires that surrogate measures
such as intracellular or plasma enrichment be used for the precursor enrichment.
Transamination products released into circulation provide a useful representation
of intracellular amino acid content. A common example is using plasma KIC to
represent intracellular leucine.50 Leucine is transaminated within cells to form KIC,
which is subsequently released into blood. The relationship is reciprocal, meaning
that labeled KIC can be infused, transaminated to leucine, and used for protein synthesis. In this situation, labeled leucine is also released into circulation and is the
precursor for FSR calculations.
The looding dose technique requires much less time and provides a better representation of the true precursor, and it was widely used to calculate FSR. However,
it was realized that providing looding doses of amino acids, in particular essential
amino acids, stimulated the making of proteins through a feeding-like effect.51,52
These indings were important because they identiied that (1) the looding dose
technique can artiicially elevate FSR, and (2) essential amino acids can stimulate
protein synthesis. Therefore, the constant infusion technique is more commonly
used to determine FSR, although it must be recognized that long study designs (4–10
hours) may not fully represent a physiological steady state or acute effects following
an intervention.
Fractional breakdown rate (FBR) is determined using a reversal of FSR, meaning that the inal product is free amino acids and the precursor is bound proteins.53
Tracers are infused initially to reach isotopic steady state in circulation then the infusion is stopped. The tracer is diluted by the release of unlabeled amino acids from
protein breakdown. Regular blood samples are used along with one or two muscle
biopsies to plot the rate of plasma and intracellular tracer dilution. An essential amino
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acid tracer must be used since the method assumes that unlabeled amino acids are
coming from protein breakdown and not endogenously synthesized. Additionally,
the protein source of amino acids cannot be determined, and thus the FBR of subfractions or individual proteins cannot be determined using this method.
9.4.1.2.3 Two- and Three-Pool Models
The concept of body pools is an attempt to model the movement of amino acids
throughout the body. The simplest model is a single pool that is used for whole-body
protein turnover and provides information about overall protein turnover; however,
regional characteristics of amino acid metabolism are not known (see Section 9.4.1.1).
Two- and three-pool models allow greater understanding of amino acid transport
characteristics, although it is apparent that modeling the body as two or three pools
of amino acids is still simplistic.54 The concept of two- and three-pool models is
based on the Fick principle of tissue substrate use in which
Tissue uptake = Blood flow × (artery − venous difference)
Tissue outflow = Blood flow × (venous − artery difference)
Adolph Fick initially used the relationship between A-V differences in O2 concentration to calculate blood low across the lungs55; however, the relationship between
blood low and tissue utilization can be readily applied to other circulating substrates.
The two-pool model compartmentalizes amino acids into (1) the arteries that supply
tissues and (2) the veins that drain tissues (Figure 9.5). The concept is similar to nitrogen balance because the difference between inlow (artery) and outlow (vein) provides
a representation of net balance across a tissue. A greater net uptake of amino acid is
indicative of protein synthesis, whereas a net release indicates protein breakdown.
In the case of two-pool models, the tissue of interest is identiied along with its
appropriate artery and vein. Commonly the skeletal muscle of the leg is of primary
interest; therefore the femoral artery and vein are catheterized for periodic blood
samples. Blood low and amino acid concentrations determine the total amino acid
content delivered to the tissue bed. Arterial concentrations are constant throughout
the entire arterial system; therefore, any artery or sometimes an arterialized hand
vein can be adequate for determining circulating amino acid concentration.56 Blood
Arterial Concentration
Artery
To Muscle
Shunt to vein
Muscle
Production
Vein
Venous Concentration
Disposal
To Vein
FIGURE 9.5 The three-pool model adds more information about protein kinetics than does
the two-pool model (shaded region). Infusion of an essential amino acid tracer that is not
metabolized within the muscle will cause production to be zero and allow disposal to be only
protein synthesis.
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low must be accurately determined for A-V difference to yield reliable tissue balance results.57,58 The units of blood low (~100 mL/min at rest per leg) are much
larger than circulating amino acid concentrations (~50 nmol/mL), so a small error
in blood low measurements will have a large effect on the calculated amino acid
delivered to the tissue. The choice of vein is critical and must be located downstream
of the tissue of interest. Since veins drain blood from all tissues, the venous measurements are affected by all tissues (skeletal muscle, skin, bone, etc.) and are limited to
the extent that the tissues contribute to amino acid metabolism.
In addition to A-V differences of amino acid, an isotopic tracer can be infused
into a separate vein (commonly antecubital) to calculate amino acid Ra and Rd. Ra
is the rate of appearance of amino acids into circulation from the tissue (represents
protein breakdown) and Rd is the rate of disappearance of amino acids into the tissue
(represents protein synthesis). The choice of tracer is crucial because the calculated
Ra and Rd will relect total tissue lux, including synthesis of nonessential amino
acids. If a nonessential amino acid tracer is used, then Ra is affected by protein
breakdown and de novo amino acid synthesis. Similarly, Rd provides an indication
of amino acid uptake into tissue but cannot differentiate between nonoxidative fates
of amino acids (such as gluconeogenesis), oxidation of the amino acid (such as for
leucine), or protein synthesis. Thus, Rd for a leucine tracer includes protein synthesis
and leucine oxidation, but Rd for phenylalanine (which is not metabolized in skeletal
muscle) primarily indicates protein synthesis. An additional limitation is that amino
acids may be released into the intracellular luid and recycled for protein synthesis
without entering general circulation. The two-pool model therefore underestimates
protein synthesis depending on the degree of amino acid recycling. Thus, leg balance
using a two-pool model yields values for Ra and Rd that relect protein breakdown
and synthesis but are not direct measures.
The three-pool model adds to the two-pool model by including the intracellular
compartment of amino acids. Biolo et al. developed the model in order to evaluate
amino acid transport kinetics into and out of the intracellular luid.59 The experimental design uses a continuous infusion of stable isotopes with samples from arterial
and venous blood and muscle tissue. Amino acid transport rates can be determined
from the artery to the muscle and from the muscle to the vein (Figure 9.5). The
model also distinguishes the low of amino acids from artery to vein that is shunted
past the tissue. Rates of protein synthesis and breakdown are calculated from the net
balance of amino acids and low of blood into the muscle divided by the intracellular
tracer enrichment.
The addition of amino acid transport kinetics to calculations of protein synthesis
and breakdown are an important addition by the three-pool model. For example,
Biolo et al. showed that a bout of resistance exercise increased the rates of inward
transport for leucine, lysine, and alanine but not phenylalanine.60 Since the model
calculates both protein synthesis and breakdown, the study also identiied that protein synthesis was elevated along with protein breakdown and indicated that both
processes are affected by resistance exercise. A limitation of the three-pool model
is that any limitations on amino acid transport or diffusion kinetics is unknown and
could affect the intracellular concentration of amino acids. Previous work showed
that the diffusion of glucose through interstitial luid was a rate-limiting process for
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glucose uptake into muscle cells and identiied the possibility that amino acid transport may also be limiting.61 Microdialysis techniques can be used to add a fourth
pool to the model and distinguish transport kinetics across membranes.62
9.4.1.2.4 Labeled Water
It is possible to measure synthesis rates of proteins using a stable isotope of water
called deuterium oxide (D2O, “heavy water”). Low amounts of D2O are normally
found within the body water pool, but the method raises the enrichment to 2–3%.
The body water pool undergoes proton exchange reactions that enrich the intracellular amino acid pool, which will ultimately be incorporated into proteins.63 For
human studies, D2O is consumed in small volumes with an initial loading phase of
150 mL/day for 1 week followed by 100 mL/day for many weeks. Rodent studies
use an initial intraperitoneal injection of D2O followed by ad libitum access to an
enriched water supply.64 Tissue samples are collected before and after the study protocol and are analyzed for deuterium enrichment. Since the body water pool is used
for many exchange reactions, a variety of end products can be measured during a
single study design.65 For example, muscle biopsies can be used to determine skeletal
muscle protein synthesis rates while blood samples can yield cholesterol synthesis
rates66 or DNA synthesis rates.67 The method allows synthesis measurements to be
determined over long periods of times (weeks) as opposed to acute isotope infusion studies (hours). Although the method is well suited for long-term studies, it has
recently been reported that D2O can be injected intraperitoneally into animals as a
looding dose method.64 A beneit is that protein synthesis can be calculated without
the confounding effects of a looding dose of amino acids. Short-term studies are
helpful to understand acute effects in a well-controlled setting; however, long-term
studies can evaluate if those acute effects will continue over the longer periods of
time under less-controlled conditions. The use of deuterium oxide is not novel; however, it has regained popularity as its application to human health and nutrition is
being explored. As described in 1935 by Schoenheimer and Rittenburg, “The number of possibilities of this method appears to be almost unlimited.”68
9.4.1.2.5 Components of Skeletal Muscle
The term skeletal muscle is commonly used to distinguish it from smooth and cardiac muscle tissue. In reality, however, a tissue sample contains a wide variety of
cell types, including contractile, structural, and circulatory elements. The analysis
of muscle samples begins with homogenizing the entire sample and the calculated
synthesis or breakdown rates are a combination of all proteins of the sample (termed
mixed muscle protein synthesis [MPS] or breakdown). Protein breakdown rates
relect mixed muscle protein because they involve either tracer dilution (which cannot distinguish between proteolysis of different proteins) or release of bound tracer
(requiring adequate incorporation of tracer). Release of 3-methyl-histidine attempts
to quantify myoibrillar protein breakdown but is inluenced by other protein sources
as well.46,69
Protein synthesis rates, however, can be distinguished between subfractions of
muscle proteins by separation techniques. Improvements in the sensitivity of mass
spectrometers allow analysis of these smaller muscle subfractions. Mixed muscle
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samples are readily separated using differential centrifugation techniques into
myoibrillar, sarcoplasmic, and mitochondrial subfractions. The separation of subfractions allows more speciic analysis of muscle samples. The calculated FSR is
determined by tracer incorporation into protein products and is inluenced by the
size and turnover of the protein pool. The large size of the myoibrillar protein pool
will primarily determine MPS rates. However, separation of smaller pools such as
mitochondrial proteins reveals higher FSR, indicating that mitochondrial proteins
turn over at a higher rate than myoibrillar proteins.70 Such analysis of subfractions
yields important information regarding the response to different conditions including aging,70 exercise,48 and feeding.47 The extracellular matrix is also a protein pool
within mixed muscle that can respond to exercise stimuli along with myoibrillar and
sarcoplasmic subfractions.71 More sophisticated separation techniques identiied the
FSR of individual muscle proteins and showed variable rates within subfractions.23
9.4.2
CLINICAL EVALUATION OF PROTEIN STATUS
9.4.2.1 Dietary Records
Like most macronutrients and micronutrients, protein status can be determined by
assessing dietary intake by a food record. There are a variety of ways to complete
a food record and each has its advantages and disadvantages. The 3- or 7-day food
record has the athlete record all food consumed in a 3- or 7-day period. It is usually
recommended that the 3-day record include one weekend day. Both methods are
relatively accurate (as compared to other methods), and this accuracy can improve
with provision of a food scale. The technique works best if the athlete (or supervising dietician) records all food as it is consumed. Additional accuracy comes from
weighing the food before and after consumption (such as an apple followed by its
remaining core). However, left to their own devices, most athletes tend to underreport the amount of food consumed and the accuracy of reporting tends to decrease
as the period of time extends (out to 7 days). Even though the 3- and 7-day records
have their drawbacks, they tend to be more accurate than retrospective methods that
require an athlete to recall all that he or she ate in the past 24 hours (24-hour recall)
or interviews about the frequency of certain consumed foods (food frequency), or a
combination in which a diet history is constructed from questionnaires. Nonetheless,
there are now a variety of dietary intake software programs that can help determine
protein intake over a period of time to determine the regular habits of that athlete.
9.4.2.2 Body Mass and Body Composition
A simple but gross measurement of protein status is body mass. Over a period
of time, an athlete may gain or lose weight and this can easily be assessed by
body mass. Since lean body mass makes up the majority of total body mass, one
can assume that changes in body mass are associated with an increase or decrease
of protein tissue. A better means to assess protein mass is the addition of some
measurement of body composition. There are multiple ways to assess body composition, including underwater weighing, dual x-ray absorptiometry (DEXA), and
electrical impedance. By knowing total mass and the composition of that mass, one
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can calculate absolute lean body mass, which will roughly equate to the protein
composition of the body. For example, an increase in lean body mass, even in the
absence of an increase in total body mass, indicates a net accretion of protein. It
is important to realize, however, that these are gross assessments and do not have
the sensitivity to distinguish relatively small changes in protein status over a short
period of time.
9.5
PROTEIN TURNOVER AND EXERCISE
Exercise training causes signiicant remodeling of skeletal muscle and produces training adaptations such as increased muscular strength, power, or endurance. The training adaptations and phenotypic changes that occur in skeletal muscle are due to the
type of training stimulus placed on the muscles. For example, an endurance athlete
can use low-resistance but high-repetition movements, such as running or cycling,
to gain muscular endurance compared to an Olympic power lifter who uses highintensity but low-repetition movements to gain muscular strength and power. The
phenotypic changes relect the type of exercise training and the molecular response
of the muscle ibers to the training. Thus, the broad term of “exercise” should be
clariied to specify resistance or endurance exercise, and the speciic response of the
muscle to each of these different stimuli will be discussed.
9.5.1
PROTEIN TURNOVER AND RESISTANCE EXERCISE
Chronic resistance exercise training using high-resistance and low-repetition movements, commonly using machines or free weights causes increases in strength and
cross-sectional areas. The primary long-term adaptive response to resistance training is increased muscle strength from increased myoibrillar protein content in
addition to other adaptations including connective tissue and neuromuscular adaptations.72 Under resting and fasted conditions, FBR is greater than FSR, indicating net
catabolism.22 During a bout of strength training, it has been demonstrated that FSR is
depressed.73 In the period after strength training, FSR is increased74 and can remain
elevated up to 48 hours after the bout of exercise.22 In the absence of nutrient provision, FBR can still exceed FSR for a portion of the period.22 Importantly the increase
of both FSR and FBR indicates more protein turnover and remodeling.
9.5.2
PROTEIN TURNOVER AND ENDURANCE EXERCISE
Endurance exercise has repeated repetitions of a relatively light load and generally does
not lead to an enlargement in muscle. A lack of hypertrophy certainly does not mean
that there is a lack of increase in protein turnover since there is substantial remodeling
of the tissue to better use aerobic-derived energy sources and to resist fatigue. Increased
mitochondrial protein content is well known with endurance training, providing a general indication that endurance exercise alters protein turnover. Studies in rats indicate that muscle protein synthesis is decreased during a bout of endurance exercise.75
Unlike protein synthesis, the rate of whole-body protein breakdown increases during
aerobic exercise.76 After a bout of endurance exercise, rates of muscle protein synthesis
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increase similarly to those found following resistance exercise.71,77,78 A large contribution to these increases is that of mitochondrial proteins, which show higher FSR than
myoibrillar subfractions.48 It is worth restating that in the absence of muscle hypertrophy, signiicant turnover of muscle protein occurs following endurance exercise.
9.5.3
TIMING OF PROTEIN INTAKE
Protein must be consumed in order to supply the body’s amino acid pool over prolonged
periods. Endogenous sources can provide amino acids; however, these may not be
suficient to promote training adaptations. As discussed previously, exercise activates
a variety of pathways to promote protein turnover. This postexercise metabolic environment requires amino acids to allow adaptations. Feeding provides the necessary
amino acid and energy substrates to promote recovery. The timing of nutrient intake
around exercise is an important consideration for nutritional recommendation.
Under resting and fasting conditions, muscle protein breakdown is elevated in
order to replenish the free amino acid pool and causes a net catabolism of skeletal
muscle. Eating a mixed meal increases the availability of amino acids and promotes
protein translation in a dose-responsive fashion.79 However, the increase in protein
synthesis is not indeinite and subsides over time.47
Although exercise, at times, results in catabolic conditions, the provision of amino
acids during or after exercise ensures an overall anabolic environment. Ingestion of
amino acids after resistance exercise, either in isolated form80 or as protein,81 stimulates the rate of muscle protein synthesis more than exercise alone.82 Further, it has
been found that amino acid infusion after resistance exercise prevented the normal
postexercise rise in muscle protein breakdown.80,83 In regards to endurance exercise,
a mixed protein and carbohydrate beverage causes less negative whole-body protein
balance during exercise and in the postexercise period as compared to carbohydrate
alone.84 More recently, it was found that consuming a combination of protein and
carbohydrate after 2 hours of cycling resulted in a higher rate of mixed muscle FSR
than consuming carbohydrate alone and that whole-body protein balance was positive only in the protein-plus-carbohydrate condition.85 Thus, the addition of protein
to carbohydrate as postexercise nutrition promotes muscle anabolism more than carbohydrates or fasting.
The timing of postexercise nutrition may affect its eficacy. In older humans
performing 12 weeks of resistance exercise training, the consumption of a proteincontaining supplement immediately following each bout of exercise resulted in
greater increases in muscle strength and mass compared to delaying consumption
by 2 hours.86 Others found a greater stimulatory effect on muscle protein synthesis
when a carbohydrate and essential amino acid mixture was provided before exercise than afterwards.87 However, consumption of whey protein (as opposed to amino
acids) did not have a differential effect of timing consumption before or after exercise.88 The whey provided whole proteins instead of free amino acids; thus it appears
that both the timing and form of amino acids can inluence the recovery of muscle
protein turnover following exercise.
A summary of nutrition and exercise indicates that feeding promotes storage of
amino acids and exercise promotes adaptive remodeling, and the combination of
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nutrition and exercise stimulates maximal adaptation.1 Although simplistic, the summary is supported by nutrition and exercise effects on protein metabolism. For comparison purposes, the condition of 12-hour fasted values will be used as a baseline.
Measurements of protein synthesis and breakdown after a 12-hour fast indicate that
breakdown exceeds synthesis, so net protein balance is negative. If one is fed or
receives an infusion of mixed amino acids (AA) after a fasted period, protein synthesis increases, whereas protein breakdown remains the same or decreases slightly.
This response is indicative of a storage phenomenon in which synthesis increases
without an increase in breakdown. In the period after exercise without nutrient provision, protein synthesis and protein breakdown are increased compared with the
12-hour fasted reference values, indicating that there is a stimulus (exercise) and
remodeling (increase in synthesis and breakdown) response, although net balance
does not improve to a positive balance. When there is an exercise stimulus with
postexercise AA feeding, protein synthesis increases more than that after exercise
or AA feeding alone, and protein breakdown remains similar to exercise without
feeding. Because there is an increase in protein synthesis above the rate observed
after exercise without AA provision, it is apparent that the provision of AA enhances
protein synthesis. In addition, although protein breakdown is increased, it does not
increase more than the fasted exercise response. Therefore, the increase in protein
synthesis after feeding is a transient storage phenomenon, whereas physical exercise
stimulates a longer-term adaptive response. Providing nutrition after physical activity takes advantage of the anabolic signaling pathways that physical activity has initiated by providing energy and AA building blocks for protein synthesis.
9.6
PROTEIN REQUIREMENTS
A full discussion of protein requirements is beyond the scope of this chapter. There
is currently much discussion on the proper methods to determine protein requirements, although nitrogen balance has traditionally been used.89 Further, these recommendations are limited because they assume energy balance and do not consider
the potential role of the timing of protein nutrition on net protein balance. The current dietary reference intake (DRI) issued by the Institute of Medicine (IOM) is
0.8 grams of protein per kilogram body weight90 (g/kg bw) and is consistent with the
WHO recommendation.4 The recommendation is designed to meet protein requirements of 97.5% of the population and varies from the estimated average requirement
(EAR) of 0.66 g/kg bw that covers 50% of the population. Importantly, these values
were largely derived from a meta-analysis of studies using 235 individuals.91 It, of
course, also begs the question whether athletes, both strength and endurance, it
within the recommendations for the general population.
It can be speculated that the increased protein turnover brought about by physical
activity, whether increased amino acid oxidation or increased protein breakdown,
may increase protein needs in athletes. The vast preponderance of anecdotal and
recorded data92,93 indicates that athletes already consume protein far in excess of
current recommendations. However, early studies indicated that instead of exercise
raising protein requirements, exercise might lower protein requirements through
protein sparing mechanisms.10,33 These initial studies are supported by others that
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are not limited to the nitrogen balance technique.94 The current consensus is that
an intake of 1.1 gm/kg day in endurance athletes95 and 1.3 g/kg bw in strength athletes92 is more than adequate to meet the needs of these athletes. Accordingly, a
70-kilogram athlete would require 77 to 91 gm of protein each day, which is readily
consumed in Western culture. Additional protein intake may not induce additional
beneits for skeletal muscle anabolism. For example, the increased skeletal muscle
FSR following resistance exercise and 20 grams of protein intake was not different if
protein was increased to 40 grams, suggesting that a maximal FSR was reached with
20 grams without additional stimulation from more protein.96 Three issues, however,
remain to be solved. First, does increasing protein above requirements increase sport
performance? Second, does increasing protein intake during caloric restriction help
retain lean body mass? And third, does the timing of protein nutrition after exercise
ultimately change required habitual protein intake?
9.7
9.7.1
SPECIAL CONSIDERATIONS
SEX DIFFERENCES
Despite women having a smaller muscle mass than men,97 attempts to detect sex
differences in protein metabolism have produced little evidence of their existence.
There have been some reports of differences between sexes in the rate of leucine
oxidation at rest and during exercise,98–100 but there is no convincing evidence of
major differences in whole-body protein turnover and mixed muscle protein synthesis76,98–103 between sexes even after accounting for different sizes of fat-free mass.98,101
Furthermore, it is reported that men and women do not have different rates of muscle
protein synthesis in response to exercise.102 The lower protein mass in women may
therefore be the result of an accumulated sex-speciic hormonal effect on synthesis or
breakdown over a period of many years.104 Additionally, female sex hormones may
inluence protein synthesis muscle subfractions, which are not distinguished with
measurements of mixed muscle in the whole body. For muscle collagen this does not
seem to be the case,103 but it could be for other protein fractions such as sarcolemmal
enzymes or mitochondria. However, a more recent study has countered the argument that women have a higher decreased protein turnover than men.105 The study
was completed on thirty men and thirty-two women, thus substantially increasing
power over previous studies. The results showed that women, irrespective of their
body mass index and age, had higher FSR of muscle proteins and higher whole-body
protein turnover than men. Since women have a smaller muscle mass than men, the
increased FSR in women could be countered with increased FBR and cause no net
anabolism. The issue of differences in protein turnover between sexes does not yet
appear to be resolved, but at this point there is no reason to believe that one group,
either men or women, has different requirements.
9.7.2
AGING
Whether older adults require protein in excess of the RDA is a contentious topic.
With aging there is a progressive decline of skeletal muscle mass due to a variety of
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causes. There is no doubt that there is a net catabolism in human muscle over time,
yet current recommendations by the IOM for protein intake in older individuals are
the same as recommended for all individuals over 19 years old.90
It has been reported that whole-body protein synthesis declines with age even
after adjustment for fat-free mass.106 The same group used a large cohort of subjects
to study changes throughout the lifespan and found a decline of 3–4% per decade in
measures of whole-body protein turnover, breakdown, and synthesis.102 These studies are supported by others that indicated a decrease in muscle protein synthesis with
age.74,102,107,108 In contrast, others have not found differences in muscle protein synthesis of younger and older individuals at rest.26,109–111 Still others proposed that the muscle wasting associated with aging is due to a decreased anabolic effect of feeding in
older individuals.110,112,113 It is possible that muscle loss with age is a collective result
of a decline in exercise habits along with decreased anabolic effects of nutrition.
The question then remains, do older individuals require more protein in their
diet? Recently a large, well-controlled study using forty-two young and old individuals examined nitrogen balance during low, medium, and high levels of protein
intake.114 The results indicated that nitrogen balance at the different protein intakes
did not differ between younger and older subjects and that the current recommendation of 0.8 gm/kg body weight per day was suficient to maintain nitrogen balance
in older individuals. These data were quite convincing in that it was a very wellcontrolled study. However, as discussed, the appropriateness of nitrogen balance for
protein adequacy continues to be debated. Therefore, the diversity of opinions on the
adequacy of current recommendations for older individuals illustrates that the issue
is not yet resolved.115–117
9.8
FUTURE DIRECTIONS
There is still some discussion regarding adequate versus optimal protein metabolism. For example, can one protein intake be adequate but still fall short of additional
beneits if more was consumed? This concept gets into the very core of the athlete
psyche that more is better. To date, in a variety of athletic and special populations,
there has not been convincing data presented that chronically higher intakes (irrespective of timing of intake) results in more optimal outcomes. However, there are
still issues that need to be resolved regarding the quantity of protein required for
different populations. Next, it is dificult to determine what the appropriate intake of
protein is without the correct assessment measures. Nitrogen balance is the basis of
all current protein recommendations but has great limitations. As of right now, no
one has proposed a better alternative. Blunt clinical measures such as body composition are a way for athletes to assess their protein status but are fairly limited over
the short term or for precise measures. Laboratory methods such as stable isotopes
are capable of measuring much smaller changes in protein status but are still limited
to short time frames. The isotope method using labeled water shows great promise
in this area because of its ability to make long-term measures in free-living conditions (analogous to doubly-labeled water and energy expenditure). Finally, future
studies must continue to account for the role of energy balance in protein metabo-
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lism. Protein status cannot be assessed without consideration of energy balance since
protein turnover is tied to energetic state.
9.9
CONCLUSIONS
Although not a large contributor to energy production, dietary protein intake is
critically important for exercise-induced adaptations. Cells adapt to training with
a response designed to make the body better at performing that stimulus later. The
adaptation requires amino acid building blocks (from dietary proteins) to execute the
making of the appropriate proteins to improve function in the cell. At the same time,
proteins that are no longer necessary are removed because they are energetically
costly to maintain. In the healthy state, it is clear then that protein structures within
cells are always turning over protein for the beneit of the individual. Although some
consensus has been reached that athletes do not require additional protein in their
diet, there is a vast amount of work yet to be performed with consideration of how to
optimize function or whether different subgroups (by sex or age) of athletes require
different needs. To properly determine protein needs, there needs to be continued
development of methods and techniques to assess protein status.
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86. Esmarck, B., Andersen, J.L., Olsen, S., Richter, E.A., Mizuno, M., and Kjaer, M., Timing
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88. Tipton, K.D., Elliott, T.A., Cree, M.G., Aarsland, A.A, Sanford, A.P., and Wolfe, R.R.,
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exercise, Am. J. Physiol. Endocrinol. Metab. 292(1), E71–E76, 2007.
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94. Hartman, J.W., Moore, D.R., and Phillips, S.M., Resistance training reduces wholebody protein turnover and improves net protein retention in untrained young males,
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T., Tarnopolsky, M.A., and Phillips, S.M., Ingested protein dose response of muscle
and albumin protein synthesis after resistance exercise in young men, Am. J. Clin. Nutr.
89(1), 161–68, 2009.
97. Janssen, I., Heymsield, S.B., Wang, Z.M., and Ross, R., Skeletal muscle mass and distribution in 468 men and women aged 18–88 yr, J. Appl. Physiol. 89(1), 81–88, 2000.
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2000.
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not lysine, kinetics, J. Appl. Physiol. 91(1), 357–62, 2001.
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Tissue composition affects measures of postabsorptive human skeletal muscle metabolism: Comparison across genders, J. Clin. Endocrinol. Metab. 84(3), 1007–10, 1999.
102. Short, K.R., Vittone, J.L., Bigelow, M.L., Proctor, D.N., and Nair, S., Age and aerobic
exercise training effects on whole body and muscle protein metabolism, Am. J. Physiol.
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103. Miller, B.F., Hansen, M., Olesen, J.L., Flyvbjerg, A., Schwarz, P., Babraj, J.A., Smith,
K., Rennie, M.J., and Kjaer, M., No effect of menstrual cycle on myoibrillar and connective tissue protein synthesis in contracting skeletal muscle, Am. J. Physiol. Endocrinol.
Metab. 290(1), E163–E168, 2006.
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105. Henderson, G.C., Dhatariya, K., Ford, G.C., Klaus, K.A., Basu, R., Rizza, R.A., Jensen,
M.D., Khosla, S., O’Brien, P., and Nair, K.S., Higher muscle protein synthesis in women
than men across the lifespan, and failure of androgen administration to amend agerelated decrements, Faseb J 23(2), 631–41, 2009.
