Food Components That May Optimize Physical Performance: An Overview
For years people have routinely searched for ways to optimize physical performance, increase the amount of work that can be accomplished under various environmental extremes, and enhance recovery from a physically exhausting task. Aids that are used to increase physical performance or enhance recovery from physical exertion are referred to as ergogenic aids. The word ergogenic is derived from the Greek word ergon meaning “work” and the suffix -genic meaning “producing.” Therefore, the word ergogenic literally means “work producing” or “tending to increase work.”
Ergogenic aids are generally classified into five categories: (1) mechanical, (2) psychological, (3) physiological, (4) pharmacological, and (5) nutritional. An example of a mechanical ergogenic aid is the fiberglass pole for pole vaulting or the lightweight frame on a racing bike. A psychological ergogenic aid might be hypnosis or mental rehearsal. Blood doping or erythropoietin injections are considered powerful physiological ergogenic aids by virtue of their ability to increase red blood cell mass and increase maximum aerobic capacity. Pharmacological ergogenic aids might be the xanthines such as caffeine or the amphetamines. Carbohydrate and protein supplements are
examples of nutritional ergogenic aids. It should be noted that many ergogenic aids can be classified into more than one category. For example, caffeine can be classified as a nutritional or a pharmacological ergogenic aid. Likewise, bicarbonate could be classified as a physiological or pharmacological ergogenic aid.
Of the various aids known to have ergogenic effects, many are natural foods or derivatives of food products. This chapter identifies some of the more effective food components that have been found to enhance physical performance and describes their methods of action. Some potential yet unproved ergogenic aids are also discussed.
Food components or food derivatives that might have ergogenic effects are generally classified as either a nutritional or a pharmacological ergogenic aid. Such aids enhance performance by:
acting as a central or peripheral nervous system stimulant,
increasing the stored amount or availability of a limiting substrate,
acting as a supplemental fuel source or reducing reliance on a limiting substrate during prolonged physical exertion,
reducing or neutralizing metabolic by-products that interfere with energy-producing reactions or muscle contraction, and
ACTIONS OF SPECIFIC FOODS AND DERIVATIVES OF FOOD PRODUCTS
Ergogenic Aids That Act as Central or Peripheral Nervous System Stimulants
Several food components or substances derived from plant extracts have been used to stimulate the brain, ward off feelings of fatigue, and renew vigor and enthusiasm. These substances may stimulate the brain directly, may increase the production or release of neurotransmitters that activate certain stimulatory regions of the brain, or prevent the release of inhibitor neurotransmitters. Examples of these neurostimulating aids are caffeine, which is found in a variety of foods, and norpseudoephedrine, which is found in the leaves of the African plant Catha edulis.
Recently, it was suggested that branched-chain amino acid (BCAA) supplementation may prevent central nervous system fatigue (Blomstrand et al., 1988, 1991). One of the hypotheses proposed to explain central nervous system fatigue is related to an increase in the concentration of 5-hydroxytryptamine (serotonin) in one or more specific areas of the brain. An increase in serotonin
levels in the brain can theoretically arise from two peripheral effects of endurance exercise. First, an increase in BCAA utilization by muscle may cause a decrease in plasma BCAA levels, which would raise the plasma tryptophan/BCAA ratio. Since BCAAs compete with free tryptophan for amino acid transporters in the brain (Pardridge and Oldendorf, 1975), an increase in the tryptophan/BCAA ratio should favor the entry of tryptophan into the brain. Tryptophan is a precursor of serotonin, and therefore, as the levels of tryptophan increase in the brain, there is a proportional increase in serotonin levels (Newsholme and Leech, 1983). Second, an increase in the plasma free fatty acid concentration could compete with tryptophan for binding sites on albumin and increase the plasma free tryptophan concentration. An increase in plasma free fatty acid levels generally occurs with prolonged aerobic exercise. Whatever the circumstances, it has been suggested that BCAA supplementation may be beneficial in that it may prevent a rise in the tryptophan/BCAA ratio, thereby reducing the uptake of tryptophan by the brain and blunting or preventing a rise in brain serotonin levels. However, there has been little definitive research that supports this idea.
