Nutrition for the sprinter

Kevin D Tipton1, Asker E Jeukendrup1, Peter Hespel2

School of Sport and Exercise Sciences, University of Birmingham, England, 2 Research Center for Exercise and Health, Faculty of Kinesiology and Rehabilitation Sciences, K.U. Leuven, Belgium

Address for correspondence Kevin D Tipton, School of Sport and Exercise Sciences, University of Birmingham, England, United Kingdom B152TT Ph 44 121 414 7242 Fax 44 121 414 4121 k.d.tipton@bham.ac.uk Email

Abstract Primary roles for nutrition in sprints are for recovery from training and competition and influencing training adaptations. Sprint success is determined largely by the power to mass ratio, so sprinters aim to increase muscle mass and power. However, extra mass that does not increase power may be detrimental. Energy and protein intake are important for increasing muscle mass. If energy balance is maintained, increased mass and strength are possible on a wide range of protein intakes, so energy intake is crucial. Most sprinters likely consume ample protein. The quantity of energy and protein intake necessary for optimal training adaptations depends on the individual athlete and training demands; specific recommendations for all sprinters are, at best, useless, and are potentially harmful. However, if carbohydrate and fat intake are sufficient to maintain energy levels, then increased protein intake is unlikely to be detrimental. The type and timing of protein intake and nutrients ingested concurrently must be considered when designing optimal nutritional strategies for increasing muscle mass and power. On race day, athletes should avoid foods that result in GI discomfort, dehydration or sluggishness. Several supplements potentially influence sprint training or performance. Beta-alanine and bicarbonate may be useful as buffering agents in longer sprints. Creatine may be efficacious for increasing muscle mass and strength and perhaps increasing intensity of repeat sprint performance during training.

Introduction Sprint events include distances from 60 400 m. These sprint and hurdle events rely primarily on the development of power through anaerobic energy, the phosphocreatine (shorter events e,g, 100 m and 200 m) and glycolytic (longer events, e.g. 400 m) systems for energy. A sprint consists of an all-out effort for a short period of time; performance is determined by the ability to achieve maximal velocity and to limit the loss of power as the sprint progresses. Biomechanical, neuromuscular and metabolic factors will all influence performance. Nutritional support for athletic performance is a popular and widely covered topic. However, the bulk of sports nutrition research has focused on endurance performance. Relatively little has been written concerning nutrition for sprinting performance. Although the potential for an effect is arguably somewhat less than for endurance sports, especially during an event, nutritional choices and strategies will contribute to adaptations to training and to performance in sprinters. Early work demonstrated that elite sprinters have muscles composed predominantly of fast-twitch fibres (Costill et al., 1976). Thus, success requires large, powerful muscles. Accordingly, the major role for nutrition may be to modulate muscle hypertrophy from training. In this review, we will focus on the role of nutrition for increasing muscle mass and strength, as well as the potential for nutritional choices to influence competition day performance. Nutritional support for athletes is often considered for two general situations: training and competition. Important considerations for the sprinter are: Maintaining energy levels during training Quick recovery from training Optimising training adaptations with nutrition Achieving a high power-to-weight ratio, thus maximising muscle mass and maintaining low body fat levels Staying focused, sharp and maintaining concentration during competition days Improve reaction times Nutrition for Sprint Training Sprint training is focused on developing lean body mass capable of generating the power necessary to carry the athlete as rapidly as possible. Adaptations to training are specific to the mode, intensity and duration of the exercise. These adaptations stem primarily from the exercise stimulus on the muscle fibres, but may be influenced by nutritional factors. Nutrition most certainly will influence muscle hypertrophy and this aspect of nutrition is usually the focus for sprinters. Besides specific sprint training, weight training with the goal of developing muscle mass is the primary form of training throughout the year. However, it is important to recognise that optimum mass may not equal maximum mass for a sprinter. At some point, the power to mass ratio may begin to decline with extra mass regardless of composition. Some aspects of the nutritional influence on training adaptations are also covered in other reviews of this series (Hawley et al. 2007; Houtkooper et al. 2007). Recent evidence on the molecular and metabolic levels indicates that training adaptations occur as protein levels change due to the response to each bout of exercise (Hawley et al., 2006). Muscle mass is determined by changes in protein levels, particularly myofibrillar proteins. Increased myofibrillar proteins result from net positive balance of myofibrillar synthesis and breakdown over a given time period. The primary changes occur in response to exercise plus nutrition. The bulk of the response of net muscle protein balance occur following, rather than during exercise (Durham et al., 2004); increased muscle protein synthesis, rather than decreased breakdown, is responsible