106. Balagopal, P., Rooyackers, O.E., Adey, D.B., Ades, P.A., and Nair, K.S., Effects of aging
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© 2011 by Taylor and Francis Group, LLC
of Vitamin
10 Assessment
Status of Athletes
Mark D. Haub, Helena B. Löest,
and Kelcie L. Hubach
CONTENTS
10.1 Introduction .................................................................................................. 289
10.2 Analytical Considerations ............................................................................290
10.2.1 Stability of Vitamins......................................................................... 290
10.2.2 Vitamin Bioavailability, Active Forms, and Storage ........................290
10.2.3 Biochemical Indices to Assess Vitamin Status ................................300
10.3 Assessment Guidelines and Considerations .................................................300
10.4 Assessment Methods ....................................................................................304
10.5 Future Research ............................................................................................ 305
10.6 Conclusions ...................................................................................................306
References ..............................................................................................................306
10.1
INTRODUCTION
Vitamins are organic compounds required in small amounts not only for survival
but also necessary for athletic competitions. Vitamins cannot be synthesized in large
enough quantities endogenously to meet metabolic requirements for eficient daily
functioning and therefore must be consumed.1,2 Some vitamins must be converted to
an active form or be incorporated into coenzymes, while some are capable of functioning without modiications.2
The vitamin status of athletes is often assumed based on outcomes of estimates
of dietary intake (for example, diet recall and diet records). Given the metabolic
demands of athletes, especially athletes training and performing in events that rely
heavily on bioenergetic pathways, and the limitations of nutrition databases, it may
be an unfortunate speculation to base nutritional recommendations on guidelines
geared toward the general population. Conversely, those same athletes will not likely
experience vitamin deiciencies if consuming a balanced and varied diet to meet
their higher energy demands. For detailed insight into vitamin functions, adequate
intake values, and food sources, other resources are available.2 Also, the assumption
of vitamin status from diet records or recall does not always account for differences
in vitamin bioavailability and/or activity. The eficiency of vitamin absorption needs
to be considered, as well as the interaction of the vitamin with other nutrients or
289
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compounds that may increase or decrease availability. In addition to those physiological issues, some foods either may not be in a food database or have not been
analyzed for complete vitamin content. Moreover, food processing is known to affect
vitamin concentrations, which likely alters bioavailability.
However, given the temporal and inancial costs associated with many biochemical
assessments, not to mention the means of collecting tissue samples from athletes and
the different metabolic demands of various sports, the vitamin status of and requirements for athletes are not fully known. With increasing interest in nutritional supplements and functional foods, the area of micronutrient analysis will likely expand to
better determine their mechanisms of action. Therefore, the purpose of this chapter
is to convey vitamin assessment strategies for those wanting to better determine
vitamin status in athletes or to perform exercise interventions. Suggestions for the
appropriate biological sample type (blood, tissue, and/or urine) will be discussed for
those vitamins that potentially yield differences in concluding vitamin status. It must
be noted that few studies have examined the inluence of acute or chronic exercise
on values of speciic vitamins using human subjects. Therefore, caution and an open
mind must be used when applying the following information.
In general, two critical issues to bear in mind when analyzing samples for vitamin
content are: (1) utilize an acceptable vitamin extraction procedure and (2) ensure that
appropriate measures or precautions are made to minimize the deactivation of the
vitamins being measured. For example, when assessing biochemical vitamin status
there are many factors that may inluence the analysis, such as vitamin stability (see
Table 10.1). If these inluencing factors are not accounted for or controlled, then the
results will likely be compromised.
10.2
10.2.1
ANALYTICAL CONSIDERATIONS
STABILITY OF VITAMINS
A critical methodological issue that occurs with the analysis of vitamins is their
instability under certain conditions (exposure to light, oxygen, metals, etc.; see
Table 10.1). This instability leads to changes in the structure (inactive form) and
may ultimately yield spurious results. Therefore, it is critical to account for as
many potential sample contaminants as possible.3 For example, when vitamin D is
exposed to light, it will convert to isotachysterol and the 5,6-trans-isomer. As noted
in Table 10.2 and in the summary of assessments, most individual and multianalyte
vitamin assessments require speciic preparations and procedures; therefore, post
hoc vitamin assessments are generally dificult to perform adequately.
10.2.2
VITAMIN BIOAVAILABILITY, ACTIVE FORMS, AND STORAGE
Basing vitamin status solely on nutrient intake values may likely yield inaccurate estimations of vitamin status, which may ultimately lead to either a vitamin deiciency
or toxicity. This occurrence results from interactions that micronutrients and other
dietary consumables have on the absorption and availability of other nutrients. The
assessment of an athlete’s diet may generate a different picture of vitamin status than
© 2011 by Taylor and Francis Group, LLC
Vitamins
Influencing
Factors
A
D
E
Air (O2)b
•
•
•
•
Heat
•
•
•
•
•
•
•
•
•
•
Light, UV
•
Metals/Minerals
•
Acid
•
•
•
B1
B2
B6
•
•
Alkali
•
Water
•
•
•
•
B12
C
•
•
Niacin
Biotin
•
•
•
•
•
•
•
•
•
•
Pantothenic
Acid
•
•
•
•
Prevention
Exclude oxygen or air by replacement
of inert gas
•
•
Work at lowest temperatures possible,
store below –20°C (preferably –70°C)
Avoid sunlight (UV) and dim lights
•
•
•
Folatea
Avoid adding metals
•
•
•
•
Use acid-free solvents
•
Reducing Agents
Oxidizing Agents
•
•
Antioxidant
+
+
Other
References
K
•
+
11,
33, 34
11,
33–35
•
+
Iodine
+
Sulite
11,
33, 34
11,
33, 34
Assessment of Vitamin Status of Athletes
TABLE 10.1
Factors Responsible for Degrading or Inactivating Fat-Soluble and Some Water-Soluble Vitamins (Free Forms in Solution) That Can
Influence Analysis Results
1, 11,
20,
34, 35
Sulfurous
acid, nitrite
1, 11,
34
1, 11,
34, 35
1, 11,
15,
34, 35
1, 6,
11
11
1, 34,
35
1, 11, 15,
34
1, 34
11, 33, 34
a
Folate exists in various forms and each form is sensitive to different factors.
Try to avoid exposure to air or oxygen during sampling or analysis; the vitamins may be more stable in the absence of oxygen, and this may minimize the sensitivity to these other factors. (Data
from Lambert, W.E., Nelis, H.J., De Ruyter, M.G.M., and De Leenheer, A.P., in Modern Chromatographic Analysis of the Vitamins, De Leenheer A.P., Lambert, W.E., and De Ruyter, M.G.M.,
Eds., Marcel Dekker, New York, 1985, p. 1.)
Note: Add an antioxidant like butylated hydroxytoluene (BHT), α tocopherol, Vitamin C, propyllgallate to samples prior to analysis to protect from oxidation. (Data from Ball, G.F.M., Water-Soluble
Vitamin Assays in Human Nutrition, Chapman and Hall, London, 1994; Lambert, W.E., Nelis, H.J., De Ruyter, M.G.M., and De Leenheer, A.P., in Modern Chromatographic Analysis of the
Vitamins, De Leenheer A.P., Lambert, W.E., and De Ruyter, M.G.M., Eds., Marcel Dekker, New York, 1985, p. 1.)
Note: Exposure of some vitamins to more than one of these factors can have an additive effect: more losses might occur when exposed to more than one factor. (Data from Lambert, W.E., Nelis, H.J., De Ruyter,
M.G.M., and De Leenheer, A.P., in Modern Chromatographic Analysis of the Vitamins, De Leenheer A.P., Lambert, W.E., and De Ruyter, M.G.M., Eds., Marcel Dekker, New York, 1985, p. 1.)
b
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TABLE 10.2
Biochemical Indices to Assess Vitamin Status
Vitamin
Component
Vitamin A
Blood
Liver
Tear luid
Other
Vitamin D
Blood
Tissue
Other
Vitamin E
(α TP)
Blood
© 2011 by Taylor and Francis Group, LLC
Biochemical Tests for Status Assessment
Colorimetry, spectrophotometry, luorometry, capillary
electrophoresis (Ref. 11); high-pressure liquid
chromatography (HPLC), thin-layer chromatography (TLC)
(Refs. 11, 34); gas chromatography (GC) (Ref. 7); and
immunological or molecular biological techniques (Ref. 9)
Serum β carotene levels (Ref. 2)
Plasma retinal levels (only reduced if liver stores are depleted)
(Ref. 2)
Relative dose response (RDR) and modiied relative dose
response (MRDR) (Ref. 9); most representative of current
status, and determine liver stores in a noninvasive way (Refs.
5, 9, 41)
Retinol binding proteins (RBP) (Refs. 5, 9)
Plasma retinol (generally accepted; see Ref. 9) and carotenoid
analysis (Refs. 5, 42, 43); plasma retinol need not be adjusted
for lipoprotein concentration (Ref. 18)
Liver retinol levels (Ref. 44) (not practical; see Ref. 9)
Conjunctival impression cytology (CIC) (Ref. 9); least
representative of current status (see Refs. 5, 9)
Tear analysis (Ref. 5)
Dark adaptation test or night-blindness determination (Refs. 5, 8)
HPLC, TLC, colorimetry, radioimmunoassay, gas
chromatography-mass spectrometry (GC-MS) (Ref. 34);
ligand-binding (Ref. 11)
Plasma/serum vitamin D levels (Refs. 2, 10); need not be
adjusted for lipoprotein lipid content (Ref. 18)
Serum 25-OH-vitamin D levels is the sum of diet intake and
production from sun exposure (Ref. 10)—the most valuable
determinant of vitamin D status (Refs. 10, 11)
Speciic competitive protein binding assay for determination of
25-OH-vitamin D and 1–25(OH)2 vitamin D (of little value)
(Refs. 10, 11)
Radio receptor assay, using 3H metabolites is a speciic way to
determine 1–25(OH)2 vitamin D (Ref. 11); also of little value
(see Ref. 10)
Plasma alkaline phosphatase activity (Refs. 2, 11)
Blood and tissue vitamin D metabolites are acceptable status
indicators but are nonspeciic (Ref. 11)
Indirect determination: serum calcium levels (Ref. 2)
Clinical trial of supplementation (Ref. 5)
Colorimetry, spectrophotometry, spectroluorometry, TLC,
HPLC, and GC (Ref. 11, 14)
Serum α TP (Ref. 14) in relation to serum triglyceride levels
(Ref. 5)
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TABLE 10.2 (continued)
Biochemical Indices to Assess Vitamin Status
Vitamin
Component
Biochemical Tests for Status Assessment
Platelet α TP levels in relation to serum triglyceride levels
(Ref. 5)
Plasma α TP is not a good indicator for toxic levels, because it
reaches a plateau (Ref. 17)
Erythrocyte α TP levels (Ref. 14)
Adipose
Adipose α TP levels in relation to serum triglyceride levels
(Ref. 5)
Adipose α TP levels increase linearly with dietary intake of
vitamin E (Ref. 15). Assess long-term vitamin E status (Ref. 17)
Muscle
Urine
Other
Recommendation
Vitamin K
Blood
Muscle α TP levels (Ref. 14), in close metabolic equilibrium
with plasma α TP (Ref. 45)
Urinary excretion of vitamin E may indicate excessive vitamin
E intakes (Ref. 16)
Urinary excretion of vitamin E metabolite α CEHC is not used
to assess vitamin E status (Ref. 16)
Erythrocyte hemolysis by peroxide (Ref. 2, 5) is inversely
related to plasma α TP concentrations (Ref. 16)
Breath ethane (Ref. 16) and pentane (Ref. 13), levels are lipid
peroxidation markers, high levels show depleted stores (Ref. 17)
Functional tests: Vitamin E status can be assessed by oxidative
changes in lipids:
(1) Erythrocyte malondialdehyde test (in vitro) by H2O2
exposure (Ref. 13)
(2) Erythrocyte malondialdehyde test with thiobarbituric acid
(Ref. 13)
Evaluate vitamin E levels in conjunction with blood lipid levels
because vitamin E is carried on lipid-protein complexes
called lipoproteins. Evaluating blood vitamin E levels alone
when assessing vitamin E status is misleading (Ref. 16)
It is more useful to use more than one biochemical tests to
assess vitamin E status (Ref. 13)
HPLC, TLC, colorimetry, GC-MS (Refs. 34, 46)
Plasma prothrombin concentrations (Refs. 2, 46)
Plasma phylloquinone (Ref. 13) relects phylloquinone intakes
(Ref. 46) but does not correlate well with vitamin K status
(Ref. 46)
Plasma or serum des-γ-carboxyprothrombin (DCP); most
sensitive indicator of vitamin K status (Ref. 5, 18, 22, 46)
DCP:prothrombin ratios (Ref. 13)
Direct chromatographic vitamin K assays (Ref. 47)
Urine
Other
© 2011 by Taylor and Francis Group, LLC
Urinary γ-carboxyglutamic acid (Ref. 13)
Hydroxyapatite binding capacity of osteocalcin (Ref. 13)
(continued)
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Nutritional Assessment of Athletes, Second Edition
TABLE 10.2 (continued)
Biochemical Indices to Assess Vitamin Status
Vitamin
Component
Recommendation
Thiamin (B1)
Blood
Urine
Body luids
Other
Recommendation
Ribolavin (B2)
Blood
© 2011 by Taylor and Francis Group, LLC
Biochemical Tests for Status Assessment
Ratio of prothrombin activity to the total immunochemical
equivalents of prothrombin (Ref. 46)
Ratio of Simplastin thromboplastin activated prothrombin time
to activated by Echis carnatus venom (S:E ratio) (Ref. 46)
Bleeding and clotting time (Ref. 5)
Prothrombin time (Ref. 5); still used but is insensitive and
nonspeciic as primary method to determine vitamin K status;
Ref. 37)
Measurements of uncarboxylated osteocalcin (Ref. 46)
Use both the plasma prothrombin measurements and DCP
(Ref. 13)
Plasma or serum des-γ-carboxyprothrombin (DCP) and
osteocalcin; most sensitive indicator of vitamin K status
(Refs. 5, 18, 21, 46)
HPLC (Refs. 5, 19, 34), TLC (Ref. 34), ion exchange
chromatography (Ref. 48), colorimetry (Ref. 5), enzymatic
(Refs. 5, 20, 22), and microbiological assays (Refs. 5, 34)
ETKAC (erythrocyte transketolase activity) (Refs. 5, 19, 22);
highly reliable method to determine status (Ref. 11)
Serum thiamin levels (Refs. 5, 20, 21); insensitive status
indicator (Ref. 11)
Thiamin pyrophosphate (TPPE) test of erythrocytes (Refs.
20–22)
Blood pyruvate, lactate, and α ketoglutarate levels (Ref. 21)
Whole blood (Lactobacillus viridescens assay) (Ref. 47);
insensitive status indicator (Ref. 11)
Erythrocyte thiamin levels; insensitive status indicator (Ref. 11)
Urinary excretions of thiamin (relect thiamin status of the
previous 24 h) (Refs. 2, 5)
Urinary excretions of thiamin metabolites (Ref. 21)
Microbiological assays (Refs. 5, 34)
Ex vivo lymphocyte growth response (Ref. 5)
Cerebrospinal luid (CSF) thiamin levels (Ref. 21)
Use ETKAC and TPPE together to assess thiamin status for most
reliable results (Ref. 21)
Use more than one method or test to assess thiamin status
(Ref. 49)
HPLC (Refs. 5, 24, 34), TLC (Refs. 34, 50), luorometry (Refs.
5, 23), enzymatic (Refs. 2, 5, 24), and microbiological assays
(Refs. 5, 34)
Erythrocyte glutathione reductase activity coeficient
(EGRAC) (Refs. 2, 23, 24) is the most common and most
sensitive to tissue stores (Refs. 23, 24)
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295
TABLE 10.2 (continued)
Biochemical Indices to Assess Vitamin Status
Vitamin
Component
Urine
Body luids
Other
Recommendation
Niacin
Blood
Blood and tissue
Urine
Body luids
Other
Vitamin B6
Blood
© 2011 by Taylor and Francis Group, LLC
Biochemical Tests for Status Assessment
Blood ribolavin levels (Refs. 23) is an insensitive indicator of
ribolavin status (Ref. 24)
Erythrocyte ribolavin levels (Ref. 23) is an insensitive
indicator of ribolavin status (Ref. 24)
24 h collection of urinary excretions of ribolavin relects
dietary intake (Ref. 23) and is not a sensitive indicator for
tissue stores (Ref. 23)
Urinary excretions collected (1) at random, (2) after fasting, (3)
a 24 h specimen, and (4) after load return test (Ref. 23)
Ratio of urinary ribolavin levels to creatinine levels (Ref. 22)
Microbiological assays (Refs. 5, 34)
Ex vivo lymphocyte growth response (Ref. 5)
EGRAC together with urinary excretion test (Refs. 11, 24)
HPLC (Ref. 33), chromatography (Ref. 25), colorimetry (Ref.
51), luorometry (Ref. 25), enzymatic (Ref. 25), and
microbiological assays (Ref. 2, 5, 34)
Serum niacin level determination is not a sensitive test (Ref.
22); it relects dietary intake, not tissue stores (Ref. 11)
Erythrocyte NAD levels (Ref. 5)
Erythrocyte NAD:NADP ratio (Ref. 5) is used to evaluate
niacin status (Ref. 25)
Lowry method measures NAD and NADP by using speciic
dehydrogenase enzymes (Ref. 25)
Excretion of N′-methylnicotinamide (NMN) and 2-pyridone
(Ref. 5) after a tryptophan dose (Ref. 2); widely used method
(Ref. 22)
Ratio of 2-pyridone to NMN is a recommended method
(Ref. 24)
Microbiological assays (Refs. 5, 51); Lactobacillus plantarum
(Ref. 3)
Ex vivo lymphocyte growth response (Ref. 5)
NMN excretion expressed as mmol/mol creatinine is not an
accurate method (Ref. 22)
Dowley-1-formate chromatography is used to separate the
puridine nucleotides (NAD/H and NADP/H) and NMN
(Ref. 25)
NMN assessment done after 4–5 h after a 50 mg load of
nicotinamide (Ref. 24)
HPLC (Ref. 34), TLC (Ref. 33), GC (Ref. 52), enzymatic (5,
26), and microbiological assays (Ref. 5, 34)
Plasma pyridoxal phosphate (PLP) concentrations (Refs. 26,
53); most often used, and correlates with tissue stores (Ref. 11)
Plasma total vitamin B6 levels or plasma PL levels (Ref. 26)
(continued)
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Nutritional Assessment of Athletes, Second Edition
TABLE 10.2 (continued)
Biochemical Indices to Assess Vitamin Status
Vitamin
Component
Biochemical Tests for Status Assessment
*Plasma homocysteine levels (Ref. 5) after a methionine load
(Refs. 15, 22, 26) relect hepatic vitamin B6 status (Ref. 26)
Serum 4-PA levels (Ref. 5)
Erythrocyte PLP levels is useful as an additional index (Ref. 26)
*Erythrocyte ALT and AST activation coeficients (Refs. 5, 15,
23, 26, 54); relect long-term vitamin B6 status because of the
lifetime of the erythrocyte (Ref. 26)
Urine
Body luids
Other
Recommendation
Cobalamin (B12)
Blood
Plasma and urine
© 2011 by Taylor and Francis Group, LLC
Erythrocyte α-EGOT measurements (Ref. 53)
Urinary 4-PA excretion (Refs. 2, 15, 26), which is a short-term
indicator (Ref. 26) that relects dietary intake (Ref. 22)
Urinary total vitamin B6 (Ref. 26)
Urinary pyridoxal lactone (Ref. 15)
*Urinary metabolite (xanthurenic and kynurenic acid)
excretion (Ref. 5) after a tryptophan load (Refs. 11, 15, 22,
26); relect hepatic vitamin B6 status (Ref. 26)
*Urinary homocysteine levels (Ref. 5) after a methionine load
(Refs. 15, 22, 26) relect hepatic vitamin B6 status (Ref. 26)
Urinary PL expressed as mg per g creatinine (Ref. 11)
Microbiological assays (Refs. 5, 34, 55)
*Oxalate excretion (Ref. 26); less common method
*EEG pattern (Ref. 26); less common method
Ex vivo lymphocyte growth response (Ref. 5)
Plasma or urine amino acid levels and ratios (Ref. 5)
Use at least two biochemical indices; one must be the PLP test.
Plasma PLP and tryptophan load test together is an excellent
biochemical conirmation of vitamin B6 status (Ref. 11)
(*) These are indirect methods that do not necessarily relect
total vitamin B6 in tissue or serum; they indirectly relect PLP
in certain tissue (Refs. 22, 26)
Radioimmunoassay (Refs. 27, 34); microbiological assays, dual
isotope methods (Ref. 5)
Serum cobalamin assay is a standard method (Refs. 5, 27)
Erythrocyte vitamin B12 measurement is a common
biochemical test (Ref. 11)
Holo TC-II (vitamin B12 transporter) measurements detect
early vitamin B12 deiciency (Refs. 11, 27)
Plasma total vitamin B12 levels (Ref. 22)
Measurement of substrates, methylmalonic acid (MMA), and
homocysteine, of two vitamin B12–dependent enzymes is a
new and more accurate way of assessing intracellular
deiciencies (Refs. 5, 27)
Plasma MMA measurements are better than plasma
homocysteine measurements (Ref. 27)
Assessment of Vitamin Status of Athletes
297
TABLE 10.2 (continued)
Biochemical Indices to Assess Vitamin Status
Vitamin
Component
Biochemical Tests for Status Assessment
Urine
Biological luids
Other
Urinary total vitamin B12 levels (Ref. 22)
Microbiological assays(Refs. 5, 34)
Vitamin B12 deiciency is relected by high levels of
2-methylcitrate, N,N-dimethylglycine, N-methylglycine, and
cystathionine
Ex vivo lymphocyte growth response (Ref. 5)
Shillings test or dual isotope variations for vitamin B12
absorption (Ref. 5)
HPLC (Ref. 34), radioimmunoassay (Ref. 34), radiometry
(Ref. 28), luorometry (Refs. 28, 56), TLC (Ref. 28),
enzymatic assay (Ref. 28)
Serum folic acid levels (Refs. 2, 5, 22); should not be used by
itself (Ref. 11, 57)
Erythrocyte folic acid levels (Ref. 2, 5, 22)
Serum or erythrocyte THF by radio isotope assay (Ref. 28)
Serum or erythrocyte 5-methyl THF (Ref. 28)
Serum folate activity (Ref. 28)
Erythrocyte folate status is a reliable indicator for long term of
folate status (Ref. 22) and tissue stores (Refs. 11, 29, 57)
Serum homocysteine concentration is an ancillary indicator of
folate adequacy (Ref. 29)
Urinary folate levels (Ref. 2)
Urinary N-formimino glutamic acid indicates comprised folate
stores (Ref. 15) indirectly but is not sensitive enough and not
used frequently (Ref. 11)
Microbiological assays (Refs. 5, 34); Lactobacillus rhamnosus
(Ref. 3)
Ex vivo lymphocyte growth response (Ref. 5)
Neutrophil hypersegmentation (Refs. 5, 57)
Dihydrofolate reductase (DHFR) inhibition assay (Ref. 56)
HPLC (Ref. 29, 33), luorescent assay (Ref. 30), TLC (Ref. 34),
microbiological assay (Ref. 2, 5, 34), colorimetry (Ref. 5)
Whole-blood biotin levels; not a sensitive indicator (Ref. 11, 30)
Avidin-binding assay (Ref. 30, 58, 59)
Derivatives of biotin (Ref. 30)
Urinary biotin levels (Refs. 2, 5, 15)
Urinary excretion of 3-hydroxyisovaleric acid (inversely
related to biotin status) (Ref. 31) is a sensitive, early detector
of biotin deiciencies (Refs. 11, 31)
Microbiological assays (Refs. 5, 34)
Ex vivo lymphocyte growth response (Ref. 5)
Propionyl-CoA carboxylase and pyruvate carboxylase (biotin
dependent enzymes) activity in hair roots (Ref. 60)
(continued)
Folate
Blood
Urine
Biological luids
Other
Biotin
Blood
Urine
Biological luids
Other
© 2011 by Taylor and Francis Group, LLC
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Nutritional Assessment of Athletes, Second Edition
TABLE 10.2 (continued)
Biochemical Indices to Assess Vitamin Status
Vitamin
Component
Biochemical Tests for Status Assessment
Recommendation
Chromatographic separation of biotin analogues together with
avidin-binding assay (Ref. 30)
HPLC (Ref. 34), colorimetry (Ref. 5), microbiological assay
(Refs. 5, 34)
Whole-blood pantothenic acid levels (not very sensitive)
(Refs. 5, 11)
Serum pantothenic acid (not very sensitive) (Ref. 11)
Urinary pantothenic acid levels (not very sensitive) (Refs. 5, 11)
Microbiological assays (Refs. 1, 12), using yeast and
lactobacillus for blood and urine pantothenic acid
measurements (Refs. 2, 32)
Ex vivo lymphocyte growth response (Ref. 5)
HPLC (Refs. 5, 61), TLC (Refs. 33, 61), GC (Ref. 61),
spectrophotometry, luorometry, chromatography,
electrochemical techniques (Ref. 6)
Serum ascorbate levels (Ref. 61); easy to perform, and most
often used, also reliable (Refs. 2, 6)
Leukocyte ascorbate levels, most reliable (Ref. 6); relect tissue
and blood ascorbate content and correlates with liver
ascorbate (Refs. 6, 11, 16)
Platelet ascorbate level (Ref. 6)
Urinary ascorbate level measurement is not a good indicator
of vitamin C status because vitamin C is reabsorbed by the
kidneys (Ref. 6), but is a good indicator for current status
(Ref. 11)
Salivary ascorbate level measurement is not a good indicator of
vitamin C status (Ref. 6)
Oral loading test (Ref. 5)
The automated and microtiter plate spectrophotometric method
is used for measurement of plasma and leukocyte ascorbate; it
is fast and has high sensitivity (Ref. 6)
Whole-blood and red blood cell ascorbate measurements are
less sensitive (Ref. 6)
Pantothenic
Acid
Blood
Urine
Biological luids
Other
Vitamin C
Blood
Urine
Saliva
Other
what is derived from the analysis of biochemical samples. This conlict may go unnoticed if vitamin intake alone is assessed. This may be common in some instances,
as the availability of computer-assisted nutrient analysis programs has increased, but
the access to and costs of the numerous biochemical assessments to measure the concentration of each vitamin are likely limited for the majority of coaches and athletes.
Table 10.3 displays the tissues or sample sites that can be used for assessment, as well
as the compound and the analytical method used to verify vitamin status.
This oversight may occur with the assessment of vitamin B6. For example, two
sources of dietary vitamin B6 are pyridoxine (PN) and pyridoxine-5′-β-D-glucoside
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Assessment of Vitamin Status of Athletes
TABLE 10.3
The Active Forms and Storage Sites for Vitamins
Vitamin
Active Form(s)
Storage Site
A
(all-trans) Retinol (Refs. 2, 9)
Liver (retinol) (Refs. 2, 9, 33)
Adipose tissue (carotenois) (Ref. 8)
D
E
K
Thiamin (B1)
Ribolavin (B2)
Niacin
Pyridoxine (B6)
(Cyano)cobalamin (B12)
Vitamin C
(all-trans) Retinal (Refs. 2, 9)
Retinoic acid (Refs. 2, 9)
B-cartotene
1,25(OH)2D (Refs. 2, 36)
24,25(OH)2D (Refs. 2)
d-α-tocopherol (most active)
(Refs. 2, 12)
β- tocopherol (Ref. 2)
γ- tocopherol (Ref. 2)
δ- tocopherol (Ref. 2)
Trienols (Ref. 2)
Hydroquinone (Ref. 38)
Thiamin Pyrophosphate (TPP)
(Refs. 2, 15)
FMN, FAD (Refs. 2, 34)
NAD, NADP (Ref. 2)
Pyridoxal phosphate (PP) (Ref. 2)
Methylcobalamin (Ref. 2),
adenosylcobalamin (Ref. 2)
Reduced ascorbic acid (DHAA)
(Ref. 2) , ascorbic acid (AA)
(Refs. 6, 39)
Biotin
Folate
Biocytin (Ref. 2)
Tetrahydrofolic acid (THF) (Ref. 2)
Pantothenic acid
Portion of coenzyme A (Refs. 2, 40)
Skin (7-dehydrocholesterol) (Ref. 36)
Adipose (adipocytes) (Refs. 2, 15, 17)
Lipid fractions of membranes (Ref. 2)
Adrenals, liver, and muscles
(Ref. 2, 15)
Adrenal glands, lungs, bone marrow,
kidneys, and lymph nodes (Ref. 13)
Skeletal muscle, liver, heart, kidneys,
and brain (Refs. 2, 21)
Liver, heart, and kidneys (Refs. 2, 15)
Muscle (Refs. 2, 26), liver (Ref. 2)
Liver (Ref. 26), brain, kidney, spleen,
and muscle (Ref. 15)
Pituitary and adrenal glands (Refs.
6,15), leukocytes (Ref. 6), eye tissue
(Ref. 16), less in saliva and plasma
(Refs. 6, 16)
Muscle, brain, and liver (Ref. 15)
Small amounts in liver, cerebrospinal
luid, bone marrow, spleen, and
kidney (Ref. 2)
(PN-glucoside). Both PN and PN-glucoside are converted to vitamin B6; however, the
conversion of PN-glucoside is less than that of PN, and PN-glucoside slightly inhibits
the conversion of PN.4 Therefore, if an athlete ingests foods that contain higher levels of PN-glucoside, then the athlete’s actual vitamin B6 levels may not adequately
relect vitamin B6 intake unless the nutrient assessment procedure accounts for the
inluence of PN-glucoside.
Another complication may arise when measuring serum or plasma levels of particular vitamins. The concentrations of vitamins in circulation may only relect the
current vitamin status. Whereas, if the storage forms (if applicable) of the vitamin
were to be assessed, a deiciency may be evident. As with iron assessments, it can be
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Nutritional Assessment of Athletes, Second Edition
important to measure the stored vitamin concentration. That is, an individual may
have a limited supply of stored vitamins for continued normal functioning, even
though circulating levels appear in the normal range.
