This fourth edition continues to integrate the science and practice of sports nutrition. Each chapter is specifically formatted to combine the viewpoints of two sports nutrition experts: the scientific principles underpinning each issue are reviewed by an internationally recognized nutritionist with extensive research experience, while a sports dietitian summarizes the practice tips that can be drawn from these principles. Topics include the measurement of the nutritional status of athletes, assessing the physique of the athlete, weight loss and making weight, fluid and carbohydrate intake during exercise, supplements and sports foods, requirements for special athletic populations (i.e. diabetics and vegetarians), and the prevention, protection, and treatment of iron deficiency and depletion.

1. Chapter 1
Exercise physiology
and metabolism
Mark Hargreaves
Introduction
Physical exercise requires a coordinated physiological response involving the interplay
between systems responsible for increased energy metabolism, supply of oxygen and sub-
strates to contracting skeletal muscle, removal of metabolic waste products and heat, and
the maintenance of fluid and electrolyte status. Knowledge of these responses is important
for an understanding of the potential mechanisms by which nutrition can influence exercise
and sports performance. It is beyond the scope of this chapter to summarize all of these
responses in great detail, and readers are referred to various exercise physiology texts and
the cited review papers for a more thorough discussion. Nevertheless, this chapter attempts
to identify important aspects of the physiological and metabolic responses to exercise.
Skeletal muscle
Skeletal muscle can account for as much as 45% of the total body mass. It is the tissue
responsible for the generation of the forces required for joint movement during exercise.
By virtue of its mass and metabolic capacity, skeletal muscle has a major impact on whole-
body metabolism in health and disease. Factors influencing the ability of muscle to produce
force include total cross-sectional area, fiber type, number of active motor units, motor
neuron firing frequency, muscle length and velocity of contraction. The sequence of events
involved in muscle contraction is summarized as follows:
motor cortical activation and excitation of alpha motor neuron1.
arrival of electrical impulse at neuromuscular junction2.
propagation of muscle action potential across sarcolemma3.
excitation–contraction (EC) coupling:4.
conduction of excitation in t-tubulesa.
release of calcium from sarcoplasmic reticulumb.
action of calcium on actin myofilamentc.
1.1
1.2
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2. 2 Clinical spo rts n utritio n
actin-myosin cross-bridge formation and tension development (sliding filament theory)5.
re-uptake of calcium by sarcoplasmic reticulum (SR) and muscle relaxation6.
The chemical energy required for skeletal muscle to undertake mechanical work is pro­
vided by the hydrolysis of adenosine triphosphate (ATP), and this reaction is catalyzed by
myosin ATPase. Since the intramuscular stores of ATP are relatively small (approximately
5–6 mmol/kg wet weight), other metabolic pathways responsible for the resynthesis of ATP
must be activated in order to maintain contractile activity. These energy pathways are sum-
marized in Figure 1.1. Creatine phosphate (CrP) is a high-energy compound, stored in greater
amounts (approximately 20 mmol/kg) in skeletal muscle, and can be broken down quickly
during intense exercise to provide energy for ATP resynthesis. In addition, ATP can be formed
from adenosine diphosphate (ADP) in a reaction catalyzed by adenylate kinase. These reac-
tions form what is called the alactic or phosphagen system. The other non-oxidative energy
system is the lactacid system or ‘anaerobic’ glycolysis, in which glucose units, derived primarily
from intramuscular glycogen reserves, are broken down to lactate. These two energy systems
are maximally active during high-intensity exercise of short duration. During prolonged exer-
cise, the aerobic system becomes the predominant provider of energy for contracting skeletal
muscle, the major oxidative substrates being carbohydrate (CHO) and lipid.