for the increased balance (Tipton & Wolfe, 2004). Elevation of muscle protein synthesis is delayed following exercise (Pitkanen et al., 2003), presumably due to inhibition of translational pathways due to elevations in AMPK (Bolster et al., 2003;Koopman et al., 2006). Once activated, muscle protein synthesis and net muscle protein balance remain elevated for up to 48 h following the exercise bout (Phillips et al., 1997); however, protein balance does not become positive without provision of exogenous amino acid sources (Biolo et al., 1997). Consumption of a source of amino acids following exercise increases the response of muscle protein synthesis in an additive manner resulting in positive muscle protein balance (Borsheim et al., 2002;Biolo et al., 1997). The response of net muscle protein balance is due primarily to the essential amino acids (Borsheim et al., 2002;Tipton et al., 1999). Thus, consumption of a source of essential amino acids, be it an intact protein or a free amino acid mixture, will stimulate uptake of amino acids for synthesis of muscle proteins necessary for muscle growth. The optimum amount of amino acids has yet to be determined, but it is clear that a relatively small amount of exogenous amino acids (about 12 g) results in positive protein balance (Borsheim et al., 2002). However, it remains to be seen if chronic consumption of a small amount of amino acids capable of stimulating a transient metabolic response is enough to stimulate muscle hypertrophy in the long term. It is clear that the metabolic and thus phenotypic responses to exercise and thus training adaptations are mediated by intracellular signalling. Recent reviews have examined the response of these pathways to exercise and nutrition in detail (Rennie, 2005; Tipton & Sharp, 2005). Signalling aspects of muscle adaptation to training are also discussed elsewhere in this series of reviews (Hawley et al. 2007). Both translational (Bolster et al., 2004) and transcriptional (Creer et al., 2005;Psilander et al., 2003) mechanisms are stimulated by resistance exercise, but the bulk of the increase in muscle protein synthesis is translational (Chesley et al., 1992). Rates of muscle protein synthesis are increased with no increase in total RNA levels suggesting that it is the efficiency of translation, i.e. an increase in synthesis per molecule of RNA, that is increased by resistance exercise (Chesley et al., 1992). Resistance exercise increases phosphorylation of many translation initiation pathway components (Karlsson et al., 2004;Koopman et al., 2006;Coffey et al., 2006). Adaptations that influence muscle growth also stem from transcriptional regulation (Williamson et al., 2003;Coffey et al., 2006); transcriptional activity of genes for muscle growth factors and myosin heavy chain is stimulated by resistance exercise (Psilander et al., 2003;Raue et al., 2006). At this juncture it is somewhat difficult to discern detailed influences of these pathways due to differences in study design and methods among the studies. Much work needs to be completed to address the gaps in our knowledge. Nutrition has a clear effect on the signalling pathways related to muscle protein synthesis. Previous reviews have detailed the response of intracellular signalling to exercise and nutrition (Kimball et al., 2002;Tipton & Sharp, 2005). The influence of amino acids on muscle protein synthesis is primarily through the mTOR signalling pathways (Kimball et al., 2002;Tipton & Sharp, 2005). Leucine is particularly effective in stimulating initiation of translation following exercise (Anthony et al., 2000;Gautsch et al., 1998). In humans, administration of branched-chain amino acids following resistance exercise increased phosphorylation of p70s6k 3.5-fold above the increase due to exercise when measured at one and two hours after exercise (Karlsson et al., 2004). However, the time course of signalling events relative to muscle protein synthesis has yet to be examined in humans and much has yet to be determined. Increased insulin levels resulting from carbohydrate intake are clearly a major controller of translation initiation pathways (Kimball et al., 2002). Thus, carbohydrates seem to play a role in the response of muscle protein synthesis to feeding after exercise. Insulin stimulates these

translation signalling pathways primarily through phosphoinositol-3-kinase (PI3k), Akt and mTOR (Kimball et al., 2002). Interestingly, post-exercise hyperinsulinaemia only minimally stimulates muscle protein synthesis above normal post-exercise levels (Biolo et al., 1999). Moreover, Anthony et al. (2002) demonstrated that the response of translation initiation to amino acids is mediated by insulin. Taken together, these results suggest that combining carbohydrates and proteins may be the best strategy for stimulation of anabolic pathways. Indeed, utilisation of ingested amino acids for synthesis of muscle proteins is greatest when carbohydrates are ingested concurrently with an amino acid source (Tipton & Witard, 2007). Furthermore, leucine has been demonstrated to be an effective insulin secretagogue (Koopman et al., 2005). Carbohydrate intake may be important for muscle anabolism in other ways as well. Depletion of muscle glycogen is possible, given the multiple sprints common to a sprint training session (Gaitanos et al., 1993). Thus, carbohydrate intake should be sufficient to maintain glycogen levels, not only to prevent fatigue development and maximise training potential, but also perhaps to optimise muscle anabolism. Low glycogen availability may influence the adaptive response to training (Creer et al., 2005;Churchley et al., 2007), suggesting that the maximal anabolic response to resistance exercise may not be possible when exercise is initiated with low glycogen levels. Thus, sprinters should consume sufficient carbohydrate to maintain glycogen during training. Clearly, protein intake is important for muscle hypertrophy, but the amount of dietary protein necessary for a sprint athlete to optimise muscle gains and performance is difficult to determine. A high protein intake is often thought to be critical for muscle growth, repair and enhancement of training adaptations, and a huge supplement industry has been built upon this assumption. The scientific evidence for the efficacy of high protein intakes for increasing muscle mass is, at best, equivocal, and has been extensively debated in the scientific community. The reader is referred to previous reviews for discussions of the merits of increased protein requirements in athletes (Phillips, 2006;Rennie et al., 2004;Tipton & Wolfe, 2004;Tipton & Witard, 2007). It is likely that the disparity of opinions regarding overall protein needs arises from primarily two sources; methodological limitations (nitrogen balance and leucine oxidation) and, perhaps more fundamentally, a lack of consideration for the principal reason athletes ingest protein (Tipton & Witard, 2007). Rather than the attainment of N balance, the amount of protein that optimises muscle hypertrophy and maximises performance is the most salient factor. Attainment of N balance is unlikely to concern sprinters; rather they endeavour to consume the amount of protein necessary to optimise muscle mass and power. For many, if not most, athletes, including sprinters, the point may be inconsequential. Most athletes ingest enough protein to cover even the higher estimates of ~1.2-1.5 gkg-1d-1 (Phillips 2004, Tarnopolsky 2004). Thus, recommending increased protein intake would not be necessary for the majority of athletes consuming a well-chosen diet that meets energy needs. Moore et al. (2007) recently demonstrated that increased N balance and lean body mass result from 12 weeks of intense resistance training while consuming 1.4 gkg-1d-1. Thus, habitually high intakes, often greater than 2 gkg-1d-1, seem to be unnecessary for muscle hypertrophy and increased strength and power. It is likely that protein intake in excess of 1.7 gkg-1d-1 is simply oxidised (Tarnopolsky, 2004). Of course, it should be noted that these results come from previously untrained individuals and it is arguable that years of training may change these responses. On the other hand, a relatively high protein intake is unlikely to be detrimental, even if not entirely necessary. Given the high energy intakes necessary to support increased muscle mass, habitual protein consumption is likely to assure maximum muscle accretion. Although protein and amino