10.2.3
BIOCHEMICAL INDICES TO ASSESS VITAMIN STATUS
Determining vitamin status is dependent on the source of sample used for quantiication. For some vitamins it may be more beneicial to measure stored levels
versus amounts in circulation, as the concentrations in circulation will not relect
a deiciency until the stored levels have been suficiently diminished. Contrarily,
assessing certain samples may not be justiiable. For example, liver samples provide an accurate measurement of vitamin A (retinol) levels, but the necessary biopsy
would be excessive as similar results can be obtained by measuring plasma retinol
levels. Some have reported the assessment techniques using tear5 or saliva samples6
to assess vitamin status, but those minimally invasive techniques are generally less
representative of the individual’s vitamin status than results obtained from blood or
tissue samples. Therefore, when assessing vitamin status, it is imperative to carefully
select the sample source, preparatory methods, and analytical techniques. Otherwise,
the time and money spent for this assessment may not yield optimum results. In other
words, the assessment would not have performed up to its potential.
10.3
ASSESSMENT GUIDELINES AND CONSIDERATIONS
The following information was compiled to aid in deciding which indices and techniques to choose in order to assess the status of a particular vitamin. These guidelines are not all encompassing, as many of these procedures have not been used
in conjunction with athletes. Additionally, other modiications or adjustments not
mentioned here may need to be made given differences in analytical equipment and
skill of personnel.
Vitamin A (Retinoids). Several techniques and laboratory equipment can be
used to assess vitamin A status (Table 10.3). Different forms of vitamin A
(β-carotene, retinol, or retinal) can be determined from blood, liver, or tear
luid. Carotenoid concentrations in blood and tissue samples usually relect
dietary intakes.7 Vitamin A status can also be determined indirectly by conducting a night-blindness test.5,8 The relative dose response and modiied
relative dose response method, where liver stores are assessed by giving the
person an oral vitamin A dose, is most representative and noninvasive.9 The
conjunctival impression cytology test is the analysis of vitamin A levels of
cells taken from a person’s eye but is less representative of current vitamin
A status.9
Vitamin B1 (Thiamin). Erythrocyte (red blood cell) transketolase is an enzyme
that needs thiamin to function, and when thiamin is depleted, this enzyme’s
activity decreases. Therefore, by measuring the enzyme activity, vitamin B1
status can be determined.20 Thiamin is needed in the form of thiamin pyrophosphate (TPP).21 Erythrocyte transketolases activity can be measured by
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Assessment of Vitamin Status of Athletes
301
adding TPP to the reactions. After TPP is added, increased activity would
indicate thiamin deiciency. This suggests there was not enough thiamin for
the enzyme to function before the addition of TPP.22 Other methods, such
as serum thiamin, microbiological assays, and erythrocyte thiamin levels,
are insensitive indicators of vitamin B1 status (Table 10.3).
Vitamin B2 (Ribolavin). Erythrocyte glutathione reductase activity coeficient is a test utilizing the activity of the enzyme erythrocyte glutathione
reductase to determine vitamin B2 status (Table 10.3).23 The activity of the
enzyme is measured before and after addition of lavin-adenine dinucleotide
(FAD), a coenzyme needed for the enzyme to function.23,24 If the activity of
the enzyme is low before and higher after the addition of FAD, that would
suggest a vitamin deiciency. If there were no deiciency, the levels before
and after FAD addition would be the same. Other methods, such as blood,
red blood cell, and urinary ribolavin levels, are also used to assess vitamin
B2 levels, but are not very sensitive indicators.23
Niacin (Nicotinamide and Nicotinic Acid). Niacin is a precursor for nicotinamide adenine dinucleotide (NAD), which is very important for biological functions.25 Erythrocyte NAD levels as well as the ratio of erythrocyte
NAD:NADP can be used to determine niacin status in blood.25 The Lowry
method has been developed, using speciic dehydrogenase enzymes, to
measure NAD and NADP levels in blood and tissue. Urinary excretions of
niacin metabolites, such as N′-methylnicotinamide (NMN) and 2-pyridone,
are also widely used methods in assessing niacin status (Table 10.3).24
Vitamin B6 (Pyridoxal). Table 10.3 displays methods by which vitamin B6
can be assessed. Vitamin B6 levels and vitamin B6 metabolites in blood
and urine samples are generally used for assessing this vitamin’s status.5,26
Pyridoxyal phosphate (PLP or PP) is the active form of vitamin B6, and its
levels in blood relect tissue stores.2,11 Enzymatic tests, such as erythrocyte alanine transaminase (ALT) and erythrocyte aspartate transaminase
(AST), indirectly relect vitamin B6 status.5 A short-term indicator for vitamin B6 status is urinary 4-pyridoxic acid (4-PA), a metabolite, representing
40–60% of the daily intake of vitamin B6.26 Urinary total vitamin B6 levels
represents 8–10% of the daily intake.26
Vitamin B12 (Cobalamin). Vitamin B12 status is generally assessed using
blood samples,22 where total vitamin B12 levels are assessed (Table 10.3).
Enzymatic tests are also used where substrates, such as methylmalonic acid
(MMA), holotranscobalamin (holoTC), and homocysteine, are measured.
Vitamin B12–dependent enzymes utilize these substrates. High substrate
levels in blood or urine indicate that there is not enough vitamin B12 for
the enzymes to function, so they cannot use the substrates. Therefore high
substrate levels indicate eficiency.5,27
Vitamin C (Ascorbic and Hydroascorbic Acids). Leukocyte (white blood
cell) vitamin C (ascorbic acid) concentration is the most reliable determinant of vitamin C status and is not affected by recent luctuations in the diet
(Table 10.3).6,11 It is representative of tissue and blood vitamin C status and
is correlated with liver vitamin C stores.6,11,16 Serum and platelet vitamin C
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Nutritional Assessment of Athletes, Second Edition
levels can also be used to assess vitamin C status.6 Urinary levels are not a
good indicator because the kidney reabsorbs vitamin C.6 Blood and urinary
vitamin C levels also relect recent dietary intake.11
Vitamin D (Calciferol). Different forms of vitamin D exist in blood and tissue, such as 25-OH vitamin D and 1,25 (OH)2 vitamin D (Table 10.3). In
assessing vitamin D status of the body, it is most valuable to assess 25-OH
vitamin D levels in blood. The reason for this is because 25-OH vitamin
D is converted to 1,25 (OH)2 vitamin D (active form, Table 10.2). In the
blood, 25-OH vitamin D is generally present in much higher concentrations than 1,25 (OH)2 vitamin D,10 and therefore it will always be converted
to the active form, even though the active form appears in low, normal,
or high concentrations. Other methods, such as assessing the proteins that
carry vitamin A in the blood (retinol binding proteins), enzymatic tests, and
receptor binding tests, are also used but are not as eficient as the method
discussed earlier.11
Vitamin E (Tocopherols and Tocotrienols). Alpha tocopherol (α TP) is the
most active form of vitamin E in the body, and this form is assessed when
determining vitamin E status.2,12 In Table 10.3, the different techniques to
assess vitamin E status are listed, such as the use of colorimetry, thin-layer
chromatography (TLC), high-pressure liquid chromatography (HPLC),
and the value of different methods are mentioned. According to Groff and
Gropper,13 there is not one method that is very accurate in determining vitamin E status; therefore, it is recommended to use more than one biochemical test. Blood, erythrocyte, adipose, muscle, and urine α TP levels have
been used to determine vitamin E status.14–16 Vitamin E protects lipids in
the body against oxidative damage (peroxidation). By exposing samples to
oxidation, vitamin E status can be determined by the time it takes for these
samples to be damaged. High vitamin E levels in the samples will extend
or delay the damage, or such levels can be measured by lipid peroxidation
markers like breath ethane and pentane.13,16,17 In the latter test, high levels
of peroxidation markers show depleted vitamin E levels. Vitamin E is carried on lipid-protein complexes called lipoproteins in the blood and when
assessing vitamin E, the lipids in these lipoproteins must be taken into
account because assessment of blood vitamin E levels alone are misleading
in determining vitamin E status.18
Vitamin K (Phylloquinone, Menaquinone, Menadione and Undercarboxylated
Osteocalcin). By measuring blood prothrombin, phylloquinone, or
des-γ-carboxyprothrombin (DCP) levels (Table 10.3), vitamin K status can
be assessed. Of these three, determining DCP by utilizing antibodies is the
most valuable indicator. Other samples, such as urine, can also be used to
determine vitamin K status. The recommendation, however, is to use DCP
as well as blood prothrombin determinations.13 Bleeding and clotting time
of blood is also useful to determine vitamin K status.5 For the assessment of
bone-related levels of vitamin K, measuring the percent of undercarboxylated
osteocalcin is also performed.19
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Folate (and Folacin). Folate (folic acid) is present in the body in the form of
tetrahydrofolate, which is very important for many biological pathways in
the body.28 By measuring metabolites of these pathways, folate status can
be determined (Table 10.3). An example is urinary N-formiminoglutamic
acid. This metabolite is involved in the breakdown of histidine to glutamic
acid and requires the cofactor tetrahydrofolate. Without tetrahydrofolate,
levels of N-formiminoglutamic acid in the blood will increase and lead
to excretion in the urine.15 Assessment of serum folic acid levels by itself
should not be used for folate status determination.11 Red blood cell folate
levels represent tissue store, thus this measurement is a more reliable longterm indicator.22,29
Biotin. A reduced biotin level in urine is a determinant of biotin deiciency.30
Also, the metabolite 3-hydroxyisovaleric acid, which is excreted in urine, is
inversely related to biotin status.31 It is also a sensitive and early indicator
of biotin deiciency.11,31 Blood biotin levels are not sensitive indicators for
biotin status, even though the avidin-binding assay or bioassays were used
(Table 10.3).30
Pantothenic Acid. Pantothenic acid is present in the body as part of acetyl
coenzyme A (CoA), which plays a critical role in energy metabolism. After
blood samples are obtained, certain enzymes, called hydrolytic enzymes,
are needed to cleave pantothenic acid from CoA in order to be analyzed in
the laboratory.32 This cleavage is not needed for determining pantothenate
levels in the urine, because hydrolytic enzymes present in the body already
cleaved pantothenate from CoA.32 Another means of determining blood,
tissue, and urine pantothenate is by microbiological assays using yeast and
lactobacillus (Table 10.3).2
Although chemical assessment of physical samples is a preferred means of determining vitamin status, this process can be too costly or cumbersome for some athletes
or their coaching staff. Thus, many athletes and coaches attempt to assess vitamin
status using indirect assessments, particularly diet records or diet recalls. This is
evident especially among the scientiic community, as most published reports pertaining to vitamin status in athletes have used indirect methods to estimate nutrition
status of the population sample.
Indirect assessments provide useful information regarding what athletes from
various sports eat and shed light on the amount of each vitamin those athletes
ingest during the prescribed assessment period. For example, in a group of ultradistance runners, it was reported this group had insuficient intakes of several antioxidant vitamins and that vitamin intake was associated with low energy intake.62
Interestingly, they observed that antioxidant status of the runners was actually similar to other runners, thereby illustrating the need to measure biological samples to
substantial nutrition status instead of making assumptions based on what is eaten.
As a guide, using indirect measures of vitamin status can be useful for the watersoluble vitamins, but doing so for the fat-soluble vitamins may lead to false security
or alarm. In other words, the indirect methods can be a useful tool to determine
which vitamins may need to be analyzed directly. This screening could reduce costs
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Nutritional Assessment of Athletes, Second Edition
and time by focusing the assessments on vitamins that seem to be consumed at lower
than recommended levels. Also, many of the recent papers that have been published
regarding vitamin status have pertained almost exclusively to the antioxidant vitamins and not speciically the vitamin status.
10.4
ASSESSMENT METHODS
Absorption spectrophotometry is limited to vitamins with a strong chromaphore. Light spectrophotometry utilizes either ultraviolet or visible wavelengths to measure the sample. As the selected wavelength of light passes
through the sample, the absorption of light will vary according to the sample. Based on a standard curve or derived regression equation, the absorption is proportional to the vitamin content of the sample.
Capillary electrophoresis is a high-performance analytical technique that can
be used to separate a variety of charged and neutral components. When
voltage is applied through the run buffer, the particles present will migrate
through a tube at a velocity determined by their respective size and electric charge. This separation technique is synonymous with other forms of
electrophoresis.
Chromatography (gas, thin-layer, and paper) is a separation procedure similar
to HPLC. It is capable of separating the desired compound but is not capable of quantifying the amount or concentration of the sample. For example,
following gas chromatography, the sample is further assessed using mass
spectroscopy to quantify the amount of the desired compound.
Diet analysis is the most common method for assessing vitamin status. This
method indirectly assesses status. There are several means to analyze a
diet (for example, diet recall and food frequency questionnaire), yet each
method cannot deinitively ascertain whether the athlete is truly deicient.
Dietary analysis can be a useful tool to determine which vitamins might
be deicient in an athlete. Hence this process may help narrow down the
number of vitamins to analyze, which could signiicantly decrease analytical costs.
Electrochemical techniques are used following chromatography to quantify
vitamin content. The procedure is based on the electrochemical qualities of
each vitamin or vitamer.
Enzymatic and microbiological assays utilize chemical reagents to convert
the vitamin or vitamer to a compound that is generally measurable by luorometry or various types of spectrophotometry. Speciic to microbiological
assays, the sample is exposed to an organism that will only grow in the
presence of the speciic vitamin.
Fluorometry is similar to spectroscopy. The exception is that the luorometer
detects the luorescence of compounds at different wavelengths. Therefore,
if the assay reagent does not yield luorescent compounds, the luorometer
will not be of value.
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Gas chromatography-mass spectrometry (GC-MS), which separates the
compound of interest from other potentially interfering compounds and the
mass spectrometer, analyzes the puriied sample over a time interval.
High-pressure liquid chromatography (HPLC) can be used as a puriication method and quantitative technique. Injecting the sample onto
the column separates compounds. The various components in the sample pass through the column at different rates due to partitioning differences between the mobile liquid and stationary phases. HPLC also
provides greater chromatographic selectivity than gas chromatography.
Fluorescent detection is frequently used for quantifying several lipid and
water-soluble vitamins.
Ion exchange chromatography is commonly used in the puriication of biological materials. Charged molecules in the liquid phase pass through the
column until a binding site in the stationary phase appears. The molecule
will not elute from the column until a solution of varying pH or ionic
strength is passed through it. Separation by this method is highly selective.
Radioimmunoassay utilizes a labeled isotope to quantify a given compound.
The radio-labeled isotope binds to the compound. The sample is analyzed
in a scintillation counter. The greater the radioactive count, the greater
amount of bound isotope.
10.5
FUTURE RESEARCH
Within the realm of vitamin assessments there are a few factors that hinder advancing our understanding of the role vitamins play in exercise and sport. A general
consensus is that vitamin status does not affect exercise or sport performance in
most athletes. That does not mean they are not important, but simply that most athletes consume enough vitamins to minimize the chance of a vitamin deiciency from
affecting their ability to perform at a desired level. That said, there is little evidence
illustrating a dose response for each vitamin on athletic performance to better determine whether athletes truly need more vitamins than less-active individuals.
So what does that issue have to do with vitamin assessments? A primary issue to
address that prior point is having assessment procedures that are accurate and inancially feasible. Secondary issues are how quickly the samples can be analyzed, how
invasive the procedure is (for example, tissue, blood, or saliva samples), and the number of compounds to assess to determine vitamin status (such as β-carotene, retinol,
or retinal concentrations for vitamin A status). Currently, most of the preferred or
more valid methods to assess vitamin status require costly equipment and blood
samples at the minimum. There are some less-invasive methods, but even those can
present other barriers (time needed to conduct the test, for example).
Thus there is a great need for studies that are designed to increase the “ease”
(cost, speed, and invasiveness) of assessing vitamin status in athletes. Given the
changes that occur throughout a competitive season and the off-season for many
athletes, it would be valuable to know to what degree most athletes truly need to
concern themselves with vitamin intake beyond the concerns needed to maintain
general health.
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10.6
Nutritional Assessment of Athletes, Second Edition
CONCLUSIONS
The intent of this chapter is to provide sport scientists information regarding the
assessment techniques to biochemically determine vitamin status. The assessment
of vitamin status tends to require more analytical steps and stability-maintaining
procedures than assessments of other nutrients (glucose, non-esteriied fatty acids,
etc.). If greater detail is desired, there are several texts that fully explain and discuss
the chemical properties and analytical methods to assess each vitamin and/or vitamer.1,11,33 Given the complex interactions between micronutrients, such as vitamins
and other ingested compounds, it will be beneicial for scientists to assess vitamin
status in athletes to justify or better explain biochemical occurrences affecting training, competition, or recovery of athletes.
When initiating the process of assessing vitamin status, it is imperative that the
coach, athlete, or scientist refer to texts or articles that not only explain the methods but also discuss the confounding analytical factors that lead to the conversion
of inactive isomers or instability of the vitamins being measured. These factors,
in conjunction with the fact that few studies have demonstrated vitamin malnutrition in athletes, seem to minimize the interest in vitamin research in exercise science. However, the assessment of vitamin status may be prove beneicial in better
understanding performance outcomes of athletes with eating disorders, those who
ingest megadoses of vitamins and other supplements, and those performing high
training volumes. Therefore future research in vitamin assessment should investigate how nutrient and training status (for example, malnutrition and high training
volume) alter the circulating and stored levels of vitamins and the subsequent effect
on performance.
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© 2011 by Taylor and Francis Group, LLC
of Mineral
11 Assessment
Status of Athletes
Henry C. Lukaski and Angus G. Scrimgeour
CONTENTS
11.1
11.2
11.3
11.4
11.5
Introduction ................................................................................................ 312
11.1.1 Dietary Intake .............................................................................. 313
11.1.2 Biochemical Measures ................................................................. 313
11.1.2.1 Sample Collection ....................................................... 314
11.1.2.2 Sample Contamination ............................................... 314
11.1.2.3 Analytical Methods .................................................... 315
11.1.2.4 Quality Control ........................................................... 315
Calcium ...................................................................................................... 315
11.2.1 Methods for Assessing Calcium Status ....................................... 316
11.2.1.1 Total Serum Calcium .................................................. 316
11.2.1.2 Serum Ionized Calcium .............................................. 316
11.2.1.3 Urinary Calcium Excretion ........................................ 316
11.2.1.4 Calcium Reference Intervals and Data from Athletes ....317
Chromium .................................................................................................. 318
11.3.1 Methods for Assessment of Chromium Status ............................ 318
11.3.1.1 Chromium Reference Intervals and Data from
Athletes ....................................................................... 319
Copper ........................................................................................................ 319
11.4.1 Methods for Assessment of Copper Status .................................. 320
11.4.1.1 Serum and Plasma Copper.......................................... 320
11.4.1.2 Ceruloplasmin............................................................. 320
11.4.1.3 Copper, Zinc Superoxide Dismutases......................... 321
11.4.1.4 Cytochrome c Oxidase ............................................... 321
11.4.1.5 Copper Reference Intervals and Data from Athletes ....322
Iron ............................................................................................................. 323
11.5.1 Methods for Assessment of Iron Status ....................................... 323
11.5.1.1 Hemoglobin and Hematocrit....................................... 323
11.5.1.2 Ferritin ........................................................................ 323
11.5.1.3 Serum Iron, Total Iron-Binding Capacity,
Transferrin, and Transferrin Saturation ...................... 324
11.5.1.4 Soluble Transferrin Receptor ...................................... 324
11.5.1.5 Free Erythrocyte Protoporphyrin and Zinc
Protoporphyrin............................................................ 325
11.5.1.6 Iron Reference Intervals and Data from Athletes....... 325
311
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11.6
Magnesium ................................................................................................. 326
11.6.1 Methods for Assessment of Magnesium Status ........................... 326
11.6.1.1 Serum and Plasma Magnesium .................................. 327
11.6.1.2 Ionized Magnesium .................................................... 327
11.6.1.3 Muscle Magnesium ..................................................... 327
11.6.1.4 Blood Cells ................................................................. 327
11.6.1.5 Magnesium Load Test................................................. 328
11.6.1.6 Magnesium Reference Intervals and Data from
Athletes ....................................................................... 328
11.7 Phosphorus ................................................................................................. 328
11.7.1 Methods for Assessment of Phosphorus Status ........................... 329
11.7.1.1 Phosphorus Reference Intervals and Data from
Phosphate Supplementation Trials .............................. 329
11.8 Zinc............................................................................................................. 330
11.8.1 Methods for Assessment of Zinc Status....................................... 330
11.8.1.1 Plasma and Serum Zinc .............................................. 330
11.8.1.2 Zinc-Containing Enzymes.......................................... 330
11.8.1.3 Zinc Reference Intervals and Data from Athletes ...... 331
11.9 Inlammation and Mineral Status .............................................................. 331
11.10 Future Research Needs............................................................................... 332
11.11 Conclusions ................................................................................................ 333
Note.... .................................................................................................................... 333
References .............................................................................................................. 334
11.1
INTRODUCTION
The burgeoning awareness of the fundamental biological roles that trace elements
and minerals play in the development of physical itness and the attainment of peak
performance (Table 11.1) fuels interest in measures of assessment of mineral element
nutritional status of physically active people.1,2 Selection of an appropriate assessment
tool is complicated by theoretical and practical limitations. The ideal marker should
be speciic and sensitive, and should distinguish adequate from deicient nutritional
status. Among vigorous individuals, however, subclinical or marginal nutritional,
compared to overt or clinical, deiciency is more likely to occur and thus requires one
or more biomarkers for characterization. Biochemical indicators of subclinical deiciency should be practical, convenient, and cost effective, and relect cellular mineral
content and the function of speciic cells. Because no single method achieves all
of these criteria, a compromise is needed to achieve a valid and realistic indicator
to routinely identify subclinical mineral nutritional status in humans.3 This chapter
details some useful approaches to assess human mineral nutritional status with an
emphasis on biochemical methods and indicators. The focus is on mineral elements
that are either acknowledged to have key roles in promoting physical performance or
are used as performance-enhancing supplements; they include calcium, chromium,
copper, iron, magnesium, phosphorus, and zinc. The chapter describes traditional
and new biochemical measures of mineral element nutriture, presents values in
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TABLE 11.1
Biological Roles of Mineral Elements in Support of Physical Performance
Element
Biochemical Role
Physiological Function
Calcium
Second messenger
Organic matrix of skeleton
Insulin action
Muscle contraction
Bone health
Insulin sensitivity
Glucose and lipid metabolism
Aerobic energy production
Antioxidant protection
Aerobic energy production
Intermediary metabolism
Maintenance of ATP and CP
Muscle contraction
Formation of ATP and CP
Aerobic energy metabolism
Muscle function
Oxygen release and CO2 removal
Antioxidant protection
Chromium
Copper
Iron
Magnesium
Phosphorus
Zinc
Oxidative metabolism
Free radical breakdown
Oxygen utilization
Energy transformation
Energy storage
Oxygen release to tissues
Macronutrient metabolism
Gas transport
Free radical neutralization
diverse groups of physically active persons, and identiies alterations in physiological functions and performance linked with altered mineral nutritional status.
11.1.1
DIETARY INTAKE
The estimated daily intake of nutrients is a common indicator of nutritional status.
Self-reports or recall of food and luids consumed, in conjunction with computerized
programs and mineral nutrient data bases, permit calculation of individual nutrient
intakes from commonly consumed food and beverages. Evaluation of adequacy of
intake utilizes a comparison of self-reported intake with established national recommendations such as the Dietary Reference Intakes (DRI).4,5 This approach relies on
accurate recording or recall of amounts of food and luids consumed, reporting of
intake on multiple days of the week that are representative of usual consumption,
and nutrient databases that accurately relect nutrient contents of the food and beverages consumed. This approach can be dificult with physically active adults unless
speciic precautions are employed.6 A limitation to the use of DRI is that physical
activity is considered only in calculating recommendations for calcium, iron, and
magnesium intakes.7 The tendency of individuals to report less food than they actually consume limits the accuracy of this approach.8,9
11.1.2
BIOCHEMICAL MEASURES
Use of blood biochemical analyses to assess nutritional status provides an objective alternative to self-reported food intakes. The concentrations of minerals in
serum or plasma, mineral concentrations in the cellular components of blood, and
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the activities of mineral-containing enzymes (metalloenzymes) in blood or cells
are routine assessment measures. The rationale for these measurements is the
assumption that these variables are proportional to their intracellular contents and
relect tissue or organ content and function. Some factors moderate the validity
of these measures to index nutritional status. Mineral element concentrations may
be affected by factors unrelated to whole-body mineral status (hormones, stress,
inlammation, injury, etc.). Also, changes in the extracellular luid volume affect
concentration values.10,11
11.1.2.1 Sample Collection
Accurate determination of mineral elements in biological specimens requires special
precautions and attention to potential analytical concerns.12,13 Analysis of seemingly
homogenous specimens such as blood may be markedly affected by sampling and
processing procedures. Hemolysis or microhemolysis of a whole-blood sample can
yield erroneously high plasma or serum concentrations of iron or zinc because erythrocyte concentrations of these and other minerals are more than ten times greater
than those in plasma.14 Also, concentrations of zinc are 5 to 15% greater in serum
than plasma due to the release of zinc from platelets during clotting. Selection of an
anticoagulant also is important because of the potential expansion of plasma volume
associated with intracellular luid shifts that occurs during exercise and the possible
contamination of heparin with zinc.13
11.1.2.2 Sample Contamination
The critical problem affecting the validity of mineral element analyses is sample
contamination from external sources. Sources of contamination in the laboratory
include dust, rubber, paper products, wood, metal surfaces, skin, dandruff, and hair.
In experimental and laboratory environments, mineral elements exist in nanogram
(ng) and milligram (mg) amounts. Thus, a signiicant portion of an analytical value
may be the result of contamination unless appropriate precautions are followed.
Contamination, therefore, contributes to the wide variation of reported reference values, speciically in the mineral elements reported in very low concentration ranges
(for example, part per billion ranges or ng/g).
Plastic and borosilicate glass are best suited for trace element analysis. Speciically,
luorocarbon, polyethylene, and polypropylene plastics are recommended. Surfaces
in contact with samples for analysis should be cleaned of adherent mineral elements
by soaking with dilute, analytical-grade nitric acid or commercial, metal-binding
solutions. Water should meet or exceed American Chemical Society standards of
14 MΩ/cm2 for elemental contamination or resistivity.13 Reagents and anticoagulants
should be free of mineral elements. Disposable syringes and stainless steel needles
should be used for blood collection. Stainless steel contains high chromium and
nickel contents; therefore stainless steel needles are not acceptable for phlebotomy
when measuring chromium, nickel, and other ultra-trace elements unless they are
siliconized. Commercially available, evacuated, blood collection tubes may be problematic if specimens come in contact with the stopper. Mineral elements may leach
from the stopper into the blood, thus contaminating the specimen. Use of commer-
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cial, trace-element-free, evacuated tubes should be examined for mineral element
contamination before use.
11.1.2.3 Analytical Methods
Measurement of mineral elements in biological specimens requires analytical sensitivity, speciicity, precision, accuracy, and expedience. Analytical sensitivity is paramount because concentrations of trace and ultra-trace elements occur in the mg to
ng/g range.
Although a variety of analytical techniques are available, atomic absorption spectroscopy (AAS) and emission spectroscopy, including inductively coupled plasma
emission spectroscopy (ICPES) and inductively coupled plasma mass spectroscopy
(ICPMS), are the most commonly used in clinical settings. The AAS method is the
routine assessment tool of single mineral element analysis. Samples may be diluted
and aspirated directly into the lame. Electrothermal or lameless AAS methods
are available for microsample volumes and very low concentrations (< 50 ng/g).
Background correction using Zeeman or deuterium arc techniques is often necessary
with electrothermal AAS to overcome matrix or background interferences.15 The
ICPES is a multielemental method that is replacing AAS for many mineral element
applications. It enables simultaneous multielemental measurements in small sample
volumes and over a wide analytical range.
11.1.2.4 Quality Control
Effective quality assurance procedures must be included in mineral element analysis
plans because methods for mineral analysis are susceptible to interferences with biological matrices and external contamination. In each batch of samples, there should
be reagent blanks, replicate analyses to estimate precision, and reference materials
with known or certiied concentrations of mineral elements prepared similarly to the
unknown samples to enable assessment of accuracy and batch-to-batch precision.15
Importantly, the reference material should possess the same matrix and approximately the same amounts of analytes as the unknown samples. A variety of reference
or control materials are available commercially.
11.2
CALCIUM
Calcium is a major mineral in the body, serving to provide body structure with more
than 99% of body calcium stored in bone. The remainder of body calcium exists in
tissues and extracellular luid, and acts to regulate a wide variety of body functions
including muscle contraction, blood coagulation, enzyme activation, nerve transmission, signal transduction in hormone actions, and membrane transport.
Calcium in the serum exists in three different physiological forms. Approximately
47% of calcium is free or ionized, making it available for incorporation into intracellular compartments. Another 47% is bound to proteins, mainly albumin; this binding
is highly dependent on pH. About 20% of the protein-bound calcium is bound to
globulins. The remaining 6% of calcium is associated with diffusible anions, including bicarbonate, lactate, citrate, and phosphate. Factors such as diet, stress, or illness
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alter the distribution of calcium among these three metabolic pools and thus affects
the amounts of total and ionized calcium in the circulation.