Another possible mechanism of action of food components is the facilitation of excitation-contraction-coupling. This facilitating effect could occur at the neuromuscular junction by increasing the release of the neurotransmitter acetylcholine or, possibly, by preventing the depletion of this neurotransmitter by providing choline supplements (R.T.Wurtman, Massachusetts Institute of Technology, personal communication, 1992). As with BCAA supplementation, however, there has been no definitive research that supports this idea.
Ergogenic Aids That Increase the Stored Amount or Availability of a Limiting Substrate
Carbohydrate is an essential fuel source for prolonged exercise of moderate intensity. At intensities ranging between 60 and 80 percent of maximum aerobic power (maximum oxygen uptake ), the major source of carbohydrate is muscle glycogen. Numerous studies have demonstrated that the capacity to exercise at exercise intensities ranging from 60 to 80 percent is directly related to the preexercise muscle glycogen level (Ahlborg et al., 1967; Bergström and Hultman, 1967; Bergström et al., 1967). Because of the paramount importance of muscle glycogen during prolonged, moderate-intensity exercise, the regulation of muscle glycogen synthesis and mechanisms for increasing the muscle glycogen stores have been studied extensively. For years it has been known that the consumption of a high-carbohydrate diet will elevate glycogen stores above normal levels. To maximize muscle glycogen
stores, however, a specific regimen of exercise and diet must be followed. Although several regimens have been developed, the 7-day protocol developed by Sherman et al. (1981) is the most practical. First, the muscle glycogen level is depleted by exercise. During the next 3 days, exercise should be of moderate intensity and duration and a well-balanced mixed diet composed of about 45 percent carbohydrate should be consumed. During the last 3 days, the exercise duration is tapered and the carbohydrate content of the diet is increased to 70 percent. This protocol has been found to double the normal muscle glycogen concentration.
Oxygen availability is also an important determinant of aerobic endurance. Increasing oxygen delivery or availability to the working muscles has been found to increase maximum aerobic power and aerobic endurance. The increase in aerobic endurance is thought to be due to a reduced reliance on carbohydrate stores and/or reduced lactate production during submaximal exercise. Blood doping and erythropoietin injections have been used to increase the oxygen-carrying capacity of the blood and to increase by increasing the red blood cell mass (Spriet, 1991). These procedures, however, are potentially dangerous because of the possibility of infection and increased blood viscosity, which can place undue stress on the exercising heart.
Phosphate loading, which has been found to increase is an alternative to blood doping and other procedures that increase red blood cell mass (Cade et al., 1984; Kreider et al., 1990; Stewart et al., 1990). Typically, this procedure consists of consuming between 600 and 1,000 mg of sodium phosphate three to four times per day for 3 to 6 days. It has been reported that this procedure will increase by 6 to 12 percent, increase the anaerobic threshold, and increase the run time to exhaustion during a continuous ramp protocol on the treadmill (Cade et al., 1984; Kreider et al., 1990; Stewart et al., 1990). It is believed that the increased phosphate consumption elevates the 2,3-diphosphoglycerate concentration of the blood and that this improves tissue oxygen extraction from blood by reducing the affinity of oxygen for hemoglobin (Bredle et al., 1988; Cade et al., 1984; Stewart et al., 1990). It should be mentioned, however, that other possibilities for the ergogenic effects of phosphate loading have been suggested (Bredle et al., 1988; Kreider et al., 1990) and that positive effects have not always been found (Bredle et al., 1988; Duffy and Conlee, 1986).
