ACUTE HEMODYNAMIC CHANGES ASSOCIATED WITH
DANCE EXERCISES IN FEMALES OF LUSAKA, ZAMBIA
By:
Chanda Grace Chisunka
A dissertation submitted to the University of Zambia in partial fulfilment of the
requirements of the degree of Master of Science in Human Physiology.
THE UNIVERSITY OF ZAMBIA
SCHOOL OF MEDICINE
LUSAKA
2019
ABSTRACT
The research was titled; Acute Hemodynamic Changes Associated with Dance Exercises
in Females of Lusaka, Zambia. Dynamic exercises are known to elicit hemodynamic
changes in the cardiovascular system. Zumba and ZOCA are part of a fast growing
group of dance fitness programmes designed to provide a cardiovascular dynamic
workout by moving the large muscle groups rhythmically, repetitively and continuously
following choreography in synchrony to music. However, despite their growing
popularity, very few studies have been done to provide knowledge regarding the
hemodynamic changes associated with these dance exercises. The study was a case
study in which 27 female participants took part in 60 minutes of either a Zumba or
ZOCA class. Using digital blood pressure monitors, recordings of blood pressure and
heart rate were taken at three different points. The first readings were taken before
commencement of the exercise (baseline measures), the second measurements were
taken 30 minutes after exercise (peak exercise time) and at the end of the class (after the
cool down choreography which is performed slowly in order to gradually restore the
body back to its resting state before exercise). The results obtained were as follows;
Mean baseline blood pressures were 118
and 77
7 mmHg, systolic and
diastolic blood pressure, respectively. After 30 minutes of dancing, mean systolic blood
pressure increased to 130
to an average of 80
mmHg (p˂ 0.05) while diastolic blood pressure only rose
mmHg (p˃ 0.05). At the end of the class (after the cool down
phase) mean systolic blood pressure reduced to 109
mmHg (p˂ 0.05). Heart rate increased from
diastolic blood pressure reduced to 74
a baseline value of 83
16 beats/min to 124
exercise (p˂ 0.05) and reduced to 110
mmHg (p˂0.05) while
beats/min after 30 minutes of dance
17 beats/min at the end of the class (p˂ 0.05).
From the heart rate at 30 minutes, the average percentage of maximum heart rate (%
HRmax) was calculated to be 65
%. The researchers concluded that Zumba and
ZOCA elicited significant hemodynamic changes that can be attributed to these
exercises stimulating the cardiovascular regulatory mechanisms sufficiently and hence
resulting in autonomic adjustments that were concurrent with dynamic exercise.
i
DECLARATION
I declare that this research is my own work and that it has not been submitted by any
other person for the acquisition of another postgraduate degree. All the sources of
information that were used have been acknowledged appropriately.
................................
................................
Chanda Grace Chisunka.
Date
ii
DEDICATION
To my children, I hope this inspires you to achieve greater things.
iii
ACKNOWLEDGEMENTS
I give thanks to my God for His sufficient grace.
To my supervisor, Dr. G. Sijumbila and Professor F. Goma, I am grateful for the
academic guidance and support.
I give thanks to the Zumba and ZOCA Instructors, Tendayi Chapoto, Hanifa and Ghada
for the opportunity to conduct this research during their classes.
And I acknowledge the help of all my friends and family members.
iv
Table of Contents
ABSTRACT……………………………………………………………………………………………………………….………………….i
DECLARATION ................................................................................................................................. ii
DEDICATION ................................................................................................................................... iii
ACKNOWLEDGEMENT……………………………………………………………………………………………………………….iv
TABLE OF CONTENTS……………………………………………………………………………………………………………......v
LIST OF TABLES…………………………………………………………………………………………………………………………vii
LIST OF FIGURES……………………………………………………………………………………………………………..………viii
CHAPTER ONE ................................................................................................................................. 1
INTRODUCTION .............................................................................................................................. 1
1.1 BACKGROUND……………………………………………………………………………………..…………………….….1
1.1.1 ARTERIAL BLOOD PRESSURE AT REST AND IN RESPONSCE TO EXERCISE……..……….2
1.1.2 HEART RATE AT REST AND IN RESPONSE TO EXERCISE………………………………………...5
1.2 STATEMENT OF THE PROBLEM.......................................................................................... .6
1.3 JUSTIFICATION……………………………………………………………………………………………………………….7
1.4 RESEARCH QUESTION………………………………………………………………………………………………….…8
1.5 OBJECTIVES…………………………………………………………………………………………………………………...8
1.5.1 MAIN OBJECTIVES……………………………………………………………………………………………..…8
1.5.2 SPECIFIC OBJECTIVES……………………………………………………………………………………….….8
1.6 ORGANISATION OF DISSERTATION………………………………………………………………………..………9
CHAPTER TWO………………………………………………………………………………………………………………………..10
LITERATURE REVIEW……………………………………………………………………………………………………………….10
2.1 PHYSIOLOGY OF HEMODYNAMIC CHANGES ………………………….………………………………….10
v
2.2 CARDIOVASCULAR ADAPTATIONS TO REGULAR EXERCISE…………………………..……………..14
2.3 REVIEW OF CURRENT STUDIES ASSESSING EFFECTS OF DANCE AEROBICS………………....16
CHAPTER THREE………………………………………………………………………………………………….…………….….18
METHODOLOGY…………………………………………………………………………………………..…………………..….….18
3.1 STUDY DESIGN ………………………………………………………………………………………….………………18
3.2 STUDY SETTING …………………………………………………………………………………...….……………….18
3.3 STUDY POPULATION ………………………………………………………………………………….………………18
3.4 PARTICIPANT RECRUITMENT ……………………………………………………………………….……………19
3.5 INCLUSION CRITERION ………………………………………………………………………………………………19
3.6 EXCLUSION CRITERION ………………………………………………………………………………………………19
3.7 DATA COLLECTION PROCEDURE ………………………………………………………………………………..19
3.8 DATA RECORDING PROCEDURE …………………………………………………………………………………21
3.9 DATA ANALYSIS………………………………………………………………………………………………………….21
3.10 LIMITATIONS……………………………………………………………………………………………………………21
3.11 ETHICAL CONSIDERATION ……………………………………………………………………………………….21
CHAPTER FOUR ………………………………………………………………………………………………………………………23
RESULTS …………………………………………………………………………………………………………………………………23
4.1 BASIC CHARACTERISTIC S OF THE STUDY PARTICIPANTS……………………………………………23
4.2 HEMODYNAMIC PARAMETERS…………………………………………………………………………………23
4.2.1 SYSTOLIC BLOOD PRESSURE………………………………………………………….…………………23
4.2.2 DIASTOLIC BLOOD PRESSURE…………………………………………………………………………..25
4.2.3 HEART RATE, MAXIMUM HEART RATE (HRmax) AND PERCENTAGE OF HRmax..26
CHAPTER FIVE ………..……………………………………………………………………………………………………….……..28
DISCUSSION ..………………………………………………………………………..……………………………………………….28
vi
5.1 ASSESSMENT OF BLOOD PRESSURE CHANGES……………..……………………………………….28
5.1.1 SYSTOLIC BLOOD PRESSURE CHANGES………………………………………………………….28
5.1.2 DIASTOLIC BLOOD PRESSURE CHANGES…….………………………………………………….30
5.2 ASSESSMENT OF HEART RATE CHANGES ……….……………………………………………………..31
5.2.1 BASELINE HEART RATE………………………………………………………………………………….31
5.2.2 HEART RATE DURING THE AEROBIC PHASE………………..…………………………………34
5.2.3 HEART RATE AFTER THE COOL DOWN CHOREOGRAPHY.………………………..…….36
CHAPTER SIX …………………………………………………………………………………………………………………………..38
CONCLUSION AND RECOMMENDATION ……………………..……...…………………………..…………………….38
6.1 CONCLUSION…………………..…………………………………………………………………………………………..38
6.2 RECOMMENDATIONS ……………………………………………………………………………………………..….39
REFERENCES …………..………………………………………………………………………………………………………………40
APPENDICES
APPENDIX I ................TABLE OF PERSONAL INFORMATION, BLOOD PRESSURE AND HEART RATE
APPENDIX II ………………………..…………………………………………………………………...INFORMATION SHEET
APPENDIX III…………………………………………………………………………………..INFORMED CONSENT FORM
LIST OF TABLES
TABLE 4-1: SYSTOLIC BLOOD PRESSURE CHANGES……………..……………………………………………………23
TABLE 4-2: DIASTOLIC BLOOD PRESSURE CHANGES……………………………………………………………..….25
TABLE4-3: HEART RATE, HEART RATE MAXIMUM AND PERCENTAGE OF HEART RATE
MAXIMUM..................................................................................................................................27
vii
LIST OF FIGURES
FIGURE 2:1: FACTORS THAT INTEGRATE AND RESULT IN CARDIOVASCULAR ADJUSTMENTS
DURING DYNAMIC EXERCISE……………………………………………………………………………………………………14
FIGURE 4-1: MEAN SYSTOLIC BLOOD PRESSURES AT BASELINE (0MIN), DURING THE AEROBIC
(30 MIN) AND COOL DOWN PHASES (60 MIN) OF THE DANCE EXERCISES…………………….………...24
FIGURE 4-2: MEAN DIASTOLIC BLOOD PRESSURES AT BASELINE (0MIN), DURING THE AEROBIC
(30 MIN) AND COOL DOWN PHASES (60 MIN) OF THE DANCE EXERCISES………………..……………..26
viii
CHAPTER ONE
INTRODUCTION
1.1 Background
During the performance of muscular exercise, the cardiovascular system undergoes
important adaptive changes depending on the type of exercise. There are broadly two
types of muscular activity; dynamic or isotonic exercise and static or isometric exercise.
Exercise in which skeletal muscle contraction causes principally a change in length with
little change in tension is termed dynamic or isotonic exercise. It involves repetition of
low resistance motion and performance of external work; frequent performance
increases endurance. Static exercise on the other hand is muscular activity in which the
contraction causes principally a change in tension with little change in length, it involves
sustained contraction of skeletal muscles against a fixed resistance and does not involve
movement of the joints or axial skeleton and hence no external work is performed;
regular performance does not increase endurance (Lavie et al., 2001). Most muscular
exercise is neither purely dynamic nor purely static. Activities that are predominantly
dynamic include walking, running and cycling while those predominantly static include
lifting or pushing heavy weights (Punia et al., 2016).
Acute hemodynamic changes during dynamic exercise include increases in heart rate,
stroke volume and cardiac output, with relatively little change in mean arterial pressure
because systolic blood pressure tends to increase markedly while diastolic blood
pressure does not. Thus dynamic exercise may be thought of as causing primarily a
volume load on the heart as opposed to a pressure load caused by static exercise
(Weippert et al., 2013). With regular endurance exercise, there can be chronic
adaptations in the cardiovascular system that improve cardiovascular health such as
increase in left ventricular mass and chamber volume without ventricular wall
thickening, a phenomenon known as eccentric cardiac hypertrophy (Joyner and Casey,
2015). These adaptations augment stroke volume and thus maximum cardiac output.