11.2.1
METHODS FOR ASSESSING CALCIUM STATUS
The skeleton is the major reserve of calcium in the body. Thus calcium is mobilized
from bone to ensure cellular functions and maintain extracellular luid concentrations when dietary intake is inadequate. Assessment of calcium status is problematic
because serum calcium levels are tightly controlled by hormones and remain constant under most conditions.16 Serum ionized calcium (> 50% of total serum calcium), also termed free calcium, is generally considered to be the physiological form
of calcium because it is biologically active and is highly controlled by calcium-regulating hormones. Because approximately 47% of serum calcium is bound to proteins,
total calcium concentrations are markedly affected by alterations in blood protein
concentrations, principally albumin.
11.2.1.1 Total Serum Calcium
Three methods currently used to determine total calcium in biological luids include
photometric analysis, titration of a luorescent calcium complex with ethylenediaminetetraacetic acid (EDTA) or ethylene glycol tetraacetic acid (EGTA), or AAS. The
approved reference method for measuring serum concentrations of calcium is AAS17; it
provides improved accuracy and precision compared to the spectrophotometric methods. Detailed procedures for the determination of calcium in serum are available.18
11.2.1.2 Serum Ionized Calcium
Serum ionized calcium, which represents the majority of calcium in the circulation,
is the physiologically active form of calcium. In contrast to total serum calcium that
may be normal in conditions characterized by neuromuscular irritability, such as
vitamin D deicient rickets and hypoparathyroidism, serum ionized calcium concentration is reduced.
Physiological and measurement conditions, including changes in the specimen pH,
the use of EDTA or heparin, and high concentrations of magnesium and sodium, affect
serum ionized calcium concentrations.19 Because most anticoagulants bind calcium,
serum is the preferred specimen for measuring ionized or free calcium. Common biologically active anions, including citrate, phosphate, oxalate, and sulfate, form complexes with free calcium and thus may reduce its apparent concentration. The binding
of free calcium by protein and relatively small anions is affected by pH both in vivo
and in vitro. Biological specimens should be analyzed at the pH of the blood because of
the inverse relationship between pH and ionized or free calcium. Anaerobic conditions
should be maintained because specimens lose carbon dioxide and become more alkaline when exposed to air. Also, specimens should be handled with care to minimize
metabolism of erythrocyte and leukocytes, which produce acids and decrease pH.
11.2.1.3 Urinary Calcium Excretion
Under certain conditions, urinary calcium measurements, which are correlated with
calcium intake,4 are used to assess changes in calcium metabolism. Urinary calcium
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collected over a 24-hour period may be affected by antecedent diet, metabolic disorders, and or dehydration. Diets high in calcium and/or vitamin D, dehydration,
hyperthyroidism, hyperparathyroidism, Paget’s disease, osteoporosis, sarcoidosis, or
kidney disease may result in high levels (250–300 mg/24 hour sample) of calcium in
the urine. Low urine calcium levels (< 150 mg/24-hour sample) may indicate problems with the parathyroid glands (hypoparathyroidism), low amounts of calcium or
vitamin D in the diet, poor absorption of calcium or vitamin D by the intestines, or
kidney disease.
11.2.1.4 Calcium Reference Intervals and Data from Athletes
In healthy adults, serum calcium concentrations range from 8.6 to 10.2 mg/dL, or 2.15
to 2.55 mmol/L.18 Concentrations decrease with age in men; females have slightly
lower concentrations than males. Serum ionized calcium concentrations range from
4.64 to 5.28 mg/dL (1.16 to 1.32 mmol/L) in healthy adults. Calcium in urine ranges
from 150 to 300 mg/24-hour sample. Because circulating calcium levels are maintained homeostatically with calcium luxes from bone, there is no good indicator of
calcium status for adults (see Table 11.1).
Supplemental calcium in conjunction with a program of weight-bearing activity
has been used to prevent and to treat bone loss in adolescent girls20 and nonosteoporotic women.21 However, when both treatments have been applied, no additive
effects were found in elderly women.22 Supplementation of healthy boys with 1000 mg
calcium/d resulted in greater bone mineral content (BMC) of the whole body, and this
BMC response was greater in subjects with high physical activity.23 Supplementation
of female recruits in the U.S. Navy with 2000 mg calcium and 800 IU of vitamin D/d
for 8 weeks signiicantly reduced stress fractures by 21%.24 These indings contrast
with those of a supplementation study involving male military recruits receiving 500
mg of calcium/d in which the supplement, compared to a placebo, had no effect on
the frequency of overuse injuries during 9 weeks of physical training.25 Because total
daily calcium intake was at least 800 mg/d, the authors concluded that this amount of
calcium was adequate to protect against overuse bone injuries in men. Urinary calcium excretion decreased ~15% in healthy, moderately active men participating in a
3-week program of daily high-impact and resistance training activities.12 The authors
suggested that the reduction in urinary loss of calcium might be at least partially
responsible for improved bone mineralization that has been observed during periods
of greater physical activity.
Although the importance of measuring blood biochemical indicators of calcium
status is well established in the evaluation of endocrine control of bone metabolism, measurements of calcium status in physically active persons are not common
(Table 11.1). Crespo et al.26 measured biological markers of nutrition in 18 marathon
runners and 22 sedentary controls and reported no differences in serum calcium
levels between the groups. Assessment of bone status, which is a long-term indicator
of the adequacy of calcium status, relies on determinations of bone mass and quality
with dual x-ray absorptiometry and determinations of circulating hormones involved
in maintenance of bone accretion and turnover (Table 11.2).
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TABLE 11.2
Indicators of Subclinical Deficiency of Selected Minerals and Functional
Impairments
Values Linked with
Impaired Function
Impaired Function
Not established
No reliable indicator
Not established
Low bone mineral density
Impaired glucose/insulin metabolism?
Increased oxidative damage
> 8.5 mg/L
Magnesium
None
Serum chromium?
Superoxide dismutase
activity: serum and
RBCa
Soluble transferrin
receptors
RBC magnesium
Phosphorus
Zinc
Serum phosphate?
Serum or plasma zinc
Not established
< 11.0 µmol/L
Decreased endurance, Reduced
energy eficiency
Reduced energy eficiency, Reduced
cardiorespiratory function
Decreased cell energy intermediates?
Reduced cardiorespiratory function,
Decreased endurance and strength
Element
Indicator
Calcium
Chromium
Copper
Iron
a
< 6.0 mmol/g Hbb
RBC = red blood cells or erythrocytes; b Hb = hemoglobin.
11.3
CHROMIUM
Chromium is an ultra-trace element; it facilitates the biological action of insulin
in carbohydrate, protein, and lipid metabolism.27 Chromium, which binds to an
intracellular, low-molecular-weight chromium-binding protein, potentiates the autoampliication of insulin signaling by stimulating the insulin receptor kinase activity
in insulin-sensitive cells.28 Insulin resistance may be a consequence of chromium
deiciency because insulin apparently is ineficient as a regulator of glucose uptake
and utilization without chromium. Because of analytical problems with measurements of very small concentrations of chromium in foods, beverages, and biological
samples as well as interferences with chromium contamination, human metabolic
studies of chromium are very limited. Thus, inference of human chromium deiciency relies on improvement in glucose tolerance after supplementation.27
11.3.1
METHODS FOR ASSESSMENT OF CHROMIUM STATUS
Analytical limitations because of trace concentrations of chromium in human tissues
and luids have limited the identiication of a reliable measure of body chromium
status.27 Early reports of serum and urinary chromium concentration were erroneous
because of contaminations and other analytical problems. With improved method
sensitivity and capability of identiication and elimination of external chromium
contamination, substantially decreased estimates of chromium concentration in biological and food samples appeared.
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The preferred method for determination of chromium in biological samples is
AAS with a graphite furnace and Zeeman correction.29 Caution is advised to avoid
any contact of a sample with any metal surface, including the use of stainless steel
needles unless they are siliconized.
11.3.1.1 Chromium Reference Intervals and Data from Athletes
The current adult reference range for serum chromium concentration is < 0.05 to
0.52 μg/L or 1 to 10 nmol/L. Urinary chromium excretion is referenced at 100 to
200 ng/24 h. Consumption of chromium supplements will increase daily urinary
chromium output depending on the dose and duration of the supplement usage.
Data describing serum chromium concentrations and urinary chromium excretion
of athletes are limited.30 Anderson and co-workers31 reported signiicantly increased
serum chromium concentrations in men consuming self-selected diets and after
running 10 km. Basal values were 2.3 ± 1.2 nmol/L, increased to 3.3 ± 1.7 nmol/L
immediately after running, then to 3.6 ± 1.7 nmol/L 2 hr after exercise. Urinary
chromium output also increased signiicantly from nonexercise values of 200 ± 120
to 370 ± 240 ng/d on the day of running. Among young men consuming self-selected
diets and participating in an 8-week resistance training program, serum chromium
concentrations increased from 13 ± 4 to 14.5 ± 4 nmol/L.32 With chromium supplementation (~180 mcg chromium daily as chromium picolinate), serum chromium
increased from 13 ± 4 to 16 ± 3 nmol/L. Concomitantly, urinary chromium excretion increased only with chromium supplementation. Similarly, serum and urinary
chromium increased signiicantly in healthy women fed a diet containing 29 ± 2 µg
chromium daily for 12 weeks and supplemented with ~190 mcg chromium as chromium picolinate (45 µg/L and ~300 nmol/24 hr) compared to placebo or picolinic
acid (1720 µg) [~27 µg/L and ~40 nmol/24 hr].33 Dificulties in collecting and analyzing samples, and the direct inluences of exercise and chromium intakes affecting
serum and urinary chromium, contribute to the lack of an acceptable indicator of
chromium status in humans (Table 11.2).
11.4
COPPER
The biochemical role for copper is primarily catalytic with many copper metalloenzymes acting as oxidases to reduce molecular oxygen. In these oxidation-reduction reactions, copper serves as the reactive center in the copper metalloenzymes.
Some copper metalloenzymes include ceruloplasmin, superoxide dismutase,
dopamine-β-hydroxylase, lysyl oxidase, cytochrome c oxidase, and tyrosinase.34
Thus, copper plays a key role in supporting increased energy expenditure, antioxidant
protection, and synthesis of important protein needed to sustain physical activity.
Copper deiciency decreases the activity of copper metalloenzymes and results
in marked biological impairments.34 Defective connective tissue cross-links
in heart, muscle, and bone may be attributed to decreased lysyl oxidase activity.
Hypopigmentation has been associated with depressed tyrosinase activity because
copper is required for melanin synthesis. Oxidative damage in various organs, tissues,
and organelles has been shown to be the result of decreased superoxide dismutase
activity. Low copper intake in humans has been associated with exaggerated blood
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pressure responses during isometric exercise and attributed to altered dopamine-βhydroxylase activity in vascular tissue.35
11.4.1
METHODS FOR ASSESSMENT OF COPPER STATUS
Biochemical indicators of copper nutritional status continue to undergo evaluation
and validation.36 Despite the lack of an unequivocal marker of human copper nutritional status, a number of indices can be useful in the diagnosis of subclinical copper
deiciency (Table 11.2).
11.4.1.1 Serum and Plasma Copper
A common measure of copper status is serum or plasma copper concentration, with
low copper concentration in plasma or serum indicative of depleted body copper
stores. However, plasma copper concentrations are not reliable indicators of shortterm marginal copper status in humans. Homeostatic mechanisms regulate plasma
copper concentrations within a narrow range. Thus, plasma copper concentrations
decrease only after signiicant depletion of body copper stores.37 Factors independent of copper intake affect circulating copper concentrations. Women generally
have higher plasma or serum copper concentrations than men; estrogen increases
plasma copper concentrations in women taking oral contraceptive agents and postmenopausal women receiving estrogen therapy.38 Plasma copper concentrations are
increased in pregnancy, inlammation, infection, and rheumatoid arthritis.39 In contrast, general stress and glucocorticoid hormones decrease plasma copper concentrations.39 Thus conditions that elevate serum copper may belie decreased serum
copper even during copper deprivation. Also, circumstances that reduce serum copper should be eliminated before a valid assessment of copper nutritional status may
be undertaken.
The method of choice for determination of plasma or serum copper is AAS after
dilution of the specimen with deionized water. Hemolysis is not a major concern for
copper determinations because concentrations of copper in erythrocytes and plasma
are similar.
11.4.1.2 Ceruloplasmin
More than 80% of the copper in plasma is associated with the protein ceruloplasmin;
changes in plasma copper are relected in changes in the amount of this protein in the
circulation. Both the enzymatic activity of ceruloplasmin and the immunoreactive
protein ceruloplasmin respond similarly to age, sex, and hormone use; they increase
in pregnancy and in response to inlammation. Enzymatic activity of ceruloplasmin
has been shown to be an indicator of copper status in animals and humans deprived
of copper.37
Serum ceruloplasmin may be measured immunochemically or by its oxidase
activity. The copper-depleted, apo-ceruloplasmin is likely present in normal and
copper-deicient serum.37 Thus, chemical assays of its oxidase activity are preferred
as an index of copper status. The speciic activity of ceruloplasmin, deined as the
ratio of enzymatic activity to the immunoreactive protein, may be a sensitive marker
of copper status because it was inversely related to blood pressure response to hand-
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grip work.35 This ratio, which is not affected by age, sex, or hormone use,37 should
be used to assess copper status of athletes.
11.4.1.3 Copper, Zinc Superoxide Dismutases
Superoxide dismutases (SOD) belong to a family of antioxidant enzymes that catalyze the dismutation of the superoxide radical to yield hydrogen peroxide and oxygen. There are two distinct forms of SOD in mammals and each utilizes copper
in its reactive center. These isozymes are characterized by their cellular location
and distribution among various tissues. The erythrocyte isoform (SOD1) is localized in the nucleus and cytoplasm and found principally in erythrocytes and liver
cells.40 However, the extracellular isoform (SOD3) is concentrated in the extracellular matrix of tissues, speciically lung and kidney, and is the dominant extracellular
antioxidant enzyme found in the serum.41
11.4.1.3.1 Erythrocyte Superoxide Dismutase
Erythrocyte superoxide dismutase activity decreases during copper deiciency in
humans and some animal species. It also is sensitive to changes in copper status
as shown in several studies of experimental copper deprivation.37 Compared to
other biochemical markers of copper status such as plasma copper and ceruloplasmin, erythrocyte superoxide dismutase activity is independent of age, sex, and
hormone use.42
11.4.1.3.2 Extracellular Superoxide Dismutase
The extracellular superoxide dismutase is a secretory protein present in relatively
reduced amounts in the circulation relative to its tissue source.41 It is responsive to
changes in copper43 and zinc44,45 intake in animal models. Some controversy exists
regarding the speciicity of the activity of extracellular superoxide dismutase as a
functional indicator of copper or zinc status, as both conditions have been shown to
reduce its activity.46,47
Biochemical assays for superoxide dismutase are based on the indirect measurement
of activity that consists of a superoxide generating system and a superoxide indicator
that is measured spectrophotometrically.48 Addition of copper (zinc superoxide dismutase, speciically SOD1) inhibits the absorption change. The use of the autoxidation
of pyrogallol has been the principal method for determination of erythrocyte superoxide dismutase activity.49 In contrast, the autoxidation of xanthine by xanthine oxidase
is the recommended method for determination of extracellular superoxide dismutase.50
Recent indings reveal that the determination of SOD3 activity in serum with xanthine
and xanthine oxidase at pH 10 is a very sensitive indicator of copper status.51
A practical problem arises from the use of superoxide dismutase activities to
assess copper status; there are no uniform reference ranges available. To facilitate
the use of superoxide dismutase, it is suggested that reference ranges be developed in
each laboratory and the conditions used for analysis be maintained.
11.4.1.4 Cytochrome c Oxidase
Decreased tissue cytochrome c oxidase activity is an early and consistent trait of
copper deiciency in animals. Reductions of 50% of normal cytochrome c oxidase
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activity are associated with impaired neurological, cardiac, and muscle functions.52 Studies in humans report that cytochrome c oxidase activities in platelets
are decreased when dietary copper is restricted.37,53 Cytochrome c oxidase activity
in platelets and leukocytes paralleled copper status in animals54; the cytochrome c
oxidase activity correlated directly with liver copper concentration, an established
index of copper status in animals.
Available methods for determination of cytochrome c oxidase activity in blood
cells and tissues utilize the spectrophotometric analysis of the oxidation of ferricytochrome c. A microassay has been described that uses a coupled reaction between
cytochrome c and 3-3′-diaminobenzidine tetrachloride in microwell plates.55
Age affects cytochrome c oxidase activity.37,53 Platelet and leukocyte cytochrome c
oxidase activity are higher in older than in young adults but are not affected by sex or
hormone use. Other factors that may limit the use of this marker include considerable
between-individual variability, the labile nature of this enzyme, and its sensitivity to
minor variations in technique.
11.4.1.5 Copper Reference Intervals and Data from Athletes
Serum copper concentrations are higher in women of child-bearing age, 80 to 190 µg / dL
or 12.6 to 24.4 μmol/L, than in men, 70 to 140 µg/dL or 11 to 22 μmol/L. Serum copper is highest in pregnant women, 118 to 302 µg/dL or 18.5 to 47.4 μmol/L. The range
of normal values for children 6 to 12 years of age is 80 to 90 µg/dL or 12.6 to 29.9
μmol/L.17
There is a paucity of data describing the copper status of athletes. In a sample of
44 male university athletes, plasma copper was 90 ± 14 µg/dL with hypocupremia
(< 70 µg/dL) present in four of the men.56 Plasma copper (95 ± 11 and 94 ± 10 µg / dL)
and enzymatic ceruloplasmin (419 ± 37 and 397 ± 38 mg/L) were unchanged from
precompetition to end of the competitive season in 12 elite female university swimmers.57 Similarly, plasma copper and enzymatic ceruloplasmin were within the range
of normal values for male and female swimmers before and during a competitive
season.58 Interestingly, SOD1 activity increased signiicantly in response to swim
training, despite reduced copper intake.58 Thus, the increased activity of SOD1 was
an adaptation to increased oxidative stress associated with aerobic training.
Copper status of runners also has been assessed. Anderson et al.31 reported serum
copper of 93 ± 15 µg/dL for 9 trained runners. In contrast, Singh et al.59 found
increased plasma copper (122.2 ± 12.5 vs. 106.6 ± 15.6 µg/dL), decreased erythrocyte copper (1.06 ± 0.02 vs. 1.26 ± 0.03 µg/g), and similar enzymatic ceruloplasmin
(287 ± 49 vs. 281 ± 50 mg/L) in 45 female runners compared to 27 nonrunners. Thus
exercise apparently induced a redistribution of copper in the women.
The use of more than one biochemical measure of copper status will increase
the probability of reliably identifying an individual as copper deicient or adequate.
Thus, the use of multiple indicators, such as serum copper, platelet cytochrome c
oxidase, and superoxide dismutase activities, will enhance success of a valid assessment of copper nutritional status in physically active persons (Table 11.2).
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11.5
323
IRON
Iron serves as a component of a number of proteins hemoglobin and myoglobin for
oxygen transport and intracellular oxygen storage, and enzymes required for cellular
energy production. More than 60% of iron in the body is found in hemoglobin in circulating erythrocytes, 25% as a readily mobilizable iron store, and the remaining 15% in
myoglobin of muscle and a variety of iron-containing enzymes (such as cytochromes).
Iron deiciency is one of the most prevalent micronutrient deiciencies in both
industrialized and developing countries.60 It is most common among children and
women during their reproductive years; it may be seen among men as the result of
chronic blood loss associated with parasitic load. Severe iron deiciency is manifest
as anemia with adverse consequences such as impaired immune function, decreased
work capacity, cold intolerance, and compromised learning ability. In contrast, iron
overload, which may be caused by progressive accumulation of iron in tissues (idiopathic hemochromatosis), may contribute to ischemic heart disease and cancer. It
also may be the result of excessive use of iron supplements, injections of therapeutic
iron, or blood transfusions.
11.5.1
METHODS FOR ASSESSMENT OF IRON STATUS
A variety of biochemical measures is available to assess iron status because it ranges
from deiciency states to iron overload in humans. Some common measurements
include hemoglobin, hematocrit, various erythrocyte indices, ferritin, serum iron,
total iron-binding capacity, transferrin, transferrin saturation, soluble transferrin
receptors, free erythrocyte protoporphyrin, and zinc protoporphyrin. These status
indicators vary in their sensitivity and speciicity.
11.5.1.1 Hemoglobin and Hematocrit
Measurement of hemoglobin concentration in whole blood is the most widely used
assessment tool for iron deiciency anemia. As an indicator of iron deiciency, it
is relatively insensitive and exhibits low speciicity. Hemoglobin concentrations
decrease only during the late stages of iron deiciency after tissue iron stores have
been greatly reduced. Moreover, hemoglobin concentration may be affected by other
nutritional perturbations, such as folic acid, copper, and vitamin B12 deiciency, and
other conditions including pregnancy, tobacco smoking, infection, and inlammation, as well as dehydration.61 A common method for measurement of hemoglobin in
blood includes spectrophotometry after anticoagulation with heparin or EDTA and
conversion to cyanomethemoglobin.
Hematocrit or packed erythrocyte volume decreases after erythrocyte production has been reduced. Thus it also is relatively insensitive and nonspeciic because
hematocrit is inluenced by the same factors that affect hemoglobin concentrations,
mainly changes in plasma volume.
11.5.1.2 Ferritin
Serum ferritin concentration is in equilibrium with body stores, and variations in
the quantity of iron in the storage compartment affect serum ferritin concentration.62
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Serum ferritin concentration declines very early in the development of iron deiciency, well in advance of any reductions in hemoglobin or serum iron concentration. Thus serum ferritin may serve as a useful indicator of tissue iron deiciency.
However, certain chronic conditions, including chronic infections, inlammatory
diseases, some malignancies, and liver damage, increase serum ferritin concentrations independently of iron intake. Among healthy women depleted of iron by diet
and phlebotomy, then repleted with iron, serum ferritin was the most sensitive measure of changes in iron status and body iron stores.63 Serum ferritin concentrations
are currently determined by using immunological techniques. Commercial radioimmunoassay and enzyme-linked immunosorbent assay kits are available.
11.5.1.3
Serum Iron, Total Iron-Binding Capacity,
Transferrin, and Transferrin Saturation
Measurement of iron and iron bound to transport proteins in blood provides another
indicator of iron nutritional status. Serum iron and total iron-binding capacity
relect the transit of iron from the reticuloendothelial system to the bone marrow.
Transferrin is the transport protein for iron in blood (serum) and is generally only
one third saturated with iron in normal circumstances. Transferrin may be measured
immunologically, but practically it is determined as total iron-binding capacity. The
most useful measure of iron transport capacity is transferrin saturation, which is
calculated as the ratio of serum iron to total iron-binding capacity. Importantly,
serum iron and iron-binding capacity respond in reciprocal manner during iron
deiciency and overload. A transferrin saturation less than 16% indicates an inadequate iron intake, whereas iron saturation exceeding 55% relects iron overload
and possibly hemochromatosis.64
Serum or plasma iron is measured using chromogens, such as banthophenanthroline sulfonate and ferrozine, and spectrophotometry. The use of AAS to measure
serum or plasma iron is not recommended because AAS will determine the heme
iron released during hemolysis; the colorimetric procedure does not detect heme
iron. Total iron-binding capacity is determined by initially saturating the serum with
excess iron and then adding magnesium carbonate to adsorb and remove excess iron
not bound to transferrin.
11.5.1.4 Soluble Transferrin Receptor
The cell membranes of the developing erythrocyte precursors in bone marrow are
very rich in transferrin receptors to which the iron-transferrin complex binds before
it is internalized to deliver iron in cells. Measurement of transferrin receptor concentration in blood is a useful index of subclinical iron deiciency because the number
of transferrin receptors increases during iron deiciency and decreases during iron
excess.65 Studies in humans show that soluble transferrin receptor concentrations
in blood discriminate tissue iron deiciency better than ferritin concentrations and
are not inluenced by inlammation.66–68 Circulating serum transferrin receptor concentrations decrease only after iron stores are replenished and in advance of other
markers of iron deiciency. Also the ratio of soluble transferrin receptor to ferritin
concentrations is a practical index of iron overload.69 Soluble transferrin receptor
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concentrations can be determined by using commercially available enzyme linked
immunosorbent assay (ELISA); however, care is required to minimize betweenbatch variability.
11.5.1.5 Free Erythrocyte Protoporphyrin and Zinc Protoporphyrin
The concentrations of these proteins have been found to be sensitive indicators of
iron-deicient erythrocyte production.70 Changes in free erythrocyte protoporphyrin
or zinc protoporphyrin are relatively insensitive to acute changes in iron status due to
the slow turnover rate of erythrocytes, 90 to 120 days. Free erythrocyte protoporphyrin and zinc protoporphyrin concentrations are measured spectrophotometrically.
11.5.1.6 Iron Reference Intervals and Data from Athletes
Serum iron concentrations range from 65 to 165 µg/dL or 11.6 to 31.3 μmol/L in men
and 50 to 170 µg/dL or 9.0 to 30.4 μmol/L in women.17 Total serum iron-binding
capacity in healthy adults ranges from 250 to 425 µg/dL or 44.8 to 76.1 μmol/L.
Serum ferritin concentrations range from 20 to 250 µg/L in men and 10 to 120 μg/L
in women. Ferritin concentrations less than 10 µg/L indicate depleted iron stores,
whereas concentrations greater than 300 mcg/L suggest iron overload.
Iron status in athletes and physically active persons has been summarized in several reviews.71,72 Iron deiciency anemia, deined as hemoglobin concentrations less
than 110 and 120 g/L in women and men, respectively, has been reported in physically active persons.73 This severe iron deiciency is associated with reduced aerobic capacity in athletes and decreased work productivity in agricultural laborers. In
some studies, the anemia is present in all of the subjects.74 Generally anemia is present in a small percentage (~2%) of athletes examined.75–78 More common (25–50%)
is subclinical iron deiciency, characterized by decreased iron stores and increased
iron-binding capacity without anemia. Since the initial inding that depleted body
iron stores adversely affect work metabolism,79 there has been increased awareness
that subclinical iron deiciency is associated with impaired endurance and muscle
function. Studies of adolescent girls with decreased serum ferritin and normal hemoglobin concentrations experienced decreases in training and impaired endurance.80,81
Medical treatment with iron supplementation (100 mg/d) improved training duration
and endurance performance.
Despite these positive indings, experimental data do not reveal a consensus on
the effects of iron supplementation on performance of adults with subclinical iron
deiciency deined as low ferritin (< 12 µg/L) or increased soluble transferrin receptor
concentration (> 8.5 mg/L). Women supplemented with iron (100 mg/d for 8 weeks)
signiicantly increased peak oxygen uptake and endurance and decreased blood lactate with signiicant increases in ferritin (22.5 vs. 14.3 µg/L) and hemoglobin (141
vs. 128 g/L) compared to placebo-treated subjects.82 Other supplementation trials of
iron-deicient adults, however, only report signiicant increases in ferritin or soluble
transferrin receptor concentrations without improvements in peak work capacity
but signiicant reductions in lactate or increased endurance.79,83 One key factor that
could explain these divergent indings is the confounding effect of inlammation that
sequesters iron and reduces circulating ferritin levels.66,67
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Accumulating evidence reveals the beneicial effects of iron supplementation on
performance of adults with subclinical iron deiciency. Women with subclinical iron
deiciency supplemented with iron (8 mg/d for 6 wk) and trained on cycle ergometers
signiicantly increased serum ferritin (10.4 ± 0.82 to 14.52 ± 1.5 µg/L) and decreased
soluble transferrin receptor (7.92 ± 0.87 to 6.78 ± 0.42 mg/L) concentrations without a change in hemoglobin compared to placebo-treated controls (8.07 ± 0.77 to
8.11 ± 0.90 µg/L and 7.94 ± 0.73 to 7.93 ± 0.77 mg/L, respectively).84 Although both
iron-supplemented and placebo-treated women reduced 15-km time trial times, the
improved endurance was signiicant only in the women supplemented with iron. A
follow-up study showed that the iron-supplemented women with initial subclinical
iron deiciency completed a simulated 15 km time trial is signiicantly less time,
consistent with the previous observation, and exercised a signiicantly higher work
rate with a lower percent of aerobic capacity than the placebo-treated women.85
Similarly, iron supplementation (10 mg/d for 8 weeks) of female soldiers engaged in
military training signiicantly attenuated the decline in iron status (that is, decreased
ferritin and increased soluble transferrin receptor concentrations) and was associated
with improved endurance and mood compared to placebo-treated female controls.86
Among women with subclinical iron deiciency, iron supplementation (10 mg/d for
6 weeks) maintained soluble transferrin receptor concentrations and signiicantly
increased progressive fatigue resistance during dynamic knee extensor exercise
(such as muscle force at voluntary fatigue) to exhaustion compared to unsupplemented women whose soluble transferrin receptor concentrations increased signiicantly.87 In these studies, soluble transferrin receptor concentrations in serum were
a discriminating indicator of subclinical iron deiciency and physical performance
(Table 11.2).
