Introduction

Humans have courted the challenge of athletic performance and competition since the days of the early Greeks.  The science of nutrition emerged much later, spurred by the expanding knowledge of metabolism and the biochemistry on which it is based.  Because the energy for physical performance must be derived from nutrient intake, it was only a matter of time before these areas of interest would be linked.

The heavy emphasis on the enhancement of health and physical performance in today’s society has led sports nutrition to emerge as an important science.  Nutrition, as a means of positively affecting physical performance, has become a topic of great interest to all those involved in human performance, the scientist as well as the athlete and athletic trainer.

The human body converts the potential energy of nutrients to usable chemical energy, part of which drives muscle contraction, a process fundamental to athletic prowess.  Fluctuations in the body’s demand for energy – for example, changes in exertion level among resting, mild exercise, and strenuous exercise – are accompanied by shifts in the rate of catabolism of the different stored forms of nutrients.

It follows that an understanding of sports nutrition requires an understanding of the integration of the metabolic pathways that furnish the needed energy.

Biochemical Assessment of Physical Exertion

To fully understand sports nutrition, we need to examine different types of skeletal muscle.  Muscle is generally classified as one of three distinct types, each emphasising a different metabolic pathway:

  1. Type I;
  2. Type IIa; or
  3. Type IIb.

Type I muscle, sometimes called red muscle, is oxidative and red in colour.  It has a large number of mitochondria and therefore is capable of oxidizing glucose to CO2 and H2O and carrying out β-oxidation of fatty acids.  This muscle typically is used for aerobic endurance events.

Type IIa muscle and Type IIb muscle have been called white muscle.  Type IIb has fewer mitochondria, has a very active glycolytic pathway, and is white in appearance.  This type of muscle is used primarily for short-duration anaerobic events and power events.  Type IIa muscle can be considered a hybrid of Type I and Type IIb muscle, with some characteristics of each.  Endurance training can make Type IIa muscle act more like Type I muscle, whereas strength training or sprint training can make it look more like Type IIb.

Much more could be said about the muscle types and their response to nervous system stimulation and training, but this brief description provides sufficient information to foster an understanding of the resemblance of sports nutrition to the fed-fast cycle.  The portion (relative number) of each type of muscle fibres a person has is defined by genetics.

Training can increase the size (volume) of a muscle fibre type but does not alter the actual number of fibres of that type.  Because some sports rely on a specific muscle type, some people are genetically better fit for a specific type of sport activity based on their muscle type makeup.  Interestingly, women have more Type I muscle than men.  The result of that difference is that, under usual conditions of long-term aerobic exercise, women burn lipid at higher percentages of VO2 max than do men (Tarnoplosky, 1999).

To understand how the muscle types relate to physical exercise at the cellular level, we need to examine two common measurements used by the exercise physiologist (Romijn et al., 1993):

  • The respiratory quotient (RQ); and
  • The maximal oxygen consumption (VO2 max).

Respiratory quotient is called the respiratory exchange ratio (R or RER) by exercise physiologists.  It is the ratio of CO2 production to O2 consumption.  Typical RQs for carbohydrate, fat, and protein are 1.0, 0.70, and 0.82, respectively.  A newer generation of procedures (e.g., the isotope infusion method) has been developed to measure the relative contribution of substrates to energy supply during exercise and these measurements are described briefly here.

Further details of how the duration and intensity of physical conditioning influence which muscle cell type is used, and which metabolic pathways are active, are discussed later.  The respiratory quotient (RQ) has served for nearly a century as the basis for determining the relative participation of carbohydrates and fats in exercise (Hermansen et al., 1967; Powers & Howley, 2007).

The amount of protein being oxidised can be estimated from the amount of urinary nitrogen produced, and the remainder of the metabolic energy must made up of a combination of carbohydrate and fat.  Should the principal fuel source shift from mainly fat to carbohydrate, the RQ correspondingly increases, and a shift from carbohydrate to fat lowers the RQ.

Tables exist that permit the estimation of the relative percentage of either carbohydrate or lipid being used as a metabolic fuel based on the RQ at any given time (for short-term exercise activities, it is often assumed that no amino acids are used for energy).  However, during the past 20 years such knowledge has been advanced by invasive techniques such as arteriovenous measurements and the use of needle biopsies to quantify tissue stores of the energy nutrients.  These measurements are used clinically to evaluate elevated rates of metabolism.

The concept of maximum oxygen (VO2 max) uptake is fundamental.  As work increases in intensity, the volume of oxygen taken up by the body also increases.  The VO2 max is defined as the point at which a further increase in the intensity of the exercise no longer results in an increase in the volume of oxygen uptake.

The intensity level of a particular workload is most commonly expressed in terms of the percentage of the VO2 max that it induces.  As discussed later, the metabolic pathway that supplies energy for work is determined by the availability of metabolic energy (carbohydrate or lipid) and oxygen as well as by the duration of the activity and the conditioned state of the person performing the work.

As a person goes from an untrained state to a trained state the VO2 max increases.  Isotope infusion can be used to quantify the contribution of the major energy substrates, plasma glucose and fatty acids, and muscle triacylglycerols and glycogen to energy expenditure during exercise.  It involves the intravenous infusion of stable isotope (e.g., 2H [deuterium])-labelled glucose, palmitate, and glycerol during periods of rest and exercise.  By monitoring the uptake of infused labelled glucose and palmitate and knowing whole-body substrate oxidation, the contribution of muscle triacylglycerol and glycogen to overall energy supply can be estimated (Romijn et al., 1993).