Ergogenic Aids That Act as a Supplemental Fuel Source or Reduce Reliance on a Limiting Fuel Store
Several nutritional supplements have been used as a supplemental fuel source. The most popular and probably the most effective is simple carbohy-
drates. Generally, these supplements are composed of glucose or a combination of maltodextrins, glucose, and fructose. The mechanism by which carbohydrate supplements improve aerobic endurance performance may be determined by the intensity of the exercise. During the onset of moderate-intensity aerobic exercise (60–75 percent ), muscle glycogen is a primary fuel source (Ahlborg et al., 1967; Bergström and Hultman, 1967; Bergström et al., 1967). As exercise continues and the muscle glycogen stores decline, the muscle becomes increasingly more dependent on blood glucose for its carbohydrate needs (Gollnick et al., 1981). This, however, does not appear to be a problem as long as the liver is able to maintain an adequate blood glucose concentration of approximately 3.5 mM (Coyle et al., 1986). However, when the muscle glycogen stores have been depleted and the blood glucose concentration falls below 3.5 mM, muscle glucose uptake cannot meet the carbohydrate requirements of the active muscle. Once the carbohydrate requirement cannot be met, muscle fatigue rapidly ensues. Carbohydrate supplements taken during the activity are able to maintain the blood glucose concentration above a critical level and prolong the time to fatigue during exercise of moderate intensity (Coyle et al., 1983, 1986).
Carbohydrate supplementation has also been found to be beneficial during low-intensity exercise (40–50 percent ) (Ivy et al., 1983; Yaspelkis and Ivy, 1991). However, the mechanism of action of the carbohydrate supplementation during low-intensity exercise appears to differ from that during moderate-intensity exercise. During low-intensity exercise, the rate of muscle glycogen utilization is significantly reduced by carbohydrate supplementation (Yaspelkis and Ivy, 1991). The difference in the muscle glycogen response elicited by a carbohydrate supplement during moderate- and low-intensity steady-state exercise is likely due to the differences in the plasma glucose and insulin responses. Ingestion of carbohydrate supplements during low-intensity exercise increases insulin and plasma glucose concentrations and maintains these variables at elevated levels throughout the exercise bout (Ivy et al., 1983; Yaspelkis and Ivy, 1991). In contrast, carbohydrate supplementation during moderate-intensity exercise aids only in the maintenance of plasma glucose and insulin concentrations (Coyle et al., 1983, 1986; Ivy et al., 1979). Recently, Yaspelkis et al., 1993) observed that carbohydrate supplementation elevated plasma glucose and insulin levels during prolonged, continuous variable-intensity exercise (45–75 percent ) and enhanced aerobic endurance. The increase in plasma insulin levels was the highest that those investigators had observed during exercise. Associated with the increase in endurance was a sparing of muscle glycogen (Yaspelkis et al., 1993). Therefore, it appears that when exercise intensity is fluctuating between low and moderate intensity, carbohydrate supplementation may enhance aerobic endurance by reducing dependency on muscle glycogen as a fuel source.
Another approach to increasing aerobic endurance is to increase the blood free fatty acid concentration prior to the onset of aerobic exercise. Raising the blood free fatty acid concentration increases the amount of fatty acid uptake by the muscle and reduces reliance on muscle glycogen and blood glucose for energy production. This process has been found to be effective in both rats and humans (Costill et al., 1977; Hickson et al., 1977). The most effective procedure for the elevation of plasma free fatty acid is to ingest a high-fat meal several hours prior to exercise. This elevates the plasma triglyceride level. Once plasma triglycerides are elevated, heparin is injected intravenously to activate lipoprotein lipase, which hydrolyzes the triglycerides to glycerol and free fatty acids. This can effectively raise the free fatty acid concentration in the blood to more than 1 mM. However, this mechanism is impractical and potentially dangerous because of the anticlotting effect of the heparin.