11.6
MAGNESIUM
Magnesium is an intracellular cation; it is required in a wide variety of fundamental cellular processes that support diverse physiological functions.4,88 Magnesium is
involved in more than 300 enzymatic reactions in which food is metabolized and
new products are formed. Some of these reactions are involved in glycolysis, fat
and protein metabolism, hydrolysis of adenosine triphosphate (ATP), and second
messenger system and signal transduction. Magnesium also regulates membrane stability and neuromuscular, cardiovascular, immune, and hormonal functions. Thus
magnesium may be a limiting factor in physical performance.89
11.6.1
METHODS FOR ASSESSMENT OF MAGNESIUM STATUS
Evaluation of human magnesium status is challenging; there is no simple, rapid,
and accurate laboratory test to indicate subclinical magnesium status.88 A number of
approaches have been used to assess magnesium status, including determination of
circulating magnesium, measurement of cellular magnesium content, and indirect
assessment of body magnesium stores.
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11.6.1.1 Serum and Plasma Magnesium
Serum magnesium is the most commonly used indicator of magnesium status.
Although a practical tool, serum or plasma magnesium is only an index of the
presence or absence of severe magnesium deiciency. Low magnesium concentration or hypomagnesemia reliably indicates magnesium deiciency; however, its
absence does not exclude signiicant magnesium depletion. The concentration of
magnesium in serum has not been shown to be correlated with the concentration
of magnesium in any other tissue pools except interstitial luid, a component of the
extracellular luid.90
Serum, rather than plasma, is preferred because anticoagulants may be contaminated with magnesium or affect the assay procedure. It is critical to avoid hemolysis because the magnesium concentration of erythrocytes is three times as great as
serum. Magnesium concentration in serum is determined directly by lame AAS
after diluting ifty-fold with a lanthanum chloride or oxide diluent.
11.6.1.2 Ionized Magnesium
Magnesium in serum exists in several forms at physiological pH: protein-bound
(19–34% of total), free magnesium ion (61–67% of the total), and complexed to certain anions (5–14% of the total).91 The free or ionized magnesium is considered to
be the physiologically active form, but it also is not adequate to detect subclinical
magnesium deiciency.92 Ionized magnesium is measured in serum with ion-speciic
electrodes. Magnetic resonance spectroscopy provides the unique opportunity to
measure intracellular magnesium in tissues in vivo at rest and during exercise93; however, this novel technology is restricted to a few research laboratories.
11.6.1.3 Muscle Magnesium
More than 26% of magnesium is localized in muscle. Knowledge of the fundamental biological roles of magnesium in metabolism suggests that muscle is an appropriate tissue to sample in healthy and ill persons to assess magnesium nutriture.
Percutaneous skeletal muscle biopsy has been used to assess magnesium status in
humans.93,94 However, because this is an invasive procedure and requires special
skills and equipment, it has not been widely used.
11.6.1.4 Blood Cells
The mononucleated white blood cell has been proposed as a possible indicator of
cellular magnesium status. Indeed, several studies reported a signiicant correlation
between the magnesium concentration of the mononucleated cells and skeletal muscle magnesium but not serum magnesium.92,93
Erythrocyte magnesium concentration has been associated with hypertension,
chronic fatigue syndrome, and premenstrual syndrome,92 but its value as an indicator
of cellular magnesium content has only recently been examined. Among women fed
controlled diets containing adequate, low, and supplemental magnesium (322, ~140,
and 360 mg/d), erythrocyte magnesium decreased signiicantly (6.8 to 5.8 µmol/g
hemoglobin) and then increased (6.6 µmol/g hemoglobin), in contrast to serum magnesium that only decreased from 0.85 to 0.81 mmol/L with restricted magnesium
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intake.94 Importantly, the changes in erythrocyte magnesium paralleled the signiicant reductions in skeletal muscle magnesium with low magnesium intakes and the
signiicant increases in response to supplemental magnesium (52, 48, and 54 mmol/
kg dry weight, respectively). Thus erythrocyte magnesium concentrations are a practical alternative for assessing muscle magnesium.
11.6.1.5 Magnesium Load Test
Oral and intravenous magnesium loading tests have been described and perhaps are
more widely used as a diagnostic tool of body depletion of magnesium than measures of intracellular magnesium.88 Persons with adequate magnesium in body pools
generally excrete the vast majority (75 to 100%) of the administered dose within
24 to 48 hours, compared to persons with depleted magnesium pools who retain a
signiicant proportion of the dose. Sensitivity of the response as well as the need for
normal kidney function and the lack of any disturbances in myocardial conductivity
hamper the application of this test.
11.6.1.6 Magnesium Reference Intervals and Data from Athletes
Total magnesium concentrations, as determined by AAS, range from 1.6 to 2.6 mg/
dL or 0.66 to 1.07 mmol/L.17 There is no apparent diurnal variation in total serum
magnesium concentration.
Impetus for the measurement of magnesium status of physically active persons
began with a report of hypomagnesemia (plasma magnesium < 0.60 mmol/L) associated with muscle spasms in a competitive tennis player.95 Surveys of adult athletes
participating in a variety of sports indicate values of plasma or serum magnesium in
the range of normal values.56,96–101 Similarly, children participating in swim training
had normal values for plasma magnesium concentrations.102 Intense, anaerobic training transiently decreases plasma magnesium concentration with a parallel increase
in urinary magnesium excretion.103,104 Routine assessment of erythrocyte magnesium
concentration is recommended because it relects decreased cellular magnesium status and its adverse impact on muscle function (Table 11.2).
11.7
PHOSPHORUS
Phosphorus in the form of inorganic or organic phosphate is the second most abundant mineral in the body. More than 85% of the phosphorus in the adult is present
in the skeleton as either hydroxyapatite or as calcium phosphate. The remainder is
in cells of the soft tissues (14%) and the extracellular luid (1%); it is present as
inorganic phosphate or in nucleic acids, phosphoproteins, phospholipids, and highenergy compounds including phosphocreatine (CP) and adenosine mono-, di-, and
triphosphates (AMP, ADP, and ATP). Phosphorous is an essential factor in most
energy-producing reactions of cells.4
Phosphorus depletion results in low intracellular concentrations of phosphoglycerate, ATP, and CP that impair muscle function, work capacity, and overall cardiorespiratory function. Impaired phosphorus status is associated with long-term total
parenteral nutrition, metabolic perturbations resulting in ketoacidosis, and excessive
use of antacids containing aluminum hydroxide or aluminum carbonate.
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329
METHODS FOR ASSESSMENT OF PHOSPHORUS STATUS
Serum phosphorus, measured as phosphate, is used most frequently to assess phosphorus status (Table 11.2). Phosphate in serum exists both as the monovalent and divalent
anion. The ratio of H2PO4–1 to HPO4–2 varies from 1:1 in acidosis to 1:4 at physiological
pH and 1:9 in alkalosis. Approximately 55% of the phosphate in serum is free; 35% is
complexed with sodium, calcium, and magnesium; and 10% is bound to protein.
Serum phosphorus concentrations are generally measured colorimetrically.105 It
is critical to separate blood cells from the serum as soon as possible because high
concentrations of organic phosphate esters in cells may be hydrolyzed to inorganic
phosphate during storage.
11.7.1.1
Phosphorus Reference Intervals and Data from
Phosphate Supplementation Trials
Age affects the range of normal values of serum phosphorus. Values are higher in
infancy and then decline throughout childhood until adulthood concentrations are
reached. Serum phosphate, expressed as phosphorus, ranges from 4.0 to 7.0 mg / dL
or 1.29 to 2.26 mmol/L in children, and from 2.5 to 4.5 mg/dL or 0.81 to 1.45 mmol/L
in healthy adults. Serum phosphate concentrations are dependent on timing of food
and luid intake and are sensitive to changes in hormone status, particularly parathyroid hormone.
The effects of phosphate loading on exercise performance have been labeled
as both inconsistent106 and equivocal.107 This conclusion was drawn from about a
dozen studies conducted with phosphate supplementation and its effect on physical performance, and the results were clearly ambiguous. However, no study had
reported decreases in performance, and ive studies from independent laboratories
have now shown remarkable similarities relative to increased levels of VO2max following phosphate supplementation and improved performance on bicycle ergometer
exercise tests such as a simulated 40-km cycle time trial.108–112 Serum phosphate
has been used to evaluate the effects of phosphate supplements on compliance and
physical performance.106,113 Phosphate loading increases both plasma and erythrocyte phosphate pools and the rise in erythrocyte 2,3-bisphosphoglycerate levels
(2,3-BPG) is probably a consequence of the rise in cellular inorganic phosphate concentration [Pi].114 As compared to placebo, ingestion of 1 g of tribasic sodium phosphate for 4 days signiicantly increased basal serum phosphate concentration from
0.95 ± 0.17 to 1.11 ± 0.32 mmol/L in six male endurance athletes.112 However, at peak
exercise, there was no difference in serum phosphate concentrations (1.50 ± 0.19 vs.
1.48 ± 0.21 mmol/L). Interestingly, most studies report greater increases in serum
phosphate after a bout of acute exercise than after ingestion of phosphate-containing
supplements.106 Finally, Goss et al. recently reported that although phosphate supplementation did not affect physiological responses during exercise at about 70–80% of
VO2max, the rating of perceived exertion (RPE) was lower, suggesting a beneicial
psychological effect.115
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11.8
Nutritional Assessment of Athletes, Second Edition
ZINC
The vital role of zinc for optimal growth and well-being of animals and plants
emphasizes its biological importance. Zinc is required for the activity of more than
300 metalloenzymes participating in essentially all aspects of metabolism. These
zinc-containing enzymes include RNA and DNA polymerase, carboxypeptidase,
carbonic anhydrase, and alcohol dehydrogenase.116 Zinc also plays a regulatory role
in gene expression by affecting gene structure and enzymatic activity.116
Zinc deiciency occurs at various stages with different signs. Severe deiciency presents with alopecia, weight loss, clinical behavioral and neurophysiological disorders,
and ultimately death, if untreated. Moderate deiciency is characterized by growth
retardation, mild dermatitis, impaired cognition, poor appetite, impaired immune
function, and abnormal light-to-dark visual adaptation. In contrast, signs of subclinical zinc deiciency generally require a stressor for presentation and may include
impaired cognitive function, altered behavior, and low resistance to infection.
11.8.1
METHODS FOR ASSESSMENT OF ZINC STATUS
Laboratory assessment of zinc status includes measurement of zinc in a body luid
and determination of the activity of a speciic zinc-dependent enzyme. Although
practical, the determination of the zinc concentration of plasma or serum is not a reliable indicator of subclinical zinc status of an individual.117 Functional assessments
of the activity of zinc-containing enzymes (for example, 5-nucleotidase in plasma),
metallothionein mRNA in monocytes and erythrocytes, certain zinc transporters
in blood cells, and responses to controlled stressors such as exercise and ethanol
administration are promising indicators of subclinical zinc status of humans.118 No
single test has been proven to be a deinitive indicator of zinc status.119
11.8.1.1 Plasma and Serum Zinc
Although the zinc concentration in plasma or serum often has been interpreted
to indicate human zinc deiciency, it does not relect whole-body zinc status.117, 118
Concurrent conditions that decrease plasma zinc concentration without causing zinc
depletion including nonfasting conditions, infection, inlammation, steroid use, pregnancy, low serum albumin associated with liver disease, and malnutrition.117
The most practical and reliable analytical method to determine plasma or serum
zinc is AAS. The recommended approach is to use a ivefold dilution of plasma
or serum and standards with 5% glycerol matrix with AAS.120 Measurement of
plasma or serum zinc by inductively coupled plasma–optical emission spectroscopy
(ICP-OES)121 enables improved sensitivity with smaller volumes than AAS and is
restricted to a few research laboratories. Hemolysis must be avoided during sample
collection and preparation to avoid aberrant zinc values because erythrocytes contain greater than ten times more zinc than plasma.
11.8.1.2 Zinc-Containing Enzymes
Several zinc-containing enzymes, such as alkaline phosphatase, carbonic anhydrase,
nucleoside phosphorylase, and ribonuclease, are useful indicators of zinc adequacy.
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Decreased alkaline phosphatase activity in either serum or neutrophils has been
shown in a number of human zinc-deicient conditions. Zinc-deicient patients
supplemented with zinc also increased alkaline phosphatase activity in response to
zinc supplementation. Similarly, carbonic anhydrase and nucleoside phosphorylase
activities increased in sickle anemia patients treated with zinc. Importantly, these
positive responses in enzyme activity occurred in subjects with severe, not subclinical, zinc deiciency.
11.8.1.3 Zinc Reference Intervals and Data from Athletes
The accepted reference interval for zinc in plasma is 70 to 150 µg/dL or 10.7 to 22.9
μmol/L. Serum zinc concentrations are generally 5 to 15% higher than plasma values
because of osmotic shifts of luid into the extracellular luid when various anticoagulants are used. Because of diurnal variation and signiicant effects of recent food
ingestion, a fasting morning blood sample is recommended for routine assessment
of human zinc status.
Because of the potential of subclinical zinc deiciency to adversely affect all
aspects of metabolism, there has been an effort to assess zinc status in many groups
of athletes. Twenty-ive percent of 76 experienced marathon runners had serum zinc
concentration less than 11.5 μmol/L.122 In a survey of elite German athletes, 25%
of the men and women were characterized as hypozincemic deined as serum zinc
concentrations less than 12.0 μmol/L.123 Among male participants in a 500-km road
race, prerace serum concentrations were markedly depressed, with the majority of
the values less than 11 μmol/L.124 A similar pattern of low plasma zinc concentrations was found in elite female endurance runners.125 Other studies did not identify
low zinc concentrations in runners,31,59,98 swimmers,59,101 skiers,127 and volleyball
players.128 However, some longitudinal studies of athletes did not report signiicant
decreases in serum zinc during intensive training.126,128
Low serum zinc concentrations have been associated with decreased muscle
strength and diminished exercise capacity.129 Adolescent gymnasts, screened for
delayed pubertal maturation and growth, had serum zinc concentrations signiicantly
less than age-matched nontraining adolescents (9.2 ± 0.4 vs. 12.4 ± 0.2 μmol/L).130
Among the 21 gymnasts, the 12 girls had lower serum zinc than the 9 boys (8.5 ± 0.3
vs. 10.1 ± 0.6 μmol/L). Serum zinc concentrations were signiicantly correlated
(r = 0.465) with isometric adductor strength. Similarly, a screening of 21 male soccer players revealed that 9 had low serum zinc concentrations (8.3 ± 0.2 μmol/L) and
12 had normal serum zinc (11.3 ± 0.2 μmol/L).131 The hypozincemic men had signiicantly decreased peak power output and a lower lactate threshold. Thus serum or
plasma zinc concentration, speciically hypozincemia, may be a speciic indicator of
impaired physiological function associated with either inadequate (low) zinc intake
and/or excessive zinc losses (Table 11.2).
11.9
INFLAMMATION AND MINERAL STATUS
Heavy and prolonged exercise can cause an acute phase response.132 This response is
characterized by secretion of many diverse immunological proteins such as C-reactive
protein, ferritin and cytokines including interleukin-6 (IL-6).133 The net effect of this
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inlammatory action is to sequester trace elements that have been released into the
circulation because of exercise-induced breakdown of erythrocytes, muscle damage,
or mobilized from storage depots in the liver. Increased production of IL-6 induces
expression of hepcidin in the liver134,135 and the uptake of iron into macrophages.
Thus, exercise-induced inlammation alters blood biochemical markers of iron status
by increasing ferritin and decreasing iron concentrations in blood.136
Exercise also affects zinc status. Metallothionein is a ubiquitous, zinc-binding
intracellular protein. Its expression is up-regulated by oxidative and inlammatory
stressors, such as strenuous exercise.137,138 Metallothionein also serves as a potent
antioxidant during strenuous exercise.139,140 Increases in tissue metallothionein result
in decreases in circulating zinc concentrations.137
These indings demonstrate that inlammatory stressors, such as exercise, affect
traditional blood biochemical measures of iron and zinc nutritional status independently of intake. Importantly, they indicate the need to standardize the timing of
blood sampling to control for the moderating effects of physical training.
11.10
FUTURE RESEARCH NEEDS
There is increasing evidence that many mineral elements regulate key biological
activities required to develop and maintain human physical work capacity, sustain
training, and optimize performance (Figure 11.1). One factor confounding research
on the interaction of mineral intake and physiological function has been the lack of
appreciation of the need for standardization of collection practices (such as fasting
and before physical activity). Appropriate guidelines are available to minimize contamination during phlebotomy and processing of blood samples. Development and
implementation of contemporary analytical methods are needed to minimize blood
volumes that will facilitate future research and regular nutritional monitoring. There
Inadequate
Intake
Sub-Clinical
Deficiency
Calcium
Chromium
Copper
Iron
Magnesium
Phosphorus
Zinc
Decreased
Bone density
Endurance
Time to fatigue
Work efficiency
Antioxidant protection
Work capacity
Strength
Diminished
Training
Recovery
Performance
Increased
Losses
FIGURE 11.1 Summary of factors contributing to sub-clinical mineral element deiciencies
and functional impairments leading to diminished capacity for physical performance.
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also is a critical need to incorporate multiple markers, rather than reliance on a single
marker, to identify subclinical deiciency because moderate nutrient deprivation can
adversely affect several metabolic functions.
The most pressing issues center on the identiication of valid and sensitive markers of subclinical deiciency of certain mineral elements. Although calcium plays
pervasive roles in muscle function, assessments only focus on the calcium reserve
in bone. Reliable indicators of magnesium and phosphorus status also are needed.
Measures of cellular contents such as sublingual epithelial cells for magnesium and
noninvasive determinations of phosphorylated energy intermediates (ADP/ATP, etc.)
in skeletal muscle are opportunities to explore. Practical analytical and sophisticated
instrumentation are available to meet this challenge. Assessment of chromium status
requires a novel biochemical indicator that relects tissue levels of chromium and
cellular function. Although some measures of copper (superoxide dismutase activity)
and zinc (serum/plasma zinc) have been found in some cases to discriminate physiological impairments, consensus is lacking. Utilization of advanced molecular and
cell biology approaches that focus on measurements of gene expression (for example, protein and mRNA levels) should be encouraged in addressing the imminent
need for reliable and sensitive indicators of subclinical mineral element deiciency in
physically active people.
11.11
CONCLUSIONS
There is increasing evidence that many of the trace and macro elements have important roles in facilitating biochemical and physiological functions operational in the
development and maintenance of physical work capacity and performance. One
factor restricting further research on the interaction of mineral intake and physical
activity has been the availability of valid indicators of subclinical mineral nutritional
status. Recent indings indicate that two markers of magnesium and iron status merit
incorporation in the biochemical assessment of mineral nutriture. Red blood cell
magnesium is a surrogate marker for skeletal muscle magnesium and soluble serum
transferrin receptor concentration is a biomarker of tissue iron depletion. Each of these
nutritional markers is linked to perturbations in energy metabolism and impairments
in work capacity and endurance. Although plasma zinc concentration is inversely
related to muscle strength and endurance, its validity as a precise marker of zinc
status remains controversial. The lack of acceptable indicators of calcium, copper,
phosphorus, and chromium status hinders research to ascertain whether restricted
or supplemental intakes affect biological processes (such as antioxidant protection,
muscle function, and energy production) in response to physical training.
NOTE
The opinions or assertions contained herein are the private views of the authors
and are not to be construed as oficial or as relecting the views of the Army or the
Department of Defense.
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136. Peeling, P., Dawson, B., Goodman, C., Landers, G., and Trinder, D., Athletic induced
iron deiciency: New insights into the role of inlammation, cytokines and hormones.
Eur. J. Appl. Physiol. 103, 381–91, 2008.
137. Oh, S.H., Deagen, J.T., Whanger, P.D., and Weswig, P.H., Biological function of
metallothionein. Part 5. Its induction in rats by various stresses, Am. J. Physiol. 234,
E282–E285, 1978.
138. Penkowa, M., Keller, P., Keller, C., Hidalgo, J., Giralt, M., and Pedersen, B.K., Exerciseinduced metallothionein expression in human skeletal muscle ibres, Exp. Physiol. 90,
477–86, 2005.
139. Ji, L.L., Antioxidants and oxidative stress in exercise, Proc. Soc. Exp. Biol. Med. 222,
283–92, 1999.
140. Viarengo, A., Burlando, B., Ceratto, N., and Panfoli, I., Antioxidant role of metallothioneins: A comparative overview, Cell Mol. Biol. 46, 407–17, 2000.
© 2011 by Taylor and Francis Group, LLC
of
12 Assessment
Hydration of Athletes
Fiona E. Pelly, Gary J. Slater, and Tanya M. King
CONTENTS
12.1
12.2
Introduction ................................................................................................ 341
Impact of Hypohydration ........................................................................... 342
12.2.1 The Effects of Hypohydration on Thermoregulatory and
Cardiovascular Function .............................................................. 342
12.2.2 The Effect of Hypohydration on Exercise Performance .............. 343
12.2.3 Hydration and Health ...................................................................344
12.2.4 Current Drinking Practices of Athletes ....................................... 345
12.3 Assessment of Hydration Status ................................................................. 345
12.3.1 Body Mass Changes.....................................................................348
12.3.2 Urinary Indices ............................................................................ 349
12.3.2.1 Urine Speciic Gravity ................................................ 349
12.3.2.2 Urine Osmolality ........................................................ 350
12.3.2.3 Urine Color ................................................................. 350
12.3.2.4 Urine Volume.............................................................. 351
12.3.2.5 Interpretation of Urinary Indices................................ 351
12.3.3 Hematological Indices ................................................................. 352
12.3.4 Salivary Parameters ..................................................................... 353
12.3.5 Total Body Water Assessment ..................................................... 353
12.4 Assessment of Sweat Rate and Composition ............................................. 354
12.4.1 Sweat Rate Assessment ................................................................ 354
12.4.2 Sweat Composition Assessment................................................... 358
12.5 Recommendations for Fluid Intake ............................................................ 359
12.5.1 Pre-Exercise Hydration ................................................................360
12.5.2 Fluid Replacement during Exercise .............................................360
12.5.3 Postexercise Fluid Replacement................................................... 362
12.6 Conclusions and Future Directions ............................................................364
12.7 Practical Recommendations ....................................................................... 365
References .............................................................................................................. 366
12.1
INTRODUCTION
Exercise associated with an increase in metabolic rate results in a subsequent rise in
body temperature. Increases in skin blood low and sweat production occur in response
341
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Nutritional Assessment of Athletes, Second Edition
to elevated body temperature as a means of dissipating heat. Sweat losses during vigorous exercise, particularly in warm to hot conditions, can be signiicant. If not adequately
replaced, loss of body water (dehydration) can reduce exercise performance, decrease
time to exhaustion, and increase heat storage.1 A loss of 2% or greater of body mass can
adversely affect exercise performance in both temperate and hot environments, particularly when the exercise duration is greater than 90 minutes.2 With a loss of 3–5% of body
weight, sweat production and skin blood low decline, which can subsequently compromise physiological function (stroke volume, cardiac output, core temperature, and heart
rate).3 This can lead to exertional heat illness, which ultimately can be fatal.4,5
There is increasing evidence that water and electrolyte losses during exercise vary
greatly between individuals.6 Consequently the American College of Sports Medicine
position stand for luid and electrolyte replacement recommends that hydration strategies should be prescribed on an individual basis.7 Hydration testing is an essential tool
in the development of individual luid intake guidelines, allowing the measurement of
individual sweat rates and the adequacy of luid and electrolyte replacement strategies.
Common techniques used to monitor hydration status include body mass changes, urinary and hematological indices, salivary parameters, and total body water assessment.
There is currently no gold-standard hydration assessment tool. Each method has both
advantages and disadvantages relating to precision, accuracy, technical requirements,
safety, cost, and convenience. Each of these factors should be taken into consideration
when selecting the most appropriate tool for testing the hydration status of the athlete.
This chapter provides an overview of the impact of hypohydration, the various methods for assessing hydration status, factors that have an impact on rehydration, and current luid intake guidelines. The chapter highlights the advantages and disadvantages
of each hydration assessment technique and provides a guide for selecting the most
appropriate tool for the individual athlete and the testing environment. Finally, there
are practical recommendations in regard to application of the assessment techniques.
Throughout this chapter, the term “euhydration” refers to a state of luid balance
or normal body water content, that is, an adequate luid intake to sustain normal
urinary volume and concentration and relative stability of total body water (TBW),
extracellular water, and intracellular water. “Hypohydration” and “hyperhydration”
are deined as body water content deicits and excesses beyond normal luctuations,
while “dehydration” refers to the loss of body water as part of the process of becoming dehydrated. “Rehydration” is deined as the process of regaining body luids
from a dehydrated state toward euhydration.
12.2
12.2.1
IMPACT OF HYPOHYDRATION
THE EFFECTS OF HYPOHYDRATION ON THERMOREGULATORY
AND CARDIOVASCULAR FUNCTION
Hypohydration occurs more rapidly in hot environments and during prolonged
exercise.1 Hypohydration reduces skin blood low and sweating responses during
exercise.8 Water lost through sweating originates from the intracellular (ICF) and
extracellular luid (ECF) compartments, and causes a reduction in plasma volume
(hypovolemia).9–12 Reduced plasma volume can increase cardiovascular strain as
© 2011 by Taylor and Francis Group, LLC
Assessment of Hydration of Athletes
343
indicated by a reduced stroke volume and a consequent elevation in heart rate during
exercise.11,13 This compromises the ability to dissipate heat from contracting muscles
to the skin surface, thereby causing body temperature to rise, and increases the rate
of body heat storage. At high ambient temperatures, evaporation of luid from the
respiratory tract and sweat from the skin surface provide the only means by which
heat can be lost from the body.14 However, if the relative humidity is high, sweating
contributes little to evaporative heat loss because high vapor pressure impairs evaporative cooling. Despite the relative ineficiency of sweating under these conditions,
sweat formation continues, and the risk of heat injury increases.15
As dehydration progresses, there are negative effects on heart rate,11,16–18 stroke
volume,11,13,19 cardiac output,11,13 fatigue,20 skin blood low,21 plasma volume,9,13,22
and rate of perceived exertion.17,23 The type of exercise can also contribute to the
thermoregulatory response. Sporting activities with variable exercise intensities (that
is, intermittent high-intensity exercise with short recovery bouts) have been shown
to increase thermoregulatory (body temperature), cardiovascular (heart rate), and
metabolic (lactate) stresses24 when compared to steady-state exercise.
12.2.2
THE EFFECT OF HYPOHYDRATION ON EXERCISE PERFORMANCE
It is well known that even small body luid deicits incurred before or during exercise
can compromise performance16,23,25 well before they negatively affect health. The
greater the body water deicit, the greater the physiological strain.13 Fluid losses in
excess of 2% of body mass have been shown to have a substantial impact on physical and cognitive performance in a variety of climatic conditions.2,25,26 However,
the critical level of luid deicit that may have physical and cognitive performance
implications varies from 1% to 10% of body mass loss.6 The magnitude of the performance deicit may vary according to variations in how performance is measured,
environmental conditions, type of exercise, and individual characteristics such as
differences in sweat rates and sweat composition.6 Nevertheless, it is widely known
that the performance implications of hypohydration are exacerbated when undertaking prolonged exercise in the heat.27 Physiological factors that impair exercise
performance include increased core temperature, increased cardiovascular strain,
increased glycogen utilization, and possibly altered central nervous system function.3 Impairment of physiological function and exercise performance caused by
dehydration appear to be much greater when the luid deicit is induced prior to25
rather than during exercise.23
Cognitive/mental performance such as complex skill execution and coordination
as required in team sports have also been shown to be impaired by mild dehydration.17,28,29 Evidence suggests that luid ingestion during exercise helps to attenuate
the rise in heart rate and core temperature,16 delay the onset of fatigue,20 prevent the
deterioration of sport-speciic skills,17 and ultimately increase time to exhaustion.23
The means by which the body luid loss occurs also determines the adverse effects
experienced. For example, diuretic-induced dehydration results in a greater ratio of
plasma volume loss to total body water loss compared with sweating.30 However,
exercise performance is not always impaired.31 Similarly, heat-induced dehydration
results in a greater plasma volume reduction for a given body water deicit than
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Nutritional Assessment of Athletes, Second Edition
exercise-induced dehydration.32 It appears that there is a highly individual response
as some athletes appear to tolerate hot conditions and dehydration, while others have
to discontinue exercise.1
It should be noted that while athletes might tolerate moderate luid deicits in
cool environments without signiicant impairment to exercise performance,33 hypohydration is associated with serious health and physiological consequences and all
attempts should be made to maintain physiological capacity.