Energy Sources during Exercise

The hydrolysis of the terminal phosphate group of ATP (adenosine triphosphate, metabolic energy produced in cells) ultimately provides the energy for conducting biological work.  In terms of physical performance, the form of work that is of greatest interest is the mechanical contraction of skeletal muscles.  The physical exertion depends on a reservoir of ATP, which is in an ever-changing state of metabolic turnover.  Whereas ATP is consumed by physical exertion, its stores are supplemented by the metabolic pathway, discussed next, and are repleted during periods of rest.  The key to optimising physical performance lies in nutritional strategies that maximise cellular levels of stored nutrients as fuels for ATP production.  Three energy systems supply ATP during different forms of exercise (Powers & Howley, 2007):

  • The ATP-CP (creatine phosphate) system;
  • The lactic acid system (anaerobic glycolysis); and
  • The aerobic system (aerobic glycolysis, TCA cycle, and β-oxidation of fatty acids).

The ATP-CP (Phosphagen) System

The ATP-CP system is a cooperative system in muscle cells using the high-energy phosphate bond of creatine phosphate (CP) together with ATP.

When the body is at rest, energy needs are fulfilled by aerobic catabolism (see The Aerobic System below) because the low demand for oxygen can easily be met by oxygen exchange in the lungs and by the oxygen carried to the muscle by the cardiovascular system (The ATP-CP system also operates continuously during this time, though at a slow pace).

If physical activity is initiated, the energy requirements of contracting muscle are met by existing ATP.  However, stores of ATP in muscle are limited, providing enough energy for only a few seconds of maximal exercise.  As ATP levels diminish, they are replenished rapidly by the transfer of high-energy phosphate from CP to form ATP in the ATP-CP system.  The muscle cell concentration of CP is only four to five times greater than that of ATP, and therefore all energy furnished by this system is expended after approximately 10 to 25 seconds of strenuous exercise.

When the ATP-CP is expended, the lactic acid system (anaerobic glycolysis) kicks in to produce more ATP.  Performance demands of high intensity and short duration such as weightlifting, 100 metre sprinting, some positions in football, and various short-duration field events benefit most from the ATP-CP system.  Lower-intensity activity may allow a person to use this system for up to 3 minutes.

The Lactic Acid System (The Famous Burn Sensation!)

This system involves the glycolytic pathway by which ATP is produced in skeletal muscle by the incomplete breakdown of glucose anaerobically into 2 mol of lactate.  The source of glucose is primarily muscle glycogen and, to a lesser extent, circulating glucose and the lactic acid system can generate ATP quickly for high intensity exercise.

The lactate system is not efficient from the standpoint of the quantity of ATP produced.  However, because the process is so rapid, the small amount of ATP is produced quickly and absolutely by substrate-level phosphorylation of ADP (adenosine diphosphate).  The lactate produced by this system quickly crosses the muscle cell membrane into the bloodstream, from which it can be cleared by other tissues (primarily the liver) for aerobic production of ATP or gluconeogenesis.  If the rate of production of lactate exceeds its rate of clearance by the liver, blood lactic acid accumulates.

This accumulation lowers the pH of the blood and is one cause of fatigue.  Under such circumstances, exercise cannot be continued for long periods.  The lactic acid system is engaged to provide a rapid source of energy.  When an inadequate supply of oxygen prevents the aerobic system from furnishing sufficient ATP to meet the demands of exercise, the lactic acid system will continue to function.  Although the lactic acid system is operative as soon as strenuous exercise begins, it becomes the primary supplier of energy only after CP stores in the muscle are depleted.

As a backup to the ATP-CP system, the lactic acid system becomes very important in high-intensity anaerobic power events that last from 20 seconds to a few minutes, such as sprints of up to 800 metres and swimming events of 100 or 200 metres.

The Aerobic System

This system involves the TCA cycle, through which carbohydrates, fats, and some amino acids are completely oxidised to CO2 and H2O.  The system, which requires oxygen, is highly efficient from the standpoint of the quantity of ATP produced.

Because oxygen is necessary for the system to function, a person’s VO2 max becomes an important factor in performance capacity.  Contributing to the VO2 max are the cardiovascular system’s ability to deliver blood (which carries the oxygen) to exercising muscle, pulmonary ventilation, oxygenation of haemoglobin, release of oxygen from haemoglobin at the muscle, and use of the oxygen by skeletal muscle mitochondria.  Matching these contributors to the cellular need for oxygen in exercising muscle is complex, because low efficiency of any of them becomes rate limiting for the entire process.

In terms of cellular metabolism, the aerobic pathway is slow to become activated and begins to dominate the course of activity only after about five minutes of continuous activity.  The aerobic system is an important supplier of energy for forms of exercise lasting longer than 3 or 4 minutes, depending on the intensity of the exercise.  Both intracellular triacylglycerols and plasma fatty acids also contribute to the overall energy supply.  Many types of exercise or sports meet these criteria, for example, distance running, distance swimming, and cross country skiing, just a few of the so-called endurance feats.

Current thinking is that the three energy systems do not simply take turns serially, and that no particular system is skipped in meeting the demands of exercise.  Rather, all systems function at all times, and as one predominates, the others participate to varying degrees.  The interaction of the three systems over the course of the first two minutes of exercise is complex but appears to involve the following energy contributions: ATP-CP system initially supplies energy, and as ATP begins to be depleted after ten seconds or so, the lactic acid system phases in and becomes the major supplier of energy.  After three minutes or so, aerobic glycolysis starts to be the major supplier energy.  It takes about 20 minutes of moderate exercise for fatty acids to be a major contributor.

Fuel Sources during Exercise

Carbohydrate, fat, and protein are the dietary sources that provide the fuel for energy transformation in the muscle.  At rest, and during normal daily activities, fats are the primary source of energy, providing 80% to 90% of the energy.  Carbohydrates provide 5% to 18%, and protein provides 2% to 5% of energy during the resting state (Wolinsky, 1998).