Because of the lipolytic effect of caffeine, the use of this xanthine to elevate plasma free fatty acid levels prior to exercise has also been investigated. Several studies have found that ingestion of caffeine approximately 1 h prior to exercise increased the plasma free fatty acid concentration (Costill et al., 1978; Essig et al., 1980). This was accompanied by a decrease in the exercising respiratory exchange ratio and an increase in aerobic endurance. However, other studies have found an increase in aerobic performance following caffeine ingestion without an increase in plasma free fatty acid concentrations (Graham and Spriet, 1991; Ivy et al., 1979; Spriet et al., 1992). For example, Ivy et al. (1979) used nine trained cyclists to study the effects of caffeine on work production during 2 h of isokinetic cycling exercise. Ingestion of 250 mg of caffeine 60 min before the ride and ingestion of an additional 250 mg of caffeine at 15-min intervals over the first 90 min of exercise increased work production by 7.4 percent without increasing the subjects’ perception of exertion. Of interest was the observation that the subjects started exercising at a higher work rate from the start of exercise and maintained a higher work rate than the controls during the course of the 2-h ride. Plasma free fatty acid levels in the test subjects were not significantly different from those in the controls although fat oxidation, based on the respiratory exchange ratio, in the test subjects became significantly greater than those in the controls after 60 min of exercise. It was concluded that the ergogenic effect of caffeine was both neurological and metabolic in nature and independent of an increase in plasma free fatty acid levels.
Recently, Spriet et al. (1991, 1992) performed a series of studies investigating the mechanism of caffeine’s ergogenic effects on running and cycling performance at a relatively high aerobic exercise intensity (80–85 percent ). It was found that high concentrations of caffeine ingested prior to exercise resulted in an elevation in plasma epinephrine levels and a sparing of muscle glycogen early in exercise. This spared glycogen was
available late in exercise and coincided with a prolonged time to exhaustion. It was further suggested that increased utilization of intramuscular triglyceride and/or extramuscular free fatty acids after caffeine ingestion may have inhibited carbohydrate oxidation early in exercise via elevations in muscle citrate and the acetyl-coenzyme A to coenzyme A ratio (acetyl CoA/CoA-SH) ratio. Plasma free fatty acid levels, however, were not significantly different during the caffeine and control treatments.
The combination of pyruvate and dihydroxyacetone (PD) is another food component that has potential as an ergogenic aid. Stanko et al. (1990a) found that consumption of pyruvate and dihydroxyacetone as part of a standard diet improved submaximal arm endurance by 20 percent. The experimental paradigm called for substituting 100 g of PD (1:3) for an isocaloric amount of carbohydrate in the diet over 7 consecutive days. Both arteriovenous glucose difference and blood fractional glucose extraction were higher after dietary consumption of the PD than after consumption of the control diet, suggesting an enhanced muscle glucose uptake. In addition, the muscle glycogen concentration was higher for the PD treatment compared with that for the control treatment before exercise but did not differ between the two groups at exhaustion. It was suggested that the greater muscle glycogen stores and the increased muscle glucose uptake delayed the onset of fatigue and extended the submaximal endurance capacity during the PD trial.
In a subsequent study by the same group, the ergogenic effects of PD were investigated during cycling at an exercise intensity of 70 percent (Stanko et al., 1990b). The experimental paradigm used was similar to that of their first study, except that the PD and the placebo were provided separately from the meals. This resulted in similar muscle glycogen concentrations for the two treatment groups at the onset of exercise. Time to fatigue was 20 percent longer for the PD treatment group compared with that for the placebo group. The whole-leg arteriovenous glucose difference was greater for the PD treatment group than for the placebo group at rest and during the first 30 min of exercise, but there was no difference in the respiratory exchange ratio between the two groups. There was also no difference in muscle glycogen levels at the time of exhaustion between the treatment groups. It was suggested that the greater glucose extraction may have spared muscle glycogen and that the spared muscle glycogen and/or the increased glucose extraction provided the necessary fuel for prolongation of exercise endurance capacity. A potential problem with this supplement, however, is that pyruvate is available only as a sodium or a calcium salt. Therefore, the high concentrations of pyruvate required for the ergogenic effect may produce a mineral overload.