During maximum exercise, heart rate increases to values of 200 beats per minute (bpm)
while stroke volume may also increase from 70ml per beat at rest to 100ml per beat.
1
Thus maximum cardiac output may reach a value of 20 liters per minute. This increase
in stroke volume is also enhanced by training induced increases in blood volume. Blood
volume increases due an increase in both red cell mass and plasma volume (Convertino,
2007).
A fairly new phenomenon in the types of dynamic exercises are aerobic dancing classes
such as Zumba (Luettgen et al., 2014) and Zambia’s own Carribean and African dance
(ZOCA). The typical format of a class begins with a warm up dance of 3 to 5 minutes.
The dance starts slowly to music and gradually increases in speed for the next 30 to 45
minutes. Heart rate elevates to the target as one performs the dance based movements.
The class ends with a 3 to 4 minutes of slow music in order to gradually restore heart
rate to resting levels, this is referred to as the cool down and is then followed by
stretches (Wolfe, 2016).
Zumba and ZOCA are aerobic dances which involve moving the large muscle groups (in
the arms and legs) rhythmically, repetitively and continuously following choreography
in synchrony to music. Zumba uses mainly Latin music while ZOCA uses mainly
Zambian and Caribbean music. The aim is to offer fun and a high energy cardiovascular
workout. Both offer the social aspects of group fitness and support as well as a certified
instructor to lead the class. In this study, acute hemodynamic changes in clients taking
part in Zumba and ZOCA were measured following their participation in a session of
either one of these dance aerobics in order to generate knowledge about the acute effects
of dance exercises on hemodynamic parameters in females of Lusaka, Zambia.
1.1.1
Arterial Blood Pressure At Rest And In Response To Exercise
Arterial blood pressure regulation like other cardiovascular functions is controlled by the
autonomic nervous system. However, the autonomic nervous system is organized as
functional reflexes in which sensory signals from receptors is relayed to integrating
centers in the central nervous system, the impulses are then transmitted via efferent
pathways to the visceral organs to control their activity (Gordan, Gwathmey and Xie,
2015). Integration of cardiovascular reflexes occurs within specialised groups of neurons
2
in the medulla oblongata collectively known as the vasomotor center (Ganong, 2001).
The terminations of the afferent fibers (via the vagus and glossopharyngeal nerves) of
the cardiovascular reflex are located in the nucleus tractus solitarii (NTS). From the
nucleus solitarii, secondary neurons project directly to groups of neurons which
formulate modulatory autonomic signals (Shariff and Hou, 2017). Neurons of the caudal
ventrolateral medulla (CVLM) and rostral ventrolateral medulla (RVLM) determine the
sympathetic tone. They generate excitatory action potentials to the sympathetic
preganglionic neurons (SPN) in the spinal cord. Activation of sympathetic efferent
nerves to the heart increases heart contractility, rate of relaxation and conduction
velocity. In blood vessels, sympathetic activity constricts arteries and arterioles
(resistance vessels) which increases vascular resistance and decreases blood flow. When
this occurs, the increased vascular resistance causes an increase in arterial pressure. The
nucleus ambiguous (NA) and the dorsal motor nucleus of vagus (DMV) have cell bodies
of parasympathetic preganglionic neurons. These mediate the parasympathetic
component of the cardiovascular reflexes which is opposite from sympathetic activity
(Martins-Pinje, 2011). The parasympathetic nervous system acts to decrease cardiac
activity in response to fast increases in blood pressure. At rest, the sympathetic and
parasympathetic nervous systems function reciprocally and maintain an average normal
blood pressure of 120/80mmHg, but it can range from 90/60 mmHg to 130/80 mmHg
(Mallett and Dougherly, 2000).
The most important reflex mechanism that moderates the neural regulation explained
above and plays an important role in short term control of blood pressure during
pathologic and physiologic conditions such as dynamic exercise is known as the
baroreceptor reflex. Mechanoreceptors located in the aorta, carotid sinus, atria,
ventricles and pulmonary vessels are sensitive to the stretch of the walls of these
structures. When the walls are stretched by increased transmural pressure, receptor firing
rate increases and this initiates reflex responses of the autonomic nervous system that
alter cardiac output and systemic vascular resistance (Swenne, 2013). Increased pressure
in the carotid sinus and aorta stretches the carotid sinus baroreceptors and aortic
baroreceptors and raises their firing rate. The increased firing rate leads to excitation of
the nucleus ambiguous neurons and inhibition of firing of the rostral ventrolateral
3
neurons. This results in increased parasympathetic neural activity to the heart and
resistance vessels causing decreased cardiac output and decreased systemic vascular
resistance. Since arterial pressure is the product of systemic vascular resistance and
cardiac output, arterial pressure is returned toward the normal level. Conversely,
decreases in arterial pressure leads to decreased stretch of the baroreceptors and
increased sympathetic neural activity and decreased parasympathetic neural activity
resulting in increased heart rate, stroke volume and systemic vascular resistance, this
raises blood pressure toward the normal level. The primary purpose of the arterial
baroreflex is to provide rapid and efficient stabilization of arterial blood pressure on a
short term basis. Impaired baroreflexes leads to increased blood pressure variability
(Irigoyen and Krieger, 1998).
During exercise, in order to allow for the increase in heart rate and arterial blood
pressure that occur with exercise, the arterial (aortic and carotid) baroreflexes are reset
to function at the higher prevailing arterial blood pressure of exercise (Michelini et al.,
2015).The central command and the exercise- pressor reflex both play a role in the
resetting (Gallagher et al., 2001). Resetting of the operating pressure of the baroreflex to
a higher pressure enables the baroreflex control of sympathetic nerve activity to be
maintained at the resting level despite an increase in pressure produced by a rise in heart
rate and cardiac output (Sheriff, 2006).
Typical maximal values of systolic blood pressure during exercise range from 160 to
220 mmHg. Any further increase in systolic blood pressure during exercise is commonly
interpreted as hypertensive response. On the contrary, a failure of systolic blood pressure
to increase is a hypotensive response. Clinically, both responses may be associated with
underlying risk or presence of cardiovascular disease (Porcari, Bryant and Comana,
2015).
The diastolic blood pressure does not change significantly during exercise in spite of the
increase in systolic blood pressure. This is because diastolic blood pressure is a
parameter mainly determined by cardiac output and peripheral vascular resistance and as
the exercise becomes more intense, systemic vascular resistance normally decreases due
4
to exercise- induced metabolite local vasodilation in the exercising muscles (Kubozono
et al., 2005). This local vasodilation necessitates the hyperemia in the muscles in order
to increase the blood flow to these exercising muscles.
1.1.2 Heart Rate At Rest And In Response To Exercise
Heart rate is normally determined by the sinuatrial node (SA) which exhibits
automaticity. This intrinsic automaticity, if left unmodified by neurohumoral factors,
exhibits a spontaneous firing rate of 100- 115 beats/min. At rest, there is significant
vagal tone on the SA node so that the resting heart rate is between 60 to 100 beats per
minute (Klabunde, 2012).
During exercise, there is both a withdrawal of vagal tone and an activation of
sympathetic activity innervating the SA node. This reciprocal change in sympathetic and
parasympathetic activity permits heart rate to increase during exercise. This neural
activity is also modified by other regulatory factors such as mechanical input from the
muscles (Klabunde, 2012).
In as much as heart rate increases linearly with workload and oxygen consumption, there
is a maximum heart rate that an individual can attain known as the maximum heart rate
(HRmax). Maximal heart rate is often used in exercise physiology and clinical practice
in order to develop exercise prescriptions, estimate aerobic fitness levels and as a
criterion for achieving maximal exertion in the determination of maximal aerobic
capacity (Sarzynski, 2013).
In the determination of an individuals’ maximum heart rate, researchers, clinicians,
fitness instructors and exercise practitioners often use age-based prediction equations to
calculate HRmax. Although many age- based formulae have been proposed, the most
commonly used equation is the age- predicted maximal heart rate calculated by
subtracting an individuals’ age in years from 220 (Zhang et al., 2016). Or more
specifically according to Edwards (2015) 226 - age in years (for women) and 220 – age
in years (for men).
In order for an individual to achieve a particular benefit of an
5
aerobic exercise, one needs to exercise within a percentage of the maximum heart rate
known as the target heart rate.
Target heart rate is a specific age- based pulse rate to be achieved and maintained
during aerobic exercise to ensure optimal cardiovascular function and to ensure an
exercise intensity that maintains the heart rate at 60 % to 85% of the maximum (Fletcher
et al., 1995).
Another physiological measure of work and exercise intensity is the rate pressure
product (RPP), also known as the double product. RPP is an estimate myocardial work
(and the resulting oxygen consumption). It is calculated by multiplying the heart rate
(number of the times the heart needs to beat) and the systolic blood pressure (the arterial
pressure against which the heart is pumping). This index of relative cardiac work relates
closely to directly measured myocardial oxygen consumption and coronary blood flow
in healthy subjects over a wide range of exercise intensities. Changes in heart rate and
blood pressure contribute equally to changes in RPP. Typical values for RPP range from
6000 at rest (HR=50 beats/min; SBP=120 mmHg) to 40,000 (HR= 200 beats/min; SBP=
200mmHg) or above, depending on intensity and exercise mode. Resistance training and
upper body exercise produce substantially higher heart rate and blood pressure responses
(hence higher RPPs) than more rhythmic exercise with the lower body. This added
myocardial work poses an unnecessary risk for coronary heart disease patients with
compromised myocardial oxygen supply. The RPP thus provides an objective measure
to evaluate the effects on cardiac performance of various clinical, surgical, or exercise
interventions (McArdle et al., 2010).
1.2 Statement Of The Problem
Non-communicable diseases (NCDs) such as cardiovascular disease, diabetes mellitus,
chronic obstructive pulmonary diseases (COPD) and cancers are among the leading
causes of morbidity and mortality in the world, with higher rates in developing countries
(Islam et al., 2014). The risk of these diseases is significantly reduced by appropriate
lifestyle modifications such as increased physical activity (Golbidi and Laher, 2012).
6
Aerobic exercises result in autonomic modulation of hemodynamic parameters mainly
mediated by parasympathetic withdrawal and sympathetic activation. This results in
acute cardiovascular changes such as an increase in heart rate, stroke volume, cardiac
output and mean arterial blood pressure (Klabunde, 2012). With regular aerobic training,
chronic adaptations in the cardiovascular system take place e.g. eccentric cardiac
hypertrophy (Joyner and Casey, 2015). In order to produce noticeable or measurable
training effects that then result in these adaptations, principles of exercise entail
exposing the organism (human systems) to an exercise load or work stress of sufficient
intensity, duration and frequency (Åstrand, 2003). Dance exercises are principally
dynamic type of exercises that are performed in synchrony to music. The choreography
of Zumba and ZOCA dances utilizes mainly the large muscle groups of the arms and
legs rhythmically and repetively for an average of 60 minutes per class (Wolfe, 2016).