12.2.3 HYDRATION AND HEALTH
Dehydration increases the risk of exertional heat illnesses such as heat cramps,
heat exhaustion, and heat stroke that occur as a result of a signiicant rise in body
temperature accompanying intense exercise. Predisposing factors leading to heat
exhaustion and heat stroke include lack of heat acclimatization, inadequate training, medications, genetic predisposition, and viral illnesses that can potentially be
fatal.34 Athletes are at increased risk of developing exertional heat illnesses,35 and
in extreme cases rhabdomyolysis, a potentially life-threatening condition resulting
from the breakdown of muscle ibers and the leakage of their contents into the circulation when exercising in a hypohydrated state.36,37 Hypohydration in combination
with rhabdomyolysis (deined as serum creatine kinase greater than ten times normal) also appears to increase the risk of acute renal failure.1
There may also be a relationship between exercise associated muscle cramps and
high losses of both luid and sodium, particularly in susceptible individuals who
undertake prolonged strenuous exercise in the heat.38,39 Furthermore, hypohydration
has been associated with reduced blood low to the brain,40 and altered intracranial
volume.41
Conversely, overdrinking (drinking luid volumes in excess of sweat losses) can
result in exercise-associated hyponatremia, a condition characterized by low blood
sodium concentrations. Plasma sodium levels below 125 mmol.L –1 increase the risk
of dilutional encephalopathy and pulmonary edema and result in symptoms of headache, vomiting, swollen hands and feet, fatigue, confusion, and disorientation, while
plasma sodium levels below 120 mmol.L –1 can be fatal.42 This has been shown to
occur most commonly in smaller, nonelite individuals who run slowly, have lower
sweat rates, and overdrink in competitive endurance events42 but has also been evident in sports where athletes are trying to prevent heat cramps and as a result drink
excessive amounts of hypotonic luids or water.42,43 To prevent hyponatremia occurring, Noakes44 argues that athletes should drink according to thirst and not according
to prescribed guidelines. An alternative strategy is to individualize recommendations
on luid intake based on sweat rate calculations (Section 12.4). Female athletes also
appear to be more at risk of hyponatremia as they typically have lower sweat rates.45
Age and gender differences also play a role on the impact of hypohydration on
health. Females have lower sweat and electrolyte losses, while older adults have
decreased thirst sensitivity and are slower to restore body luid homeostasis due to
reduced renal responses.46 Children have lower sweat rates (less than 400 mL.h–1)
due to a smaller body surface area and faster rise in core temperature than adults.47
© 2011 by Taylor and Francis Group, LLC
Assessment of Hydration of Athletes
12.2.4
345
CURRENT DRINKING PRACTICES OF ATHLETES
Although thirst is a suficient stimulus for luid intake under resting conditions,48
athletes’ drinking patterns are inluenced by other factors such as habitual or social
behaviors and recommended guidelines rather than physiological need.35,49,50 During
exercise, however, dehydration usually occurs before luid is consumed, demonstrating the inadequacy of thirst to stimulate suficient drinking when luid losses are
high.48,51 This delay in voluntary luid intake with the initiation of exercise has been
termed “involuntary dehydration.”48 As a result, most athletes can expect to complete
an exercise session with a mild to moderate degree of dehydration.
Athletes exposed to warm weather environments or hot/humid conditions can
lose in excess of 3 L of sweat per hour, and can range from 0.5–2.0 L.hr–17 and at
best, replace only 30–70% of these losses.52–54 Euhydration can only be maintained
during exercise if the rate of luid ingestion and absorption equals the rate of luid
loss. Accordingly, some degree of hypohydration is likely during exercise because
maximal sweat rates often exceed potential gastric emptying rates (greater than
1000 mL.h–1).53,55,56 Although a reduction in body mass may appear to be of beneit
in sports where power-to-weight ratio is important, there is evidence that modest
dehydration does not provide an advantage of a reduced metabolic cost. Ebert and
colleagues57 demonstrated that uphill cycling performance in the heat was signiicantly compromised in athletes when hypohydrated by approximately 2 kg.
In many sports, particularly team sports, the opportunity to ingest luids may be
limited by the rules of competition, the number of breaks or substitutions in play, and
luid availability.53,58 For this reason, strategies such as pre-exercise hyperhydration
may be warranted (see Section 12.5.1).
Many athletes start exercise hypohydrated due to attempts to make weight or
inadequate time to fully rehydrate between sessions.7 Studies reporting the hydration status of athletes prior to elite-level competition have shown that hypohydration is prevalent among competitors.59 Within weight-category sports, this scenario
may be even more exacerbated where athletes may be “habitually hypohydrated” to
assist with body mass management.60 Despite acknowledgment of the importance of
adequate rehydration strategies, many athletes fail to adhere to current sports nutrition guidelines for luid replacement.37,53,60 Maintaining hydration status is a major
challenge to the athlete, and particular efforts should be made to limit dehydration
and the potential impairment to physiological function and health.
12.3
ASSESSMENT OF HYDRATION STATUS
An awareness of the performance implications of a compromise in hydration status
has led to the pursuit of identifying tools that can be used to assess hydration status.
Body mass changes,61 bioelectrical impedance analysis and dilution techniques,62
hematological indices (plasma osmolality, sodium, chloride, potassium, total plasma
protein, blood-urea nitrogen, hematocrit, hemoglobin,63 aldosterone,64 and arginine
vasopressin concentrations62), urinary indices (osmolality, speciic gravity, color,
volume, sodium,65 and conductivity66,67), and salivary parameters (osmolality, total
protein concentration, and low rate)68,69 have all been trialed to assess hydration
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Nutritional Assessment of Athletes, Second Edition
status. A summary of the most common techniques available to assess hydration
status, including their strengths and weaknesses, equipment requirements, and reference ranges, is presented in Table 12.1.77–79
While plasma osmolality (OSM) has been cited as a criterion method for assessing
hydration status,70 the choice of marker will be inluenced by the sensitivity and accuracy with which hydration status needs to be established,71 together with factors such
as availability, expense, portability, invasiveness, time effectiveness, and technical
expertise necessary to conduct procedures.72–74 preferred tool should be noninvasive,
TABLE 12.1
Hydration Assessment Techniques, Their Strengths and Weaknesses,
Equipment Requirements, and Reference Ranges
Euhydrated
Reference Range
Method
Advantages
Disadvantages
Equipment
Body mass
Simple,
noninvasive,
inexpensive,
portable
Able to selfmonitor
Immediate
feedback
Beneicial for
estimating sweat
rates when
assessed pre- and
postexercise,
after accounting
for during
exercise nutrient
intake, urine/
fecal losses, etc.
Precise, accurate
Can detect acute
dehydration
Does not measure
body luid
absorption
Requires
knowledge of
euhydrated mass
Provides little
information
about presenting
hydration status
due to diurnal
variations in
body mass
Limited to acute
assessments
across no more
than 14 days
Professional
quality digital
scales, lat,
nonabsorbent
surface
< 1% variance in
body mass from
one day to the next
Requires trained
phlebotomist
Invasive,
expensive
Does not provide
immediate
feedback
Inluenced by diet,
medications,
illness, exercise,
vitamins, acute
ingestion of
luids
Osmometer,
centrifuge
< 290 mOsm.kg–1
Urine color chart
Very pale yellow,
pale yellow,
straw-colored (< 3
on urine color
chart although
rarely 1)
Plasma/serum
osmolality
Urine color
Simple,
noninvasive,
inexpensive
Able to selfmonitor
Immediate
feedback
Portable
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Assessment of Hydration of Athletes
TABLE 12.1 (continued)
Hydration Assessment Techniques, Their Strengths and Weaknesses,
Equipment Requirements, and Reference Ranges
Euhydrated
Reference Range
Method
Advantages
Disadvantages
Equipment
Urine speciic
gravity
Noninvasive,
convenient,
inexpensive
Immediate
feedback
Portable
Refractometer
(preferred)
Dipsticks
< 1.020, although
rarely below 1.010
Urine
osmolality
Noninvasive
Precise
Osmometer
< 700 mOsm.kg–1
Saliva
Simple,
noninvasive
Inluenced by acute
ingestion of luids
and presence of
glucose and
protein in urine
Delayed response
to acute
dehydration
Expensive
Does not provide
immediate
feedback
Delayed response
to acute
dehydration
Flow rate less
sensitive
Possible effect of
food and luid
intake on saliva
low rate
Large
interindividual
variation
Expensive if
measuring
osmolality
Polyester swab/
tube, osmometer
(osmolality),
digital scales
(volume),
spectrophotometer (total
protein)
< 61 mOsm.kg–1
although
euhydrated
reference range
should be
determined
individually
Sources: Casa, D.J., Armstrong, L.E., Hillman, S.K., Montain, S.J., Reiff, R.V., Rich, B.S.E. et al., J. Athl.
Train. 35, 212–24, 2000; Armstrong, L.E., Maresh, C.M., Castellani, J.W., Bergeron, M.F.,
Keneick, R.W., LaGasse, K.E. et al., Int. J. Sport Nutr. 4, 265–79, 1994; Kovacs, E.M., Senden,
J.M., and Brouns, F., J. Sport Med. Phys. Fitness. 39, 47–53, 1999; Shirreffs, S.M. and Maughan,
R.J., Med. Sci. Sports Exerc. 30, 1598–1602, 1998; Walsh, N.P., Montague, J.C., Callow, N., and
Rowlands, A.V., Arch. Oral Biol. 49, 149–54, 2004; Walsh, N.P., Laing, S.J., Oliver, S.J., Montague,
J C., Walters, R., and Bilzon, J.L., Med. Sci. Sports Exerc. 36, 1535–42, 2004; Oppliger, R.A.,
Magnes, S.A., Popowski, L.A., and Gisoli, C.V., Int. J. Sport Nutr. Exerc. Meth. 15, 236–51, 2005;
Oppliger, R.A. and Bartok, C., Sports Med. 32, 959–71, 2002; Armstrong, L.E., Nutr. Rev. 63 (6 Pt
2), S40–S54, 2005; Popowski, L.A., Oppliger, R.A., Patrick Lambert, G., Johnson, R.F., Kim
Johnson, A., and Gisoli, C.V., Med. Sci. Sports Exerc. 33, 747–53, 2001; Pagana, K.D. and Pagana,
T.J., Mosby’s Diagnostic and Laboratory Test Reference, 4th ed., Mosby Inc, St. Louis, Missouri,
1999; Casa, D.J., Armstrong, L.E., Ganio, M.S., and Yeargin, S.W., Curr. Sports Med. Rep. 4,
309–17, 2005; Oliver, S.J., Laing, S.J., Wilson, S., Bilzon, J.L., and Walsh, N.P., Arch. Oral Biol.
53, 975–80, 2008; Armstrong, L.E. Pumerantz, A.C., Fiola, K.A., Roti, M.W., Kavouras S.A.,
Casa, D.J., Maresh, C.M., Int. J. Sport Nutr. Ex Metab. 20, 145–153, 2010..
© 2011 by Taylor and Francis Group, LLC
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Nutritional Assessment of Athletes, Second Edition
economical with minimal consumable requirements, technically simple, portable,
valid, precise, and not inluenced by factors unrelated to hydration status. Given
this, urinary indices are generally the preferred method to assess hydration status,
particularly in ield situations, as urinary tests are simple, noninvasive, inexpensive,
provide immediate feedback to the athlete, and are amenable to self-monitoring.72–73
Periodic monitoring of hydration status creates an awareness of whether athletes
are meeting their luid intake needs and identiies those individuals most at risk of
dehydration, such as those with high sweat rates or reluctant drinking behaviors.58
Hydration assessments also complement the education process associated with good
hydration strategies, providing feedback to athletes on how adjustments in drinking behavior inluence hydration status. The assessment of hydration status has also
become ingrained in the procedures used in the annual weight classiication of athletes competing in weight category sports like wrestling.35,62,73,75 This has evolved as
a result of athletes attempting to achieve rapid weight loss by aggressive dehydration
practices to “make weight.”76
12.3.1
BODY MASS CHANGES
It is assumed that body mass changes over short periods of time (that is, throughout
an exercise session) or from one day to the next are due to water gained (food and
luid intake, substrate metabolism) or lost (via sweat and respiration) since no other
body component can be gained or lost at such a rapid rate.80 Supporting this assumption, it has been shown that changes in body mass and total body water generally
move in the same direction and magnitude.62,81 Random variation in body mass from
one day to the next is within the range of ±1%.80,82 This information has been used
to suggest a reduction in body mass in excess of this could be used in the ield to
indicate a state of hypohydration.
While day-to-day body mass changes may offer insight into acute changes in luid
balance, it cannot be used to accurately specify the state of hydration. This is because
acute body mass changes merely indicate the degree of luid deicit with reference to
a baseline body mass measurement, which may not necessarily represent euhydration. As such, this tool should be used in conjunction with other hydration markers
to conirm a baseline euhydrated body mass. Furthermore, body mass measurements
should be made at the same time of day (preferably before breakfast or training but
after voiding the bladder and bowel) and wearing minimal clothing,49 so as to minimize the inluence of factors other than hydration status that can have an impact on
day-to-day variation in body mass. Other issues to consider include consistency in
scales used,83 menstrual cycle phase84 in females, and chronic energy imbalance,
which can inluence body mass independent of hydration status.85 As such, a euhydrated baseline body mass should not be used for any longer than 2 weeks.80 The use
of body mass change from one day to the next as an index of hydration status should
not be confused with the acute measurement of body mass over an exercise session
as part of procedures for measuring sweat rates.
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Assessment of Hydration of Athletes
12.3.2
URINARY INDICES
Urine is composed of a complex mixture of minerals, salts, and ionic and nonionic
compounds, the relative proportions of which can vary markedly.86,87 Urea accounts
for almost half the total solute composition of urine, followed by the major inorganic solutes of chloride, sodium, and potassium.87 Other main constituents of urine
include creatinine, uric acid, calcium, magnesium, phosphate, sulfate, and ammonia.
The amber-yellow color of normal urine is due to the presence of several pigments,
with urochrome being the predominant pigment.88
With acute hypohydration, urine demonstrates acute changes in volume, color,66,89
speciic gravity,72,89 osmolality,66,67,72 and conductance,66,67 creating an opportunity to
assess hydration status via relatively noninvasive urinary indices.
12.3.2.1 Urine Specific Gravity
Urine speciic gravity (Usg) is a measure of the density of a urine sample compared
with the density of pure water.86,90 It is dependent on the molecular weight and number of particles (osmolality) in urine86,91 as well as the concentration of urea, protein,
and glucose.73,91 As a result, the presence of heavy molecules, such as radiocontrast
agents, and abnormal concentrations of protein and glucose can cause disproportionate
increases in Usg with a minimal effect on urine osmolality (Uosm).86,91,92 Therefore,
when present, these constituents may invalidate the use of Usg as an indicator of hydration status. Medical conditions in which Usg should not be used to assess hydration
status are described in Table 12.2.98 Similarly, athletes with large muscle mass may be
incorrectly classiied as hypohydrated and a higher usg cutoff may be warranted.99
Several methods have been used to measure Usg, including hydrometry, refractometry, and reagent strips (dipsticks),73,86,90 although hydrometry is no longer considered
TABLE 12.2
Medical Conditions and Diagnostic Tests That May Affect Urine Specific
Gravity Measurements
Condition/Test
Resultant Urinary
Substance
Diabetes mellitus with glucosuria
Hyperparathyroidism/hypercalciuria
Salt-losing nephropathy
Nephrotic syndrome
High dose of mannitol
Use of radiocontrast media
Saline diuresis
Uremia
Glucose
Calcium
Abnormal urinary salts
Albumin
Mannitol
Radiocontrast media
Sodium
Urea
Consequences
Urine speciic gravity underestimates
total body water
Urine speciic gravity overestimates
total body water
Sources: Data from Chadha, V., Garg, U., and Alon, U.S., Ped. Neph. 16, 374–82, 2001; Voinescu, G.C.,
Shoemaker, M., Moore, H., Khanna, R., and Nolph, K.D., Am. J. Med. Sci. 323, 39–42, 2002;
Bakhshandeh, S. and Morita, Y., Michigan Med. 74, 399–403, 1975.
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Nutritional Assessment of Athletes, Second Edition
a valid or reliable measuring device to determine Usg.90 Refractometry is an indirect
estimation of speciic gravity by measurement of the urine’s refractive index.86 The
amount of refraction is proportional to the number, mass, and chemical structure of the
dissolved particles.86 The refractometer requires only a small volume of urine,73,90,93 is
temperature compensated,73,93 and can be used as a general guide to an athlete’s hydration status.35,90 Furthermore, as refractometry is portable, noninvasive, inexpensive,
objective, and simple to use by clinicians,73,75,90 it has become the preferred method for
hydration assessment by many investigators.63,65,75,89,94,95 Manual hand-held units and
digital refractometers are commercially available, with the manual unit being both
cheaper and more robust. Both techniques provide almost identical results.
Research assessing the reliability and validity of using commercial reagent strips
(dipsticks) to measure Usg has provided mixed results.90,93,96,97 Dipsticks lack the resolution of other techniques with graduations of 0.005 compared to 0.001 for refractometry.86,90 Consequently they are no longer considered an acceptable measuring
device to determine Usg in wrestlers during minimal weight certiication procedures
due to concerns with accuracy, reliability, and precision.97 Nevertheless, dipsticks
offer a simple inexpensive method that athletes can use in the ield to monitor substantial changes in hydration status.
12.3.2.2 Urine Osmolality
Osmolality is a measure of total urine solute concentration. Osmolality is measured
using the freezing point depression technique on an osmometer, a laboratory-based
piece of equipment that does not lend itself to being easily portable. Physiologically,
urine osmolality (Uosm) is considered the most accurate measure of urine concentration.86 This is because Uosm is less affected by solutes such as glucose, protein,
and urea compared to Usg.86,91 Urine concentration is dependent on the presence of
small solutes (for example, electrolytes, phosphate, urea, uric acid) and large solutes
(such as protein, glucose)93 and tends to increase with a reduction in urine volume.
However, it should be noted that the composition and concentration of urine vary
independently.100 Therefore, when either large volumes of dilute urine are produced
or when only small volumes of concentrated urine are produced, the total amount of
solute excreted can be identical.100
12.3.2.3 Urine Color
In an attempt to simplify urinalysis, Armstrong et al.65 developed an eight-color scale
including colors ranging from very pale yellow to brownish-green, which provides
both clinicians and athletes a validated, simple, and inexpensive method to assess
hydration status.35 Using this scale, urine color (Ucol) has been shown to provide a
reasonable index of hydration status in athletic or industrial settings when compared
to Usg and Uosm,65 at least when assessed by experienced personnel. However urine
color can be inluenced by an array of factors other than hydration status; details of
this are speciied in Table 12.3.
Ucol should be assessed in a well-lit room with samples collected into inert,
clear polypropylene containers and contrasted against the Ucol chart in the presence of a white background. It is not appropriate to assess Ucol from samples passed
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TABLE 12.3
Common Foods/Drugs That May Affect Urine Color
Common Foods/Drugs
Resultant Urine Color
Specific Test for Differential Diagnosis
Ibuprofen
Anthraquinone laxative
(Senna)
Ribolavin (vitamin B2)
supplementation
Carrots
Red/Red-brown
Yellow-brown
No speciic test. Seek medication history
No speciic test. Seek medication history
Yellow
No speciic test. Seek dietary supplementation/
medication history
Urine petroleum ether extraction/seek dietary
history
No speciic test. Seek dietary history
No speciic test. Seek dietary history
No speciic test. Seek dietary history
Chlorophyll breath mints
Rhubarb
Beet
Yellow-orange
Blue-green
Yellow-brown
Yellow
Source: Raymond, J.R. and Yarger, W.E., South. Med. J. 81, 837–41, 1988.
directly into a toilet. Finally, athletes may require training to assist in the accurate
interpretation of hydration status via Ucol.
12.3.2.4 Urine Volume
Urine volume is another index that has the advantage of allowing athletes to independently monitor their own hydration status.73 Athletes are often advised to monitor
urine volume and frequency of urination when assessing their hydration status.101
This is particularly important during training camps and warm weather environments
where signiicant luid deicits can occur. However, urine volume is inconvenient to
collect and assess,35 necessitates compliance by the athlete,73 is inluenced by recent
luid intake, and provides little information about hydration status at a particular time
point during the day.65 In addition, subjectively monitoring daily urine frequency
is only useful if the data collected can be compared to normal micturition patterns
that have been established prior to competition, while assuming the athlete is in a
euhydrated state.49,101 Urine samples relect all urine that has collected in the bladder
since the previous void, possibly explaining why urinary indices “lag behind” blood
indices during acute changes in hydration status, as occurs throughout exercise.70
12.3.2.5 Interpretation of Urinary Indices
The interpretation of urinary results can be complex because of the many factors that
inluence urine formation and composition. Factors that are known to inluence urinary
indices independent of hydration status include attempted rapid rehydration with hypotonic luids,66 severe dehydration,77 intravenous saline infusion,102 and the consumption
of caffeine103 and alcohol.104 Moreover, the presence of normal or abnormal urinary
constituents, certain disease states, diet (beets, carrots), temperature, and pH can also
inluence urinary indices of hydration status, the magnitude of which varies with the
technique.86,105 Storage of urine samples between the point of micturition and analysis
can also inluence results, with sample analysis recommended within 30–60 minutes.106
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When sample analyses cannot be undertaken within this time frame, they should be
refrigerated as soon as possible after micturition at 2–8°C. However this may promote
crystal formation, rendering samples invalid for assessment via Ucol.106
Urinary values may vary signiicantly with certain medications (for example, antibiotics, diuretics), supplements, fever, endocrine function, metabolism, exercise, and the
presence of bacteria.77,87 Furthermore, atypical dietary patterns such as strict vegetarianism86,107 and exclusive milk consumption in children can alter urinary solute composition and affect both Usg and Uosm results.86,105,107 Usg speciicity is also reduced
in athletes with large muscle mass due to an increase in urine protein metabolites.99
When attempting to undertake hydration assessments, it is important to be aware of the
potential limitations of each technique before selecting an assessment tool.
Ucol, Uosm, and speciic electrical conductance may be poor indicators of hydration status in athletes during the irst 6 hours after exercise-induced hypohydration (3% body mass loss) as a result of rapid ad libitum rehydration.66 Athletes who
attempt to aggressively rehydrate with large volumes of hypotonic luids during a
brief period will produce large volumes of dilute, pale-colored urine even if the body
is still in a state of dehydration.66,108 Excessive urine production can occur before total
body luid deicits have been completely replenished in the intracellular and extracellular spaces, thus masking hydration status. Fluid ingestion can temporarily produce
a urine sample that does not accurately relect hydration status.72,108,109 Consequently,
urinalysis is best undertaken on upon-waking samples, eliminating the inluence of
acute food and luid intake.65,67 Despite this, there may still be value in “spot checks”
at other time points during the day to conirm a state of dehydration given that while
false negatives are possible (hypohydrated yet urine sample indicates a state of euhydration), false positives (euhydrated yet urine sample indicates a state of dehydration)
are unlikely at any stage during the day for the majority of athletes.
In summary, Ucol, Usg, Uosm, and urine volume can be used either independently
or simultaneously to assess an athlete’s hydration status. While Uosm may be considered the preferred urinary index of hydration status within a clinical environment
where elevations in urinary solute load are possible independent of hydration status (for
example, presence or elevation of glucose, protein and urea in urine), healthy athletes
do not require such a precise and sophisticated measurement.67 Consequently monitoring Ucol or Usg provides an inexpensive, noninvasive, practical, and effective method
of assessing hydration status that can be easily used by athletes.35,73
12.3.3
HEMATOLOGICAL INDICES
Numerous blood-borne indices have been used to assess hydration status. Changes
in hemoglobin and hematocrit concentrations may be used to assess intra- and extracellular luid shifts provided baseline/euhydrated values are established.9,71,73,95,110
However, to ensure comparable results, a standardized posture must be assumed for
about 15–20 minutes89,95,101,110 to remove the inluence of posture on luid compartment shifts.87 If baseline values are known, relative changes in plasma volume can be
estimated from changes in hematocrit and hemoglobin concentrations.111
In order for markers of hydration status to be of practical use, they must be capable
of detecting a body water deicit of 2–3% of body mass.101 Indeed, plasma osmolality
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is sensitive enough to identify acute body luid deicits of as little as 1–5% body
mass, as can occur during exercise.70,72 Furthermore, unlike urinary indices, there
does not appear to be a delayed response to the effect of hypohydration on plasma
osmolality. However, changes in plasma osmolality in response to moderate hypohydration (< 3% of body mass) may dissipate over time as plasma volume is defended
to maintain cardiovascular stability.95
While the immediate measurement of osmolality is preferred, serum and plasma
samples can be left at room temperature for upwards of 3 days without inluencing osmolality data.112 Despite this, the measurement of blood parameters in the ield is impractical, requires a qualiied phlebotomist, and is expensive and invasive.73 In addition, blood
collection can cause discomfort to the athlete and introduces the risk of infection, bruising, and vein damage.73,101 Clearly, these limitations restrict the use of this method to
regularly monitor hydration status. Such tests may be considered more appropriate in
research and clinical settings where reliability, accuracy, and precision are essential.
12.3.4
SALIVARY PARAMETERS
Recently, salivary parameters have been identiied as potential indices of hydration
status during progressive acute hypohydration to 3% body mass loss.68,69,79 Strong correlations between percent body mass loss and saliva osmolality and total protein concentration were found (mean r = 0.94 and 0.97, respectively; P < 0.01).68 However, changes
in saliva low rate were less sensitive to changes in hydration status measured by percent body mass loss (mean r = –0.88; P < 0.01)68 and urine and plasma osmolality.69
Compared with blood collection procedures, collecting saliva samples using a
polyester swab is simple, noninvasive, and inexpensive.68 Nonetheless, other factors
may inluence the validity of saliva parameters as a potential marker of hydration
status, including a possible short-term effect of food and luid ingestion on saliva
low rate. There is a need for further research to elucidate the mechanisms responsible for salivary responses during progressive acute hypohydration and to determine
the sensitivity of salivary parameters in a ield setting.68
12.3.5
TOTAL BODY WATER ASSESSMENT
Biochemical parameters and body mass changes are indirect markers of hydration
status and do not indicate total body water (TBW) change.82 Measuring TBW by
dilution techniques such as deuterium oxide62,110,113,114 and bioelectrical impedance
analysis or spectroscopy allows the determination/estimation of TBW content.62
Total body water levels can be measured by administering an oral dose of an isotope
tracer such as deuterium oxide (2H2O or D2O) and measuring the isotope enrichment
in saliva, urine, or serum samples.115,116 The dilution technique assumes the distribution and diffusion of the isotope tracer in the body luid compartments are comparable to the distribution and diffusion of water.115 Deuterium dilution has been the
preferred technique62,65,110,113,117 and has served as the gold standard to validate blood
and urine indices of hydration status110 and bioimpedance spectroscopy analyses.118
With careful attention to administration and measurement procedures, TBW can
be determined by isotope dilution with a precision of 1–2%.114,115 Despite its small
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measurement error,114 TBW measurements are generally restricted to laboratorybased assessments, as they are time consuming and expensive. In addition, an equilibrium period of 3 to 4 hours is required after dose administration, without food,
luid, or exercise,114,115 making it inadequate to track acute changes in TBW.
Bioelectrical impedance analysis and spectroscopy use electrical current to estimate
TBW content. Electrical current passing through the human body is resisted by body
tissues and water. This technique represents a noninvasive, safe, and relatively easy
means to assess TBW.73,119,120 However, the accuracy and reliability of impedance testing requires strictly standardized and controlled conditions, particularly electrode placement, subject position, recent exercise, previous food and luid intake, hydration status,
skin temperature,121,122 and plasma tonicity.120 Even when these conditions are achieved,
bioelectrical impedance analysis is only able to identify half of acute changes in luid
balance.123 Estimates of TBW may also be compromised if the prediction equations
used are not applicable to the speciic individual or population under investigation.121
As such, the current consensus is that bioelectrical impedance analysis can provide an
indication of total body water but lacks the precision, accuracy, and resolution for monitoring small changes in hydration status, as occur within the athletic setting.73,78,118,120
In summary, impedance and dilution techniques appear to be of limited practical use to monitor the hydration status of athletes. This is mainly because athletes
are commonly in an “uncontrolled” or postexercise state.119 Although dilution techniques are considered the gold standard for estimating TBW, the analytical requirements, expense, and degree of control required limit the routine use of this technique
for hydration assessment.
12.4
12.4.1
ASSESSMENT OF SWEAT RATE AND COMPOSITION
SWEAT RATE ASSESSMENT
Assessment of an athlete’s individual sweat rate is a practical way to obtain information
about his or her current hydration status and can assist with prescription of individual
luid requirements. Sweat rate assessment requires the use of two measurements: (1)
upon-waking Usg and (2) luid intake and body mass changes during exercise. The
equipment needed to conduct sweat rate assessment is listed in Table 12.4.
TABLE 12.4
Equipment Checklist for Sweat Rate Assessment
Urine Specific Gravity
Body Mass Changes
Portable refractometer
Sample jars for urine
Pipettes
Plastic gloves
Sterile wipes
Water (sterile or tap)
Plastic covering for table
Scale accurate to 100 g for body mass
Scale accurate to 5 g for bottle/food weight
Towels for wiping down athletes
Board to place scales on
Weather monitor for temperature and humidity
Chart to record data
Stopwatch/clock
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The following procedure describes the steps required to conduct a sweat rate
assessment.
1. Pre-exercise:
• The athlete presents with upon-waking urine sample to assess hydration
status pre-exercise.
• Refractometer Usg test is conducted. Ensure the refractometer is zeroed
with distilled water. Pipette a sample of at least 1 mL of urine onto the
reading surface and record result. Wipe the reading area clean with a
sterile wipe and repeat.
• Record the air temperature and relative humidity.
• Weigh the athlete in minimal clothing with bladder voided. Record any
luid consumed in the 30 minutes prior to being weighed.
• Weigh drink bottles that are to be consumed during the exercise session. Record the type of luid in each bottle.
• Take note of the time the exercise session commences.