acid supplements may be convenient sources of essential amino acids, no evidence exists to suggest the anabolic response to protein from food sources is inferior to commercially-available supplements (Elliot et al., 2006;Phillips, 2006). It is not possible to make a broad recommendation for a specific amount of protein for all sprinters based on current scientific evidence. Any such recommendations are based on the presumption that muscle protein accretion is linear in relation to amount of ingested protein (Tipton & Witard, 2007). In fact, much of the evidencecasts doubt upon such broad recommendations. Metabolic studies clearly demonstrate that the anabolic response to feeding is dependent on many factors, including, but not limited to, the amount of protein ingested. The type of protein ingested will affect the utilisation of the amino acids for synthesis of muscle proteins (Wilkinson et al., 2007), the anabolic response to protein ingestion will vary with ingestion of other concurrently ingested nutrients (Borsheim et al., 2004a);(Elliot et al., 2006) and, finally, the timing of ingestion of an amino acid source will influence the anabolic response of muscle (Tipton et al., 2001;Tipton et al., 2006). Taken together, it is clear that ingestion of a given amount of protein may result in a variable metabolic response depending on several factors other than solely the amount of protein. Training adaptations may depend less on the amount of protein ingested, and more on the type of proteins ingested, timing of ingestion and other nutrients ingested in the same meal. Perhaps a risk/benefit approach may offer some insights for recommendations of protein intake for athletes. If risk is minimal and there is a rationale for potential benefit, then there is no reason to recommend against increasing protein intake. Health problems, such as kidney damage and bone loss, have often been given as reasons for avoiding high protein intakes. Whereas these issues are theoretically associated with high protein intake, to date there is no evidence for kidney damage from high protein in those with no predisposing kidney maladies (Zello, 2006). A major component of bone is protein and, in fact, synthesis of bone collagen responds similarly to muscle proteins following ingestion of an amino acid source (Babraj et al., 2005). Thus, it appears that reasonably high protein intakes offer little in the way of health dangers to sprinters and other athletes. The relationship between high protein intake and chronic diseases has not been firmly established, but it should be noted that individuals with preexisting kidney disease, should not consume high-protein diets (Zello, 2006). For many athletes, the primary risk of high protein intakes is a necessary reduction in carbohydrate intake which may then affect performance. (Macdermid & Stannard, 2006). Glycogen depletion is likely during training sessions involving repeated sprints (Balsom et al., 1999;Gaitanos et al., 1993) and so sufficient carbohydrate intake to support these training sessions is clearly necessary. However, sprint athletes habitually consume ample carbohydrate and protein (Burke 2007) to support training. Protein nutrition is most often the focus of athletes whose goals include increased muscle mass. However, it is clear that energy balance is just as, if not much more, important for muscle hypertrophy than is protein intake. It is not possible to maintain positive N balance during an energy deficit (Todd et al., 1984). Up to about one third of the variability in N balance is likely due to energy intake (Pellett & Young, 1992). As early as 100 years ago, Chittenden (1907) demonstrated that as long as energy intake is sufficient athletes will gain muscle mass and increase strength even during periods of low protein intake. More recently, positive energy balance has been demonstrated to be more important than level of protein intake for gains in lean body mass during resistance training (Rozenek et al., 2002). The arguments rendered above are contingent upon one primary assumption, namely that the acute metabolic response of muscle to exercise and nutrition represents the potential for long-term muscle gain. Clearly, the ideal study to determine the effect of various feeding strategies on sprinters would be to measure changes in muscle mass, strength, power and speed

ultimately sprint performance during periods with different feeding strategies. Unfortunately, these studies are virtually impossible to perform, primarily due to difficulties in controlling all variables (Tipton & Wolfe, 2004;Tipton & Witard, 2007). A series of recent investigations suggests that results from acute metabolic studies adequately represent the potential for changes in muscle mass in response to training and nutrition (Paddon-Jones et al., 2004;Tipton et al., 2003;Tipton & Witard, 2007). Results from studies at the molecular level support this contention (Coffey et al., 2006;Hawley et al., 2006;Psilander et al., 2003). Since the balance between synthesis and breakdown ultimately determines the amount of each protein in muscle, a decrease in muscle protein breakdown rates should contribute to increased muscle mass. Thus, nutritional strategies aimed at decreasing rates of muscle protein breakdown following exercise are often recommended. Amino acid ingestion following resistance exercise can reduce muscle protein breakdown (Biolo et al., 1997;Tipton et al., 1999). Utilisation of amino acids from ingested amino acid sources by muscle has been shown to increase when carbohydrates are ingested simultaneously (Borsheim et al., 2004b;Borsheim et al., 2004a). The effect of carbohydrates is presumably due to the associated insulin release. Insulin increases net muscle protein balance following resistance exercise primarily by blocking the rise in muscle protein breakdown (Biolo et al., 1999). Thus, it is often recommended to consume protein plus carbohydrates following exercise to maximise net muscle protein balance and increase muscle mass. Recent data suggest that the role of protein breakdown for muscle hypertrophy may not be so clear. Following a resistance exercise bout, rates of muscle protein breakdown increase and are associated with the increased rates of synthesis (Biolo et al., 1995;Phillips et al., 1997). Furthermore, transient changes in gene expression and mRNA levels of both myogenic (Psilander et al., 2003) and atrogenic (Churchley et al., 2007;Jones et al., 2004) genes following resistance exercise suggest that increases in both synthesis and breakdown of proteins are important for changes in protein levels. These data suggest that muscle protein breakdown may play an important role for accretion of muscle. Clearly, more research on the effect of nutrient intake on specific muscle degradative pathways is warranted. Nutrition for Racing The acute influence of nutritional intake for sprinting is not likely to be as great as with endurance events. The length of the race alone prevents large influence from acute intakes. Although sprint events only last seconds, competition can be rather drawn out. A typical competition day involves a number of heats and finals with variable amounts of waiting around in between. For example at the World Championships in Osaka in 2007 the schedule for 100 m is: Day 1 12:10 M 100 Metres HEATS Day 1 20:15 M 100 Metres QUARTER-FINAL Day 3 20:10 M 100 Metres SEMI-FINAL Day 3 22:20 M 100 Metres FINAL On day 1 there are 8 hours between round 1 and 2, on the third day only 2 h between semi-final and final! During the time in between heats athletes should stay hydrated but avoid over-drinking, maintain blood glucose levels and avoid behaviours, including feeding, that may contribute to discomfort, particularly gastrointestinal discomfort. Careful consideration of what NOT to eat is probably more important than what to eat. It is likely that there is no common way to achieve these goals in every athlete. There is almost certainly large individual variation and preference in ways to achieve these goals. Experimenting in training is therefore essential to develop a good routine on race day.