One aspect of muscle physiology that has received great attention over the years is the
potential link between skeletal muscle fiber composition and exercise performance (Zierath
& Hawley 2004). Human skeletal muscle is composed of two main fiber types: slow twitch
(ST) and fast twitch (FT). The FT fibers have been further divided into FTa and FTb on the
basis of differences in their glycolytic and oxidative potential. The fiber types differ in their
contractile, morphological and metabolic characteristics, and are usually differentiated
using histochemical staining for myosin ATPase (Saltin & Gollnick 1983). The ST fibers
rely primarily on oxidative metabolism, are well supplied by capillaries and are fatigue
resistant. Not surprisingly, they are well suited to prolonged, low-intensity activity. In
contrast, FT fibers have a higher glycolytic capacity (FTb > FTa), a lower oxidative ­capacity
(FTb < FTa) and are more fatigable. They are more suited to high-intensity exercise. During
CHO
LAC CP
Glycolysis
ATP ADP
Oxidative metabolism
CO2
lipid protein
Figure 1.1 Metabolic pathways and sources of ATP generation in skeletal muscle
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3. Ch apt er 1 Exercise ph ysiology and metabolism 3
progressive exercise, ST fibers are involved at the lower intensities and as exercise intensity
increases there is progressive recruitment of more ST and FT fiber populations.
This general pattern of muscle fiber recruitment during exercise has been confirmed in
humans using histochemically determined glycogen depletion patterns as an index of fiber
involvement. During prolonged, submaximal exercise, the ST fibers are preferentially recruited,
although there may be involvement of FTa fibers in the latter stages (Vøllestad et al. 1984).
As exercise intensity increases, the FT fibers are recruited so that during maximal
exercise all fiber types are involved (Vøllestad & Blom 1985; Vøllestad et al. 1992). These
patterns of recruitment have resulted in interest in the link between muscle fiber com-
position and exercise performance in specially trained athletes. Indeed, elite endurance
athletes possess a high percentage of ST muscle fibers (70–90%), while sprint and explo-
sive athletes possess relatively more FT fibers (Costill et al. 1975; Saltin & Gollnick 1983).
This appears to be due to a combination of genetic factors and possible training-induced
alterations in muscle fiber composition (Saltin & Gollnick 1983; Schantz 1986).
Exercise metabolism
During high-intensity, dynamic exercise (such as sprinting, track cycling and interval train-
ing), the breakdown of ATP and CrP and the degradation of glycogen to lactic acid are
the major sources of energy. These substrates are also important during static exercise,
particularly above 30–40% maximum voluntary contraction (MVC), since an increase
in intramuscular pressure will impair muscle blood flow, thereby reducing oxygen and
substrate delivery to contracting skeletal muscle. Activation of muscle phosphagen and
glycogen degradation occurs with the onset of exercise. Although the capacity for ATP gen-
eration is greater for the glycolytic system (190–300 mmol ATP/kg dry muscle) than for the
phosphagen system (55–95 mmol ATP/kg), the power output is lower (4.5 mmol ATP/kg/s
compared with 9 mmol/kg/s). For this reason, when the levels of CrP decline with maximal
exercise, the rate of anaerobic turnover cannot be sustained (see Fig. 1.2 overleaf), and this
contributes to the decline in power output that is observed during all-out exercise.
During prolonged exercise, the oxidative metabolism of CHO and lipid provides the
vast majority of ATP for muscle contraction. Although amino acid oxidation occurs to a
limited extent during exercise, CHO and lipid are the most important oxidative substrates.
The relative contribution of CHO and lipid is influenced by exercise intensity and dura-
tion, preceding diet and substrate availability, training status and environmental factors.