2. During exercise:
• Record a second reading of air temperature and humidity.
• Weigh each drink bottle as it is emptied and reweigh if reilled.
• Note the number and timing of drink breaks.
• If the athlete visits the bathroom, ensure that he or she is weighed before
and after emptying bladder. Alternatively, collect urine and weigh.
3. Postexercise:
• Record the inish time of the exercise session.
• Ask athlete to wipe off any residual sweat from his or her body, hair,
and clothing. Record the weight of the athlete in identical clothing to
pre-exercise weight.
• Ask the athlete to empty his or her bladder (if possible) and record the
post–bladder voided weight.
• Reweigh any remaining drink bottles and unconsumed food with
packaging.
• Record a inal reading of air temperature and humidity. Calculate an
average of all three readings.
Practitioners can enter the results obtained from the sweat rate assessment into
the data entry sheet provided in Table 12.5.
This data can be used to calculate sweat rate and obtain information on luid
intake and drinking behaviors during exercise. The calculations required to determine sweat rate are as follows:
1.
2.
3.
4.
5.
6.
Fluid intake (absolute) = (luid 1 + luid 2 + luid 3) mL
Fluid intake (relative) = [absolute luid (mL) / exercise time (min)] × 60 mL/hr
Weight loss (kg) = Pre-exercise weight – postexercise bladder voided weight
Urine loss (mL) = weight pre-bladder void – weight post–bladder void
Sweat losses (absolute) = (Weight loss + luid intake – urine loss) mL
Sweat rate = [absolute sweat loss (mL) / exercise time (min)] × 60 mL/hr
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7. Percent luid replaced (%) = [luid intake (mL) / sweat loss (mL)] × 100
8. Percent body weight change (%) = (weight loss/pre-exercise weight) ×100
Sweat rate calculations are based the assumption that 1 g of weight loss is equal to
1 mL of luid, and the majority of the luid loss is sweat. It does not account for respiratory and metabolic water or fuel losses. In distance events such as marathons, weight
TABLE 12.5
Sweat Rate Assessment Data Entry
Name:
Test day USG:
Sport:
Euhydrated:
Yes / No
Bladder voided:
Yes / No
Comments:
Temperature:
Temperature:
Temperature:
Humidity (%):
Humidity (%):
Humidity (%):
Average:
Start time:
Finish time:
Total time =
A. Pre-exercise wt
(kg):
A. Pre–bladder void
wt (kg):
B. Postexercise wt
(kg):
B. Post–bladder void
wt (kg):
Postexercise bladder
void (kg):
Urine volume
(A – B) =
A. Weight pre:
B. Weight post:
Fluid 1: A – B =
A. Weight pre:
B. Weight post:
Fluid 2: A – B=
A. Weight pre:
B. Weight post:
Fluid 3: A – B =
Conditions
Reading 1 (pre)
Reading 2 (during)
Reading 3 (post)
Training
Type:
Weight
During exercise
bladder void
Time:
Fluid
Bottle 1
Type luid:
Bottle 2
Type luid:
Bottle 3
Type luid:
Drink breaks
(mark off)
Time
Comments
1
2
3
4
5
6
7
8
9
Food
Type =
A. Weight food
pre (g)=
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B. Weight food
post (g) =
A–B=
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Assessment of Hydration of Athletes
loss from other sources may account for 1.5 to 2 kg of weight loss.124 Nevertheless,
sweat rate assessment of the athlete can assist with the development of individual
luid replacement guidelines. The guidelines should consist of advice on estimated
luid requirements before, during, and after exercise as well as goals and strategies for
luid replacement over the remainder of the day. Information on the most appropriate
type of luid and the volume and timing of intake can also be addressed. Table 12.6
provides a template for a sweat rate assessment report that can be provided to athletes to complement advice on speciic strategies to improve drinking practices.125
Feedback should take into account factors that are relevant to the individual athlete
and his or her sport (such as taste preferences, opportunities to consume luid, rules
of the sport, playing position in team sports). Speciic recommendations for luid
intake pre-, during, and post-exercise are provided in Section 12.5.
Although there is a need for individualized sweat rate assessment and luid replacement guidelines, estimating sweat losses can assist with planning needs for sporting
populations and military personnel, particularly when exposed to heat stress. Sweat
rate can be predicted from a range of parameters, including the environmental conditions, metabolic rate, and clothing. The original Shapiro prediction equation,126 formulated 25 years ago, was based on laboratory experiments that determined energy
expenditure of men at rest and up to moderate exercise intensities over a range of
environmental conditions while wearing a range of clothing.126 This equation has
been used to determine the U.S. dietary reference intakes (DRI) standards for water
and electrolytes.127 More recently this equation has been shown to overpredict sweat
TABLE 12.6
Sweat Rate Assessment Report
Name:
Sport:
Environmental conditions
Urine speciic gravity:
(A reading < 1.020 is considered well hydrated)
Sweat losses:
Urinary losses
Total luid loss
Fluid intake
Fluid replacement
Comments
Date:
Training session :
Duration:
Temperature:
Humidity (%):
Total (mL) =
Hourly loss (mL/hr) =
Urine losses
Total (mL) =
Total (mL)
Hourly loss (mL/hr) =
Total (mL) =
Hourly intake (estimate) (mL/hr) =
% of your sweat loss
Source: Adapted from Gatorade Sports Science Institute, Australian Institute of Sport, and Sports Dietitians
Australia, 2006.
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rates, resulting in a new prediction equation that more accurately estimates sweat
losses.128 As previously suggested, there may be speciic situations where use of this
equation is warranted. However, the preferred option for the practitioner is to conduct a sweat rate assessment as outlined above.
12.4.2
SWEAT COMPOSITION ASSESSMENT
Knowledge of sweat composition can complement sweat rate assessment and assist
with development of luid intake guidelines. Sodium and chloride are the primary
electrolytes lost in sweat, with calcium, magnesium, and potassium present in
smaller amounts.129 There is a large individual variability in the concentration of
electrolytes in sweat130 with sodium and potassium concentrations ranging from 20
to 80 mmol.L –1 and 4 to 8 mmol.L –1, respectively.130,131 Profuse sweating can lead to
signiicant luid and electrolyte loss, and potentially results in exercise-associated
hyponatremia during endurance activity.131 However, higher sodium intakes have
been associated with elevated blood pressure and cardiovascular risk,132 and therefore it would be unwise to recommend that all athletes consume a high-sodium diet.
Rather, speciic prescription of suficient sodium to replace losses experienced during exercise in the postexercise period will assist with aggressive rehydration while
avoiding any of the complications associated with a habitually high dietary sodium
intake. Sweat composition analysis can help to identify athletes who have a high concentration of electrolytes in their sweat, allowing individual prescription of sodium
and other electrolytes.
Two methods are used to assess sweat composition: whole-body wash down and
regional skin surface collection (sweat patches).130 A comparison of the two methods
is shown in Table 12.7. Whole-body wash down is considered the criterion method to
determine electrolyte losses because all sweat runoff is collected and accounted for.
Sweat patch analysis involves collecting sweat from a number of locations on the body
and using these results to predict whole-body sweat composition (Table 12.8). This
method must be conducted in conjunction with the sweat rate assessment described
above. Although this is a practical approach to determining sweat composition in the
TABLE 12.7
Comparison of Sweat Composition Analysis Methods
Sweat Composition Analysis Technique
Whole-Body Wash Down
Testing environment
Exercise modality
Accuracy
Laboratory
Cycling
Criterion method
All sweat accounted for
Degree of dificulty
Complex and impractical
Sweat Patches
Laboratory or ield
All sports
Use of equation weighted for
local sweat rate and body
surface area
Simple and practical
Source: Sports Dietitians Australia, Fact Sheet, Sports Drinks, Sports Dieticians Australia, Melbourne, 2009.
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TABLE 12.8
Sweat Patch Technique
Step
1
2
3
4
Method
Clean skin with deionized water, wiping dry with sterile gauze
Apply an absorbent sterile patch pad to a speciied body parts (e.g., forearm) ensuring that the
patch adheres to the skin
After exercise, carefully remove patch with dry forceps and place into a small (30 mL) sealed
container (centrifuge tube), ensuring that no sweat evaporates from the patch after removal.
The sweat can be removed by centrifugation and the concentration of electrolytes determined
using lame photometry, ion chromatography, or ion-selective electrode.131 To work out
sweat sodium losses, combine results with sweat rate calculations.
ield, it has been shown to generally overestimate sodium and potassium sweat concentration.133 The sites most commonly used include the forehead, forearm, chest, back,
thigh, and calf.6 Patterson et al.134 found that sodium collections from the calf and thigh
were the most closely correlated to the whole-body wash down technique. However,
Baker et al.133 found the thigh and chest to be the best sites in both males and females. It
is likely that a large number of sites will enhance reliability of sweat patch techniques,
but this needs to be balanced against the additional cost associated with multiple site
analysis. Equations are available to predict whole-body sweat electrolyte losses from
regional skin surface collections133 with a single site (forearm) often used. While the
validity of regional skin surface collections as a direct measure of whole-body sweat
electrolyte concentration remains debatable,135 its application in the ield across a broad
range of exercise modalities ensures it remains an attractive option for practitioners.
The interpretation of sweat composition assessment should be considered along
with the results of sweat rate, luid intake, level of dehydration, exercise intensity and
duration, and environmental conditions. Within a normal population, sweat sodium
will range from 10–80 mmol/L and potassium from 4 to 8 mmol/L. Values outside
of this range are likely to represent an error in the collection technique. However,
individuals with cystic ibrosis will have higher concentrations of sweat sodium, and
there are a few rare genetic conditions where the value may fall outside this range.
Heat acclimatization improves the ability to reabsorb sodium and chloride, resulting
in lower sweat sodium concentrations.136
12.5
RECOMMENDATIONS FOR FLUID INTAKE
Euhydration is particularly important to the athlete when there is short recovery
between sessions, there are multiple competition events during the day, or the athlete
is identiied as being hypohydrated in the morning prior to training. In each of these
circumstances, it is worth considering the various factors that inluence the rate of
rehydration, including beverage composition, temperature, and rate of consumption.
Recent studies have shown that the rate of luid consumption is one of the key factors
in successful rehydration.10,137 Ingestion of large volumes of luid in a short space
of time leads to greater diuresis compared to when the volume is consumed over a
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longer time span.10,138 The electrolyte content, palatability, and temperature of the
beverage also play a role.139 Furthermore, the rate of luid absorption needs to be
considered when rapid rehydration is imperative to performance during exercise,
particularly in the heat. Factors that have an impact on the rate of luid availability
include the speed of gastric emptying, the intestinal absorption, and retention of the
luid within the intra- and extracellular space.15,140 The following section outlines the
current recommendations on luid intake before, during, and post-exercise and the
various factors that inluence luid availability.
12.5.1
PRE-EXERCISE HYDRATION
Athletes should aim to start exercise in a euhydrated state with minimal gastrointestinal discomfort. If an athlete has consumed adequate luid throughout the day and
suficient time has elapsed since the last exercise bout, he or she is more likely to be
euhydrated. However, if there have been substantial luid deicits and the individual
has not had adequate time to replace losses, then more aggressive pre-exercise hydration strategies may be required. There is currently no consensus on the optimal preexercise hydration strategies for athletes. The American College of Sports Medicine
recommends consuming beverages 4 hours before the exercise bout at around
5–7 mL.kg–1. If the individual does not produce urine or it is very concentrated,
then 3–5 mL.kg–1 should be consumed around 2 hours before the event.7 Consuming
beverages or food containing sodium may offer some advantage as it will stimulate
thirst, reduce urine output, and thus promote greater retention of ingested luids. As
rehydration during exercise depends upon maximizing the rate of delivery from the
stomach to the intestine, there is an advantage in starting exercise with a comfortable
volume of luid in the stomach.141 Distension of the stomach will assist with gastric
emptying provided that luid is consumed periodically once exercise commences.
Pre-exercise sodium loading has been investigated as a means of hyperhydrating
prior to exercise. There is evidence that consuming beverages containing higher levels
of sodium than standard sports drinks (164 mmol Na L –1) consumed approximately
1.5 hours before exercise can lead to increased plasma volume and exercise capacity
in the heat in both men and women.142,143 However, it is currently unclear whether
this is related to cardiovascular or thermoregulatory mechanisms. Beverage temperature can also lead to an improvement in exercise capacity in the heat. Ingestion of
cold luids (4°C) before (or during) exercise has been shown to improve performance
and attenuate the increase in core temperature that occurs in a hot environment.144
Precooling techniques, such as whole-body precooling,145 have previously been used
in athletes undertaking endurance exercise in the heat to lessen the strain on the thermoregulatory system. The ingestion of cold beverages may provide a more practical
and comfortable approach that can lead to increased endurance capacity by assisting
with the management of core temperature.
12.5.2
FLUID REPLACEMENT DURING EXERCISE
The main aim of drinking during exercise is to maintain physiological capacity and
minimize any risk of exertional heat illness. The factors that have an impact on luid
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availability include the rate of gastric emptying, intestinal absorption, and retention
of the luid within the intra- and extracellular space.15,140 Maximizing the rate of gastric emptying and delivery to the intestines is most important during exercise in the
heat when rapid delivery of luid is required. Gastric emptying has been shown to
be inluenced predominantly by the energy density and also the osmolality of the
luid.146 Most sports drinks are formulated to have an osmolality close to body luids;
however, a drink that is slightly hypotonic (dilute glucose-electrolyte solutions) may
result in a greater rate of water uptake due to the osmotic gradient created between
the intestinal contents and the intracellular luid in the cells of the intestinal wall.147
As carbohydrate intake at a rate of 30–60 g.hr–1 (approximately 1 L of sports drink)
has been shown to beneit performance through sustained exercise intensity,148 and is
independent and additive to water alone,16 there is merit in adding moderate amounts
of carbohydrate to sports drinks. Therefore, if the primary concern of the exercise bout
is to provide energy, and dehydration is of less concern, then addition of carbohydrate
as an exogenous fuel source is warranted. There is also some evidence that there is a
greater rate of carbohydrate delivery and improved endurance performance with the
consumption of multiple transportable carbohydrates (for example, glucose, sucrose,
maltodextrin, and fructose) compared with a single carbohydrate source.149,150
Many factors inluence the degree of luid and electrolyte losses during exercise
such as ambient temperature, clothing, humidity, heat acclimatization, training status,
and genetic predisposition.7 Relying on thirst alone may not give a true indication of
actual needs and may lead to dehydration, whereas overdrinking can result in hyponatremia, which can have potentially fatal consequences.42 There is also evidence that
athletes may experience gastrointestinal discomfort if they attempt to replace luid
at a rate that matches sweat loss.151 Daries and colleagues151 demonstrated that luid
consumption at a rate of approximately 330 mL every 15–20 minutes (1.0 to 1.4 L)
over 2 hours of running in a thermoneutral environment did not improve performance
and resulted in abdominal discomfort in most subjects. However, there is evidence
that athletes can “train” themselves to tolerate larger luid volumes. Lambert and colleagues152 demonstrated that trained runners could better tolerate drinking an isotonic
carbohydrate-electrolyte drink that nearly matched their sweat rate when they consumed the same volume over repeated sessions in a moderate environment. This was
not related to an improvement in gastric emptying. Although the mechanism remains
unclear, it has been proposed that this is related to gastric distension.153
All athletes should develop their own hydration strategy for luid replacement during exercise based on assessment of sweat rate and luid balance in a variety of training
and competition situations and environmental conditions.6,153 This will help the athlete
to determine whether a more aggressive approach to hydration is required. Athletes
should drink as much as practically and comfortably possible, and attempt to consume
around 70–80% of luid losses but never more than their sweat losses. The athlete will
need to be advised on the volume of luid he or she needs to consume, the type of luid,
the timing of intake based on the opportunities he or she has to drink during the activity, and gastrointestinal comfort. In team sports, the athlete must take opportunities
such as quarter/half time, pauses in play, timeouts, and substitutions to access luid.
Some examples of the composition of different types of luids are provided in
Table 12.9.154
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Nutritional Assessment of Athletes, Second Edition
TABLE 12.9
Composition of Different Types of Fluids
Fluid
Carbohydrate
(%, Type)
Sodium
(mg per 100 mL)
Water
Nil
3–5
4–8 sucrose,
glucose
20–60
(10–25 mmol.L–1)
Soft drink
11 sucrose
10
Slowly absorbed, negligible electrolytes;
cola provides caffeine; lavor alternative in
long events
Fruit juice
8–12 fructose,
glucose
7
Slowly absorbed; negligible electrolytes;
may cause gastrointestinal (GI) upset due
to high fructose load
Sports water
0–4% sucrose
0–12
Negligible electrolytes; addition of
vitamins and herbs; may be suitable for
short-duration activity
Energy drink
10–13 Sucrose,
glucose
10–120
May contain caffeine, taurine, guarana,
vitamins, herbs or other additives; lavor
alternative in long events
Sports drinks
Comments
Suitable for short-duration activity; assists
with meeting hydration needs; No
carbohydrate or electrolyte replacement.
Best choice during exercise; moderate
electrolytes; meets luid and fuel needs
Source: Adapted from Sports Dietitians Australia, Fact Sheet, Sports Drinks, Sports Dietitians Australia,
Melbourne, Australia, 2009.
12.5.3
POSTEXERCISE FLUID REPLACEMENT
The goal of postexercise luid replacement is to restore luid and electrolyte deicits.
If recovery time is suficient, consumption of water and normal meals will restore
euhydration.7 However, if recovery time is short and dehydration is substantial, more
aggressive strategies are warranted. The main factors inluencing the postexercise
rehydration process are the volume and sodium content of the ingested luid.108,155
Obligatory sweat, respiratory, metabolic, and urinary losses persist throughout the
recovery phase, even in the hypohydrated state.103 Therefore, a volume corresponding to 150% of the luid deicit must be ingested to acutely restore luid balance (i.e.,
1.5 L for every kilogram lost).108
The inclusion of sodium in oral rehydration solutions is recommended since it
is lost in sweat and should be replaced for rapid restoration of luid balance.155–157
Sodium, in combination with carbohydrate, improves palatability while also stimulating the osmotically dependent dipsogenic factors that increase voluntary luid
intake.139,156,159 Moderately high sodium intakes (50–60 mmol.L –1) to levels found
above those in sports drinks (10–25 mmol.L –1) are justiied when effective luid
replacement must be achieved within several hours after completing exercise.108,159
A study that evaluated the effect of varying levels of drink sodium content (2, 26,
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Assessment of Hydration of Athletes
52, or 100 mmol.L –1) on the rehydration process found that the subjects who consumed the two higher-sodium beverages were euhydrated 5.5 hours after the end
of the rehydration period.155 Despite the ingestion of a drink volume equivalent to
1.5 times their estimated sweat losses, subjects were in net-negative luid balance
after the consumption of the two low-sodium luids. Cumulative urine output was
inversely related to the sodium concentration of the ingested luid. Furthermore, a
study by Nose and colleagues156 found a delay in rehydration following the ingestion
of plain water and attributed this to the removal of the osmotic drive to drink and a
rise in free water clearance. Thus, unless the rehydration beverage contains suficient
sodium, luid intake will merely increase urinary output, delaying full restoration of
luid balance.101,108,158
To promote rehydration and correct luid deicits, athletes are encouraged to consume a combination of sodium-containing foods and luids (Table 12.10), which have
the potential to decrease cumulative urine output.155,160 Despite this, solid food is not
always appealing to athletes following strenuous exercise as a result of gastrointestinal discomfort109 and optimal rehydration beverages will be just as effective and
convenient. However, consumption of meals may be necessary to ensure full hydration is ultimately achieved,108 as solid food provides additional luid and electrolytes,
and assists with luid retention.161
Consumption of skim milk has been shown to effectively restore luid balance
postexercise.162 This has been attributed to its relatively large quantities of electrolytes (Na+ 32 mmol/L, K+ 42 mmol/L and Cl– 36 mmol/L) in comparison to sports
drinks, resulting in decreased urine production. Furthermore, milk can provide both
carbohydrate and protein, which can contribute to restoration of muscle glycogen
stores. However, milk is not a suitable alternative for athletes who are lactose intolerant. Alcohol can act as a diuretic and increase luid output, and therefore should be
TABLE 12.10
Sodium Content of Common Fluid and Foods
for Athletes Who Have High Sodium Losses
Food/ fluid
Sports drinks (4 cups : 1 liter)
Milk (4 cups : 1 liter)
Bread (2 slices : 80 g)
Corn Flakes cereal (1 cup : 30 g)
Noodles (1 cup cooked : 170 g)
Cheese (2 slices : 60 g)
Ham (1 slice : 20 g)
Salmon, tinned (2 tabs : 40 g)
Olives (10 medium : 40 g)
Tomato juice (1 cup : 250 mL)
mg per Serve
~ 330
457
249
320
434
390
325
211
387
750
Source: Adapted from Maughan, R.J. and Shirreffs, S.M., Int. J.
Sport Nutr. Exerc. Meth. 18, 457–72, 2008.
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Nutritional Assessment of Athletes, Second Edition
consumed in moderation during postexercise recovery.104 Caffeine is a common additive in many beverages and some sports foods. It has been implicated as potentially
increasing urine output and contributing to dehydration.7 It appears that small doses
of caffeine are unlikely to increase urine output and cause dehydration,163 although
this has not been tested during exercise or in already hypohydrated individuals.
The value of including other electrolytes in sports drinks is unclear.164 Potassium
may be necessary for intracellular luid compartment restoration; however, further
investigation is required to provide conclusive evidence.11
Individual luid replacement protocols should be implemented considering the
athlete’s sweat rate, exercise intensity, nature of the sport, recovery time between
exercise bouts, and environmental conditions to ensure optimal recovery and maintenance of exercise capacity.35
The impact of the carbohydrate content and osmolality of luid consumed postexercise appears to be of less importance when the primary aim is to restore luid
balance. In a recent study by Evans et al.,137 hypertonic carbohydrate-electrolyte
beverages (10% glucose, osmolality of 654 mosm.kg–1) were as effective as hypotonic beverages (2% glucose and 188 mosm.kg–1) and carbohydrate-free beverages
(74 mosm.kg–1) in restoring luid balance when subjects consumed luid ad libitum.
The palatability or taste of the luid will dictate the amount consumed. Thirst
mechanisms are inadequate to promote full luid replacement when plain water is
consumed.156,165 Several studies have shown that both adults52 and young children47
consume more luid when the beverage is lavored. In children, taste preferences
dictate drinking volume, with suficient consumption of luid only occurring when
a lavored beverage was consumed.47 In adults, the addition of sodium to a rehydration beverage increases voluntary intake139; however, high levels of sodium can
make the drink unpalatable.164 The addition of carbohydrate can offset the palatability issues with beverages that contain sodium. A study investigating the effect of
palatability on voluntary intake of luid after exercise found that participants drank
123% of their sweat losses with lavored water alone, 163% with lavored water and
25 mmol.L –1 sodium, and 133% with lavored water and 50 mmol.L –1 sodium.139
Commercial sports drinks are designed to provide a balance between the eficacy
of a higher sodium content and palatability through addition of carbohydrate. Other
drinks, such as skim milk, can provide higher levels of electrolytes without issues
of palatability.162 The athlete must weigh the beneits of consuming large volumes
of a lavored beverage for adequate rehydration against the additional energy intake.
Taste fatigue can also occur, particularly in endurance events when a single lavored
drink is the only option available over an extensive period of time, or postexercise
when a large volume needs to be consumed in a short time period. Including a variety of beverage lavors may encourage increased luid consumption.
12.6
CONCLUSIONS AND FUTURE DIRECTIONS
Maintaining hydration status is a major challenge to the athlete, and particular efforts
should be made to limit hypohydration and the potential impairment to physiological function and health. Fluid losses in excess of 2% of body mass have been shown
to have a substantial impact on physical and cognitive performance in a variety of
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Assessment of Hydration of Athletes
365
climatic conditions. Despite knowledge of the importance of adequate rehydration
strategies, many athletes fail to hydrate adequately before, during, and after exercise.
Conversely, some athletes have a tendency to overdrink and risk developing hyponatremia. Therefore, all athletes should develop their own hydration strategy based on
individual sweat losses in a variety of training and competition situations. Athletes
should drink as much as practically possible but not more than their sweat loss. The
palatability, temperature, and electrolyte content of the beverages they are consuming should be carefully considered, as this may play an important role in determining
the amount of luid consumed.
A wide variety of tools are available to assess hydration status, including body
mass changes, bioelectrical impedance analysis and dilution techniques, hematological and urinary indices, and salivary parameters. A preferred tool should be
noninvasive, economical with minimal consumables, technically simple to operate, stable, portable and robust, valid, precise, and not inluenced by factors unrelated to hydration status. Given this, urinary indices (especially speciic gravity and
color) are generally the preferred method to assess hydration status, particularly in
ield settings. Upon waking urine samples are preferred as this avoids the potential
confounding inluence of acute food and luid intake prior to urine sample collection. Hydration assessments can be undertaken at any time of the year but may have
particular application during periods in which environmental conditions or training
loads change. Assessments prior to competition may be best undertaken the day
before competition, allowing hypohydrated athletes an opportunity to fully rehydrate prior to competition.
Although hydration assessment tools are becoming increasingly available,
research supporting the interpretation of results is lacking. Cutoff points to identify
a state of dehydration have been proposed, but little is known about the degree of
total body water deicit associated with results from these ield tools. Future research
should investigate the association between changes in indirect indices of hydration
status and total body water. This would afford a much more prescriptive approach to
luid intake following hydration assessments.
Ucol analyses reported in the literature have been based upon analysis by
researchers rather than athletes. This approach lacks practicality because in practice, athletes are performing the analysis. Therefore, the relationship between
Ucol (analyzed by athletes) and Uosm/Usg, and the strength of association
between Ucol measured by a trained investigator in comparison to athletes should
be investigated.
12.7
PRACTICAL RECOMMENDATIONS
• Assess individual hydration status and sweat rate to assist in the development of individualized luid intake plans that are speciic to different environmental conditions, exercise intensities, and sporting disciplines.
• Establish a routine of weighing in before and after training to determine
sweat loss. This is particularly important when the individual is new to the
training environment, there are high-intensity training sessions, or the envi-
© 2011 by Taylor and Francis Group, LLC
366
•
•
•
•
Nutritional Assessment of Athletes, Second Edition
ronmental conditions change. This allows prescription of individualized
rehydration needs (that is, 150% of weight loss).
Urine color is a simple, practical tool that requires minimal equipment and
can be used for daily monitoring by the athlete.
Biochemical indices of hydration status can be particularly valuable in providing an objective assessment of the athlete’s ability to match luid intake
with luid losses. However, given the cost, invasiveness, and dificulty with
obtaining a blood sample, a measure of the speciic gravity of an uponwaking urine sample can be a practical alternative.
Collect and analyze sweat samples, and observe salt crusts on skin or
clothing, and the taste of salt. Estimate the need for sodium replacement.
Prescribe sodium replacement by adjusting food/luid recommendations
based on individual needs.
Consider the needs of speciic groups such as women, children and adolescents, and older individuals
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Section V
Clinical Assessment of Athletes
© 2011 by Taylor and Francis Group, LLC
Assessment
13 Clinical
of Athletes
Khursheed N. Jeejeebhoy and
Farida M. Jeejeebhoy
CONTENTS
13.1
13.2
13.3
13.4
Introduction ................................................................................................ 378
Nutritional Status ....................................................................................... 378
13.2.1 History ......................................................................................... 379
13.2.2 Physical Examination .................................................................. 379
Medical Status ............................................................................................ 380
13.3.1 Medical History ........................................................................... 380
13.3.1.1 Competitive Athletes .................................................. 380
13.3.1.2 Sedentary and Elderly Athletes .................................. 382
13.3.2 Physical Examination .................................................................. 382
13.3.3 Hematology .................................................................................. 383
13.3.4 Blood Biochemistry ..................................................................... 383
13.3.5 Micronutrient Levels .................................................................... 383
13.3.6 Urine Analysis ............................................................................. 384
13.3.7 Stool Examination ....................................................................... 384
13.3.8 Electrocardiographic and Echocardiographic Examination ........ 384
13.3.8.1 Competitive Athletes .................................................. 384
13.3.8.2 Sedentary and Elderly Athletes .................................. 385
13.3.9 Bone Mass .................................................................................... 386
13.3.9.1 Competitive Athletes .................................................. 386
13.3.9.2 Sedentary and Elderly Athletes .................................. 386
13.3.10 Muscle Function ........................................................................... 386
13.3.10.1 Strength ....................................................................... 386
13.3.10.2 Endurance ................................................................... 387
13.3.10.3 Peak Performance and Duration ................................. 387
Clinical Conditions Associated with Athletic Activities ........................... 387
13.4.1 Eligibility Recommendations for Competitive Athletes .............. 387
13.4.2 Eligibility Recommendations for Competitive Athletes with
Cardiovascular Abnormalities ..................................................... 388
13.4.3 Dehydration and Electrolyte Deiciencies.................................... 388
13.4.4 Asthma ......................................................................................... 388
13.4.5 Arrhythmia .................................................................................. 389
13.4.6 Renal Failure ................................................................................ 389
377
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13.4.7 Gastrointestinal Disturbances ...................................................... 389
13.4.8 Anemia ......................................................................................... 389
13.4.9 Immune Deiciency ...................................................................... 390
13.5 Summary .................................................................................................... 390
References .............................................................................................................. 390
13.1
INTRODUCTION
Athletic activities have been a part of competitive amateur and professional sports
for years. Recently, the health beneits of exercise have resulted in an increasing
number of previously sedentary persons participating in athletic activities. Older
sedentary individuals are engaging in athletic activities to lose weight, reduce the
risk of cardiovascular diseases, prevent diabetes, and correct progressive muscle
wasting referred to as sarcopenia.