During exercise, the oxidation of amino acids contributes only minimally to the total amount of ATP used by working muscles.  Significant breakdown of amino acids occurs only toward the end of a long endurance event, when carbohydrate (glycogen) stores are somewhat depleted.

Amino acids can be transaminated to form alanine (an amino acid) from pyruvate.  The alanine is transported to the liver and is a primary substrate for gluconeogenesis; this process is termed the glucose-alanine cycle or Cori cycle.  The carbon skeleton of some amino acids can be oxidised directly in the muscle.  During exercise, the four major endogenous sources of energy are:

  • Muscle glycogen;
  • Plasma glucose;
  • Plasma fatty acids; and
  • Intramuscular triacylglycerols.

The extent to which each of these substrates contributes energy for exercise depends on several factors, including:

  • The intensity and duration of exercise;
  • The level of exercise training;
  • Initial muscle glycogen levels; and
  • Supplementation with carbohydrates through the intestinal tract during exercise.

This section describes the relationship between these factors and the ‘substrate of choice’ for energy supply.

Exercise Intensity and Duration

In the fasting state, much of the energy required for low intensity levels of exercise (25%–30% VO2 max) is derived from muscle triacylglycerols and plasma fatty acid oxidation, with a small contribution from plasma glucose.  The pattern does not change significantly over a period of up to two hours at this exercise level, which is equivalent to walking.

During this time, the consumed plasma fatty acids are replaced by fatty acids mobilised from the large triacylglycerol stores in adipocytes throughout the body.  However, as exercise intensity increases to 65% and on up to 85% VO2 max, fewer adipocyte fatty acids are released into the plasma, resulting in a decreased concentration of plasma fatty acids.  This decrease occurs despite a continuing high rate of lipolysis in adipocytes.  The decreased replacement of plasma fatty acids from fat stores at higher levels of exercise has been attributed to insufficient blood flow and albumin delivery of fatty acids from adipose tissue into the systemic circulation (Hodgetts et al., 1991).

Therefore, it is predicted that fatty acids become trapped in adipose tissue and accumulate there during high levels of exercise, a theory supported by research (Romijn et al., 1993).  With moderate-intensity exercise (~65% VO2 max) equivalent to running for 1 to 3 hours, total fat oxidation increases, despite the reduced rate of return of adipose fatty acids into the circulation.  This increase is attributed to an increase in the oxidation of muscle triacylglycerols.  In fact, plasma fatty acids and muscle triacylglycerols contribute equally to energy expenditure at this level of exertion in endurance-trained athletes.

Within the exertion range of 60% to 75% VO2 max, however, fat cannot be oxidised at a rate sufficiently rapid to provide needed energy, and therefore nearly half of the required energy must be furnished by carbohydrate oxidation.  Note that fatty acids have only two oxygen molecules, compared to carbohydrates’ equal number of oxygen and carbon molecules.  This characteristic means that fatty acids require more oxygen to be delivered by the cardiovascular system.

Also, the transfer of fatty acids into mitochondria is slow, and this may be a rate-limiting event.  The result is that when tissue oxygen levels begin to be low or high intensity exercise calls for a large quantity of energy, carbohydrate becomes a more favoured substrate.  Fatty acids are the favoured substrates for intensities of up to about 50% VO2 max.

As exercise intensity increases to 85% VO2 max, the relative contribution of carbohydrate oxidation to total metabolism increases sharply.  At VO2 max, carbohydrate in the form of blood glucose (derived from glycogenolysis of hepatic glycogen stores) and muscle glycogen essentially become the sole suppliers of energy.  Like muscle glycogen the concentration of blood glucose falls progressively during prolonged, strenuous exercise.  This decrease occurs because glucose uptake by working muscle (independent of insulin) may increase to as much as 20-fold or more above resting levels, while hepatic glucose output decreases with exercise duration.

Interestingly, however, hypoglycemia is not always observed at exhaustion, particularly at exercise intensities >70% VO2 max.  Hypoglycemia following liver glycogen depletion apparently can be postponed by an inhibition of glucose uptake and accelerated gluconeogenesis in the liver, using the glycerol produced in lipolysis, and by lactate and pyruvate (which was carried to the liver as alanine) produced by the glycolytic activity of the working muscles.

Accompanying high rates of carbohydrate catabolism is a rise in the production of lactic acid, which accumulates in muscle and blood.  This increase in lactic acid is particularly evident in situations of oxygen debt, in which insufficient oxygen to complete the oxidation of pyruvate to CO2 and H2O instead favours its reduction to lactate.  Carbohydrate is an essential energy substrate at moderate to high levels of exercise because of the need for TCA cycle intermediates from carbohydrates to oxidise the fatty acids, the slow rate of fat oxidation, and the limited ability of muscle to oxidise fat at high rates.

Muscle fatigue occurs when the supply of glucose is inadequate, such as occurs with muscle glycogen depletion or hypoglycemia.  To delay muscle fatigue, a person must reduce workload intensity to a level that matches his or her ability to oxidise fat predominantly, possibly as low as 30% VO2 max.

The reason for this limitation, and thus the dependence of muscle on carbohydrate as an energy source, is not fully understood.  However, traditional thinking is that the limitation may be based on two factors:

  1. Oxidation of fatty acids is limited by the enzyme carnitine acyltransferase (CAT), which catalyses the transport of fatty acids across the mitochondrial membrane; and
  2. CAT is known to be inhibited by malonyl CoA. When availability of carbohydrate to the muscle is high, fatty acid oxidation may be reduced by the inhibition of CAT by glucose-derived malonyl CoA (Elayan & Winder, 1991).