Muscle glycogen is the important substrate during both intense, short-duration exer-
cise and prolonged exercise. Its rate of utilization is most rapid during the early part of
exercise and is related to exercise intensity (Vøllestad et al. 1984; Vøllestad & Blom 1985;
Vøllestad et al. 1992). As muscle glycogen declines with continued exercise, blood glucose
becomes more important as a CHO fuel source. Muscle glucose uptake increases in both
an exercise-intensity and duration-dependent manner. This is a consequence of increased
sarcolemmal glucose transport, due to translocation of the GLUT-4 glucose transporter
isoform to the plasma membrane, activation of the metabolic pathways responsible for
glucose metabolism and enhanced glucose delivery due to increased skeletal muscle
blood flow (Hargreaves 2000). Accompanying the increased muscle glucose uptake is an
increase in liver glucose output, so that blood glucose levels usually remain at, or slightly
above, resting levels. Liver glycogenolysis supplies the majority of liver glucose output;
however, during the latter stages of prolonged exercise, when liver glycogen levels are
1.3
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4. 4 Clinical spo rts n utritio n
low, gluconeogenesis is an important source of glucose. Under such circumstances, liver
glucose output may fall behind muscle glucose uptake, resulting in hypoglycemia. Fatigue
during prolonged exercise is often, but not always, associated with muscle glycogen deple-
tion and/or hypoglycemia (Hargreaves 1999). Thus considerable attention has focused on
CHO nutrition and exercise performance, and athletes are encouraged to adopt nutritional
strategies that maximize CHO availability before, during and after exercise (Hargreaves
1999; Hawley et al. 1997). These strategies are reviewed in Chapters 12, 13 and 14. There
is increasing evidence that lactate, derived from contracting and inactive muscle, is an
important oxidative and gluconeogenic precursor and is a valuable metabolic intermedi-
ate, rather than simply being a waste product of anaerobic glycolysis (Brooks 1986).
Contracting skeletal muscle also derives energy from the ß-oxidation of plasma free
fatty acids (FFA), derived from adipose tissue lipolysis. Plasma FFA levels usually peak
after 2–4 hours of exercise, at which time they are a major substrate for muscle (Coyle
1995). The muscle uptake and utilization of FFA is determined, in part, by the arterial
FFA concentration and the ability of the muscle to take up and oxidize FFA. Increasing
plasma FFA availability and utilization may reduce the reliance on muscle glycogen and
blood glucose, and this has resulted in interest in strategies designed to enhance FFA
oxidation (e.g. high-fat diets, caffeine lipid ingestion and carnitine supplementation),
although results in the literature remain equivocal (Hawley et al. 1998). These strategies
are reviewed in greater detail in Chapter 15.
Figure 1.2 Anaerobic ATP utilization during maximal cycling exercise of varying duration (From
ME Nevill, GC Bogdanis, LH Boobis, HKA Lakomy and C Williams, 1996, Chapter 19: Muscle
metabolism and performance during sprinting. In Biochemistry of exercise IX, edited by RJ
Maughan and SM Shirreffs, page 249, Figure 19.3 © 1996 by Human Kinetics Publishers, Inc.
Reprinted with permission from Human Kinetics (Champaign, IL).)
6 10 20 30
15
10
5
0
Sprint duration (seconds)
AnaerobicATPutilization
(mmol.kg1.s1drymuscle)
ATP
CrP
glycolysis
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5. Ch apt er 1 Exercise ph ysiology and metabolism 5
It should be noted that a major metabolic adaptation to endurance training is an
increased capacity for lipid oxidation. Muscle triglyceride stores can also be used by con-
tracting muscle (Van Loon 2004; Watt et al. 2002) and are believed to be more important
early in exercise and during exercise at higher intensities where mobilization of FFA from
adipose tissue is inhibited (see Fig. 1.3; Coyle 1995). During high-intensity exercise, mito-
chondrial oxidation of FFA derived from both adipose tissue and muscle triglycerides is
reduced and CHO, predominantly muscle glycogen, is the main fuel.
Amino acids, particularly the branched-chain amino acids, can also be oxidized during
prolonged exercise, but their overall contribution is small. The contribution from amino acids
is enhanced when CHO reserves are low. This is particularly important for athletes in heavy
training, who are likely to place a large stress on their endogenous CHO reserves and in whom
the training-based adaptations (e.g. increased metabolic enzymes, myofibrillar mass and buffer
capacity) are protein dependent. Protein requirements for exercise are reviewed in Chapter 4.
Oxygen transport system
The increased oxidative metabolism during exercise is dependent upon the adequate
delivery of oxygen to active skeletal muscle and, thus, upon the functional capacities of
the cardiovascular and respiratory systems. The most widely accepted measure of aerobic
fitness is maximal oxygen uptake (VO2 max
), and over the years there has been considerable
interest in the physiological determinants ofVO2 max
.