However, investigations into physiological and fitness components of dance and aerobic
exercises has mainly concentrated on classical forms such as ballet dancing (Koutedakis
and Jamurtas, 2014). Relatively little has been published in relation to modern dance
exercises despite their growing popularity (Luettgen et al., 2014). This study sought to
generate knowledge about the hemodynamic changes associated with Zumba and ZOCA
dance exercises in females of Lusaka, Zambia.
1.3 Study Justification
Exercise is an important factor in the prevention and management of obesity and noncommunicable diseases (NCDs). According to the African Health Observatory (2010),
there are some interventions that have been identified to reduce the prevalence of NCDs,
these include: introducing and strengthening physical activities in all schools,
community physical/sporting activities and promotion of healthy diets. This study
contributes to awareness about the types of exercises that Zambians are already
engaging into even as implementation of the above interventions is undertaken.
7
The study can be used in the formulation of hypotheses for further research related to
dance aerobics and similar dance exercises and contributes to The University of
Zambia’s information in the section of exercise therapy research.
Understanding the hemodynamic changes that occur during dance exercise provides
dance aerobics instructors and their client’s information needed for them to be more
effective in achieving their desired goals of the exercises.
In addition, as far as the researcher’s literature review went, there are no documented
studies that have been done in Zambia to either quantify or describe the health benefits
of dance.
Dance is well received as is evidenced from how fast it’s spreading. The way to credit its
contribution as an exercise is through research. This study contributes to this.
1.4 Research Question
What are the acute hemodynamic changes associated with dance exercises in females of
Lusaka, Zambia?
1.5 Objectives
1.5.1 Main Objective
To determine the acute hemodynamic changes of female participants during a dance
exercise session.
1.5.2 Specific Objectives
To assess the blood pressure changes of female participants during a dance exercise
session
To assess the heart rate changes of female participants during a dance exercise session
8
1.6 Organisation Of Dissertation
The study is presented under six chapters. Chapter one introduces the study by giving
the background of the study, which also elaborates the relevance of the study, the
problem identified and the objectives. Chapter two presents a review of some literature
that relates to the study. Chapter three presents the methodology used in the study and
gives a description of the study population, participant recruitment and the study tools
used. Chapter four presents the results obtained during the study as they relate to the
main and specific objectives of the study. Chapter five discusses the findings of the
study and compares and contrasts them to other studies and relevant literature. Chapter
six gives a summary of the study findings or conclusions and recommendations for
further research.
9
CHAPTER TWO
LITERATURE REVIEW
2.1 Physiology Of Hemodynamic Changes During Exercise
Cardiovascular responses during exercise are due to autonomic modulations that consist
of nervous system regulation (parasympathetic withdrawal and sympathetic activation)
and of mechanical mechanisms (skeletal and respiratory pumps) (Nobrega et al., 2014).
The neural regulation of cardiovascular response during exercise is due to
parasympathetic withdrawal and sympathetic activation. Both of these are a function of
exercise intensity and the total muscle mass recruited (Fisher, 2013).
The sympathetic system (thoracolumbar division) consists of nerves that originate from
the thoracolumbar division of the spinal cord (T1- T4) and innervate target organs while
nerves of the parasympathetic originate within the midbrain, pons and medulla
oblongata of the brain stem and part of the spinal sacral region (S2 –S4). This autonomic
nervous system in turn receives input from the reflex cardiovascular mechanisms via the
neurons of vasomotor center in the medulla oblongata.
The cardiac sympathetic preganglionic nerves originate from the upper thoracic
segments (T1-T4). These secrete the neurotransmitter acetylcholine. The postganglionic
neurons of the sympathetic nervous system release norepinephrine which attaches to
adrenergic receptors in the cardiovascular system. β1 receptors are expressed in the heart
(in the sinuatrial (SA) node, atrioventricular (AV) node and on atrial and ventricular
cardiomyocytes). Activation of β1 receptors increases heart rate (via increased action
potentials from the sinuatrial node), increases cardiac contractility as a result of
increased intracellular calcium concentrations and increased calcium release from the
sarcoplasmic reticulum and increased AV conduction velocity. In addition, activation of
sympathetic β1 receptors induces renin release by the kidneys which activates the reninangiotensin- aldosterone system for the long term regulation of blood pressure, plasma
sodium concentration and blood volume. α1 adrenergic receptors are expressed mainly
10
in vascular smooth muscle proximal to sympathetic nerve terminals. Activation elicits
vascoconstriction. Low expression is also present in cardiomyocytes, activation of which
increases contractility. α2 receptors are expressed in vascular smooth muscles distal to
sympathetic nerve terminals. Activation of these receptors also results in
vasoconstriction. In summary, the sympathetic nervous system to the cardiovascular
system functions to increase heart rate, increase cardiomyocyte contractility, enhance
conduction velocity and vasoconstriction (Gordan, Gwathmey and Xie, 2015).
Cardiac parasympathetic preganglionic neurons are located in the motor nuclei of cranial
nerves and sacral nerves. These receive activation from the nucleus ambiguous and
dorsal nucleus of vagus in the medulla oblongata. Parasympathetic nerves associated
with parts of the head are carried by occulomotor, facial and glossopharyngeal nerves.
Fibers that innervate organs of the thorax and abdomen are part of the vagus nerve
which carries about 75% of all parasympathetic nerve fibers to the heart, lungs and
stomach. Sacral nerves S2 – S4 carry impulses to viscera in the pelvic cavity. Both the
preganglionic and postganglionic neurons release acetylcholine which binds to
muscarinic receptors. In relation to the cardiovascular system, the parasympathetic
nervous system has two kinds of muscarinic receptors, M2 and M3 receptors. M2
receptors are expressed in the heart, abundant in nodal and atrial tissue but sparse in the
ventricles. Binding of acetylcholine to M2 receptors slows heart rate back to resting
sinus rhythm by slowing the rate of depolarization and reducing conduction velocity
through the AV node. Parasympathetic activity also reduces contractility of atrial
cardiomyocytes thus reducing cardiac output as a result of reducing cardiomyocyte
contractility, reducing stroke volume and slowing heart rate. M3 receptors are mainly
expressed in vascular endothelium. M3 receptor activation causes dilation of vessels by
stimulating nitric oxide production by vascular endothelial cells (Gordan, Gwathmey
and Xie, 2015).
Parasympathetic withdrawal and sympathetic activation during exercise therefore results
in an increase in cardiac chronotropy (increased heart rate), increase in cardiac inotropy
(increased myocardial
contractility) to increase stroke volume,
at inducing
venoconstriction to improve venous return, at increasing vascular resistance in the
11
abdominal viscera and nonactive skeletal muscles and at preserving most of the
available cardiac output for the perfusion of the active muscles where metabolicmediated vasodilation takes place. This neural regulation is also referred to as central
command (Fisher, 2013). However, the heart rate increase accounts for a greater
proportion of the increase in cardiac output than does the increase in stroke volume
during strenuous exercise. The stroke volume normally reaches its maximum by the time
the cardiac output has increased only halfway to its maximum. Any further increase in
cardiac output must occur by an increase in heart rate (Guyton and Hall, 2006).
Mechanical mechanisms consist of the contribution of respiratory and skeletal pumps.
The skeletal pumps play the most important role. The muscle rhythms of contraction
occurring during dynamic exercise create intramuscular oscillations which facilitate
blood flow to the heart and enhance cardiac preload, thus increasing stroke volume (SV)
and also cardiac output (CO), this is achieved by recruiting The Frank-Starling
mechanism. In addition, mechanoreceptors and metaboreceptors within muscle
reflexively modulate sympathetic tone on the basis of the mechanic and metabolic
conditions of the contracting muscle. This is referred to as the exercise pressor reflex
(Nobrega et al., 2014). Hypoxia and metabolites produced within endothelial cells of
exercising muscles during dynamic exercise stimulate afferent fibers to the medullary
regulatory centers. Metabolites include adenosine, prostaglandins and nitric oxide
(Casey and Joyner, 2011). These metabolites also increase blood flow in the exercising
muscles by causing vasodilation. This vasodilation lowers peripheral resistance.
In the architecture of skeletal muscle vasculature, the skeletal muscle is perfused by a
feed artery branching off a major conduit artery. There are then four or six branch orders
before the terminal arterioles give rise to capillaries. When the microcirculation is
visualized using imaging and video techniques in contracting skeletal muscle, there is
marked dilation in all elements of the arteriolar tree, with the most pronounced elements
seen in the smallest arterioles (VanTeeffelen and Segal, 2006). However, vasodilation
does not only take place in small arterioles, vasodilation occurs even in feed arteries.
Vasodilation that starts in the smallest arterioles closest to capillaries in the contracting
muscles can ascend to the largest elements of the arteriolar network including feed
12
arteries. This mechanism is dependent on an intact endothelium and appears to be an
active process that includes calcium and electrical signaling along the endothelium and
between the smooth muscle cells and endothelial cells. And finally, with muscle
contractions, the smallest arterioles that vasodilate most vigorously are relatively
resistant to sympathetically mediated vasoconstriction (VanTeeffelen and Segal, 2006).
Arterioles’ being the major site of vascular resistance, their dilation significantly lowers
peripheral resistance and maintains diastolic blood pressure at near resting values during
exercise. This is because as mentioned earlier, diastolic blood pressure is determined
mainly by cardiac output and peripheral resistance. A marked increase in diastolic blood
pressure during exercise could therefore result from an inappropriately high cardiac
output or impaired vasodilation of resistance vessels within skeletal musculature (Brett,
Chowienczyk and Ritter, 1999).
Thus, the hemodynamic changes/adjustments shown during dynamic exercise are
achieved by an integration of several inputs from the motor cortex, arterials and skeletal
muscle receptors. The cardiovascular controlling center integrates this information and
generates hemodynamic adjustments such as an increase in heart rate, increase in
myocardial contractility, increase in blood pressure and constriction of the vascular beds
of organs and tissues not involved in exercise. Figure 2-1 illustrates some of the factors
that contribute to the cardiovascular adjustments occurring during dynamic exercise.
13
Figure 2:1 Factors that integrate and result in cardiovascular adjustments during
dynamic exercise (Nobrega et al., 2014).
2.2 Cardiovascular Adaptations To Regular Exercise
Regular dynamic exercise promotes several cardiovascular adjustments, including
remodeling of the heart and skeletal muscle circulation, improvement of autonomic
control of the heart, and resting bradycardia, a marker of exercise training. Trained
individuals exhibit faster ventricular filling, increased myocardial contractility with
larger stroke volumes, increased capillary supply, predominance of arteriole vasodilator
responses with larger exercise induced muscle blood flow. These cardiac and skeletal
muscle adaptations maintain cardiac output with less energy expenditure and thus a
lower heart rate (Martins- Pinge, 2011).
Fagard (2003) reported that athlete’s had larger left ventricular diameters, larger left
ventricular mass and higher ventricular wall thickness, significant higher posterior wall
thickness and interventricular septal thickness. Apart from these structural adaptations,
athlete’s also had high stroke volumes which were attributed to them having higher end14
diastolic volumes. Therefore, at rest, cardiac output of trained (well exercised)
individuals is reached by higher stroke volumes and lower heart rates.