Supplements for the Sprinter There are a few supplements that should be addressed in relation to sprint performance. We will concentrate primarily on supplements for which there is sufficient evidence of their efficacy. Others that are often considered to be important for aspects related to sprint performance, e.g. hydroxymethylbutyrate, ribose, etc., will not be included in this discussion. The results from studies on most supplements is equivocal and it is difficult to recommend usage by sprinters at this time. More detail on these and other supplements can be found in another review in this series by Maughan et al. (2007) and in previous reviews (Hespel et al., 2006;Maughan et al., 2004). When maximal exercise is performed for more than 30 seconds, most of the energy is derived from anaerobic glycolysis. These high rates of glycolysis have been associated with increased muscle acidity and this may eventually impair muscle contraction. Increasing the buffering capacity is theoretically a way of improving performance in such events (>30 sec up to about 7 min; 400m running may just be long enough to benefit from an increased buffering capacity). Beta-alanine (-alanyl-L-histidine) Beta-alanine is a non-essential amino acid that is common in many foods, especially meats. Beta-alanine is believed to be the rate-limiting substrate for synthesis of carnosine, which is an important intracellular buffer (Dunnett & Harris, 1999). Carnosine is found primarily in type IIa and type IIx fibres in skeletal muscle and contributes to intracellular buffering of H+. Thus carnosine attenuates the decrease in intracellular pH associated with anaerobic metabolism. Interestingly, carnosine concentrations in athletes, such as sprinters, appear to be higher than those of marathoners or untrained individuals (Abe, 2000;Tallon et al., 2005). Furthermore, intense physical training may increase muscle carnosine levels (Hill et al., 2007). Four weeks of beta-alanine supplementation increased muscle carnosine by 59% and 10 weeks of supplementation increased it by 80% (Hill et al., 2007). In theory, increasing skeletal muscle carnosine levels (via betaalanine supplementation or intense training) should increase buffering capacity, delay fatigue, and increase exercise performance. Higher carnosine concentration in muscle was associated with higher mean power from a 30 second maximal sprint on a cycle ergometer(Suzuki et al., 2002). Betaalanine supplementation has been demonstrated to increased muscle carnosine content and to be associated with increased performance (Stout et al., 2007). Future studies need to confirm the limited results that are available and examine the combined effect of beta-alanine supplementation and training on muscle carnosine levels in highly trained athletes. Sodium Bicarbonate The primary buffers in the muscle are phosphates and tissue proteins. The most important buffers in the blood are proteins, including haemoglobin, and bicarbonate. During intense exercise, the intracellular buffers (including carnosine) are insufficient to buffer all the hydrogen ions formed. The efflux of H+ into the circulation increases, and bicarbonate has a role in buffering these H+ ions. Bicarbonate ingestion (in the form of sodium bicarbonate) is the traditional method of increasing the extracellular buffering capacity, although sodium citrate is often used as well. The mechanism by which bicarbonate supposedly exerts its action is through this buffering of H+ in the extracellular fluid. This increases the H+ gradient and increases efflux of H+ from the muscle. Reviews of the available literature suggest a dose-response relationship between the amount of bicarbonate ingested and the observed performance effect (Horswill, 1995). A dose of 200 mg/kg bw ingested 1 hour to 2 hours before exercise seems to improve performance in most studies, but 300 mg/kg bw seems to be the optimum dose (with tolerable side effects for most athletes). Doses of less than 100 mg/kg bw do not affect

performance. Intakes of more than 300 mg/kg bw tend to result in gastrointestinal problems. Most of these studies have, however, been performed with exercise lasting longer than a minute and in most of the studies the exercise intensity and duration is comparable to middle distance running, not sprints. No studies show an effect on exercise performance in high-intensity exercise lasting less than 1 minute. Therefore, a window for efficacy of bicarbonate has been identified between approximately 1 minute and 7 minutes and sprint events are not likely to be affected. Nevertheless, the use of bicarbonate is common in 400m running, with anecdotal support for its efficacy. CREATINE Creatine is a natural guanidine compound occurring in meat and fish in concentrations ranging between 3 to 7 gram per kg (Walker, 1979). Synthetic creatine supplements exist as creatine monohydrate or various creatine salts, such as creatine-citrate or creatine-pyruvate. The latter are soluble and stable in solution and thus can be included in sports drinks or gels. On the other hand, creatine monohydrate must be consumed soon after it is brought into solution. The effects of creatine intake on strength and power, primary determinants of sprint running performance, have been extensively investigated since Harris and co-workers first reported that a few days of high-dose oral creatine supplementation can increase muscle creatine content(Harris et al., 1992) However, to the best of our knowledge, only two well-controlled studies have specifically looked at performance in well-trained sprint athletes. Skare et al. (2001) investigated the effect of creatine intake on sprint velocity during a 100m sprint followed by 6 x 60m in locally competitive sprinters. Creatine intake (5 days, 20g/day) marginally increased running velocity in the initial 100m sprint and in five of the 60m sprints. Conversely, performance in sprinters at national level was not increased by creatine intake (0.35g/kg bw, 7 days) in a 6 x 40m (2min rest intervals) intermittent exercise test (Delecluse et al., 2003). Other studies utilizing various types of athletes provide equivocal results (Glaister et al., 2006;Mujika et al., 2000). Importantly, none of the available studies has reported impaired performance. Direct determination of a beneficial effect of creatine supplementation on sprint performance is difficult. First, the performance benefit of creatine intake as a rule is very small, and conceivably within the limits of day-to-day variability in performance, thus reliability of sprint tests in the field may be too small to demonstrate a significant effect of creatine in a small sample of subjects. Second, available data predominantly refer to very short sprints (15-60m) where start reaction time as well as running skill (~coordination) are major determinant of performance. Creatine intake is unlikely to beneficially affect either of these important factors. Finally, it is important to emphasise that results from well-controlled laboratory studies consistently indicate that creatine supplementation can enhance power output during short maximal exercise (Terjung et al., 2000), in particular during intermittent series (10-30sec) of maximal muscle contractions (Casey et al., 1996;Greenhaff et al., 1993) interspersed by 1-2min rest intervals. Heavy resistance training, accounts for an important fraction of the total training volume in elite sprinters. It has been well documented that creatine supplementation can potentiate the gains in fat free mass and muscle force and power output that accompany resistance training (Hespel et al., 2001;Volek et al., 1997). Thus, creatine supplementation conceivably could contribute to improving sprint performance by enhancing the efficacy of resistance training. A classical creatine loading regimen consists of an initial loading phase (15-20g per day, 4-7 days) followed by a maintenance dose (2-5g per day) (Terjung et al., 2000). However, individual responses vary and there are