1.4
Figure 1.3 Relative contributions of the various CHO and lipid substrates for oxidative
metabolism during exercise of increasing intensity in trained men (from Romijn et al. 1993)
muscle glycogen
muscle triglycerides
plasma FFA
plasma glucose
6525 85
300
200
100
0
cal.kg1.min1
% of VO2 max
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6. 6 Clinical spo rts n utritio n
The cardiovascular system is regulated during exercise to ensure that oxygen delivery to
contracting skeletal and cardiac muscle is increased, that metabolic waste products such as
CO2
and heat are removed, and that mean arterial blood pressure and cerebral perfusion
are maintained. Skeletal muscle vasodilation occurs rapidly with the onset of exercise and is
closely coupled to the metabolic demands. Muscle blood flow is determined by the balance
between neural activity (vasoconstrictor) and local vasodilation mediated by vasoactive
substances released from contracting skeletal muscle, vascular endothelium and/or red
blood cells (Clifford & Hellsten 2004). Such substances include ATP, potassium, hydrogen
ions, adenosine, nitric oxide (NO) and prostanoids. No single substance can account entirely
for exercise hyperemia and considerable redundancy exists (Clifford & Hellsten 2004).
Mean arterial pressure (MAP) is maintained, despite the decrease in skeletal muscle vascu-
lar resistance, by an increase in cardiac output (increased heart rate and stroke volume) and
vasoconstriction in the splanchnic, renal and inactive muscle vascular beds. The cutaneous
circulation receives increased flow for the dissipation of heat, although it becomes a target
of sympathetic vasoconstriction at higher exercise intensities. Active skeletal muscle may
also be a target for sympathetic vasoconstriction in order to maintain MAP as maximal
cardiac output approaches (Calbet et al. 2004; Saltin et al. 1998). The regulation of the car-
diovascular response to exercise involves a number of neurohumoral factors. The general
pattern of cardiovascular effector activity is set by descending neural activity from the car-
diovascular centre (central command), increased in parallel with motor cortical activation
of skeletal muscle (Mitchell 1990). This activity is influenced by feedback from muscle and
arterial chemoreflexes, arterial baroreflexes, hypovolemia and hyperthermia.
An increase in pulmonary ventilation is essential for maintaining arterial oxygenation
and eliminating carbon dioxide, produced by oxidative metabolism in contracting muscle.
During incremental exercise, ventilation increases in proportion to the increases in oxygen
consumption and carbon dioxide production; however, at higher intensities a point is reached
where there is an abrupt increase in ventilation. This is often referred to as the ventilatory or
anaerobic threshold and it has been suggested that it arises from stimulation of the periph-
eral chemoreceptors by increased carbon dioxide, due to bicarbonate buffering of lactic acid
produced by contracting skeletal muscle (Wasserman et al. 1986). There is considerable debate
and controversy in the literature regarding the mechanisms of lactate production during exer-
cise, and the link between hyperventilation and blood lactate accumulation (Brooks 1986;
Wasserman et al. 1986; Katz & Sahlin 1988). Despite the controversy, measurement of lactate
threshold and lactate/ventilatory variables remains commonplace in endurance athlete assess-
ment, given the strong links between such variables and endurance exercise performance
(Coyle et al. 1988). The ventilatory responses to exercise are regulated by a number of neural
and humoral factors. These include carbon dioxide flux to the lung, descending activity from
respiratory neurons in the hindbrain, increased body temperature, alterations in arterial H+
, K+
and adrenaline levels, and feedback from muscle chemoreceptors and proprioceptors.