In achieving adaptations due to exercise, the overload principle needs to be applied.
Principles of physical training entail exposing the body systems to a training load or
work stress of sufficient intensity, duration and frequency in order to produce a
noticeable or measurable training effect i.e. an improvement of the function for which
one is training. In order to achieve such a training effect, it is necessary to expose the
organism to an overload, that is, to a stress which is greater than the one regularly
encountered during activities of daily living (Åstrand et al., 2003).This principle is based
on the need to train the body at a level beyond that at which it normally performs.
Therefore, overload should be a training stimulus, sufficient for chronic adaptations to
occur.
Exercise frequency, duration and intensity are the variables most often
manipulated to provide overload to the systems of the body with specific consideration
given to the mode of exercise (Frontera, 2007). These variables are given under the basic
recommendations for the quality and quantity of cardiorespiratory exercise for
apparently healthy adults as laid down by the American College of Sports Medicine
(ACSM) given below;
Adults should get at least 150 minutes of moderate-intensity exercise per week.
Exercise recommendations can be met through 30-60 minutes of moderateintensity exercise (five days per week) or 20-60 minutes of vigorous-intensity
exercise (three days per week).
One continuous session or multiple shorter sessions (of at least 10 minutes) are
both acceptable to accumulate desired amount of daily exercise (American
College of Sports Medicine [ACSM], 2011).
The American Heart Association (2014) also recommends that emphasis should be on
aerobic physical activities at moderate intensity, as part of an active lifestyle, for at least
150 minutes per week in bouts of 10 minutes or more. Or 75 minutes per week of
vigorous physical activity, or a combination of the two.
15
2.3 Review Of Current Studies Assessing Effects Of Dance Aerobics On The
Cardiovascular System
Dance exercise is principally an isotonic type of exercise that is performed in synchrony
to music. In particular, dance exercise classes utilize mainly the large muscle groups in
the arms and legs rhythmically and repetitively for an average of 60 minutes. During this
time, there are acute hemodynamic changes that occur (such as an increase in heart rate,
increase in stroke volume and cardiac output). With regular aerobic training, chronic
adaptations in the cardiovascular system take place such as eccentric cardiac
hypertrophy (Fernandes and Oliveira, 2011). It is on this basis that exercise programmes
are undertaken. However, investigations into physiological and fitness components of
dance and dancers has mainly concentrated on classical forms of dance such as ballet
(koutedakis and Jamurtas, 2004). Relatively little has been published in relation to
modern types of dance such as Zumba and ZOCA. The following are some studies
which the researcher reviewed relating to these dance aerobics.
In a study carried out by the American Council on Exercise to determine the average
exercise intensity and energy expenditure during a typical Zumba fitness class,
researchers found that the average heart rate (HR) of their participants during the class
was 154 beats per minute (bpm), which was roughly 80 percent of the average predicted
maximum heart rate (HRmax) for the subjects. The researchers reported that this was
within the fitness industry guidelines which suggest exercising in the range of 64 percent
to 94 percent of HRmax in order to improve cardio endurance. The researchers
concluded that Zumba may feel like a party, but that it’s also a highly effective workout
(Luettgen et al., 2014).
Donath et al. (2013) carried out a study in which they provided instructed Zumba
training to thirty female college students twice per week for eight weeks. They found
that clients performed better on a six minutes walk test after the eight weeks of Zumba
than they had done prior to it (p˂0.001). They concluded that Zumba training had
resulted in an improvement in cardiovascular endurance. However, in the same study,
trunk flexibily and lower extremity strength did not change significantly (p˂0.05). This
16
was in accordance with the findings of Barene et al. (2014) in which they found that
after 9 months of Zumba training (two to three one hour sessions of Zumba per week for
the first three months and once a week for another 6 months), no significant intervention
effects were revealed in trunk flexibility (p˂0.05) nor in vertical jump height (p˂0.05)
among the participants.
The health enhancing effects of Zumba are also supported by the work of Domene et al.
(2015) in which they evaluated, among other things, the physiological effects of Zumba
on cardiovascular risk factors and inflammatory biomarkers in overweight and
physically inactive women. Participants were randomly assigned to either engaging in
one or two one hour classes of Zumba fitness weekly. Laboratory assessments were
conducted pre (week 0) and post- intervention (week 8). In the intervention group,
maximal oxygen uptake significantly increased (p˂0.05), percentage of body fat
significantly decreased (p˂0.05) and interleukin 6 and white blood cell count both
significantly decreased (p˂0.05). They concluded that Zumba fitness was an efficacious
health-enhancing activity for adults.
More studies need to be done in order to have comparable results from which
conclusions can be made about the physiological and metabolic effects of dance
exercises such as Zumba and ZOCA.
17
CHAPTER THREE
METHODOLOGY
3.1 Study Design
The research was a case study.
3.2 Study Setting
The study was conducted at Chez Nthemba Sports Club, Intercontinental Hotel Gym and
Olympia Fitness Centre. Study sites were identified by visiting Gyms/Fitness centres
closest to the University of Zambia, Ridgeway Campus and by referral from the
instructors at the visited Gyms/Fitness centres. The researcher then paid a visit to the
different gyms to find out whether they had a dance class, after which permission to
conduct the study was sought from the management at the study sites and from the
respective instructors who offered dance exercise classes.
The three selected study sites were found to have dance exercise instructors with either a
Zumba Fitness or ZOCA Dance instructor licence.
3.3 Study Population
The study population included all members of the selected study sites attending dance
exercise classes. These were between the ages of 18 and 56. A preliminary visit to the
study sites revealed that only females were taking part in both Zumba Fitness and ZOCA
Dance classes.
Therefore, the study population included adult female members of Zumba Fitness or
ZOCA dance exercise classes who met the inclusion criterion and gave consent to taking
part in the study.
18
3.4 Participant Recruitment
Convenience sampling was the method used in this study. In every session that data
were collected, the first two volunteering clients were selected to take part in the study
for that day. Data were collected within a period of one month at each study site. During
this duration, 27 dance exercise clients were recruited and took part in this study.
3.5 Inclusion Criterion
The inclusion criterion was all dance exercise class members above the age of 18 who
had normal measures of blood pressure and heart rate at rest, had attended at least one
dance exercise class prior to the day of data collection and gave consent to taking part in
the study.
Normal blood pressure at rest was taken to be in the range of 90/60 mmHg to 130/80
mmHg (Malett and Dougherly, 2000).
Normal range of heart rate was considered to be 60 to 100 beats per minute (Edward,
2014).
3.6 Exclusion Criterion
Dance exercise class members who were below the age of 18 and those who did not
have normal measures of blood pressure and heart rate at baseline were excluded from
the study.
3.7 Data Collection Procedure
All consenting participants were given a table to fill in demographic information before
the start of the dance exercise session (appendix I). Demographic information included
information such as date of birth, age, gender and how long that client had been taking
dance as an exercise.
Blood pressure and heart rate measurements were collected using a Digital Wrist Blood
Pressure Monitor (Brand; Citizen Micro HumanTech, Model; CH- 618). Each time
measurements were taken, the client was asked to sit down and rest their hand on a table
19
so that their hand was approximately at the level of the heart. The sphygmomanometer
was then strapped at the wrist and the measurement taken. Each session in which data
were collected lasted approximately 60 minutes and all participants in a particular
session started the exercise at the same time. Dance classes were on average, three times
per week. Measurements of blood pressure and heart rate were collected three times for
each participant during a single session.
The first measurements were taken before the start of the exercise session. A consenting
client was asked to take a five minutes rest on a chair before these baseline
measurements were taken. These were also taken in order to exclude participants who
might have blood pressures and heart rates outside the normal resting ranges for a
normal adult. Such clients were advised to consult with a Physician for medical advice.
The second measurement was taken after 30 minutes of exercise. At this time, it was
expected that the client would have exercised for enough time to reach their aerobic
target heart rate and exercising blood pressure. The measurements at this time are
referred to as the aerobic measurements in this study to indicate that these measurements
were taken during the aerobic phase of the dance exercise session. Instructors also gave
a one minute break at this time for clients to refresh and it was immediately at the start
of this break that measurements were taken.
The third measurement was taken after 60 minutes, that is, at the end of the session, after
the cool down choreography. Towards the end of the dance exercise class, for the last
approximately 5 minutes, the instructor reduces the tempo of the choreography, this is
referred to as the ‘cool down’ phase. This is important because an effective cool down
aims to restore the body back to its resting state before exercise. Aside from bringing
body temperature and heart rate down, the cool down helps the body to dispose of waste
products (such as lactic acid) and toxins produced during exercise which would
otherwise contribute to muscle soreness (Weippert et al., 2013).
20
3.8 Data Recording Procedure
Demographic information and measurements of blood pressure and heart rate were
recorded in a table (Appendix I). The information was then entered in a Microsoft Excel
Spreadsheet in readiness for analysis.
3.9 Data Analysis
Continuous variables (such as age, systolic blood pressure, diastolic blood pressure and
heart rate) were summarized using means, medians and standard deviations.
Paired t-tests were used to determine statistical significance of the change in the
variables between baseline and 30 minutes, between 30 minutes and 60 minutes and
between baseline and 60 minutes.
Data analyses were done using STATA version 12.
Data were presented in tables and graphs for clearer display of the results.
3.10 Limitations
The hemodynamic parameters were measured only once for each phase of exercise.
Taking atleast three measurements and then calculating the average would have
minimised possible errors made during the procedure of taking measurements. However,
the necessary client preparation was done precisely to minimise errors. This included
asking the client to sit with the arm resting at the level of the heart, showing the
sphygmomanometer to the client in advance and assuring them that the sensation of
tightening on the wrist was safe (to avoid anxiety) and explaining that they were to avoid
unnecessary movements and talking while measurements were being taken.
3.11 Ethical Considerations
Participation in the study was voluntary and participants were informed that they were
not obliged to continue exercising for the purpose of the study in an event that they
experienced symptoms such as dizziness, shortness of breath or chest discomfort. It was
21
explained that although it is rare in healthy adult individuals, certain changes may occur
during aerobic exercise, including abnormal blood pressure, fainting, abnormal heart rate
and other side effects of exercise and that if this happened, it would be advisable for that
client to stop the exercise and thereafter, to consult with their doctor.
Measurements were taken using a digital blood pressure monitor both to optimise the
accuracy of the change in hemodynamic measurements and also to ensure that the
participants were only minimally disturbed during their exercise session.
All sessions in which data were collected were choreographed by a licensed dance
instructor to ensure that the session was typical of the dance exercise and to ensure the
safety of the clients as the licensed instructors are taught how to monitor their clients.
Participants were not identified by name but using numbers and written consent was
obtained for each participant.
Participants were also told that the information obtained would be used by the researcher
as partial fulfillment for the obtainment of a Master of Science in Human Physiology
Degree, and would also be published for statistical or /and scientific purposes.
Permission to carry out the study was sought from ERES COVERGE and from the
Fitness Instructors of the Zumba Fitness and ZOCA at the different study sites.