Medium-chain triglycerides (MCTs) have also been experimented with as a substitute fuel source during prolonged moderate-intensity exercise. MCTs have been described as a food fat that can be more rapidly hydrolyzed,
absorbed, and metabolized than ordinary long-chain triglycerides (Greenberger et al., 1966; Schwabe et al., 1964). Since MCTs are absorbed into the blood as medium-chain fatty acids (Greenberger et al., 1966) and metabolized as quickly as glucose (Schwabe et al., 1964), it has been speculated that they might provide an alternate carbon source for muscle metabolism during prolonged exercise. To date, however, there have been no studies that have demonstrated an advantage to ingesting large amounts of MCTs before or during prolonged aerobic exercise. In addition, there is a significant problem with the oral administration of MCTs. By themselves, MCTs are highly unpalatable and produce stomach discomfort and diarrhea when taken in high concentrations (Ivy et al., 1980). Therefore, even if they appeared to enhance aerobic endurance, their use is questionable.
Ergogenic Aids That Reduce or Neutralize Metabolic By-Products
During intense exercise, in which glycolysis is primarily responsible for resynthesis of ATP, lactic acid is formed and accumulates in the muscle and blood. The decrease in muscle pH because of lactic acid accumulation is assumed to be one of the major factors limiting exercise performance. The inhibitory effect of an increase in the intramuscular hydrogen ion concentration (H+) has been related to impairment of glycolytic enzyme activity (Chasiotis et al., 1983; Trivedi and Danforth, 1966), direct interference with excitation-contraction-coupling (Fuchs et al., 1970; Nakamura and Schwartz, 1972), and alterations in the plasma membrane potential because of excessive potassium ion (K+) efflux (Heigenhauser and Jones, 1991). The magnitude of the decrease in muscle pH is determined by the amount of lactic acid accumulation, the muscle buffering capacity, and the flux rate of lactic acid from muscle to blood.
Early studies by Dennig and colleagues (1931) suggested that administration of buffering substances such as sodium bicarbonate (NaHCO3) could improve high-intensity exercise performance, whereas substances that compromised the buffering capacity of the blood would worsen intense exercise performance. Those early studies, however, were conducted on only one subject, and several subsequent studies from other laboratories found no effect of NaHCO3 on exercise performance (Asmussen et al., 1948; Johnson and Black, 1953). It was not until 1976 that a well-controlled study on the ergogenic effects of NaHCO3 was conducted. Sutton et al. (1976) found that, in comparison with a control condition, the ingestion of NaHCO3 increased by approximately 65 percent the duration of time subjects could cycle at 90 percent . In a second study, the same group evaluated the effects of
metabolic acidosis and metabolic alkalosis on high-intensity exercise performance (Jones et al., 1977). Subjects were provided calcium carbonate (CaCO3) as a control (placebo), ammonium chloride (NH4Cl) to induce acidosis, and NaHCO3 to induce alkalosis. Compared with the control, acidosis reduced exercise duration by 70 percent while alkalosis increased exercise duration by 63 percent. Of interest was the observation that the blood pH and plasma lactate concentration were highest during the NaHCO3 trial and lowest during the NH4Cl trial. It was suggested that the endurance performances associated with NH4Cl and NaHCO3 treatments were due, in part, to their effect on the efflux rate of lactate from muscle. That is, NH4Cl impaired muscle lactate efflux and increased the rate of muscle lactate accumulation, and NaHCO3 facilitated muscle lactate efflux and decreased the rate of muscle lactate accumulation. It has been demonstrated in various animal models that a low blood pH impairs and that a high blood pH facilitates lactate efflux from muscle to blood (Hirche et al., 1975).
Another approach to increasing high-intensity exercise performance is to reduce the rate of muscle lactate production. Pangamic acid, which is also referred to as vitamin B15, is a naturally occurring substance with vitamin-like properties. The active agent in pangamic acid is thought to be dichloroacetate (DCA). DCA stimulates pyruvate dehydrogenase indirectly by inhibiting pyruvate dehydrogenase kinase (Whitehouse et al., 1974). Pyruvate dehydrogenase catalyzes the rate-limiting step in the aerobic oxidation of pyruvate and lactate. Maximal stimulation of pyruvate dehydrogenase activity by DCA has been shown to lower blood lactate concentrations during exercise in animals and during postexercise recovery in humans (Carraro et al., 1989; Schneider et al., 1981). Schneider et al. (1981) found that DCA-treated rats were able to swim approximately 40 percent longer than controls when the exercise intensity was near the maximal work load. This increase in performance was associated with lower levels of blood and muscle lactate at rest and during the swim. At exhaustion, blood lactate was the same in the two groups, even though the DCA-treated rats had worked for a significantly longer period of time.