The ability of the muscles to consume oxygen in metabolism, and the combined
abilities of the cardiovascular and respiratory systems to deliver oxygen to the muscle
mitochondria, are reflected in VO2 max
, the most widely accepted measure of aerobic fit-
ness. Values for VO2 max
range from 30–40 mL/kg/min in inactive sedentary individuals
to as high as 80–90 mL/kg/min in highly trained endurance athletes. Such high values
reflect a combination of genetic endowment and vigorous physical training. There has
been much interest in the physiological factors that limit VO2 max
(see Fig. 1.4), with rea-
sonably general agreement that it is oxygen supply to muscle that represents the major
limiting factor (Richardson 2003; Saltin & Rowell 1980). It is likely that all components
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7. Ch apt er 1 Exercise ph ysiology and metabolism 7
of the oxygen transport system, by influencing either oxygen delivery to muscle or tissue
diffusion of oxygen, will play a role in determining VO2 max
(Richardson 2003). Strategies
(like blood doping and erythropoietin supplementation) designed to increase red blood
cell mass and arterial hemoglobin, and therefore arterial oxygen-carrying capacity, have
received attention from endurance athletes over the years. Furthermore, since iron is an
important component of hemoglobin, myoglobin and the cytochromes within the respi-
ratory chain, there has been much interest in the iron status of endurance athletes and
the potential effects of iron deficiency, and subsequent supplementation, on endurance
exercise performance. Iron requirements for training are reviewed in Chapter 10.
Temperature regulation and fluid balance
The metabolic heat that is produced during exercise must be dissipated so as to avoid
hyperthermia. During exercise in air, as much as 75% of this heat loss is achieved by the
evaporation of sweat, with approximately 580 kcal of heat being dissipated for each liter
of sweat evaporated. Sweat rates can be as high as 1–2 L/h during prolonged exercise and
under extreme conditions may reach 2–3 L/h for short periods. The transfer of heat to the
skin is achieved by vasodilation of the cutaneous circulation, thereby displacing blood to
1.5
Figure 1.4 Physiological determinants of maximal oxygen uptake
Respiration
Ventilation
VA/ Q
Diffusion
HbO2 affinity
Peripheral circulation
Muscle blood flow
Capillary density and
recruitment O2 extraction
Muscle metabolism
Oxidative capacity
(mitochondrial density, %ST fibres)
Substrates (CHO and lipid)
Muscle mass
Central circulation
Hb level and HbO2
Cardiac output
Maximal oxygen uptake
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8. 8 Clinical spo rts n utritio n
the periphery (Fortney & Vroman 1985). A fall in central blood volume is thought to result
in a decrease in stroke volume and a concomitant increase in heart rate during prolonged
exercise or exercise in the heat. Furthermore, there is the possibility that blood flow to active
muscle is reduced due to this‘circulatory conflict’, which is exacerbated by the hypovolemia
that develops as a result of the sweating-induced fluid losses (González-Alonso et al. 1998).
Core temperature stabilizes at a new, elevated level, depending upon the exercise intensity;
however, if the rate of metabolic heat production is maintained, or if heat loss is impaired
due to extreme environmental conditions, hyperthermia can develop. Hyperthermia not
only impairs exercise performance (González-Alonso et al. 1999; Parkin et al. 1999), but can
also have potentially life-threatening consequences. Exercise in the heat is also associated
with accelerated liver and muscle glycogenolysis and muscle and blood lactate accumula-
tion (Febbraio et al. 1994; Hargreaves et al. 1996). Although CHO depletion is not thought
to contribute to the premature fatigue observed with heat stress (Parkin et al. 1999), the
greater CHO use during exercise in the heat has nutritional implications for athletes who
regularly train and compete in hot environments (see Chapter 23).
In order to minimize the risk of hyperthermia, athletes are encouraged to become
acclimatized to hot environments and to ingest fluids during exercise. Acclimatization can
be achieved, in part, by passive exposure to heat and through exercise training; however,
most benefit is gained from exercising in the heat. The physiological adaptations to accli-
matization include an expanded plasma volume, reduced heart rate and body temperature
during exercise, increased volume of dilute sweat, earlier onset of sweating and reduced
glycogenolysis (Febbraio et al. 1994). Pre-cooling, resulting in a lower body core tempera-
ture, has also been shown to enhance exercise tolerance in the heat (González-Alonso
et al. 1999). The ingestion of fluids during exercise attenuates the increases in heart rate
and body temperature that are observed during prolonged exercise (Hamilton et al. 1991).
This seems to be due, in part, to the maintenance of a higher blood volume and lower
plasma osmolality during exercise (Coyle & Montain 1992).