22
CHAPTER FOUR
RESULTS
4.1 Basic Characteristics Of The Study Participants
The total sample consisted of 27 adult females. The age range was 18 to 56 with a mean
of 36 years. Of these, 12 (44.4%) had been taking dance exercise for a period of more
than one year, 11 (40.7%) for a period of 1-12 months and 4 (14.8%) for less than 4
weeks.
4.2 Hemodynamic Parameters
4.2.1 Systolic Blood Pressure
Systolic blood pressure was measured at baseline, 30 minutes and also 60 minutes after
exercise. Baseline mean systolic blood pressure was 118
. After 30 minutes
of exercise (during aerobic phase), mean systolic blood pressure increased to 130
mmHg (p˂ 0.05). 60 minutes after exercise (cool down phase), mean systolic blood
pressure reduced to 109
mmHg (p˂0.05).
Table 4-1: Systolic Blood Pressure Changes
Characteristics
Baseline systolic BP, (mmHg)
Mean
118
Median
116
Range
SD
P-value
14
0.0052a
19
<0.0001sc
13
0.0005b
93-142
Systolic BP 30min after training
(mmHg)
130
132
97-165
Cool down systolic BP (mmHg)
109
106
88-129
SD (standard deviation). SBP (Systolic blood pressure). aPaired t-test p-value for
baseline mean and 30 minutes after training systolic blood pressures. scPaired t-test p23
value for systolic BP 30min after training and cool down systolic BP. bPaired t-test pvalue for baseline and cool down systolic blood pressures
140
120
100
Systolic
Blood
Pressure
(mmHg)
80
60
40
20
0
0 min
Baseline
30 min
Aerobic
Time (minutes)
60 min
Cool down
Figure 4-1: Mean systolic blood pressures at baseline (0min), during the aerobic (30
min) and cool down phases (60 min) of the dance exercise.
24
4.2.2 Diastolic Blood Pressure
Diastolic blood pressure was measured at baseline, 30 minutes and 60 minutes after
exercise. The mean diastolic blood pressure at baseline was 77
7 mmHg and showed
no significant change after 30 minutes of dance exercise as it only rose to 80
mmHg
(p˃ 0.05). At the end of the class, diastolic blood pressure reduced to 74
mmHg
(p˂0.05).
Table 4-2: Diastolic Blood Pressure Changes
Characteristics
Mean
Median
Range
SD
P-value
Baseline diastolic BP (mmHg)
77
79
64-86
7
0.1237c
Diastolic BP 30min after training
(mmHg)
80
81
67-110
8
0.0012dc
Cool down diastolic BP (mmHg)
74
74
53-106
12
0.1123d
SD (standard deviation). DBP (diastolic blood pressure). cPaired t-test p-value for
baseline mean DBP and mean DBP 30 minutes after exercise. dcPaired t-test for mean
DBP 30min after exercise and mean DBP after 60 minutes of exercise. dPaired t-test pvalue for mean DBP at baseline and mean DBP 60 minutes after exercise.
25
90
80
70
60
Diastolic
Blood
Pressure
(mmHg)
50
40
30
20
10
0
0 min
Baseline
30 min
Aerobic
Time (minutes)
60 min
Cool down
Figure 4-2: Mean diastolic blood pressures at baseline (0min), during the aerobic (30
min) and cool down phases (60 min) of the dance exercise.
4.2.3 Heart Rate (HR), Maximum Heart Rate (HRmax) And Percentage Of
Maximum Heart Rate (%HRmax)
Heart rate was measured three times for each participant, at baseline, 30 minutes after
exercise and 60 minutes after exercise. The means for heart rate were 83
and 110
, 124
beats per minute (bpm) respectively. The mean heart rates recorded
30 minutes after exercise and also 60 minutes after exercise were statistically higher than
the mean heart rate at baseline (p˂0.05). Using the age-predicted formula for women
(i.e., 226- age), the maximum heart rate was calculated first for each participant and then
the mean maximum heart rate for the participants was calculated and found to be 190
bpm. Furthermore, using the heart rates measured at 30 minutes after exercise, and the
maximum heart rates of the participants, the percentage of maximum heart rate during
the aerobic phase of exercise was calculated for each participant. The average
26
percentage of maximum heart rate was 65% (41-96) in this study. Details of these
characteristics are outlined in table 4-3.
Table 4-3: Heart rate, maximum heart rate and percentage of maximum heart rate
Characteristics
Mean
Median
Range
SD
P-value
Baseline heart rate (bpm)
83
80
59-109
16
Heart 30min after exercise (bpm)
124
119
80-184
25
<0.0001e
Cool down heart rate (bpm)
110
110
68-139
17
<0.0001f
Maximum heart rate (HRmax)
190
189
68-208
10
Percentage (%) of Maximum
heart rate
65
63
41-96
12
SD (standard deviation). ePaired t-test p-value for mean baseline HR and mean HR 30
minutes after exercise. fPaired t-test p-value for mean baseline HR and mean HR after 60
minutes.
27
CHAPTER FIVE
DISCUSSION
5.1 Assessment Of Blood Pressure Changes
5.1.1 Systolic Blood Pressure Changes
In healthy adults, during acute aerobic exercise, systolic blood pressure increases
linearly in relation to the exercise intensity (Kokkinos, 2010). The systolic blood
pressure of the participants in this study showed a significant increase between baseline
and the aerobic phase of exercise (p˂0.05) and also between the aerobic phase and the
cool down phase of the exercise session (p˂0.05). This significant increase in systolic
blood pressure during the aerobic phase of dance exercise demonstrates that the exercise
intensity of Zumba and ZOCA was sufficient to elicit cardiovascular reflex activity that
influenced the autonomic nervous system to increase cardiovascular activity. This is
because the neural regulatory mechanism’s (central command) response of the
cardiovascular system to acute exercise is a result of an integration of information from
the metaboreflex of the exercising muscles and the arterial baroreflex (Michelini et al.,
2015). The neural regulation of the cardiovascular system responds to acute exercise by
parasympathetic withdrawal and sympathetic activation. Sympathetic activation results
in activation of β1 adrenergic receptors in the sinuatrial node, atrioventricular node,
atrial and ventricular cardiomyocytes resulting in increased action potentials from the
sinuatrial node, increased atrioventricular conductivity and increased cardiac
contractility (Gordan, Gwathmey and Xie, 2015). The resultant effect is increased heart
rate, stroke volume and hence cardiac output. Sympathetic activation also results in
vasoconstriction via activation of α1 and α2 receptors of vascular smooth muscle.
Vasoconstriction then leads to increased venous return and increased vascular resistance.
A further increase in venous return is caused by the muscle pumps of exercising muscle
groups’, these are muscle rhythms of contraction and relaxation which facilitate blood
flow to the heart. An increase in venous return increases end-diastolic volume which
increases resting fiber length of cardiomyocytes and results in a further increase in the
force of contraction. This increase in the force of contraction results in an increased
28
stroke volume and subsequently an increased cardiac output, a phenomenon explained
by The Frank-Starling mechanism (Nobrega et al., 2014). Apart from increasing venous
return, vasoconstriction increases vascular resistance in abdominal viscera, this is
important so that cardiac output can be preserved for the exercising muscles were local
vasodilation occurs due to the effect of local metabolites (such as nitric oxide,
prostaglandins and adenosine) produced during muscular activity. The metabolites also
activate
metaboreceptors
in
the
exercising
muscles,
these
together
with
mechanoreceptors, send afferent input to the vasomotor center to reflexively increase
sympathetic tone (exercise-pressor reflex). Both the increased cardiac output and
increased vascular resistance contribute to the increased arterial blood pressure observed
during dynamic exercise (Martins-Pinge, 2011). In addition to the contribution of the
central command and exercise-pressor reflex, an increase in systolic blood pressure is
also possible due to an effective baroreflex resetting. The arterial baroreflex is
responsible for maintaining a stable arterial blood pressure on a short term basis and
therefore, to allow the physiological increase in arterial blood pressure that occurs with
dynamic exercise, this reflex is reset to operate at the prevailing higher arterial blood
pressure (Michelini et al., 2015). In this study, an effective increase in systolic blood
pressure during the aerobic phase of dance exercise suggests that effective baroreflex
resetting occurred in the study participants. In summary, the significant increase in
systolic blood pressure from baseline to the aerobic phase of this study suggest that the
intensity of the Zumba and ZOCA exercises was sufficient to stimulate the exercisepressor reflex input to the vasomotor center with resultant neural modulation and
baroreflex resetting that facilitated the increase in systolic blood pressure.
In order to promote and integrate scientific research and practical application of sport
and exercise science for the maintenance and enhancement of physical performance,
fitness, health and quality of life, certain membership organizations formulate guidelines
for professionals and individuals to adhere to. The American College of Sports Medicine
is one such organization and its guidelines in the field of sport and exercise are
considered to be the ‘gold standard’ in the health and exercise industry. According to the
American College of Sports Medicine (2011), adults should get at least 150 minutes of
29
moderate-intensity exercise per week for the maintenance and improvement of
cardiorespiratory health. In this study, Zumba and ZOCA sessions were routinely
offered for 60 minutes per session, three times per week. With the significant increase in
mean systolic blood pressure recorded during the aerobic phase of exercise, it can be
said that the guidelines of Zumba and ZOCA comply with the guidelines for the duration
and intensity of exercise for adults.
5.1.2 Diastolic Blood Pressure Changes
In this study, the means of diastolic blood pressure before the dance exercises and during
the aerobic phase of exercise were not statistically different (p˃0.05), showing that
diastolic blood pressure did not change significantly during this period of exercise. This
finding is in agreement with literature reviewed that states that in healthy individuals,
diastolic blood pressure does not change significantly during dynamic exercise in spite
of the increase in systolic blood pressure (Kubozono et al., 2005).
The diastolic blood pressure is defined as the minimum pressure experienced in the aorta
when the heart is relaxing before ejecting blood into the aorta from the left ventricle,
often approximately 80mmHg (Homan and Cichowski, 2018). Together with cardiac
output, one of the important determinants of arterial blood pressure is total peripheral
resistance. It a reflection of the countervailing force against cardiac blood flow in the
microvasculature. Multiple factors affect total peripheral resistance and those directly
proportional to it include vessel diameter, total vessel length, blood volume and blood
viscosity. An increase in any of these parameters results in an increase in total peripheral
resistance and hence an increase in blood pressure and vise versa (Hill et al., 2018).
During diastole, the heart is relaxed, not ejecting a stroke volume and hence during this
part of the cardiac cycle, the blood pressure is mainly affected by the peripheral
resistance.