indications that a positive effect on muscle mass may diminish after 8-10 weeks (Derave et al., 2003). Although solid data are lacking, it may be advisable to add wash-out periods to periods of creatine supplementation for optimum impact. Individuals with a low initial muscle creatine content, such as vegetarians (Burke et al., 2003), respond better to creatine supplementation than others with high a natural muscle creatine content. Therefore, creatine intake probably is an adequate adjuvant to a vegetarian diet in sprinters. Furthermore, ingesting creatine in conjunction with training sessions can stimulate muscle creatine uptake, as exercise is known to facilitate the disposal of ingested creatine into musculature (Harris et al., 1992). It is probably also worthwhile considering the possibility of ingesting creatine supplements in combination with post-exercise carbohydrate-amino acid-protein supplements in order to enhance muscle creatine retention due to increased insulin concentrations (Steenge et al., 2000). Creatine is not on the doping list and its intake is generally found to be safe in healthy adults provided the aforementioned guidelines are followed (Terjung et al., 2000). Creatine intake does result in increased body weight from intracellular water accumulation. Increased water content may be problematic for some athletes, particularly sprinters desiring optimal power-to-mass ratios. The physiological mechanisms underlying the effects of creatine supplementation are only partly understood. There are data indicating that the increased muscle creatine content can facilitate flux through the creatine kinase reaction and thereby prevent net ATP degradation during high intensity muscle contractions (Casey et al., 1996). This flux could also explain the shortening of muscle relaxation time seen after creatine loading (Van et al., 1999) possibly contributing to increased stride frequency during sprinting with creatine intake (Schedel et al., 2000). Given that the importance of phosphocreatine (PCr) to energy production (relative to muscle glycogen) increases as the duration of a sprint is shortened, the ergogenic effect of creatine may be more important in 60 and 100m sprint than in the longer sprint events (200-400m). Furthermore, stimulation of muscle PCr resynthesis may contribute to enhanced recovery between intermittent sprint bouts (Casey et al., 1996;Greenhaff et al., 1994), thus enhancing sprint training. The mechanisms underlying the potential of creatine to stimulate muscle anabolism during resistance training are unclear. Creatine intake may increase stimulation of satellite cell proliferation (Olsen et al., 2006) or intracellular signalling pathways (Deldicque et al., 2005;Louis et al., 2004). Still, direct evidence that creatine can stimulate net protein synthesis in human muscle is lacking (Louis et al., 2003;Parise et al., 2001). Alternatively, changes in muscle protein accretion can occur as a consequence of individuals performing more work during high intensity training programs whilst consuming creatine (Kreider et al., 1998). CAFFEINE Caffeine is a popular stimulant used by most individuals, including athletes. Caffeine is contained in coffee, tea, chocolate and many other caffeinated food sources like cola and so-called energy-booster drinks. The primary mechanism of action by which caffeine can beneficially affect performance probably is by enhancing central drive, and/or improving muscle fibre recruitment (Graham, 2001). It is well known that small doses of caffeine (1-2 mg/kg body weight) can beneficially influence mental alertness and thereby shorten reaction time (Haskell et al., 2005), which is obviously crucial to sprint success. However, care must be taken to determine the optimum dose during training because overdosing will negatively affect reaction time. Because sprinters typically compete on an empty stomach, caffeine will be very rapidly absorbed, and if ingested during the precompetition warm up period the potential performance benefits may be reduced during the competition to follow (Bell & McLellan, 2002). Caffeine should be ingested in an isolated formulation (capsules or tablets) rather than

in the form of strong coffee because the latter is more likely to cause gastrointestinal distress (Tarnopolsky, 1994). Responses to caffeine intake and withdrawal vary greatly amongst individuals depending on the degree of habituation (Bell & McLellan, 2002;Magkos & Kavouras, 2004). Therefore, individual tuning of the dosage in the context of training is very important. Frequent high-dose caffeine intake results in rapid desensitization and will will require use of an even higher dose. The common use of caffeine as a social stimulant probably proves that low dose caffeine intake should be considered to be safe. However, high-dose caffeine intake is well known to be associated with adverse health effects, in particular at the level of the cardiovascular system (Tarnopolsky, 1994). In 2004 the World Anti Doping Agency (WADA) removed caffeine from the list of banned substances and its use is currently being monitored. Summary of nutritional guidelines for sprinters Clear consensus for Carbohydrate intake should be sufficient (~5g/kg body wt) to maintain glycogen stores during training. Energy intake should be carefully considered if increased muscle mass is desired, energy intake should be increased; if muscle mass is optimal, energy intake should be maintained and perhaps monitored. Protein intake is likely adequate for the majority of sprinters, but if energy intake is increased a portion of this increase could, and perhaps should, be protein. Type of protein and timing of protein ingestion should be considered if increased muscle mass is the goal. Race day nutrition should be developed individually with the goal of avoiding GI distress and dehydration. Creatine supplementation may enhance increases in muscle mass and strength, but sprinters must consider the extra weight gain associated with creatine use. Clear consensus against A single broad recommendation for protein intake for all sprint athletes is nonsensical. Since power/mass is the most critical element of sprinting success, automatically assuming strategies that may increase muscle mass are desirable could be a mistake if increased mass decreases the power/mass ratio. Use of supplements as sources of protein and amino acids in the belief that they provide superior quality to foods. There is insufficient evidence to recommend other supplements, e.g. ribose, hydroxymethylbutyrate, vanadyl sulphate, etc. to sprinters at this time.

Issues that are equivocal

Relationship of type of protein and timing of ingestion of proteins for muscle anabolism. The role of muscle degradative pathways for adaptation to training. The impact of nutrition on muscle degradative

pathways for training adaptations. Effect of nutrients and the interaction with training on signalling pathways and gene expression in muscle. Efficacy of beta-alanine for increasing muscle carnosine in well-trained sprinters. Efficacy of bicarbonate in sprinters.