Level of Exercise Training

Endurance training increases an athlete’s ability to perform more aerobically at the same absolute exercise intensity.  Several factors aid in this increase.

Endurance-trained muscle exhibits an increase in the number and size of mitochondria.  Cardiovascular and lung capacity also increase, and Type I muscle hypertrophies.  This hypertrophy is an increase in the size of the Type I muscle, not the number of muscle fibres.

The activity of oxidative enzymes in endurance-trained subjects has been shown to be 100% greater than in untrained subjects at 65% VO2 max.  Endurance training also results in an increased use of fat as an energy source during sub-maximal exercise.

In skeletal muscle, fatty acid oxidation inhibits glucose uptake and glycolysis.  For this reason, the trained athlete benefits from the carbohydrate-sparing effect of enhanced fatty acid oxidation during competition, because muscle glycogen and plasma glucose are depleted more slowly.

This effect largely accounts for the training-induced increase in endurance for exercise over a prolonged period.  Trained athletes have been reported to have lower plasma fatty acid concentrations and reduced adipose tissue lipolysis than untrained counterparts do at similar exercise intensity.

This finding suggests that the primary source of fatty acids used by the trained athlete is intramuscular triacylglycerol stores, rather than adipocyte triacylglycerols.  After exercise, the intramuscular triacylglycerols are replaced with the fatty acids coming from plasma.  Lipolysis from adipocytes increases the free fatty acid levels in plasma.  This process can result in shrinking the size of the adipose tissue.

Endurance training appears to result in an increased capacity for muscle glycogen storage.  Therefore, the trained athlete benefits not only from a slower use of muscle glycogen (as explained earlier) but also from the capacity to have higher glycogen stores at the onset of competition.

Initial Muscle Glycogen Levels

The ability to sustain prolonged moderate-to-heavy exercise largely depends on the initial content of skeletal muscle glycogen, and the depletion of muscle glycogen is the single most consistently observed factor that contributes to fatigue.

High muscle glycogen levels allow exercise to continue longer at a sub-maximal workload.  Even in the absence of carbohydrate loading (see the following section), a strong positive correlation exists between initial glycogen level and time to exhaustion, level of performance, or both during exercise periods that last more than one hour.  The correlation does not apply at low levels of exertion (25%–35% VO2 max), or at high levels of exertion for short periods, because glycogen depletion is not a limiting factor under these conditions.

It has been suggested that the importance of initial muscle glycogen stores is related to the inability of glucose and fatty acids to cross the cell membrane rapidly enough to provide adequate substrate for mitochondrial respiration (Saltin & Gollnick, 1988).  Let us now review the changes in the source of energy during long endurance events.

If a well-trained person were to run a marathon (a 26.2 mile run), their source of biological fuel and metabolic pathway to supply the energy would change.  These changes do not occur abruptly, but one source (or pathway) begins to decrease while the next one begins to increase.

During the first ten seconds or so, most of the energy is supplied by preformed muscle ATP.  As the ATP begins to be used, the CrP-ATP system kicks in and creatine phosphate starts to resupply the ATP.  After 20 to 30 seconds, the lactic acid system starts.  This system uses muscle glucose in the beginning, followed by a rapid breakdown of muscle glycogen.  The anaerobic glycolysis continues for about the next five minutes and then metabolism shifts to aerobic metabolism.  The glucose comes from muscle glycogen and from blood glucose absorbed by the muscle fibre by a non-insulin dependent process.  During this time, the β-oxidation of fatty acids begins.  It takes about twenty minutes into the exercise before fatty acid oxidation proceeds at its maximum rate.  Depending upon the level of exertion (the % VO2 max), this energy can continue for a long time.  If the person is well trained, it can last for two to three hours or more.

At the midpoint of the marathon the person will be burning aerobically about a 40/60 split between carbohydrate and lipid.  Which one dominates depends on the level of training, the level of exertion, the availability of oxygen to the muscle, and the availability of each of the biological fuels.  At this point, the lipid comes mostly from muscle triacylglycerol.  Once glucose becomes limited, the oxidation of fatty acid cannot continue.  Some (but a limited amount) of fatty acids are absorbed from blood from the increased free fatty acids that have been released from adipose tissue.  At the midpoint, glucose comes mostly from gluconeogenesis by the liver.

During the last phase of the marathon (about the last 10 to 15 minutes), skeletal muscle protein begins to break down.  The amino acids transfer their amino group to ∞-ketoglutarate and then to alanine.  The alanine is transported to the liver, where it will be converted to glucose by gluconeogenesis.  During this time, branched chain amino acids (from skeletal muscle protein) will be used directly by the muscle for energy.

Finally, during the last minute or so, the runner will make a final effort, using the last of their glucose anaerobically.  Until that last effort, the athlete must maintain an intensity that permits an adequate supply of oxygen, maintain body temperature by drinking enough water, and maintain sufficient glucose to supply energy.

Carbohydrate Supplementation (Super-compensation)

When muscle glycogen was identified as the limiting factor for the capacity to exercise at intensities requiring 70% to 85% VO2 max, dietary manipulation to maximise glycogen stores followed naturally.  The most popular subject for research of this nature has been the marathon runner or cross-country skier, because of the prolonged physical taxation of these events and the fact that the athlete’s performance is readily measurable by the time required to complete the course.