During dynamic exercise, local metabolites produced in the exercising muscles cause
vasodilation which then lowers peripheral resistance. Although the vasomotor center is
the nervous control center of vessel diameter, arterioles and precapillary sphincters are
affected by accumulation of local vasodilator metabolites such as adenosine, potassium,
30
nitric oxide, prostanoids and adenosine triphosphate (Clifford and Hellsten, 2004). These
local effects override the vasomotor center through a process called autoregulation and
increase the rate of exchange of materials between tissue cells and the capillaries. In
addition to vasodilator metabolites, local mechanisms maintaining vasodilation and
hence a high blood flow in exercising muscle include a fall in partial pressure of oxygen,
a rise in tissue partial pressure of carbondioxide, a decreased pH and an increased
temperature (Ganong, 2001). A marked increase in diastolic blood pressure during
dynamic exercise could therefore result from an inappropriately high cardiac output or
impaired vasodilation of resistance vessels within skeletal musculature (Brett,
Chowienczyk and Ritter, 1999). Apart from the short term vasodilation, sustained
postexercise vasodilation (resulting in postexercise reduction in blood pressure) typically
lasts in excess of 2 hours following moderate-intensity aerobic exercise (Halliwill et al.
(2013). Previous work by McCord and Halliwill (2006) had demonstrated that the
sustained postexercise vasodilation is dependent on the activation of histamine H1 and
H2 receptors and that combined antagonism of these receptors reduces postexercise
vasodilation by 80% and postexercise hypotension by 65% following 60 min of
moderate-intensity cycle ergometry in both sedentary and endurance-trained athletes.
These findings are important because they prompt further investigations into possible
benefits that may result from such responses to aerobic exercise.
5.2 Assessment Of Acute Heart Rate Changes
5.2.1 Baseline Heart Rate
The heart’s electrical activity is initiated by specialized cardiac pacemaker cells residing
in the sinoatrial node, often referred to as the SA node (Yanjiv, Tsutsui and Lakatta,
2015). The electrical impulse is then transmitted by perinodal cells to the right atrium
and then through the rest of the heart’s electrical conduction system, resulting in
myocardial contraction (Kashou and Kaushou, 2017). The intrinsic electrical
automaticity of the SA node determines the heart rate (Klabunde, 2012). At rest, the SA
nodal myocytes depolarize at a regular rate between 60 and 100 impulses/minute which
is considered the normal resting heart rate (Kashou and Kashou, 2017). In this study,
participants had an average baseline heart rate of 83 beats per minute which was within
31
the physiological limits. It was important that all participants have heart rate within the
normal range at baseline so that changes measured during the course of the exercise
session could be attributed to the physiological effects of the dance exercises.
The rate and rhythm of spontaneous action potential firing of sinoatrial nodal cells
(SANC) are regulated by stochastic mechanisms that determine the level of coupling of
chemical to electrical clocks within cardiac pacemaker cells. These rhythmic clocks are
the ion channels (and currents) on the surface membrane of the SA node referred to as
the membrane clock (M clock) or voltage clock and calcium channels and currents on
the sarcoplasmic reticulum referred to as the calcium clock (Ca2+ clock). In
spontaneously firing SANC, the M and Ca2+ clocks do not operate in isolation, but
work together and are called a coupled clock system. These clocks work together via
numerous interactions modulated by membrane voltage, subsarcolemmal Ca2+, protein
kinase A (PKA) and Calcium/clamodulin protein kinase II (CaMKII)-dependent protein
phosphorylation. Through these interactions the two subsystem clocks become mutually
entrained to form a robust, stable, coupled-clock system that drives normal cardiac
pacemaker cell automaticity. The coupled- clock system is modulated by autonomic
signaling from the brain via neurotransmitter release from the vagus and sympathetic
nerves (Yanjiv, Tsutsui and Lakatta, 2015). The influence of the autonomic modulation
allows heart rate to vary depending on various environmental and physiological factors.
During exercise, there is both a withdrawal of vagal tone and an activation of
sympathetic activity innervating the SA node. This reciprocal change in sympathetic and
parasympathetic activity permits heart rate to increase during exercise. This neural
activity is also modified by other regulatory factors such as mechanical input from the
muscles (Klabunde, 2012).
Spontaneous diastolic depolarization (DD) is the essence of cardiac pacemaker cell
automaticity. This is the absence of a stable resting potential during diastole, but instead,
there is a smooth transition from maximum diastolic (resting) potential (MDP, -70mV)
to the threshold (-40mV) for the initiation of a new action potential. The diastolic
depolarization is also referred to as the pacemaker phase or phase 4. The contributions of
32
the membrane clock and calcium clocks to cardiac pacemaker cell automaticity are
discussed in the following paragraphs.
Voltage clock. The voltage clock is mainly governed by the ‘funny current’, which is an
inward influx of sodium and potassium. The hyperpolarisation- activated cyclicnucleotide gated (HCN) channel is responsible for the funny current. This pump is
activated by hyperpolarization which occurs during the last phase of the SA node action
potential. This current provides an inward depolarizing current that contributes to
diastolic depolarization. At the same time, there is a reduction in outward K+ currents
that occurs during hyperpolarisation. Additionally, the delayed rectifier K+ currents
which are responsible for repolarisation of the SA node action potential decay following
repolarisaton, allowing the funny currents and other inward currents to depolarize the
cell. SA node myocytes express both L-type and T-type Ca2+ channels. During the last
phase of diastolic depolarization, the T-type Ca2+ channels are activated and this inward
Ca2+ current contributes to the final phase of diastolic depolarization (Bartos, Grandi
and Ripplinger, 2015).
Calcium clock. During late diastolic depolarisation (DD), there is occurrence of
subsarcolemmal local Ca2+ releases (LCR’s). SANC have vast sarcoplasmic reticulum
calcium (SERCA) 2 pumps in the cytoplasm and ryanodine receptors (RyR) in the
subsarcolemmal space. Local calcium releases emanate from sarcoplasmic reticulum via
RyRs following the dissipation of a prior action potential and peak during the late DD,
as they merge with the cytosolic Ca2+ transient triggered by the next AP. This means
local calcium releases induce late diastolic Ca2+ elevations (LDCAE). This Ca2+
elevation results in activation of soldium-calcium exchange channels (NCX). Sodium is
transported into the cell as calcium is transported out of the cell.. Due to this calcium
going out while sodium comes in, the activation threshold of L-type calcium channels is
reached at -50mV to -40mV. Activation of L-type Ca2+ channels during the late DD
results in the generation of the AP rapid upstroke, which then triggers a global SR CA2+
release. This coupled system of intracellelular Ca2+ clocks and surface membrane
voltage clocks controls the timekeeping mechanism of the hearts pacemaker (Lakatta,
Maltsey and Vinogradova, 2010).
33
5.2.2 Heart Rate During The Aerobic Phase Of Exercise
The mean heart rate of the study participants during the aerobic phase of the exercise (at
30 min) was significantly higher than the baseline (0 min) value (P˂0.05). During
aerobic exercise, heart rate increases primarily due to reduced cardiac parasympathetic
neural activity (cPNA), i.e. parasympathetic withdrawal. Central command and rapid
feedback from muscle mechanoreceptors contributes to initial parasympathetic
withdrawal, while loading of the cardiopulmonary baroreceptors (due to an increase in
venous return secondary to muscle pump action) likely also elicits parasympathetic
withdrawal as well cardiac sympathetic neural activation (cSNA). Both parasympathetic
and sympathetic neural activity regulate heart rate throughout the entire exercise
continuum with the relative balance shifting from predominantly parasympathetic
control at rest and low intensities to mainly sympathetic control at higher intensities
(Michael, Graham and Davis, 2017). The sinuatrial node has both sympathetic and
parasympathetic innervations. Sympathetic β1 adrenergic receptors of the SA node,
when activated by norepinephrine, increase its action potential firing rate and thus
results in an increase in heart rate. Activation of β1 receptors also increases contractility
as a result of increased intracellular calcium concentrations and increased calcium
release by the sarcoplasmic reticulum and increased atrioventricular node conduction
velocity. The sinus node also has parasympathetic muscarinic (M2) receptors, the
binding of acetylcholine to M2 receptors serves to slow heart rate till it reaches normal
sinus rhythm (Gordan, Gwathmey and Xie, 2015). As exercise intensity increases
further, progressive baroreceptor resetting as well as afferent feedback from muscle
metaboreceptors trigger further cardiac parasympathetic withdrawal and sympathetic
activation, the latter of which is increasingly augmented from moderate to maximal
intensity by systemic-adrenal activation. This is because as intensity increases, the
augmented activity of the adrenergic neurons stimulates increased adrenal gland release
of epinephrine (and to a lesser extent norepinephrine) into the bloodstream. These
adrenal hormones perpetuate and broaden the sympathetic response to exercise by
increasing energy mobilization, energy redistribution and cardiovascular responsivity.
Catecholamines do so rapidly by activating glycogenolysis and gluconeogenesis.
Epinephrine also augments the supply of free fatty acids to the heart and to the muscles.
34
Adrenal hormones also raise blood pressure and cardiac output (Berne et al., 2007). The
above review emphasizes the knowledge that the muscle activity is the trigger of the
reflex response to exercise, a significant increase in heart rate during Zumba and ZOCA
suggest that the intensity of the dance participants was adequate to elicit the above
mentioned mechanisms of aerobic exercise.
A further extrapolation of the heart rate during the aerobic phase of exercise is the
analysis of the maximum heart rate during this phase of exercise. Zakynthinaki (2015)
explains that if the heart is viewed as a simple pumping machine, it would be expected
to have a minimum and maximum pumping capacity. These would depend on factors
such as its size, shape and its intrinsic mechanical characteristics which defer among
individuals. As long as there is life, the minimum is never zero but operates at a
minimum to sustain bodily functions in the absence of movement. This can be referred
to as the mimimum heart rate or resting heart rate. The maximum heart rate (HRmax) on
the other hand is the highest value that can be achieved in an all-out effort to the point of
exhaustion. It is a highly reliable value that remains constant for a particular subject and
changes only slightly with age (a slight but steady decrease of about one beat/min per
year, beginning at 10 to 15 years of age has been observed). Based on this explanation,
for a person who starts moving from rest (HRmin), the temporal change in heart rate
depends on the intensity of the exercise, as well as on a number of other factors, such as
temperature, heat, fatigue, age, over-training, nutrition and hydration, altitude,
medication, infectious disease or even mental activity. In this study, it was assumed that
all other factors remained constant between the time the baseline measurement of heart
rate and the subsequent readings measured during the 60 minutes that the participant
took part in either a Zumba or ZOCA class and therefore suggests that the changes in
heart rate observed were as a result of the dance exercise choreography and intensity.
Any kind of movement of a particular intensity imposes a circulatory demand on the
body which the heart is called to meet and is rarely equal to HRmax but a fraction of it.
This is referred to as the percentage of heart rate maximum (% HRmax) or target heart
rate of the physical activity. Percentage of heart rate maximum can thus be used as a
measure of exercise intensity and also in developing exercise prescriptions. The
American College of Sports Medicine (2011) recommends that individuals should
35
exercise between 64 and 94% of the HRmax to improve cardiovascular fitness. The
average percentage of maximum heart rate during the aerobic phase (at 30 minutes) of
the study participants was 65
%, therefore, the intensity of the Zumba and ZOCA
dance classes undertaken by these female participants was sufficient to meet the
guidelines of the ACSM regarding the intensity of aerobic exercise that should be
engaged in by healthy adults for improvement of cardiovascular health. The findings of
this study were comparable with those of Luettgen et al. (2014) in which they found that
the average percentage of heart rate maximum of their study subjects was 79 7.0%.