Reference List

Abe H (2000). Role of histidine-related compounds as intracellular proton buffering constituents in vertebrate muscle. Biochemistry (Mosc ) 65, 757765. Anthony JC, Yoshizawa F, Anthony TG, Vary TC, Jefferson LS, & Kimball SR (2000). Leucine stimulates translation initiation in skeletal muscle of postabsorptive rats via a rapamycin-sensitive pathway. J Nutr 130, 24132419. Babraj JA, Smith K, Cuthbertson DJ, Rickhuss P, Dorling JS, & Rennie MJ (2005). Human Bone Collagen Synthesis Is a Rapid, Nutritionally Modulated Process. J Bone Miner Res 20, 930-937. Balsom PD, Gaitanos GC, Soderlund K, & Ekblom B (1999). High-intensity exercise and muscle glycogen availability in humans. Acta Physiol Scand 165, 337-345. Bell DG & McLellan TM (2002). Exercise endurance 1, 3, and 6 h after caffeine ingestion in caffeine users and nonusers. J Appl Physiol 93, 12271234. Biolo G, Maggi SP, Williams BD, Tipton KD, & Wolfe RR (1995). Increased rates of muscle protein turnover and amino acid transport after resistance exercise in humans. Am J Physiol 268, E514-E520. Biolo G, Tipton KD, Klein S, & Wolfe RR (1997). An abundant supply of amino acids enhances the metabolic effect of exercise on muscle protein. Am J Physiol 273, E122-E129. Biolo G, Williams BD, Fleming RY, & Wolfe RR (1999). Insulin action on muscle protein kinetics and amino acid transport during recovery after resistance exercise. Diabetes 48, 949-957. Bolster DR, Jefferson LS, & Kimball SR (2004). Regulation of protein synthesis associated with skeletal muscle hypertrophy by insulin-, amino acid- and exercise-induced signalling. Proc Nutr Soc 63, 351-356.

Bolster DR, Kubica N, Crozier SJ, Williamson DL, Farrell PA, Kimball SR, & Jefferson LS (2003). Immediate Response of mTOR-Mediated Signaling Following Acute Resistance Exercise In Rat Skeletal Muscle. J Physiol. Borsheim E, Aarsland A, & Wolfe RR (2004a). Effect of an amino acid, protein, and carbohydrate mixture on net muscle protein balance after resistance exercise. Int J Sport Nutr Exerc Metab 14, 255-271. Borsheim E, Cree MG, Tipton KD, Elliott TA, Aarsland A, & Wolfe RR (2004b). Effect of carbohydrate intake on net muscle protein synthesis during recovery from resistance exercise. J Appl Physiol 96, 674-678. Borsheim E, Tipton KD, Wolf SE, & Wolfe RR (2002). Essential amino acids and muscle protein recovery from resistance exercise. Am J Physiol Endocrinol Metab 283, E648-E657. Burke DG, Chilibeck PD, Parise G, Candow DG, Mahoney D, & Tarnopolsky M (2003). Effect of creatine and weight training on muscle creatine and performance in vegetarians. Med Sci Sports Exerc 35, 1946-1955. Casey A, Short AH, Curtis S, & Greenhaff PL (1996). The effect of glycogen availability on power output and the metabolic response to repeated bouts of maximal, isokinetic exercise in man. Eur J Appl Physiol Occup Physiol 72, 249-255. Chesley A, MacDougall JD, Tarnopolsky MA, Atkinson SA, & Smith K (1992). Changes in human muscle protein synthesis after resistance exercise. Journal of Applied Physiology 73, 1383-1388. Churchley EG, Coffey VG, Pedersen DJ, Shield A, Carey KA, CameronSmith D, & Hawley JA (2007). Influence of Pre-exercise Muscle Glycogen Content on Transcriptional Activity of Metabolic and Myogenic Genes in WellTrained Humans. J Appl Physiol. Coffey VG, Zhong Z, Shield A, Canny BJ, Chibalin AV, Zierath JR, & Hawley JA (2006). Early signaling responses to divergent exercise stimuli in skeletal muscle from well-trained humans. FASEB J 20, 190-192. Costill DL, Daniels J, Evans W, Fink W, Krahenbuhl G, & Saltin B (1976). Skeletal muscle enzymes and fiber composition in male and female track athletes. J Appl Physiol 40, 149-154. Creer A, Gallagher P, Slivka D, Jemiolo B, Fink W, & Trappe S (2005). Influence of muscle glycogen availability on ERK1/2 and Akt signaling after resistance exercise in human skeletal muscle. J Appl Physiol 99, 950-956.

Deldicque L, Louis M, Theisen D, Nielens H, Dehoux M, Thissen JP, Rennie MJ, & Francaux M (2005). Increased IGF mRNA in human skeletal muscle after creatine supplementation. Med Sci Sports Exerc 37, 731-736. Delecluse C, Diels R, & Goris M (2003). Effect of creatine supplementation on intermittent sprint running performance in highly trained athletes. J Strength Cond Res 17, 446-454. Derave W, Eijnde BO, & Hespel P (2003). Creatine supplementation in health and disease: what is the evidence for long-term efficacy? Mol Cell Biochem 244, 49-55. Dunnett M & Harris RC (1999). Influence of oral beta-alanine and L-histidine supplementation on the carnosine content of the gluteus medius. Equine Vet J Suppl 30, 499-504. Durham WJ, Miller SL, Yeckel CW, Chinkes DL, Tipton KD, Rasmussen BB, & Wolfe RR (2004). Leg glucose and protein metabolism during an acute bout of resistance exercise in humans. J Appl Physiol 97, 1379-1386. Elliot TA, Cree MG, Sanford AP, Wolfe RR, & Tipton KD (2006). Milk ingestion stimulates net muscle protein synthesis following resistance exercise. Med Sci Sports Exerc 38, 667-674. Gaitanos GC, Williams C, Boobis LH, & Brooks S (1993). Human muscle metabolism during intermittent maximal exercise. J Appl Physiol 75, 712-719. Gautsch TA, Anthony JC, Kimball SR, Paul GL, Layman DK, & Jefferson LS (1998). Availability of eIF4E regulates skeletal muscle protein synthesis during recovery from exercise. Am J Physiol 274, C406-C414. Glaister M, Lockey RA, Abraham CS, Staerck A, Goodwin JE, & McInnes G (2006). Creatine supplementation and multiple sprint running performance. J Strength Cond Res 20, 273-277. Graham TE (2001). Caffeine and exercise: metabolism, endurance and performance. Sports Med 31, 785-807. Greenhaff PL, Bodin K, Soderlund K, & Hultman E (1994). Effect of oral creatine supplementation on skeletal muscle phosphocreatine resynthesis. Am J Physiol 266, E725-E730. Greenhaff PL, Casey A, Short AH, Harris R, Soderlund K, & Hultman E (1993). Influence of oral creatine supplementation on muscle torque during repeated bouts of maximal voluntary exercise in man. Clin Sci Clinical Science 84, 565-571.