However, for the purpose of clinical assessment, it should be recognized that in
competitive sports, persons tend to perform at the limits of their capabilities and relatively minor abnormalities in their cardiovascular system may result in fatal events.
Similarly, older sedentary individuals have risk factors for coronary artery disease
such as obesity, diabetes, and hypertension. In both competitive and recreational athletes, it is necessary to initially assess the person to determine whether he or she is
in a good nutritional and physical status to engage in athletic activities. The potential
competitive athlete often is underweight and on a restricted diet high in supplements
with a view to having a very low body fat content and improving performance. In
addition, he or she may have an undetected congenital heart disease. The elderly or
sedentary recreational athlete may be, in contrast, overweight and on cyclical dieting followed by binge eating. In both groups, conditions likely to increase the risk of
cardiac events and injuries need to be identiied prior to initiating training.
After starting training, ongoing assessment is desirable in both types of athletes.
In the competitive athlete there is considerable risk of malnutrition, especially in
women. In the older athletes the objective is to promote weight reduction, document
improvement in cardiovascular function, and observe a gain in muscle or lean body
mass and muscle function. The assessment has two main sections: assessments of
the nutritional status and the medical/physical status. Because cardiovascular health
is especially a consideration for athletes, there should be additional emphasis on
cardiovascular considerations.
13.2
NUTRITIONAL STATUS
The clinical assessment of nutritional status attempts to identify the initial nutritional state and the interplay of the factors inluencing the progression or regression of nutritional abnormalities. Therefore, a clinical nutritional assessment is a
dynamic process that is not limited to a single “snapshot” at the moment of measurement but provides a picture of current nutritional status and insight into the patient’s
future status. The clinical assessment of nutritional status involves a focused history and physical examination in conjunction with selected laboratory tests aimed
© 2011 by Taylor and Francis Group, LLC
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379
at detecting speciic nutrient deiciencies to identify patients who are at high risk for
future nutritional abnormalities. A number of methods of nutritional assessment rely
on measurements of height and weight and calculation of Body Mass Index1,2 (BMI):
BMI = [height (meters)]2 / weight (kg), which is a way of normalizing weight by the
height. In the West, in the Caucasian population, the mean normal BMI is 23, range
(18–25) but in Oriental persons and in those from India the mean normal is 20 and
several otherwise healthy persons have a BMI below the Western range. Hence, in
this chapter the assessment is based on a “dimensionless” algorithm applicable to all
ethnic groups, dependent on the direction of change and factors that are known to
govern the nutritional status3 rather than simply a weight-to-height index.
13.2.1
HISTORY
The nutritional history should evaluate the following questions:
1. Has there been a recent unintentional change in body weight?
2. Is dietary intake adequate? The patient should be questioned about his or
her habitual diet and any change in diet pattern. Has the number, size, and
contents of meals changed? Are nutrient supplements being taken? A diary
documenting food intake may be useful when the history is inconclusive.
In this context, the diet of competitive athletes may be inadequate despite
normal biochemical parameters.4
3. What are the reasons for the change in dietary intake? Has appetite changed?
Is there a disturbance in taste, smell, or the ability to chew or swallow food?
Has there been a change in mental status or increased depression? Has there
been a change in the ability to prepare meals? Are there gastrointestinal
symptoms, such as early satiety, postprandial pain, nausea, or vomiting? Is
the patient taking medications that affect food intake?
4. Is there evidence of malabsorption? Is there any gastrointestinal disease?
Has there been a change in bowel habits?
5. Are there symptoms of speciic nutrient deiciencies including macronutrients, micronutrients, and water?
13.2.2 PHYSICAL EXAMINATION
The physical examination corroborates and adds to the indings obtained by history.
1. Anthropometric assessment. Current body weight should be compared with
previously recorded weights, if available. If accurate weights are not available, assessment of the weight loss and whether it is continuing during the
previous 2 weeks should be undertaken. A search for evidence demonstrating depletion of body fat and muscle masses should be made. A general
loss of adipose tissue can be judged by clearly deined bony, muscular, and
venous outlines, and loose skin folds. A fold of skin, pinched between the
foreinger and thumb, can detect the adequacy of subcutaneous fat. The
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presence of hollow cheeks, buttocks, and perianal area suggests body fat
loss. An examination of the temporalis, deltoids, and quadriceps muscles
should be made to search for muscle wasting.
2. Assessment of muscle function. Strength testing of individual muscle groups
should be made to evaluate generalized and localized muscle weakness. In
addition, a general evaluation of respiratory and cardiac muscle function
should be made.
3. Fluid status appraisal. An evaluation for dehydration (hypotension, tachycardia, postural changes, mucosal xerosis, dry skin, and swollen tongue)
and excess body luid (edema, ascites) should be made.
4. Evaluation for speciic nutrient deiciencies. Rapidly proliferating tissues,
such as oral mucosa, hair, skin, and bone marrow are often more sensitive
to nutrient deiciencies than are tissues that turn over more slowly.
13.3
13.3.1
MEDICAL STATUS
MEDICAL HISTORY
Clinical assessment should start with a careful history that should inquire about factors that are likely to inluence the risks and beneits of exercise. In younger competitive athletes it is necessary to look for factors that are likely to be endangering health
or risk death in the face of strenuous exercise.
13.3.1.1 Competitive Athletes
Cardiovascular system. There is concern of sudden cardiac death and cardiac events
during athletic activities in individuals with known cardiac disease and those without. The two major groups to consider are screening of individuals who plan to
participate in competitive athletic sports without a prior history of cardiac problems
and how to advise and possibly restrict those individuals with known cardiac disease
prior to undertaking athletics.
Sudden cardiac death (SCD) and cardiac events in athletes are rare events.
Although the actual event rate is not known, it has been estimated to be in the order
of 1:200,000 young people of high school age per year.5 More recent registry data in
the United States over a 27-year period (1980–2006), has found that the rate is < 100
cardiovascular sudden deaths in young athletes per year.6 However, these events usually attract a lot of media attention as the event occurs in often young and presumed
healthy individuals. The best approach to screen individuals, especially competitive
athletes, is a source of major debate within the cardiovascular and athletic communities around the world. The purpose of preparticipation screening is to identify
those individuals who may have clinically relevant preexisting conditions, and for
the purpose of this chapter, those that are cardiac in nature. The screening process
should provide potential competitive athletes with an assessment of their medical
eligibility for competitive sports. Therefore, the purpose of the screening process is
to reduce the risk inherent in competitive sports and thereby improve the safety of
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competitive athletes in sport. It should be recognized, however, that it is not possible
to achieve a zero-risk scenario for competitive athletes with preparticipation screening. However, if an abnormality is found, then the screening process is just the irst
step for the individual as further assessment and care will need to be sought through
referral to a subspecialist. The subspecialist will need to determine if the individual
is disqualiied from competitive sport or if exercise restrictions need to be applied.
This topic is beyond the scope of this chapter.
The most common cardiovascular causes of sudden death in competitive athletes
in the United States who are less than 35 years old include hypertrophic cardiomyopathy (HCM) (36%), coronary artery anomalies (17%), indeterminate left ventricular
hypertrophy (LVH) or possible HCM (8%), myocarditis (6%) and arrhythmogenic
right ventricular dysplasia (4%).7 Sudden cardiac death in older athletes (older than
35–40 years old) is usually secondary to an arrhythmia in the setting of unsuspected
atherosclerotic coronary artery disease. The estimated combined prevalence of cardiac disease in the general athlete populations is 0.3%.
The American Heart Association (AHA) updated its scientiic statement on preparticipation screening of competitive athletes in 2007. The AHA recommendations
include a twelve-element screening tool that breaks the assessment into medical
history (including personal history and family history) and then physical examination.7 The European guidelines cite similar screening criteria based on history and
physical examination.8 A positive response to one or more of the twelve items may
be judged worrisome and indication enough to prompt a referral to a cardiologist at
the discretion of the examiner. The Lausanne recommendations under the umbrella
of the International Olympic Committee (IOC) medical commission (2004) outline
a very extensive stepwise approach to the screening of athletes.9 If based on the
preparticipation screening it is decided to refer the athlete to a cardiologist, then the
athlete should not be permitted to practice or compete in events until inal medical
clearance has been given.
Medical history. Parental veriication is recommended for middle school and
high school athletes.
1. Personal History
a. Exertional chest pain/discomfort
b. Unexplained syncope/near-syncope (judged not to be vasovagal,
and of particular concern when related to exertion)
c. Excessive exertional and unexplained dyspnea/fatigue associated
with exercise
d. Prior recognition of a heart murmur
e. Elevated systemic blood pressure
2. Family History
a. Premature death (sudden and unexplained or otherwise) before age
50 due to heart disease in > 1 relative
b. Disability from heart disease in a close relative < 50 years of age
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c. Speciic knowledge of certain cardiac conditions in family members: hypertrophic or dilated cardiomyopathy, long QT syndrome
(LQTS) or other ion channelopathies, Marfan’s syndrome, or clinically important arrhythmias
Respiratory system. History of cigarette smoking and of asthma, particularly
if intensiied by exercise, should be obtained.
Nervous system. History of dizziness, especially induced by exercise or by
lifting heavy objects should be ascertained prior to starting a program of
aerobic or strength training exercise.
Musculoskeletal systems. History of previous injuries or operations on joints
as well as the residual functional limitations should be evaluated. History
of juvenile arthritis should be determined.
Metabolic conditions. Juvenile diabetes is a concern; if present, note the dose
of insulin and control of blood glucose. Episodes of hypoglycemia should
be avoided.10
13.3.1.2 Sedentary and Elderly Athletes
In addition to the history suggested above, those who are proposing to start recreational exercise and athletics should be questioned about symptoms suggestive of
1. Angina, dyspnea on exertion, strokes, and hypertension.
2. Diabetes and renal disease.
3. Body weight changes of either weight gain or unexpected weight loss should
be obtained. The former increases the risk of exercise and the latter occurs
with the onset of serious disease.
4. The existence of arthritis and limitations in mobility.
5. The previous exercise status and a drug history should be obtained. Drugs
likely to inluence exercise ability are
a. Beta-blockers, which cause fatigue and prevent exercise-induced
tachycardia.
b. Insulin action will increase with exercise and may cause hypoglycemia.
c. Antihypertensive drugs may cause fall in blood pressure.
13.3.2
PHYSICAL EXAMINATION
Head and neck examined for enlarged nodes, thyroid enlargement. Eyes
checked for central and peripheral vision and the cornea and conjunctiva
examined for signs of vitamin A and ribolavin deiciency. Tongue and
mouth examined for glossitis and stomatitis, which can suggest iron, folate,
or vitamin B12 deiciency.
Respiratory system for any abnormalities such as evidence of asthma, chronic
bronchitis and emphysema.
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Cardiovascular system
1. Heart murmur: Auscultation should be done in both supine and standing positions (or with valsalva maneuver), speciically to identify murmurs of dynamic left ventricular outlow tract obstruction.
2. Femoral pulses to exclude aortic coarctation.
3. Physical stigmata of Marfan’s syndrome.
4. Brachial blood pressure in the sitting positions in both arms.
Abdomen for enlarged organs and for any masses or tender areas.
Central nervous system for cranial nerve function, general motor function,
general sensory function, and coordination.
Musculoskeletal system for wasting, joint swelling, joint tenderness, and
mobility both passive and active.
13.3.3
HEMATOLOGY
The hemoglobin level is essential to determine whether the person has suficient oxygen-carrying capacity to undertake exercise. Particularly in women, marginal iron
deiciency is extremely common because of menstrual blood losses. The hemoglobin
tends to be at the lower limits of normal but the mean corpuscular volume (MCV)
is reduced and the serum ferritin levels are markedly low. Since iron is an important part of a number of mitochondrial constituents such as cytochrome, deiciency
results in reduced muscle performance and fatigue even when the hemoglobin is only
slightly reduced. On the other hand, with vitamin B12 and folate deiciency, the MCV
is increased. An increase in the MCV should lead to measurements of blood B12 and
folate acid levels. An increase in white blood count and platelet levels are indicative
of any inlammation.
13.3.4
BLOOD BIOCHEMISTRY
Blood glucose levels should be measured to exclude diabetes. Creatinine levels
should be measured to exclude renal disease. Blood electrolyte levels, magnesium,
calcium, and phosphorus should be checked. Abnormalities in any of these levels
can alter muscle performance. Protein status can be assessed by the levels of prealbumin and blood urea nitrogen (BUN). In protein deiciency both these parameters
are reduced. The serum albumin level is not indicative of nutritional status, and in
adults hypoalbuminemia is an index of occult disease.11 The levels of ferritin, vitamin B12, and folate should be measured. Finally, total cholesterol, LDL cholesterol,
and HDL cholesterol should be measured.
13.3.5
MICRONUTRIENT LEVELS
During athletic training, dietary intake may become imbalanced due to inadequate
intake of foods providing micronutrients. Diets high in reined carbohydrates are
often deicient in zinc, selenium, vitamins, and perhaps other minerals and vitamins
such as magnesium. A recent study showed that there was signiicant vitamin B6
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deiciency in high-performance athletes.12 Therefore if the diet of an athlete is unbalanced, micronutrient levels should be measured.
13.3.6
URINE ANALYSIS
Urine analysis should be done to look for renal disease. The presence of protein,
casts, and red blood cells suggest kidney disease and should lead to further examination. Temporary abnormalities in the urine such as proteinuria, microscopic hematuria, and casts may be seen after prolonged vigorous exercise due to reduced renal
blood low and dehydration.
13.3.7
STOOL EXAMINATION
Stool examination for parasites such as hookworm may have to be performed in
countries where this problem is endemic. Parasites cause iron deiciency, which in
turn reduces exercise tolerance.
13.3.8
ELECTROCARDIOGRAPHIC AND ECHOCARDIOGRAPHIC EXAMINATION
13.3.8.1 Competitive Athletes
Preparticipation Screening Recommendations: It is recognized that preparticipation screening with only the history and physical examination does not
have the sensitivity to guarantee detection of all cardiovascular abnormalities that could cause SCD. This could result in false-negative results.
Electrocardiogram (ECG): The 12-lead ECG is abnormal in > 90% of patients
with HCM and can uncover ion channelopathies such as long QT syndrome
and Brugada syndrome. However, the ECG is often abnormal in the hearts
of trained athletes as a normal physiologic response.
The International Olympic Committee (IOC)9 and the European Society of
Cardiology (ESC)8 currently advocate that all young competitive athletes be screened routinely with a 12-lead ECG in addition to the history and physical examination. The rationale for the routine use of the
ECG for preparticipation screening is based on the Italian experience.
Italy has a 25-year experience with a state-subsidized national program
in which all individuals participating in sport between the ages of 12
and 35 are mandated to be screened with a history, physical examination, and ECG by an accredited sports medicine physician.13 This program has been successful for detecting cardiac disease that could result
in SCD and has resulted in the disqualiication of athletes. This action
coincided with an almost 90% reduction in the annual incidence of sudden cardiovascular deaths in competitive athletes. Currently the AHA
2007 guidelines do not make this recommendation as the routine use
of ECGs for preparticipation screening would not it in the current U.S.
model of athletics. However, for the older athlete, the routine use of the
ECG is recommended by the AHA.
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Exercise Stress Testing: Exercise stress testing can be used to detect catecholaminergic polymorphic ventricular tachycardia and for the detection
of coronary artery disease. Stress testing for the detection of congenital
anomalies of the coronary arteries can often give false-negative results. For
the detection of atherosclerotic coronary artery disease (CAD), the exercise
stress test has low speciicity in the low-risk athlete. The routine use of exercise stress testing in healthy asymptomatic athletes with a low-risk proile
is not recommended as there are problems with poor positive predictive
accuracy and false-positive tests that can have negative implications and
result in further unnecessary testing. However, the older competitive athlete
should have focused screening for previously undiagnosed atherosclerotic
coronary artery disease. If, based on the preparticipation screening tool (as
outlined above), the older athlete has no evidence of coronary artery disease
but he or she does have a moderate- to high-risk cardiovascular proile for
CAD and wishes to participate in vigorous competitive situations, he or she
should undergo exercise stress testing.14 The risk proile would include men
> 40–45, women > 50–55 years of age (or postmenopausal), with one or
more independent risk factors including the following: dyslipidemia, systemic hypertension, smoker, diabetes mellitus, family history of SCD or
myocardial infarction in a irst-degree relative < 60 years old. If there are
symptoms suggestive of CAD based on the history or if the athlete is > 65
years old regardless of his or her risk proile, and even when asymptomatic,
an exercise stress test should be performed. However, a more recent study
has found that the routine use of an exercise ECG in people seeking to
obtain clinical eligibility for competitive sports can identify those individuals with cardiac abnormalities who would have otherwise passed preparticipation screening based on history, physical exam, and resting ECG.15
This study identiied that participants over the age of 30 had a signiicantly
increased risk of having cardiac abnormalities on the exercise ECG, thus
resulting in disqualiication from competition. However, follow-up studies
are needed to show if this screening process would reduce the incidence of
cardiac events in athletes.
Echocardiogram: This test is without any risk and can be diagnostic for several conditions that cause SCD in athletes. Cardiac conditions such as
HCM, aortic stenosis, mitral valve prolapse, aortic dilatation, bicuspid aortic valve, left ventricular dysfunction, and on occasion anomalous coronary
arteries can be diagnosed with echocardiogram. However, the yield of routine echocardiography in all competitive athletes will be low.
13.3.8.2 Sedentary and Elderly Athletes
The American Heart Association recommends exercise testing with an electrocardiogram before the start of a vigorous exercise program for all individuals older
than 40 years, even if they are asymptomatic and free of cardiac risk factors.2
However, a study of more than 3,000 asymptomatic men aged 35 to 59 years, with
increased risk of coronary artery disease, casts doubt on the value of this recommendation. Each subject had an exercise test on entry and annually for 7.4 years.
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Exercise proved safe in this group, with approximately 2% experiencing exerciserelated cardiac events. Only 11 of the 62 men who experienced such events had
abnormal exercise tests on entry, a sensitivity of only 18%. The cumulative sensitivity of annual tests was also low, at 24%.16 However, exercise testing can be useful
for detecting exercise-induced arrhythmias and for determining the maximal heart
rate for the exercise prescription.
Echocardiography can be used to study the thickness of the ventricular wall, ventricular diameter, and valve function. In addition, any injury to the myocardium
can be assessed by changes in the motion of the ventricular wall. Patients who have
any history suggestive of coronary artery disease, those with signiicant risk factors
such as hypertension, hypercholesterolemia, family history of myocardial infarction
below the age of 50, diabetes, and obesity would be wise to have an echocardiographic assessment by a cardiologist prior to embarking on an exercise program for
the irst time after the age of 40.
13.3.9
BONE MASS
13.3.9.1 Competitive Athletes
In the competitive athlete, especially in women who undertake intense aerobic physical training, bone loss and even osteoporosis has been recognized.17 The so-called
triad of amenorrhea, eating disorder, and bone loss may occur. The reason is a combination of reduced estrogen levels, reduced body weight and fat, and an imbalanced
diet.18 In these women it is important to document the initial BMI and changes with
training. Marked reduction in BMI and the development of amenorrhea or disordered menstruation should lead to checking the bone mineral density (BMD) by the
use of dual energy x-ray absorptiometry (DEXA). If the BMD in an individual is
more than 2.5 standard deviations (SD) below the mean for a young matched (for age
and sex) population, the diagnosis is osteoporosis. If the BMD is below 1–2.5 SD of
the mean for a young matched population, then the diagnosis is osteopenia.
13.3.9.2 Sedentary and Elderly Athletes
In these persons there may be existing osteopenia or osteoporosis on entry to the
training program. In these subjects exercise has a beneicial effect and increases
BMD.19 During exercise training, in persons with osteopenia or osteoporosis, a
yearly record of changes in BMD is essential. Recording reduced BMD in the hip is
important as it is especially resistant to treatment. In this situation a combination of
jumping, stepping, marching, and side-stepping exercise is one of the few techniques
capable of increasing BMD of the hip.20
13.3.10
MUSCLE FUNCTION
13.3.10.1 Strength
Clinical strength in nutritional studies has been assessed in the upper limb with a
hand-held dynamometer and shown to be improved by nutritional supplementation.21
Hand-grip strength is simple and easy to do and is well correlated with skeletal
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muscle strength. Maximum grip strength and mean value of a 10-second sustained
grip are completed with the dominant hand according to the method outlined in
Sunnerhagen et al.22 Briely, the patient is seated in a chair without arm rests and
with the lowest rib level with the edge of the table. The shoulder is adducted and the
elbow lexed to 90° to 100°. The other arm rests on a table. The palm and ingers are
clasped around the handle and the force exerted against the transducer in the handle
is recorded.
Another way of measuring the effect of nutrition on the strength of different muscle groups is the maximal weight that can be lifted fully one time only (1RM).23 This
measurement can be done for different muscle groups of the upper and lower limbs.
Other methods to measure strength are the vertical jump and isokinetic extension at
different rates that correlate with performance.24
13.3.10.2 Endurance
In a nutritional study of anorexic patients,25 the effect of feeding on endurance was
tested by the an ergometric bicycle protocol (3-minute steps of 30 W) before and
after 8, 30, and 45 days of refeeding. Before refeeding, the workload reached during
the exercise was 49% lower in anorexia nervosa (AN) patients than in control subjects (P < 0.01) and was correlated with body weight, fat-free mass, and leg muscle
circumference (P < 0.002). The performance improved dramatically during refeeding (P < 0.03), reaching normal values after 45 days of refeeding, despite fat-free
mass and leg muscle circumference values that were still 20% lower in AN patients
than in control subjects (P < 0.01).
13.3.10.3 Peak Performance and Duration
Peak performance can be tested by a modiied Wingate protocol. In a study of nutritional supplements,26 volunteers were subjected to a protocol in which they were
tested for the duration of maximal performance at 110% of VO2max. The subjects
were tested for their VO2max and then placed on a bicycle ergometer. The protocol
consisted of a 3-minute warm-up, 1 minute of 40% VO2max followed by 1 minute
of 110% of VO2max for four trial times. Then the subject bicycled until exhaustion
at 110% VO2max. In this study the supplement improved peak performance above
that seen with placebo.
13.4
13.4.1
CLINICAL CONDITIONS ASSOCIATED
WITH ATHLETIC ACTIVITIES
ELIGIBILITY RECOMMENDATIONS FOR COMPETITIVE ATHLETES
Current practices differ between high schools, colleges, and Olympic athletes versus professional athletes in the United States. Professional athletes often have more
rigorous assessments compared to athletes in other venues, and in addition to the
history and physical examination, often undergo noninvasive testing such as ECG,
echocardiogram, and exercise stress testing. However, the AHA in their 2007 recommendations does not believe that it is either prudent or practical to recommend the
routine use of ECG or echocardiogram in the context of mass universal screening.
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However, when considering the individual athlete, noninvasive testing such as ECG
and echocardiogram can enhance the diagnostic power above the standard history
and physical examination without risk to the patient. Therefore, the use of such noninvasive testing should be considered. At a minimum, preparticipation screening
should include the twelve elements of the history and physical as outlined in Section
13.3, and the examination should be performed by a qualiied examiner in an environment conducive to auscultation.
13.4.2
ELIGIBILITY RECOMMENDATIONS FOR COMPETITIVE
ATHLETES WITH CARDIOVASCULAR ABNORMALITIES
For individuals with known prior cardiac disease or for those athletes who are found
to have underlying cardiac abnormalities based on preparticipation screening, specialized evaluation by a cardiologist is recommended. The patient will need to have
a complete cardiovascular evaluation to thoroughly assess the underlying cardiac
abnormality, assess the stability of the cardiac condition, and be risk stratiied for
future cardiac events. A publication of the 36th Bethesda Conference is a useful
guide for physicians and outlines recommendations based on the speciic underlying
cardiac diagnosis for the eligibility for athletics, the recommended intensity of the
sport, and patients who should be disqualiied from competitive sports.27
13.4.3
DEHYDRATION AND ELECTROLYTE DEFICIENCIES
Prolonged exercise is associated with the loss of sweat and dehydration. Dehydration
can cause reduction in reaction times and vigilance.28 Dehydration can be avoided by
ingestion of luids during endurance exercise. Hyponatremia (serum sodium < 135
mmol/L) may occur due to excessive luid intake rather than sodium loss. In a recent
prospective study, dehydration accounted for 26% and hyponatremia for 9% of individuals who sought medical care during endurance exercise. Hyponatremia was
the most common reason for hospital admission. There was an inverse relationship
between postrace sodium concentrations and percentage change in body weight, supporting the suggestion that luid overload is the cause of hyponatremia.29
Plasma potassium rises in healthy subjects by only 0.5 mmol/L when exercising
at 40–50% of VO2max. Hyperkalemia occurs during strenuous exercise and is especially likely to occur in patients with angina or hypertension on beta-blockers such
as propranolol.30 Acidosis can occur with exercise31 but feeding alkalinizing agents
does not improve performance.32
13.4.4
ASTHMA
Exercise-induced asthma is a well-recognized clinical condition. It has been shown
to occur to a greater degree in athletes who pursue strength (3.5 times more common than the general population) and endurance exercise (2.2 times more common).
It occurs more frequently in women and in those who train more than 20 hours in
the week.33
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13.4.5
389
ARRHYTHMIA
Cardiac events during exercise occur in about 2% of individuals over 40 years of
age.2 Even in those who are 75 years of age, exercise-induced arrhythmia occurred
in ~24% of males and only ~7% of females but had no lasting effects.34 However,
asymptomatic persons who develop ventricular premature depolarizations had 2.6
times the risk of coronary events on followup.35 On the other hand, exercise training
of patients who have had myocardial infarction was shown to be of signiicant clinical beneit.36
13.4.6
RENAL FAILURE
Frank renal failure may occur with severe dehydration during endurance exercise.
It may rarely occur due to muscle breakdown called rhabdomyolysis.37 On the other
hand, exercise improved physical functioning in patients on dialysis.38
13.4.7
GASTROINTESTINAL DISTURBANCES
Gastrointestinal disturbance is common among athletes during competition. These
symptoms include nausea, vomiting, belching, heartburn, chest pain, bloating,
abdominal cramps, urge to defecate, frequent defecation, and diarrhea.39 The incidence of bloating, abdominal cramps, and diarrhea was higher with running. In
contrast, all the above symptoms were equally likely to occur during bicycling.20
Measurement of occult blood in the stools showed that during endurance exercise
there was increased loss of blood in the stool.40 The magnitude of the blood loss was
small and did not alter ferritin levels. The cause of blood loss is uncertain but a possible explanation is that during intense exercise, especially during running, blood is
diverted away from the bowel to the muscles, resulting in ischemia of the intestine.41
Athletes often take nonsteroidal analgesic drugs (NSAIDS), and the intake of these
drugs has been shown to increase intestinal permeability and have more adverse
gastrointestinal symptoms.42 Therefore gastrointestinal symptoms are partly due to
exercise and partly due to drugs taken to alleviate pain.
13.4.8
ANEMIA
Plasma volume expansion occurs in athletes and contributes to the commonly occurring normocytic and normochromic anemia.43 This “anemia” did not reduce performance. In football players a study showed that individuals with a lower hematocrit
paradoxically had better aerobic capacity.44 Iron deiciency does not occur simply
due to exercise per se.45 Anemia in athletes should not be dismissed as being due
to exercise without proper investigation. Anemic athletes, especially older persons,
could have an underlying serious condition such as colon cancer. The ingestion of
NSAIDS can be associated with peptic ulceration and blood loss. Anemia could also
be due to menstrual losses in women46 when combined with a diet low in iron. In
women, continuous physical exertion as in military combat training, which would be
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equivalent to vigorous athletic training, reduces ferritin levels; iron supplementation
improved vigor and running times.47
13.4.9
IMMUNE DEFICIENCY
A heavy schedule of training has been shown to be associated with a depression of
immunity.33 The causes for immune depression are multifactorial. Imbalanced diet can
inluence immunity. During intense exercise the demand for carbohydrate by muscle
is high and competes with the needs of macrophages and for purine and pyrimidine
synthesis. A high carbohydrate intake may lead to reduced intake of proteins and lipids, which are important in the maintenance of immune function.48 Intense training
is also associated with reduced immunity due to excessive weight loss and reduced
plasma glutamine levels.49 Since glutamine is an essential nutrient for lymphocytes,
the reduction of glutamine can interfere with lymphocyte function.
13.5
SUMMARY
Clinical assessment of the athlete is a comprehensive process that involves an evaluation of the current nutritional status and the possible change in nutritional status
with athletic activity. In addition it is desirable to assess the medical condition of the
person embarking on athletic activities. While assessing the medical condition of the
potential athlete, it is necessary to differentiate the medical status required for the
competitive athlete from those who are going to undertake recreational activities.
Athletic activities can cause complications that the clinician should recognize and
prevent or treat.
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