Heat is another metabolic by-product of exercise that can also impair physical performance and endurance. If environmental conditions are extreme and the exercise period is prolonged, the increased metabolic rate that occurs during exercise can result in dehydration and hyperthermia unless adequate water is consumed. The amount of water lost during exercise is determined by the need to regulate body heat. During exercise in the heat, evaporation is the principal means of body heat loss. As sweat comes into contact with the skin, a cooling effect occurs as the sweat evaporates. For each liter of water that vaporizes, 580 kcal of heat is dissipated from the body and transferred to the environment. In a few hours of hard exercise in the heat, water loss from
sweating can reach 3 to 4 liters. A water loss equivalent to 2 percent of body weight will impair cardiovascular function and the thermal regulatory mechanisms of the body (Bijlani and Sharma, 1980; Drinkwater, 1976; Gisolfi and Copping, 1974). Water loss of 4 percent of body weight will reduce muscle endurance and work capacity (Buskirk et al., 1958; Saltin, 1964). Water loss that exceeds 6 percent of body weight will drastically hamper physical performance and possibly lead to severe heat injury. Therefore, water becomes a very important ergogenic aid during prolonged exercise in a hot environment.
Ergogenic Aids That Enhance Recovery
Because of the importance of muscle glycogen for prolonged moderate-intensity exercise, replenishment of the muscle glycogen stores is essential for high levels of daily physical activity and training. Following the depletion of muscle glycogen levels by a prolonged exercise bout, normal glycogen stores can be replenished within a 24-h period if sufficient carbohydrate is ingested. This generally requires consumption of 500 to 550 g of carbohydrate daily (Costill et al., 1981). If the carbohydrate concentration of the diet is inadequate, successive days of intense, prolonged exercise may result in a gradual reduction in the muscle glycogen stores and a deterioration in performance (Costill et al., 1971).
To optimize the rate of muscle glycogen replenishment, a carbohydrate supplement of approximately 1.0 g/kg of body weight should be consumed immediately after the cessation of exercise (Ivy et al., 1988a,b) Continuation of supplementation every 2 h will maintain a rapid rate of storage for up to 6 h after exercise (Blom et al., 1987). Increasing the amount of carbohydrate consumption above 1.0 g/kg of body weight per supplement appears to provide no additional benefit (Ivy et al., 1988b). Supplements composed of glucose or glucose polymers are more effective for the replenishment of muscle glycogen stores after exercise than supplements predominantly composed of fructose (Blom et al., 1987). However, some fructose is recommended because it is more effective than glucose in replenishing liver glycogen stores (Nilsson and Hultman, 1974). It has also been found that theaddition of protein (~ 0.3 to 0.4 g/kg of body weight) to a carbohydrate supplement will increase the rate of muscle glycogen storage (Zawadzki et al., 1992). This is due to the synergistic insulin response produced from the combination of carbohydrate and protein. Finally, carbohydrates in solid or liquid form can be consumed immediately after exercise with similar results (Reed et al., 1989). However, liquid supplements are recommended because they are easy to digest and are
less filling, and therefore do not tend to adversely affect an individual’s normal appetite. They also provide a source of fluid for rapid rehydration.