Harris RC, Soderlund K, & Hultman E (1992). Elevation of creatine in resting and exercised muscle of normal subjects by creatine supplementation. Clin Sci Clinical Science 83, 367-374. Haskell CF, Kennedy DO, Wesnes KA, & Scholey AB (2005). Cognitive and mood improvements of caffeine in habitual consumers and habitual nonconsumers of caffeine. Psychopharmacology (Berl) 179, 813-825. Hawley JA, Tipton KD, & Millard-Stafford ML (2006). Promoting training adaptations through nutritional interventions. J Sports Sci 24, 1-13. Hespel P, Maughan RJ, & Greenhaff PL (2006). Dietary supplements for football. J Sports Sci 24, 749-761. Hespel P, Op't EB, Van LM, Urso B, Greenhaff PL, Labarque V, Dymarkowski S, Van HP, & Richter EA (2001). Oral creatine supplementation facilitates the rehabilitation of disuse atrophy and alters the expression of muscle myogenic factors in humans. J Physiol 536, 625-633. Hill CA, Harris RC, Kim HJ, Harris BD, Sale C, Boobis LH, Kim CK, & Wise JA (2007). Influence of beta-alanine supplementation on skeletal muscle carnosine concentrations and high intensity cycling capacity. Amino Acids 32, 225-233. Horswill CA (1995). Effects of bicarbonate, citrate, and phosphate loading on performance. Int J Sport Nutr 5 Suppl, S111-S119. Jones SW, Hill RJ, Krasney PA, O'Conner B, Peirce N, & Greenhaff PL (2004). Disuse atrophy and exercise rehabilitation in humans profoundly affects the expression of genes associated with the regulation of skeletal muscle mass. FASEB J 18, 1025-1027. Karlsson HK, Nilsson PA, Nilsson J, Chibalin AV, Zierath JR, & Blomstrand E (2004). Branched-chain amino acids increase p70S6k phosphorylation in human skeletal muscle after resistance exercise. Am J Physiol Endocrinol Metab 287, E1-E7. Kimball SR, Farrell PA, & Jefferson LS (2002). Invited Review: Role of insulin in translational control of protein synthesis in skeletal muscle by amino acids or exercise. J Appl Physiol 93, 1168-1180. Koopman R, Wagenmakers AJ, Manders RJ, Zorenc AH, Senden JM, Gorselink M, Keizer HA, & van Loon LJ (2005). Combined ingestion of protein and free leucine with carbohydrate increases postexercise muscle protein synthesis in vivo in male subjects. Am J Physiol Endocrinol Metab 288, E645-E653.

Koopman R, Zorenc AH, Gransier RJ, Cameron-Smith D, & van Loon LJ (2006). Increase in S6K1 phosphorylation in human skeletal muscle following resistance exercise occurs mainly in type II muscle fibers. Am J Physiol Endocrinol Metab 290, E1245-E1252. Kreider RB, Ferreira M, Wilson M, Grindstaff P, Plisk S, Reinardy J, Cantler E, & Almada AL (1998). Effects of creatine supplementation on body composition, strength, and sprint performance. Med Sci Sports Exerc 30, 7382. Louis M, Poortmans JR, Francaux M, Berre J, Boisseau N, Brassine E, Cuthbertson DJ, Smith K, Babraj JA, Waddell T, & Rennie MJ (2003). No effect of creatine supplementation on human myofibrillar and sarcoplasmic protein synthesis after resistance exercise. Am J Physiol Endocrinol Metab 285, E1089-E1094. Louis M, Van BR, Dehoux M, Thissen JP, & Francaux M (2004). Creatine increases IGF-I and myogenic regulatory factor mRNA in C(2)C(12) cells. FEBS Lett 557, 243-247. Macdermid PW & Stannard SR (2006). A whey-supplemented, high-protein diet versus a high-carbohydrate diet: Effects on endurance cycling performance. Int J Sport Nutr Exerc Metab 16, 65-77. Magkos F & Kavouras SA (2004). Caffeine and ephedrine: physiological, metabolic and performance-enhancing effects. Sports Med 34, 871-889. Maughan RJ, King DS, & Lea T (2004). Dietary supplements. J Sports Sci 22, 95-113. Mujika I, Padilla S, Ibanez J, Izquierdo M, & Gorostiaga E (2000). Creatine supplementation and sprint performance in soccer players. Med Sci Sports Exerc 32, 518-525. Olsen S, Aagaard P, Kadi F, Tufekovic G, Verney J, Olesen JL, Suetta C, & Kjaer M (2006). Creatine supplementation augments the increase in satellite cell and myonuclei number in human skeletal muscle induced by strength training. J Physiol 573, 525-534. Paddon-Jones D, Sheffield-Moore M, Urban RJ, Sanford AP, Aarsland A, Wolfe RR, & Ferrando AA (2004). Essential amino acid and carbohydrate supplementation ameliorates muscle protein loss in humans during 28 days bedrest. J Clin Endocrinol Metab 89, 4351-4358. Parise G, Mihic S, MacLennan D, Yarasheski KE, & Tarnopolsky MA (2001). Effects of acute creatine monohydrate supplementation on leucine kinetics and mixed-muscle protein synthesis. J Appl Physiol 91, 1041-7.