There has been debate on the optimal volume and composition of rehydration solu-
tions during exercise (Hargreaves 1996). Since sweat is hypotonic, replacement of fluid is
a priority; however, during prolonged exercise the inclusion of CHO and a small amount
of electrolyte is recommended (Coyle & Montain 1992; Gisolfi & Duchman 1992). The
effects of fluid ingestion appear to be graded in proportion to the volume of fluid ingested
(Coyle & Montain 1992). Thus athletes should be encouraged to drink as much as is
required to minimize exercise-induced body weight loss; however, this is often a difficult
task, since fluid is not always readily available and ingestion of large fluid volumes can
result in gastrointestinal distress. Although the body has hormonal mechanisms for restor-
ing water and electrolyte levels following exercise, fluid ingestion during recovery should
be encouraged to facilitate rehydration. Solutions containing a small amount of CHO and
electrolyte appear to provide an advantage over plain water (Maughan et al. 1997). Fluid
and CHO intake during exercise is reviewed in detail in Chapter 13.
Fatigue
Fatigue is defined as a reduction in the force or power-generating capacity of muscle. The
sites of fatigue include the central nervous system and motor outflow (Gandevia 2001) and
peripheral sites such as the sarcolemma, t-tubule system, SR and myofilaments within skel-
etal muscle (Fitts 1994).These peripheral sites reflect the processes of membrane ­excitation,
1.6
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9. Ch apt er 1 Exercise ph ysiology and metabolism 9
EC coupling and uncoupling, cross-bridge formation and metabolic energy ­supply. While
central fatigue occurs during exercise, most attention has focused on peripheral mechanisms
of fatigue. It is unlikely that a single mechanism can explain fatigue under all circumstances,
but possible mechanisms include ionic disturbances, impaired EC coupling, accumulation
of metabolites and substrate depletion.
Loss of potassium from contracting skeletal muscle has been implicated in fatigue
during both intense and prolonged exercise (McKenna 1992). Potassium efflux, which is
most pronounced during intense, short-duration exercise, results in reduced membrane
excitability and contributes to intracellular acidosis. Intense exercise is also associated with
accumulation of H+
, ADP and inorganic phosphate. Acidosis has been linked to fatigue via
a number of mechanisms. These include effects on myofilament force production and ATP
generation within skeletal muscle. Ingestion of oral alkalizing agents (such as bicarbonate)
has been employed to minimize these effects of acidosis and is associated with improved
high-intensity exercise performance in many investigations (see Chapter 16). Increases in
inorganic phosphate and ADP are also believed to inhibit muscle force generation.
A failure of EC coupling is also likely to be involved in the fatigue process (Allen et al.
1995; Favero 1999). Possible mechanisms include reduced calcium release from the SR and
impaired myofibrillar calcium sensitivity (Allen et al. 1995). Impaired SR calcium release could
be due to a reduction in ATP supply in the region of the calcium release channel (Chin &
Allen 1997), increased metabolite/ion (e.g. Ca2+
, Mg2+
, H+
, lactate, inorganic phosphate) accu-
mulation (Westerblad et al. 2002), or modification by free radicals (Favero 1999). In addition,
reduced SR calcium uptake and calcium ATPase activity following both intense (Li et al. 2002)
and prolonged (Leppik et al. 2004) exercise suggest impairment of SR function.
Alterations in energy supply may also be an important factor in fatigue during exercise
(Sahlin et al. 1998). Muscle ATP levels usually fall only about 30–50% during intense exer-
cise; in contrast, CrP levels can be totally depleted following intense exercise (Söderlund &
Hultman 1991) and this could contribute to the reduced power output associated with
fatigue during such exercise. Dietary creatine supplementation is a potential intervention to
increase skeletal muscle CrP availability and enhance high-intensity exercise performance
(Greenhaff 1997) (see Chapter 16). During prolonged exercise, muscle glycogen depletion
and/or hypoglycemia are often associated with fatigue (Hargreaves 1999). Increased CHO
availability, either by muscle glycogen loading prior to exercise (see Chapter 12) or CHO
ingestion before (see Chapter 12) and during exercise (see Chapter 13), is associated with
enhanced endurance exercise performance (Hargreaves 1999; Hawley et al. 1997). Other
factors contributing to fatigue during prolonged, strenuous exercise include dehydration
and hyperthermia (see Chapter 13), and impaired SR and mitochondrial function (possibly
as a consequence of oxidative damage due to increased free radical activity). Thus, in recent
years, interest has focused on the potential relationship between anti-oxidant (vitamins C
and E) supplementation and endurance performance, although definitive evidence of their
ergogenic benefits is still required (see Chapters 11 and 16).