The major dietary concern to emerge in the endurance training of marathon runners was how to elevate muscle glycogen to above-normal (super-compensated) levels.  In sporting vernacular, maximising glycogen content by dietary manipulation is referred to as ‘carbohydrate loading.’  The so-called classical regimen for carbohydrate loading resulted from investigations in the late 1960s by Scandinavian scientists (Bergstrom & Hultman, 1967).  This regimen involved two sessions of intense exercise to exhaustion to deplete muscle glycogen stores, separated by two days of low-carbohydrate diet (<10%) to ‘starve’ the muscle of carbohydrate.  This interval was followed by three days of high carbohydrate diet (>90%) and rest.  The event would be performed on day seven of the regimen.  On completion of this regimen muscle glycogen levels approached 220 mmol/kg wet weight, expressed as glucose residues, more than double the athlete’s resting level.

However, because of various undesirable side effects of the classical regimen, such as irritability, dizziness, and a diminished exercise capacity, a less stringent regimen of diet and exercise has evolved that produces comparably high muscle glycogen levels.  In the modified regimen, runners perform ‘tapered down’ exercise sessions over the course of five days, followed by one day of rest.  During this time, three days of a 50% carbohydrate diet are followed by three days of a 70% carbohydrate diet, generally achieved by consuming large quantities of pasta, rice, or bread.

The modified regimen, which can increase muscle glycogen stores 20% to 40% above normal, has been shown to be as effective as the classical approach, with fewer adverse side effects.  Predictably, the super-compensation of muscle glycogen by either approach has been shown to improve performance in trained runners during races of 30 km and longer.  It did not improve performance in shorter races (<21 km), because glycogen depletion is not the limiting factor in such events.  Other nutritional factors involving carbohydrate intake may enhance performance, as discussed in the next section.

Diets for Exercise

A thorough discussion of all of the factors that influence the choices of food for those involved in some form of strenuous exercise is far beyond the scope of this text. A few broad issues are considered in this section and it should be noted that people who engage in strenuous exercise are extremely diverse in their nutrient needs.

A few individuals are world-class athletes who work at getting every small, but meaningful, increase in performance they can, including controlling their nutritional intake.  Many more are recreational athletes who would like to follow a similar regime for their sport and their health.  Nutritional needs and, therefore, food selection differs depending on whether one is engaged in an endurance activity or a strength activity.

Considerable advice is available about nutrition, diet, and food selection.  Some of it is reliable, but much is not, and telling the difference is not always easy.

Macronutrients

One of the first considerations in planning a diet for someone involved in strenuous exercise is its macronutrient makeup.  The diet must have adequate energy (calories) intake to balance the level of energy expenditure consistent with the desired body composition.  Endurance athletes tend to focus on carbohydrate.  If you are engaged in a long endurance activity, consuming a diet that is high in carbohydrate (>65% of calories) is desirable to maintain elevated muscle glycogen levels.  This issue is discussed more fully below.

An endurance athlete should not restrict carbohydrate intake.  Carbohydrate must be available to supply the four carbon intermediates necessary in the TCA cycle so that β-oxidation of fatty acids can take place.  Strength athletes tend to focus on protein and the body does require protein to build and repair muscle and lean body mass.  The amount of protein needed for a strength athlete is not fully agreed upon by all recommending groups.  The recommended intake for protein ranges from the RDA of 0.8 gm/kg for more sedentary people to 1.2 to 1.8 gm/kg for strength athletes like body builders and weight lifters.

Many of these athletes consume much more than the amount proven to provide a benefit in performance.  The recommendations for fat intake for athletes are generally below the intake recommended for the more sedentary population of less than 30% of calories.  For athletes in serious competition in endurance sports an intake of 10% or less of calories are common (but not recommended).  High carbohydrate intake is so strongly emphasized that they drop their fat intake to levels below the amount necessary to obtain desired amounts of essential fatty acids.  Low-fat diets are generally not very palatable and are difficult to maintain, so most athletes do not stay on these diets long enough to develop essential fatty acid deficiencies.

Meal Frequency

The eating patterns of the population are very difficult to define and quantify.  Many people in the United Kingdom eat three large meals a day, with the largest meal being the evening meal.  For athletes, the recommendations are generally to divide the day’s food intake into multiple small meals, such as six or so, of equal size.

The rationale is that this pattern prevents any sharp spike in blood insulin levels, so the muscle always has a supply of substrate to repair and build muscle and replenish glycogen following exercise.  However, verifying the value of this recommendation from, current, experimental data is difficult.

Pre-event Meal

The timing of the final meal before intense exercise is crucial, because fasting reduces the labile glycogen stores of liver.  Also, carbohydrate meals consumed too close in time to the event may cause hyperinsulinemia.  Stimulation of insulin release just before an event results in a rapid reduction in plasma glucose, which significantly impairs work capacity.

Exercise permits a rapid uptake of glucose by the muscle in addition to the insulin-stimulated uptake.  Elevated plasma insulin also inhibits liver glucose output and the normal rise of plasma free fatty acids.  Under such conditions, excessive muscle glycogen degradation occurs, resulting in early fatigue.  The final meal before intense exercise should be consumed several hours (3-4 hours) before the event so that the stomach is empty, to avoid stimulating insulin levels and to allow for rapid water absorption.

For long endurance events, the meal generally should be high in complex carbohydrates and low in fat, conditions that promote rapid emptying of the stomach.  The nature of the food consumed to meet nutritional objectives is up to the athlete.  An isotonic or hypotonic beverage containing carbohydrate 15 to 20 minutes before the event provides extra dietary glucose without stimulating insulin release.

For prolonged events (longer than 90 minutes), consuming fluid containing some carbohydrate helps to maintain fluid balance and blood glucose levels.  Balance must be maintained to allow the liquid to empty rapidly from the stomach and the carbohydrate to be rapidly absorbed.  A full discussion of these factors is beyond the scope of this text.  In brief, the beverage should be cool, not cold, be isotonic or hypotonic, and contain glucose or polyglucose.  Large amounts of fructose should not be included because of its slow absorption rate.