Pellett PL & Young VR (1992). The effects of different levels of energy intake on protein metabolism and of different levels of protein intake on energy metabolism: a statistical evaluation from the published literature. In Proteinenergy interactions, eds. Scrimshaw NS & Schurch B, pp. 81-121. IDEGG, Nestle Foundation, Lausanne, Switzerland. Phillips SM (2006). Dietary Protein for Athletes: From Requirements to Metabolic Advantage. Applied Physiology, Nutrition and Metabolism in Press. Phillips SM, Tipton KD, Aarsland A, Wolf SE, & Wolfe RR (1997). Mixed muscle protein synthesis and breakdown following resistance exercise in humans. Am J Physiol (Endocrinol Metab) 273, E99-E107. Pitkanen HT, Nykanen T, Knuutinen J, Lahti K, Keinanen O, Alen M, Komi PV, & Mero AA (2003). Free amino acid pool and muscle protein balance after resistance exercise. Med Sci Sports Exerc 35, 784-792. Psilander N, Damsgaard R, & Pilegaard H (2003). Resistance exercise alters MRF and IGF-I mRNA content in human skeletal muscle. J Appl Physiol 95, 1038-1044. Raue U, Slivka D, Jemiolo B, Hollon C, & Trappe S (2006). Myogenic gene expression at rest and after a bout of resistance exercise in young (18-30 yr) and old (80-89 yr) women. J Appl Physiol 101, 53-59. Rennie MJ (2005). Body maintenance and repair - how food and exercise and keeps the musculoskeletal system in good shape. Exp Physiol. Rennie MJ, Wackerhage H, Spangenburg EE, & Booth FW (2004). Control of the size of the human muscle mass. Annu Rev Physiol 66, 799-828. Rozenek R, Ward P, Long S, & Garhammer J (2002). Effects of high-calorie supplements on body composition and muscular strength following resistance training. J Sports Med Phys Fitness 42, 340-347. Schedel JM, Terrier P, & Schutz Y (2000). The biomechanic origin of sprint performance enhancement after one-week creatine supplementation. Jpn J Physiol 50, 273-276. Steenge GR, Simpson EJ, & Greenhaff PL (2000). Protein- and carbohydrate-induced augmentation of whole body creatine retention in humans. J Appl Physiol 89, 1165-1171. Stout JR, Cramer JT, Zoeller RF, Torok D, Costa P, Hoffman JR, Harris RC, & O'kroy J (2007). Effects of beta-alanine supplementation on the onset of neuromuscular fatigue and ventilatory threshold in women. Amino Acids 32, 381-386.

Suzuki Y, Ito O, Mukai N, Takahashi H, & Takamatsu K (2002). High level of skeletal muscle carnosine contributes to the latter half of exercise performance during 30-s maximal cycle ergometer sprinting. Jpn J Physiol 52, 199-205. Tallon MJ, Harris RC, Boobis LH, Fallowfield JL, & Wise JA (2005). The carnosine content of vastus lateralis is elevated in resistance-trained bodybuilders. J Strength Cond Res 19, 725-729. Tarnopolsky M (2004). Protein requirements for endurance athletes. Nutrition 20, 662-668. Tarnopolsky MA (1994). Caffeine and endurance performance. Sports Med 18, 109-125. Terjung RL, Clarkson P, Eichner ER, Greenhaff PL, Hespel PJ, Israel RG, Kraemer WJ, Meyer RA, Spriet LL, Tarnopolsky MA, Wagenmakers AJ, & Williams MH (2000). American College of Sports Medicine roundtable. The physiological and health effects of oral creatine supplementation. Med Sci Sports Exerc 32, 706-717. Tipton KD, Borsheim E, Wolf SE, Sanford AP, & Wolfe RR (2003). Acute response of net muscle protein balance reflects 24-h balance after exercise and amino acid ingestion. Am J Physiol Endocrinol Metab 284, E76-E89. Tipton KD, Elliott TA, Cree MG, Aarsland AA, Sanford AP, & Wolfe RR (2006). Stimulation of Net Muscle Protein Synthesis by Whey Protein Ingestion Before and After Exercise. Am J Physiol Endocrinol Metab. Tipton KD, Ferrando AA, Phillips SM, Doyle D, Jr., & Wolfe RR (1999). Postexercise net protein synthesis in human muscle from orally administered amino acids. Am J Physiol 276, E628-E634. Tipton KD, Rasmussen BB, Miller SL, Wolf SE, Owens-Stovall SK, Petrini BE, & Wolfe RR (2001). Timing of amino acid-carbohydrate ingestion alters anabolic response of muscle to resistance exercise. Am J Physiol Endocrinol Metab 281, E197-E206. Tipton KD & Sharp CP (2005). The response of intracellular signaling and muscle protein metabolism to nutrition and exercise. Eur J Sports Sci 5, 107121. Tipton KD & Witard OC (2007). Protein requirements and recommendations for athletes: relevance of ivory tower arguments for practical recommendations. Clin Sports Med 26, 17-36. Tipton KD & Wolfe RR (2004). Protein and amino acids for athletes. J Sports Sci 22, 65-79.

Todd KS, Butterfield GE, & Calloway DH (1984). Nitrogen balance in men with adequate and deficient energy intake at three levels of work. J Nutr 114, 2107-2118. Van LM, Vandenberghe K, & Hespel P (1999). Shortening of muscle relaxation time after creatine loading. J Appl Physiol 86, 840-844. Volek JS, Kraemer WJ, Bush JA, Boetes M, Incledon T, Clark KL, & Lynch JM (1997). Creatine supplementation enhances muscular performance during high-intensity resistance exercise. J Am Diet Assoc 97, 765-70. Walker JB (1979). Creatine: biosynthesis, regulation, and function. Adv Enzymol Relat Areas Mol Biol 50, 177-242. Wilkinson SB, Tarnopolsky MA, Macdonald MJ, MacDonald JR, Armstrong D, & Phillips SM (2007). Consumption of fluid skim milk promotes greater muscle protein accretion after resistance exercise than does consumption of an isonitrogenous and isoenergetic soy-protein beverage. Am J Clin Nutr 85, 1031-1040. Williamson D, Gallagher P, Harber M, Hollon C, & Trappe S (2003). Mitogenactivated protein kinase (MAPK) pathway activation: effects of age and acute exercise on human skeletal muscle. J Physiol 547, 977-987. Zello GA (2006). Dietary Reference Intakes for the macronutrients and energy: considerations for physical activity. Appl Physiol Nutr Metab 31, 7479.