Because of the adverse effects of dehydration on physical performance, it is also important to rehydrate prior to any subsequent physical exertion. Although water has generally been recommended as the fluid of choice for rehydration, recent studies have suggested that electrolyte or glucose-electrolyte solutions actually may be superior to water (Morimoto et al., 1981; Nose et al., 1988). Following exercise dehydration there is a prolonged period of delayed rehydration. This is due in part to a decreased dipsogenic drive that occurs with large amounts of water consumption. This reduced drive to consume fluid appears to be related to a disproportionate recovery of plasma volume with respect to total body water (Nose et al., 1988). Apparently, a reduced plasma osmolality or a low sodium chloride (NaCl) concentration inhibits the dipsogenic response. When carbohydrate-electrolyte solutions rather than water are ingested, this prevents the rapid decline in plasma osmolality and NaCl concentration, thus prolonging the dipsogenic response of dehydration, and increases voluntary fluid consumption. It has also been reported that plasma volume and osmolality are significantly greater after 4 h of recovery from exercise-dehydration when a carbohydrate-electrolyte solution is ingested than when an equal volume of water is ingested (González-Alonso et al., 1992). This results in reduced urine loss and significantly greater water retention. These findings strongly suggest that a carbohydrate-electrolyte solution is more effective than water for the rapid replenishment of body fluids following exercise-dehydration.
Many natural foods or derivatives of food products have ergogenic effects. Their mechanisms of action as well as the types of physical performance they enhance are quite varied. Some have been found to be beneficial during prolonged moderate-intensity exercise, whereas others enhance anaerobic performance. For maximum effectiveness, it is important to understand their limitations and the proper way in which they should be used.
Carbohydrates may be beneficial in extending the time to fatigue when taken before and during prolonged moderate-intensity aerobic exercise. In combination with protein, they stimulate the rapid recovery of muscle glycogen stores following exercise. In combination with electrolytes and water, they are effective in rehydration postexercise.
Caffeine appears to be a strong enhancer of aerobic endurance. This may be due to its ability to spare muscle glycogen and facilitate neural processes.
The chronic feeding of pyruvate-dihydroxyacetone may increase aerobic endurance, but a major disadvantage of this supplement is that the concentrations shown to be effective may result in a mineral overload.
Although it has been suggested that medium-chain triglycerides may enhance aerobic endurance, this has not been substantiated, nor have there been any definitive results demonstrating a positive effect of choline supplementation on physical performance.
Branched-chain amino acids may enhance aerobic endurance by reducing the rate of brain serotonin accumulation during prolonged exercise. However, more research is needed to substantiate this hypothesis.
For maximum performance during prolonged physical exertion in a hot and humid environment, water or fluid supplementation is essential.
For high-intensity aerobic and anaerobic performance, phosphate loading may be beneficial because of the ability of phosphate to increase the blood 2,3-diphosphoglycerate concentration and reduce the affinity of oxygen for hemoglobin.
Anaerobic capacity may be enhanced by preexercise ingestion of sodium bicarbonate or dichloroacetate. Sodium bicarbonate increases blood pH, which helps with the buffering of lactate and its efflux from the exercising muscle. Dichloroacetate increases the activity of pyruvate dehydrogenase and thus reduces the rate of lactate accumulation.
Ahlborg, B., J.Berström, L.G.Ekelund, and E.Hultman 1967 Muscle glycogen and muscle electrolytes during prolonged physical exercise. Acta Physiol. Scand. 70:129–142.
Asmussen, E., W.Van Dobelin, and M.Nielson 1948 Blood lactate and oxygen debt after exhaustive work at different oxygen tensions. Acta Physiol. Scand. 15:57–62.
Bergström, J., and E.Hultman 1967 A study of the glycogen metabolism during exercise in man. Scand. J. Clin. Lab. Invest. 19:218–226.
Bergström, J., L.Hermansen, E.Hultman, and B.Saltin 1967 Diet, muscle glycogen and physical performance. Acta Physiol. Scand. 71:140–150.
Bijlani, R.L., and K.N.Sharma 1980 Effect of dehydration and a few regimes of rehydration on human performance. Ind. J. Physiol. Pharm. 24:255–266.
Blom, P.C.S., A.T.Høstmark, O.Vaage, K.R.Kardel, and S.Maehlum 1987 Effect of different post-exercise sugar diets on the rate of muscle glycogen synthesis. Med. Sci. Sports Exerc. 19:491–496.