Glycaemic Index

The form of carbohydrate ingested is also an important consideration in optimising endurance performance.  The principal factor in this regard is the glycaemic index (GI) of the food.  Potato starch is considered to have a relatively high GI, though not as high as the simple sugars.  Generally, consuming carbohydrate with a low to moderate GI before the performance is preferable to consuming high-GI carbohydrate because the hyperinsulinemic effect of high-GI food, as mentioned earlier, rapidly reduces blood glucose, suppresses release of fatty acids from store, and inhibits hepatic glycogenolysis.

After a prolonged event, however, the reverse is true with respect to GI.  Immediately after a glycogen-depleting event, liver and muscle glycogen levels are very low, and glycogen levels recover faster if a high-GI food or beverage is consumed.  There is a period following a glycogen depleting activity when muscle glycogen can be replaced rapidly (Ivy, 2001).  The foods consumed can be as simple as wedges of orange or apple or one of the sports drinks containing glucose, sucrose, or polyglucose.  Recovery depends on replacing lost body water, rebuilding glycogen levels, rebuilding lost muscle protein, and, for very long events, restoring electrolyte balance.

Nutritional Ergogenic Aids

The word ergogenic is derived from the Greek word ergon, meaning ‘work,’ and is defined as increasing work or the potential to do work.  An ergogenic aid does not have to be nutritional; it can also be mechanical.  For example, a running shoe or body suit to improve aerodynamics can be a mechanical ergogenic aid.  This discussion is limited to nutritional ergogenic supplements, or ergogenic aids.  Often these substances are part of a normal diet, or they may be cellular metabolites that are ingested in an effort to enhance the capacity for sport, exercise, and physical performance.

Several nutritional practices have ergogenic properties that are not necessarily considered ergogenic supplementation, for example, carbohydrate loading and fat loading.  Fat loading has been purported to ‘spare’ the more limited carbohydrates.  As mentioned previously, fats are the major fuel source for exercise below 50% VO2 max; it is not commonly used.  Nutritional ergogenic supplements must also be distinguished from ergogenic drugs, such as anabolic steroids or stimulants.  The risks of using anabolic steroids are so great that they have prompted the enactment and enforcement of laws prohibiting their use.

The compulsion for improved performance among athletes has led to an enormous increase in the testing and use of nutritional ergogenic aids.  As expected, the literature dealing with the subject has expanded with equal zeal.  Many supplements that have not been fully tested for either safety or efficacy have been recommended through the lay press.  The information presented here is restricted to the theoretical basis for using them and a brief overview of what is known about the effectiveness of ergogenic supplementation.

A dichotomy appears to exist between the widespread public use of certain supplements and the lack of scientific support for such use.  A problem for researchers is the common perception of subject’s under study that they simply ‘feel better’ as a result of supplementation, even though actual physiological changes may not be documented by the research.  In other words, psychological effects are adding a new dimension to the testing of ergogenic aids.  These effects must be considered along with true physiological effects, because as mood and mental outlook improve, so does physical performance – the reason for using supplements in the first place.  For all nutritional ergogenic aids, the placebo effect is substantial.

The level of athletic performance is influenced by psychological factors.  By ‘believing’ that a certain supplement will make you perform better, you may actually perform better.  Often a theoretical ‘rationale’ exists for supplement use, but it does not necessarily translate into enhanced performance.

The following section lists micronutrient ergogenic supplements that have been consumed on a broad basis.  The supplements chosen for description were selected on the basis of their reputed efficacy from a much longer list of hit-or-miss trial substances.  In most instances, research results neither totally support nor totally refute supplement efficacy but instead are divided in their findings.  This section occasionally refers to the number of ‘pro and con’ study conclusions to help the reader evaluate a substance’s efficacy.  Although specific references are not included, they, along with many more pertinent sources of information, are available to the interested reader (Bucci, 1993; Wolinsky, 1998; Green et al., 2001).

Amino Acids

  • Arginine: in large oral doses has been reported to elicit the release of somatotropin. Somatotropin, which has been called insulin-like growth factor, stimulates protein synthesis.  Arginine also has been reported to increase the secretion of growth hormone.
  • Ornithine: oral doses of ornithine have also been shown to stimulate the release of somatotropin.  At the levels required for somatotropin release, however, the side effect of osmotic diarrhea is common.  Both arginine and ornithine are purported to be beneficial in resistance training and to increase growth hormone release.
  • Aspartate Salts: the potassium-magnesium salts of aspartate have been marketed as an antifatigue agent.  Their use has been questioned, however, and the benefit is more likely a placebo effect.  The aspartate salts may have some benefits in endurance events if taken in high doses. Time to exhaustion has been reported to be increased.
  • Branched-Chain Amino Acids: branched-chain amino acids (isoleucine, leucine, and valine) have been hypothesized to benefit endurance activities by influencing the level of serum tryptophan.  BCAAs compete with tryptophan for entry into the brain.  One theory on fatigue is that brain tryptophan is converted to serotonin, which causes fatigue.  This conversion may be one of several factors that bring about fatigue.  BCAAs are also used by muscle for energy near the end of very long endurance events.  It has been suggested that consuming BCAAs before an event provides energy toward the end of the event and thereby reduces the amount of muscle breakdown.

Antioxidants

Endurance exercise increases the amount of oxygen moving into the muscle.  Increased exposure to large volumes of oxygen in turn increases the generation of free radicals, which are involved in fatigue and damage to the muscle cell membrane.  This information provides the rationale for using antioxidants to prevent muscle damage and delay fatigue.  Many antioxidants have been used, including vitamin C, vitamin E, and selenium. Coenzyme Q10 also has antioxidant activity, though its use as an ergogenic aid is based on other properties.