This was also within the stipulated guidelines.
5.2.3 Heart Rate After The Cool Down Choreography
Upon cessation of exercise, the removal of central command together with abolished
feedback from muscle mechanoreceptors resets the arterial baroreflex to a lower level
and causes an initial heart rate decrease. The heart rate decrease is also caused by
increase in cardiac parasympathetic neural activity (cPNA). Hence, this ‘fast phase’ (i.e.,
initial minute) of HR recovery has often been attributed to parasympathetic reactivation.
As recovery continues, a more gradual ‘slow phase’ of cardio-deceleration is observed,
likely mediated by both progressive parasympathetic reactivation and sympathetic
withdrawal. These slower autonomic adjustments are believed to be elicited primarily by
an intensity-dependent combination of gradual metabolite clearance (i.e., reduced
metaboreflex
input)
and
thermoregulatory factors
a
reduction
(direct
in
circulating
thermoreceptor
catecholamines,
afferents
and/or
blood
while
flow
redistribution) may also be involved (Michael, Graham and Davis, 2017). Weippert et
al., 2013 states that cooling down before complete cessation of exercise is important in
order to gradually lower body temperature and heart rate, and to ensure disposal of waste
products (such as lactic acid) and toxins produced during exercise which would
otherwise contribute to muscle soreness. Lactic acid is produced in biochemical
processes which involve the breakdown of energy substrates such as glucose and
glycogen for the production of energy. As exercise intensity increases, the concentration
of lactate in the muscles and arterial blood increases from a basal value of about 1 mM
to about 12mM during strenuous exercise (Zakynthinaki, 2015). Upon cessation of
36
exercise, the lactic acid is cleared out of the muscles and blood by two processes; about
20 percent of lactate produced during exercise is reoxidised to pyruvate and then
dissimilated to carbondioxide and water, and the remaining lactate is taken up by the
liver and forms glucose, which can be converted into glycogen or be delivered to the
blood. A review of studies done by Astrand et al. (2003) demonstrated that this removal
of lactate, accumulated in the body after exhausting exercise, is enhanced if, during
recovery, the subject continues to exercise, but at a lower intensity which normally does
not produce any lactate. This lower intensity exercise is what is termed as the cool down
phase of exercise. During this study, the last measurement of heart rate was taken upon
cessation of exercise but the choreography of the dance exercises in the last five minutes
was of a slow tempo and reduced intensity, directed to offer the ‘cool down’ and
gradually return the body to rest. The mean heart rate after the 60 minutes was lower
than the mean heart rate during the aerobic phase of the exercise, that is to say mean
heart rate reduced after the cool down choreography (p˂0.05). Therefore, the cool down
choreography of Zumba and ZOCA effectively lowered the heart rate in the participants
of this study.
37
CHAPTER SIX
CONCLUSIONS AND RECOMMENDATIONS
6.1 CONCLUSIONS
Hemodynamic changes occurred during dance exercises; Zumba and ZOCA. This can be
attributed to these exercises stimulating the cardiovascular regulatory mechanisms
significantly resulting in autonomic adjustments that were concurrent with dynamic
exercise. The reflexes known to bring about the cardiovascular adjustments during
dynamic exercise are central command, exercise-pressor reflex and baroreflex. Each
reflex in turn activates neurons within the cardiovascular center of the medulla and
modulates the sympathetic and parasympathetic outflow to the cardiovascular system.
This autonomic modulation is mainly parasympathetic withdrawal and sympathetic
activation to the heart and blood vessels. In this study, this was reflected by significant
increases in systolic blood pressure and heart rate between baseline and peak exercise.
The increase in systolic blood pressure also indicated that the participants exhibited
baroreflex resetting to sustain the increase in systolic blood pressure due to sympathetic
activation. There was no significant change in diastolic blood pressure during exercise
from which it can be concluded that the vasodilators produced during Zumba and ZOCA
counteracted the vasoconstriction due to sympathetic activation and therefore the total
vascular resistance could have been maintained or reduced. In addition, because the
change in hemodynamic parameters from rest and during aerobic exercise are directly
proportional to the exercise intensity, the percentage of heart rate maximum, systolic
blood pressure and heart rate change measured during the aerobic phase demonstrate
that the exercise intensity of the Zumba and ZOCA classes that these female participants
engaged in was sufficient to meet the guidelines for aerobic exercise for the
improvement of cardiovascular health in healthy adults.
38
6.2 Recommendations
The hemodynamic responses to Zumba and ZOCA were measured only during one
session of exercise for each client. Longitudinal studies should be done to determine the
presence or absence of adaptation after regular sessions of dance aerobics. This would
generate even more knowledge about the hemodynamic changes and their possible
benefits.
There is need for a regulatory body to formulate national initiatives to promote aerobic
exercise in Zambia as well as to spear head local research and formulation of guidelines
that promote safe but effective aerobic exercises that are tailored to local Zambian
needs, resources and interests. Most of the regulations and guidelines used for reference
are from international bodies.
39
REFERENCES
American College of Sports Medicine [ACSM] (2011) Quantity and Quality of Exercise
for Developing and Maintaining Cardiorespiratory, Musculoskeletal and Neuromotor
Fitness in Apparently Healthy Adults: Guidance for Prescribing Exercise. ACSM
Position Stand. Retrieved from: www.pgedf.ufpr.br/ACSM
American Heart Association (2014) American Heart Association Recommendations for
Physical Activities in Adults . Retrieved from: www.heart.org/heartorg
Åstrand, P. O. et al. (2003) Textbook of Work Physiology, Physiological Bases of
Exercise. 4th Edition. McGraw-Hill International Editions. Champaign. Illinois.
Barene, S. et al. (2014) Effect,s of the Workplace Health Promotion Activities Soccer
and Zumba on Muscle Pain, Work Ability and Perceived Physical Exertion Among
Female
Hospital
Employees.
PLoS
One.
9(12)
e.115059.
doi:10.1371/journal.pone.0115059.
Bartos, D. C., Grandi, E., Ripplinger, C. M. (2015) Ion Channels in the Heart,
Comprehensive Physiology, 5(3) pp. 1423- 1464.
Berne, R. M. et al. (2007) Physiology. 5th Edition. Elsevier Incoporation. Netherlands.
Europe.
Brett, S. E., Chowienczyk, J. P and Ritter, J. M (1999) Diastolic Blood Pressure
Changes During Exercise Positively Correlate with Serum Cholesterol and Insulin
Resistance. American Heart Association. 101 (01) pp. 611- 615.
Casey, P. D and Joyner, M. J. (2011) Local Control of Skeletal Muscle Blood Flow
During Exercise, Influence of Available Oxygen. Journal of Applied Physiology. 111(6)
pp. 1527-1538.
Clifford, P. S. and Hellsten, Y. (2004) Vasodilatory Mechanisms in Contracting Skeletal
Muscle. Journal of Applied Physiology. 97(1) pp. 393-403.
40
Conceicao, L. S. et al. (2016) Effect of Dsance Therapy on Blood Pressure and Exercise
Capacity of Individuals with Hypertension: A Systemic Review and Meta-analysis.
International Journal of Cardiology. 220 (06) pp. 553- 557.
Convertino, V. A. (2007) Blood Volume Response to Physical Activity and Inactivity.
The American Journal of the Medical Sciences. 334(1) pp. 72-79.
Donath, L. et al. (2013) The Effects of Zumba Training on the Cardiovascular System
and Neuromuscular Function in Female College Students. European Journal of Sport
Science. 14(6) pp. 569-577.
Domene, P. A. et al. (2015) The Health- Enhancing Efficacy of Zumba Fitness: An 8week Randomised Controlled Study. Journal of Sports Sciences. 34(15) pp. 1396-1404.
Edwards, S. (2015) Training With 5 Exercise Heart Rate Training Zones, The Training
and Education Company [Online] Available from: http://www.howtobefit.com/fiveheart-rate-zones.htm.
Fagard, R. (2003) Athelete’s Heart. Biomedical Journal. 89(12) pp. 1455-1461.
Farjaz, C. L. M. et al. (1998) Post-Exercise Changes in Blood Pressure, Heart Rate and
Rate Pressure Product at Different Exercise Intensities in Normotensive Humans.
Brazilian Journal of Medical and Biological Research. 31(10) pp. 1247-1255.
Fernandes, T. U. P. R. and Oliveira, E. M. (2011) Eccentric and Concentric Cardiac
Hypertrophy Induced by Exercise Training; microRNAs and Molecular Determinants.
Brazilian Journal of Medical and Biological Research. 44(9) pp. 836-847.
Fisher, J. P (2013) Autonomic Control of the Heart During Exercise in Humans: Role of
Skeletal Muscle Efferents. Exercise Physiology. 99(2) pp. 300-305.
Fletcher, G. F. et al. (1995) Exercise Standards, A Statement for Health Care
Professionals from the American Heart Association. American Heart Association 91 (2).
pp. 580- 615.
41
Frontera, W. R. et al. (2007) Exercise in the Management of Cardiovascular and
Cerebrovascular Disease. Clinical Sports Medicine: Medical Management and
Rehabilitation. Elsevier Health Limited. United States of America.
Gallagher, K. M. et al. (2001) Effects of Exercise-Pressor Reflex Activation on Carotid
Baroreflex Function During Exercise in Humans. Journal of Physiology. 15(3) pp. 871880.
Ganong, F. W. (2001) Review of Medical Physiology. 20th Edition. McGraw-Hill
Medical Publishing Division. New York.
Guyton, A. and Hall, J. (2006) Textbook of Medical Physiology. 11th Edition. Saunders
Limited. Philadelphia, Pennsylvania.
Gordan, R., Gwathmey, J. K. and Xie, L. H. (2015) Autonomic and Endocrine Control
of Cardiovascular Function. World Journal of Cardiology. 7(4) pp. 204-214.
Halliwill, J. R. et al., 2012, Postexercise Hypotension and Sustained Postexercise
Vasodilatation: what happens after we exercise? The Physiological Society. 98(1).
Doi.org/10.1113/expphysiol.2011.058065.
Hill, L. K. et al. (2014) A Validation of Estimated Total Peripheral Resistance Using
Twin Data. Biomedical Sciences Instrumentation. 50: 210-218.
Homan, T. D. and Cichowski, E. (2018) Physiology, Pulse Pressure. StartPearls
Publishing. Treasure Island.
Irigoyen, M. C. and Krieger, E. M. (1998) Baroreflex Control of Sympathetic Activity in
Experimental Hypertension. Brazilian Journal of Medical and Biological Research.
31(9) pp. 1213-1220.
Islam, S. S. et al. (2014) Non-Communicable Diseases (NCDs) in Developing Countries:
a
Symposium
Report.
BioMed
Central
doi.10.1186/512992-014-0081-9.
42
Globalisation
and
Health.