Summary
This chapter provides only a brief overview of the physiological and metabolic responses
to exercise. Nevertheless, it should be apparent that nutrition can have a major impact on
many physiological aspects of exercise. The specific nutritional strategies designed to opti-
mize exercise and sports performance are described in detail in the following chapters.
1.7
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10. 10 Clinical spo rts n utritio n
Practice tips
Nick Wray
A sound knowledge of the physiology and practice of sport is critical to the understanding••
of nutritional strategies that can enhance exercise performance. A good comprehension
of the specific energy systems used in a sport and the factors limiting performance are
essential before appropriate nutritional advice can be given.
To determine this information, it is necessary to establish the characteristics of the••
athlete’s training and competition schedule. A better understanding of the specific
physiological requirements and challenges faced by each athlete allows dietary advice
to be tailored to the athlete and to the situation. The practical aspects of achieving
nutritional goals also need to be considered. Important information for the sports
dietitian to collect to assess the specific nutrition demands and challenges faced by an
athlete is summarized in Tables 1.1 (training) and 1.2 (competition).
Table 1.1 Nutrition for optimal training
This list of questions may help to identify the nutritional requirements and challenges involved in
optimizing the effectiveness of the athlete’s training program.
What are the typical exercise requirements of the athlete’s training schedule? Type of training sessions?••
Frequency? Duration? Intensity? How are training sessions periodized over the week, month, season and
year? What total energy and fuel requirements do such exercise patterns set?
What is the environment in which training sessions are undertaken? What are the typical sweat losses and••
fuel requirements of training sessions? What opportunities are available to consume fluid or foods during
the session? How are such foods or fluids made available?
What are the opportunities to practice competition intake strategies in a training session?••
What are the typical exercise patterns during the off-season or during an injury break?••
How important are body mass and composition to performance in this sport? What are the typical••
characteristics of the physique of elite performances in this sport—body mass, lean body mass, body fat
levels? What is the current physique of the athlete, and what is their history of physique changes? What
is the range of physique characteristics that should allow the athlete to achieve optimal training, and then
competition performances? Will these physique goals be achieved as a result of genetics and training or must
a special dietary program be organized to assist gain of muscle mass and/or loss of body fat?
What is the typical domestic situation in which the athlete lives? Where does the athlete eat most of their••
meals? Who does the cooking?
What are the typical dietary intakes and practices of athletes (or a particular athlete) in this sport?••
What is the risk of the athlete developing any of the following problems:••
– iron deficiency (low iron intake, increased iron requirements, increased iron losses)
– menstrual dysfunction
– compromised bone status
– disordered eating
– other nutrient deficiencies
Does the athlete undertake special training programs (e.g. altitude training and/or heat acclimatization)?••
Is there direct or indirect evidence that supplementation with ergogenic aids (e.g. creatine, caffeine and••
anti-oxidant vitamins) enhances training adaptation and performance?
What are the practical considerations or difficulties in arranging food intake during a typical training day?••
At what times does the athlete train?••
What other activities need to be timetabled into the day?••
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11. ch apt er 1 Exer cise ph ysiolog y and metabolism 1 1
Table 1.1 (continued)
What factors limit access to food during the day?••
Do gastrointestinal considerations or appetite limit food intake, particularly at strategic times?••
How often or how far does the athlete need to travel to fulfill training commitments?••
Is the athlete’s nutrition influenced by other factors such as financial constraints, or religious or social••
customs?