Herbs

Much interest has recently been directed toward herbal preparations.  Evaluating and comparing studies of these preparations is difficult, because the way herbs are collected, processed, and grown influences the active components.  One class of herb, ephedra, was previously used for its ephedrine content.  The risk of harmful side effects or death has discouraged its use and caused it to be banned in most sports. The US Food and Drug Administration (FDA) banned the sale of ephedra-containing supplements in 2004.  The ban was later removed after the FDA lost a court challenge.

The Ginsengs

The most widely used and studied herbs are the ginsengs.  Some purported ergogenic benefits of Panax (Chinese/Korean) ginseng include:

  • Increased run time to exhaustion (three out of seven studies);
  • Increased muscle strength (one out of two studies);
  • Improved recovery from exercise (three out of four studies);
  • Improved oxygen metabolism during exercise (seven out of nine studies);
  • Reduced exercise-induced lactate (five out of nine studies);
  • Improved auditory and visual reaction times (six out of seven studies); and
  • Improved vitality and feelings of well-being (six out of nine studies).

These benefits have most consistently been reported following supplementation over more than eight weeks (Mahady et al., 2000).

Caffeine

Ergogenic effects of caffeine are seen in endurance events.  The greatest effect is seen in people who do not consume caffeine on a regular basis.  Caffeine is a central nervous system (CNS) stimulant that increases blood flow to the kidneys (thus acting as a diuretic) and stimulates the release of fatty acids from adipose.  Sport regulatory bodies have changed their position on caffeine use several times.  It was banned for a period before 1972 and then removed from the banned list.  Regulators then set an upper limit for its use. Caffeine was removed from the banned list of stimulants before the 2004 Olympics.  The use of caffeine is now being reconsidered once again.

Intermediary Metabolites

  • Bicarbonate: is a primary buffering agent in the body.  Athletes competing in short anaerobic events (lasting only a few minutes) build up lactic acid.  The lowering of blood pH is one factor that leads to fatigue.  Theoretically, loading with sodium bicarbonate would delay the drop in pH and thereby delay fatigue.  Studies have supported this benefit, and it is often mentioned in reviews of ergogenic aids.  However, many sprint athletes and coaches have not reported having used sodium bicarbonate, nor did they know of anyone who did.
  • Carnitine: L-carnitine is used by the body to transfer acyl CoA from the cytoplasm of a cell into the mitochondria.  This is the theoretical basis for the use of carnitine as a nutritional ergogenic aid.  In people fed parenterally for long periods of time, fatty acid use can be enhanced by supplementation with carnitine.  People with chronic cardiovascular disease have also been shown to benefit from carnitine.  For the athlete, studies that show benefit and those that do not, is about even in number.
  • Coenzyme Q10: the theoretical basis for coenzyme Q10 as an ergogenic aid stems from its pivotal role in electron transport and production of ATP in the mitochondrion.  Clinical studies have shown its safety and use in cardiovascular disease.  Supplementation with coenzyme Q10 longer than four weeks has been purported to provide benefits for the long-term endurance athlete.  However, this benefit has not been shown conclusively.
  • Creatine: muscle creatine is part of the ATP-CP energy system that supplies the initial energy during the first few seconds to minutes of exercise.  The theoretical basis for using creatine as a nutritional ergogenic aid is that saturating muscle with creatine increases the amount of creatine phosphate in the muscle.  Creatine is effective for short, intense exercise.  However, taking it is associated with some risk. People taking creatine appear to add 1 to 2 kg of water weight.  Those taking creatine in hot, humid environments have become dehydrated and more susceptible to heat stress.  Deaths have been reported.
  • Other: many other nutritional materials have been recommended in the lay literature as possessing ergogenic properties, including minerals such as calcium, magnesium, zinc, iron, phosphates, chromium, boron, vanadium, and most vitamins.  Reviews of mineral supplements (Hermansen et al., 1967) suggest that performance enhancement is not well established and that the major benefit of mineral supplementation lies in the correction of deficiencies, should they exist.  General problems of research design remain as the popularity of nutritional ergogenic supplements surges forward.  Many ergogenic effects may be attributed to mental and psychological changes, and it behoves future researchers to rule out these effects to establish strictly physiological effects.  The fact that the number of studies finding ‘for’ performance enhancement is nearly equalled by the number of those finding ‘against’ enhancement testifies to the difficulty involved in researching this important field.

Summary

Animal survival depends on a constant internal environment maintained through specific control mechanisms.  Controls, operative at all levels (cellular, organ, and system), integrate energy metabolism and allow the body to adapt to a wide variety of environmental conditions.

Primary among the mechanisms of adaptation is the regulation of metabolism through the cooperative input of the nervous, endocrine, and vascular systems.  In the normal operation of these systems, metabolic pathways may be stimulated, maintained, or inhibited, depending on the conditions imposed on the body.

A pointed example of metabolic adaptation is the shift that occurs in substrate use and metabolic pathways in answer to changes in the body’s nourishment status (i.e., fed, fasting, and starvation states).  Metabolic syndrome is an example of the interrelation of nutrient intake and metabolism.  This syndrome is a clustering of risk factors for cardiovascular disease, chronic kidney disease, and type 2 diabetes.

The physical stress of exercise and sports presents an interesting challenge to the regulatory capacity of the body to provide the additional energy needed by exercising muscles.  Substrates fueling this energy include plasma free fatty acids, plasma glucose, muscle glycogen, and muscle triacylglycerols, and their use varies according to the intensity and duration of the exercise.