10(81)
Jensen, M. T. et al. (2013) Elevated Resting Heart Rate, Physical Fitness and All-Cause
Mortality: a 16 Year Follow Up in the Copenhagen Male Study. International Journal of
Cardiology. 151(2) pp. 148-154.
Joyner, M. J. and Casey, D. P. (2015) Regulation of Increased Blood Flow (Hyperemia)
to Muscles During Exercise: A Hierarchy of Competing Physiological Needs. American
Physiological Society| Physiological Reviews. 95(2) pp. 546-601.
Kashou, A. H. and Kashou E. H. (2017) Physiology, Sinotrial Node (SA Node). Stat
Pearls Publishing, Treasure Island. Florida.
Klabunde, R. E. (2012) Resting Heart Rate. Cardiovascular Physiology Concepts. 2nd
Edition. Lippincott Williams and Wilkins Ltd.
Kokkinos, P. (2010) The Cardiovascular System. Physical Activity and Cardiovascular
Disease Prevention. Jones and Bartlett Publishers, Burlington, United States of America.
Koutedakis, Y. and Jamurtas, A. (2014) The Dancer as a Performing Athelete:
Physiological Considerations. Sports Medicine. 34(10) pp. 651-661.
Kubozono, T. et al. (2005) High Diastolic Blood Pressure During Exercise is Associated
with Hypercholesterolemia in Patients with Coronary Artery Disease. International
Heart Journal. 46(1) pp. 79-87.
Lakatta, E. G., Maltsev, V. A. and Vinogradova, T. M. (2010) A Coupled System of
Intracelleluar Ca2+ Clocks and Membrane Voltage Clocks Controls the Timekeeping
Mechanism of the Hearts Pacemaker. Circulation Research. 106(4) pp. 659-673.
Lavie, C. J. et al. (2001) Exercise and the Heart: Risks, Benefits and Recommendations
for Providing Exercise Prescriptions. The Ochsner Journal. 3(4) pp. 207-213.
43
Luettgen, M. et al. (2014) Zumba Fitness; Sure It’s Fun But Is It Effective? The
American
Council
on
Exercise.
Retrieved
from:
www.acefitness.org/certifiednewsarticle/2813/.
Martins- Pinge, M. C. (2011) Cardiovascular and Autonomic Modulation by the Central
Nervous System after Aerobic Exercise Training. Brazillian Journal of Medical and
Biological Research. 44(9) pp. 848-854.
McCord, J. L. and Halliwill, J. R. (2006) H1 and H2 Receptors Mediate Postexercise
Hyperemia in Sedentary and Endurance Exercise-Trained Men and Women. Journal of
Applied Physiology. 101(6) pp. 1693-701.
Mallett, J. and Dougherly, L. (2000) The Royal Marsden Hospital Manual of Clinical
Nursing Procedures. 5th Edition. Blackwell Science. Oxford.
Martins- Pinje, M. C. et al. (2011) Cardiovascular and Autonomic Modulation by the
Central Nervous System after Aerobic Exercise Training. Brazilian Journal of Medical
and Biological Research. 44(9) pp. 848-854.
McArdle, W. D. et al. (2010) Exercise Physiology: Nutrition, Energy and Human
Performance. 7th Edition. Lippincott Williams and
Michael, S., Graham, K. S. and Davis, G. M. (2017) Cardiac Autonomic Responses
during Exercise and Post-exercise Recovery Using Heart Rate Variability and Systolic
Time Intervals- A Review, Frontiers in Physiology. 8. pp. 301. doi:
10.3389/fphys.2017.00301.
Michelini, L. C. et al. (2015) Neural Control of Circulation and Exercise: a Translational
Approach Disclosing Interactions Between Central Command, Arterial Baroreflex and
Muscle Metaboreflex. American Journal of Physiology, Heart and Circulatory
Physiology. 309(3) pp. 381-391.
44
Miyai, N. et al. (2002) Blood Pressure Response to Heart Rate During Exercise Test and
Risk of Future Hypertension. American Heart Association [Online]. 39 pp. 761- 766.
Nobrega, A. C. L. et al. (2014) Neural Regulation of Cardiovascular Response to
Exercise: Role of Central Command and Peripheral Afferents. Biomed Research
International. doi.org/10.1155/2014/478965.
Porcari, J., Bryant, C. and Comana, F. (2015) Exercise Physiology. E. A. Davis
Company. Philadelphia.
Punia et al. (2016) Effect of Aerobic Exercise Training on Blood Pressure in Indians:
Systemic
Review.
International
Journal
of
Chronic
Diseases.
Doi.org/10.1155/2016/1370148.
Reents, S. (2007) Exercise and Hypertension [Online] Athlete In Me. Retrieved from:
www.AtheleteInMe.com.html.
Saeid, G. and Laher, I. (2012) Exercise and the Cardiovascular System. Cardiology
Research and Practice. May 31. doi 10.1155/2012/210852.
Sarzynski, A. M. et al. (2013) Measured Maximal Heart Rates Compared to Commonly
Used Age-Based Prediction Equations in the Heritage Family Study. American Journal
of Human Biology: the Official Journal of the Human Biology Council. 25(5) pp. 695701.
Sharif, H. and Hou, S. (2017) Autonomic Dysresflexia: a Cardiovascular Disorder
Following Spinal Cord Injury. Neural Regeneration Research. 12(9) pp. 1390-1400.
Sheriff, D. D. (2006) Baroreflex Resetting During Exercise: Mechanisms and Meaning.
American Journal of Physiology. 290(4) pp. 1406-1407.
Siddiqui, A. (2011) Effects of Vasodilation and Arterial Resistance on Cardiac Output.
Journal of Clinical and Experimental Cardiology. 2 pp. 170
Swenne, C. A. (2013) Baroreflex Sensitivity: Mechanisms and Measurement.
Netherlands Heart Journal. 21(2) pp. 58-60.
45
VanTeefelen, J. W. C. E. and Segal, S. S. (2006) Rapid Dilation of Arterioles with
Single Contraction of Hamster Skeletal Muscle. American Journal of Physiology. Heart
Circulation Physiology. doi:10.1152/ajpheart.00197.2005.
Weippert, M. et al. (2013) Heart Rate Variability and Blood Pressure During Dynamic
and
Static
Exercise
at
Similar
Heart
Rate
Levels.
PLOS
ONE.
8(12)
doi.org/10.1371/journal.pone.0083690.
Wolfe, L. M. (2016) The Meaning of Aerobic Dance. Live Healthy. Available from:
http://www.livehealthy.chron.com/meaning-aerobic-dance-4905.html.
[Accessed:
1st
August, 2016].
Yanjiv, Y., Tsutsui, K. and Lakatta, E. G. (2015) Potential Effects of Intrinsic Heart
Pacemaker Cell Mechanisms on Dysrthythmic Cardiac Action Potential Firing. Frontiers
of Physiology. 6(47). Doi:10.3389/fphys.2015.00047.
Zakynthinaki M. S. (2015) Modelling Heart Rate Kinetics. PLoS ONE. 10 (4):
e0118263. Doi:10.1371/journal.pone.0118263.
Zhang, H. et al. (2016) Importance of Determining Maximal Heart Rate for Providing a
Standardised Training Stimulus. JAMA Internal Medicine. 176(12) pp. 1883-1884.
46
APPENDICES
APPENDIX I: Table Of Personal Information And Measurements Of Blood
Pressure And Heart Rate
Study Site
Date of Birth
Date
Age
Gender
Signature
˂ 4 Weeks
For how long have you been taking dance
classes as an exercise?
1-12 Months
˃ 1 Year
Participant
Baseline
30 minutes
Number
BP
HR BP
60 minutes
HR BP
47
HR
APPENDIX II: Information Sheet
My names are Chanda Chisunka Grace. I am a Physiotherapist currently pursuing a
Master of Science in Human Physiology Degree at The University of Zambia.
As part of the programme am studying, I am required to carry out a research. The title of
my study is ‘Determination of the Acute Hemodynamic Changes Associated with Dance
Exercises in Lusaka, Zambia.
In carrying out this study, I will be measuring Blood Pressure and Heart rate three times
during one of your Zumba sessions. All these measurements will be taken using a wrist
blood pressure monitor which is able to measure both blood pressure and heart rate at
the same time at the wrist.
Before participating in this study, your blood pressure and heart rate will be taken while
you are relaxed in order to determine whether or not your values are within healthy
ranges. If they are found not to be, you should consult your medical doctor as you may
have a health condition that would be causing you to have abnormal blood pressure and
heart rate at rest.
During the study, if you experience symptoms such as shortness of breath or chest
discomfort, do not feel obliged to continue exercising for the purpose of the study. You
should stop and consult a doctor. Participation is voluntary and you are free to with draw
from the study at any point.
Although it is rare in healthy adult individuals, certain changes may occur during the
exercise, including abnormal blood pressure, fainting, abnormal heart rate (too rapid, too
low, or ineffective), and other side effects of exercise.
Should you decide to take part in this study, be informed that your name will not be
documented. Your readings will be treated as confidential by the researcher who will
only use serial numbers when recording the measurements to be taken.
48
The information obtained will be used by the researcher as partial fulfillment for the
obtainment of a Master of Science in Human Physiology Degree, and will also be
published for statistical or /and scientific purposes.
If you need further clarification about this study, please contact any of the addresses
below:
Chanda Chisunka. G (Postgraduate student)
Directorate of Research and Graduate Studies,
The University of Zambia,
School of Medicine,
Department of Physiological Sciences,
P.O Box 32379,
Lusaka, Zambia.
Email: chandachisunka@gmail.com
Cell #: 0967-466021
49
ERES CONVERGE IRB,
33 JOSEPH MWILWA,
LUSAKA,
ZAMBIA.
Email:eresconverge@yahoo.co.uk
Phone numbers: 260955155633/
260955155634
APPENDIX III: Informed Consent Form
I voluntarily agree to participate in the study which is designed to determine my
hemodynamic response to Zumba. The information obtained will be used by the
researcher as partial fulfillment for obtainment of a Master of Science in Human
Physiology Degree.
I have been told that before I participate in the Zumba session, my blood pressure and
heart rate will be measured in an attempt to determine whether or not I have normal
values at rest and that I should not take part in this study but consult my doctor if my
blood pressure and heart rate are found to be outside the normal ranges at rest as this
may be an indication of a health condition.
I am told that the Zumba session I will undergo will be performed for 30minutes during
which my blood pressure and heart rate will be measured seven times. I have also been
told that if I experience symptoms such as shortness of breath, chest discomfort or
extreme fatigue, I am not obliged to continue exercising for the purpose of the study but
that I should stop and consult a Doctor.
I have been told that although it is rare in healthy individuals, certain changes may occur
during the exercise, including abnormal blood pressure, fainting, abnormal heart rate
(too rapid, too low, or ineffective), and other side effects of exercise.
I agree that the information obtained may be used and published for statistical or
scientific purposes.
I have read the above and understand it, and my questions have been answered to my
satisfaction.
Subject ……………………………………………………………
Witness …………………………………………………………...
Date ……………………………………………………………….
50
51
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Acute hemodynamic changes associated with dance exercises in females of Lusaka, Zambia
2019
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