What are the current nutritional beliefs of athletes from this sport?••
Where do athletes in this sport commonly seek their dietary advice or information?••
What is the typical level of nutrition awareness of athletes in this sport?••
Source: Burke 2007
Table 1.2 Nutrition for competition performance
This list of questions may help to identify the nutritional strategies that will help to optimize the
athlete’s competition performance.
What are the exercise requirements of competition? What is the frequency? Duration? Intensity of the••
specific activity? Is this specialized into individual events or different playing positions/styles?
Is competition undertaken as a single event or a series of activities? For example, is it a tournament, schedule••
of heats and finals, multi-day stages, or a weekly fixture?
What are the typical environmental conditions in which competition is undertaken? What is the temperature?••
Humidity? Airflow?
How often is major competition undertaken by the athlete?••
Are there competition weight limits that dictate the class of competition or overall eligibility to••
compete? How often does the athlete need to weigh in? What is the time interval between weigh-in and
competition?
What is the indirect or direct evidence that any of the following factors might limit competition••
performance:
– dehydration
– CHO availability
– gastrointestinal problems
What is the indirect or direct evidence that sports nutrition strategies such as the following may affect••
competition performance:
– CHO loading
– CHO refueling before or between events
– CHO intake in the 1–4 hours before the event
– fluid intake during the event
– CHO intake during the event
– hydration strategies before the event
– hydration strategies between events
– acute use of supplements such as caffeine, bicarbonate or creatine
– strategies to promote fat availability and utilization
What time of day does competition occur?••
Are the athletes in familiar surroundings or have they traveled to undertake competition? What is the food••
availability in these surroundings?
(continued)
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12. 12 Clinical spo rts n utritio n
PRAC TI C E TI P S
Table 1.2 (continued)
What other practical considerations affect competition nutrition strategies? Is the athlete’s nutrition affected••
by financial constraints, or religious or social practices?
Do gastrointestinal problems commonly occur? Are these affected by pre-exercise intake? Is hydration status••
markedly affected during exercise? What amount and type of fluid and/or food might be needed during
exercise?
What opportunities does the athlete have to consume fluid and foods during the event? How is such food/••
fluid made available? What strategies can be undertaken to improve availability and opportunity?
What factors interfere with post-exercise eating? How can foods and fluids be made available to the••
athlete?
What are the current nutritional beliefs of athletes in this sport?••
What are the current competition practices of the athletes, or a particular athlete, in this sport?••
Where do athletes in this sport commonly seek their nutrition information and advice?••
Source: Burke 2007
Information to provide answers to the questions raised in the tables may be obtained••
directly from the athlete or coach.However,there are other resources that allow the sports
dietitian to learn more about the physiological requirements and practical challenges of
specific sports. Many books have been written about individual sports, including texts
that may specifically address physiological and training issues. Encyclopedias of sports
are very useful in providing a brief summary of the main rules and features of the vast
array of competitive and recreational sports. The Internet provides websites prepared
by the governing bodies of various sports. In Australia, a directory of national sporting
organizations can be obtained from the Australian Sports Commission. Direct contact
with the executive or coaching directors of a sport can be useful and provide contacts
with other sports nutrition, medicine or science professionals who are involved closely
with that sport. There are also numerous reviews, textbooks and journal articles that
address the applied physiology of individual sports. The resources listed at the end of
the chapter provide useful information about the physiological and nutritional demands
of selected sports.
The following example illustrates how a sound understanding of the nutritional••
requirements and practical challenges of a sport can assist the sports dietitian to provide
relevant and accurate dietary advice to an athlete.
An Ironman triathlete requests information about the amounts of energy, CHO and
fluid intake he needs to consume during a race, providing the sports dietitian with infor-
mation about his event (3.8 km swim, 180 km cycle and 42.2 km run). More detailed
knowledge about the energy costs of the race, likely sweat losses and available race
supplies (such as foods and drinks available at aid stations) would enable the sports
dietitian to provide the athlete with specific and practical advice. Kimber and colleagues
(2002) investigated the nutritional needs and practices of triathletes participating in an
Ironman race and reported that males expended around 10 000 kcal (42 MJ) over the
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13. ch apt er 1 Ex ercise ph y siology and me tabolism 1 3
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applied physiology of sports
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