Many substances have been tested for their ergogenic properties in attempts to improve performance and muscle triacylglycerols, and their use varies according to the intensity and duration of the exercise.  In most cases, test results remain controversial, and more research is needed to establish which of the reputed ergogenic aids produce true physiological improvement.

References

Hellerstein, M., Schwarz J-M, & Neese, R. (1996) Regulation of Hepatic de Novo Lipogenesis in Humans. Annual Review of Nutrition. 16, pp.523-557.

McGarry, J.D., Kuwajima, M., & Newgard, C.B. (1987) From Dietary Glucose to Liver Glycogen: The Full Circle Round. Annual Review of Nutrition. 7, pp.51-73.

Foster, D.W. (1984) From Glycogen to Ketones and Back. Banting Lecture. Diabetes. 33, pp.1188-1199.

Lehninger, A.L., Nelson, D.L. & Cox, M.M. (1993) Principles of Biochemistry. 2nd ed. New York: Worth. pp. 757-58.

Tepperman, J. & Tepperman, H.M. (1987) Metabolic and Endocrine Physiology. 5th ed. Chicago: Year Book.

Hadely, M.E. (2000) Endocrinology. 5th ed. Upper Saddle River, NJ: Prentice Hall. pp. 16-50.

Turner, A.J. (ed) (1987) Neuropeptides and Their Peptidases. New York: VCH.

Grundy, S.M., Cleeman, J.I., Daniels, S.R., Donato, K.A., Eckel, R.H., Franklin, B.A., Gordon, D.J., Krauss, R.M., Savage, P.J., Smith, S.C., Spertus, J.A. & Costa, F. (2005) Diagnosis and Management of the Metabolic Syndrome: An American Heart Association/National Heart, Lung, and Blood Institute scientific Statement. Circulation. 112, pp.2735-2752.

Kahn, R., Buse, J., Ferrannini, E. & Stern, M. (2005) The Metabolic Syndrome: Time for a Critical Appraisal. Joint Statement from the American Diabetes Association and the European Association for the Study of Diabetes. Diabetologia. 48(9), pp.1684-1699.

McMillen, I.C. & Robinson, J.S. (2005) Developmental Origins of the Metabolic Syndrome: Prediction, Plasticity, and Programming. Physiology Review. 86, pp.571-633.

Reaven, G.M. (2005) The Insulin Resistance Syndrome: Definition and Dietary Approaches to Treatment. Annual Review of Nutrition. 25, pp.391-406.

McKeown, N.M., Meigs, J.B., Liu, S.L., Saltzman, E., Wilson, P.W.F. & Jacques, P.F. (2004) Carbohydrate Nutrition, Insulin Resistance, and the Prevalence of the Metabolic Syndrome in the Framingham off Spring Cohort. Diabetes Care. 27, pp538-546.

Tarnoplosky, M. (ed) (1993) Gender Differences in Metabolism. Boca Raton, FL: CRC Press.

Romijn, J., Coyle, E. & Sidossis, L. (1993) Regulation of Endogenous Fat and Carbohydrate Metabolism in Relation to Exercise Intensity. American Journal of Physiology. 265, pp.E380-391.

Hermansen, L., Hultman, E. & Saltin, B. (1967) Muscle Glycogen during Prolonged Severe Exercise. Acta Physiology of Scandinavia. 71, pp-129-139.

Powers, S.K. & Howley, E.T. (2007) Exercise Physiology: Theory and Application to Fitness and Performance. 6th ed. New York: McGraw Hill. Chap. 4, pp. 52-72.

Wolinsky, I. (1998) Nutrition in Exercise and Sport. 3rd ed. Boca Raton, FL: CRC Press. Chaps. 6, 13.

Hodgetts, A., Coppack, S.W., Frayn, K.N. & Hockaday, T.D.R. (1991) Factors Controlling Fat Mobilization from Human Subcutaneous Adipose Tissue during Exercise. Journal of Applied Physiology. 71, pp.445-451.

Elayan, I. & Winder, W. (1991) Effect of Glucose Infusion on Muscle Malonyl CoA during Exercise. Journal of Applied Physiology. 70, pp.1495-1499.

Saltin, B. & Gollnick, P. (1988) Fuel for Muscular Exercise: Role of Carbohydrate. In: Horton, E. & Terjung, R. (eds) Exercise, Nutrition, and Energy Metabolism. New York: MacMillan. Chap. 4.

Bergstrom, J. & Hultman, E. (1967) A Study of the Glycogen Metabolism during Exercise in Man. Scandinavian Journal of Clinical Laboratory Investigations. 19, pp.218-228.

Ivy, J.L. (2001) Dietary Strategies to Promote Glycogen Synthesis after Exercise. Canadian Journal of Applied Physiology. 26 (Suppl), pp.S236-245.

Wolinsky, I. (1998) Nutrition in Exercise and Sport. 3rd ed. Boca Raton, FL: CRC Press.

Bucci, L. (1993) Nutrients as Ergogenic Aids for Sports and Exercise. Boca Raton, FL: CRC Press.

Green, G.A., Catlin, D.H. & Starcevic, B. (2001) Analysis of Over-the-counter Dietary Supplements. Clinical Journal of Sports Medicine. 11, pp.254-259.

Mahady, G., Gyllenhall, C. & Fong, H. (2000) Ginsengs: A Review of Safety and Efficacy. Nutrition in Clinical Care. 3, pp.90-101.

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2 thoughts on “Sports Nutrition & Exercise Performance

  1. I believe that consuming foods containing good fats (especially saturated fats such as organic coconut oil or beef fat) significantly improve performance for physical endurance exercises. It is often ignored in studies of nutrition for exercise.

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