Blomstrand, E., F.Celsing, and E.A.Newsholme 1988 Changes in plasma concentrations of aromatic and branched-chain amino acids during sustained exercise in man and their possible role in fatigue. Acta Physiol. Scand. 133:115–121.
Blomstrand, E., P.Hassmén, B.Ekblom, and E.A.Newsholme 1991 Administration of branched-chain amino acids during sustained exercise—effects on performance and on plasma concentration of some amino acids. Eur. J. Appl. Physiol. 63:83–88.
Bredle, D.L., J.M.Stager, W.F.Brechue, and M.O.Farber 1988 Phosphate supplementation, cardiovascular function, and exercise performance in humans. J. Appl. Physiol. 65:1821–1826.
Buskirk, E.R., P.P.Lampietto, and D.E.Bass 1958 Work performance after dehydration: Effects of physical conditioning and heat acclimatization. J. Appl. Physiol. 12:189–197.
Cade, R., M.Conte, C.Zauner, D.Mars, J.Peterson, D.Lunne, N.Hommen, and D.Parker 1984 Effects of phosphate loading on 2,3-diphosphoglycerate and maximal oxygen uptake. Med. Sci. Sports Exerc. 16:263–268.
Carraro, F., K.Samuel, J.I.Rosenblatt, and R.R.Wolfe 1989 Effect of dichloroacetate on lactate concentration in exercising humans. J. Appl. Physiol. 66:591–597.
Chasiotis, D., E.Hultman, and K.Sahlin 1983 Acidotic depression of cyclic AMP accumulation and phosphorylase b to a transformation in skeletal muscle of men. J. Physiol. (London) 335:197–204.
Costill, D.L., R.Bowers, G.Branam, and K.Sparks 1971 Muscle glycogen utilization during prolonged exercise on successive days. J. Appl. Physiol. 31:834–838.
Costill, D.L., E.F.Coyle, G.Dalsky, W.Evans, W.Fink, and D.Hoopes 1977 Effects of elevated plasma FFA and insulin in muscle glycogen usage during exercise. J. Appl. Physiol. 43:695–699.
Costill, D.L., G.Dalsky, and W.Fink 1978 Effects of caffeine ingestion on metabolism and exercise performance. Med. Sci. Sports 10:155–158.
Costill, D.L., W.M.Sherman, W.J.Fink, C.Maresh, and M.Witten 1981 The role of dietary carbohydrate in muscle glycogen resynthesis after strenuous running. Am. J. Clin. Nutr. 34:1831–836.
Coyle, E.F., J.M.Hagberg, B.R.Hurley, W.H.Martin, A.A.Ehsani, and J.O.Holloszy 1983 Carbohydrate feeding during prolonged strenuous exercise can delay fatigue. J. Appl. Physiol. 55:230–235.
Coyle, E.F., A.R.Coggan, M.K.Hemmert, and J.L.Ivy 1986 Muscle glycogen utilization during prolonged strenuous exercise when fed carbohydrate. J. Appl. Physiol. 61:165–172.
Dennig, H., J.H.Talbott, H.T.Edwards, and D.B.Dill 1931 Effect of acidosis and alkalosis upon capacity for work. J. Clin. Invest. 9:601–613.
Drinkwater, B.L. 1976 Thermoregulatory responses of women to intermittent work in the heat. J. Appl. Physiol. 41:57–62.
Duffy, D.J., and R.K.Conlee 1986 Effects of phosphate loading on leg power and high intensity treadmill exercise. Med. Sci. Sports Exerc. 18:674–677.
Essig, D., D.L.Costill, and P.J.van Handel 1980 Effects of caffeine ingestion on utilization of muscle glycogen and lipid during leg ergometer cycling. Int. J. Sports Med. 1:86–90.
Fuchs, F., Y.Reddy, and F.N.Briggs 1970 The interaction of cations with the calcium-binding site of troponin. Biochim. Biophys. Acta 221:407–409.
Gisolfi, C.V., and J.R.Copping 1974 Thermal effects of prolonged treadmill exercise in the heat. Med. Sci. Sports 6:108–113.
Gollnick, P.D., B.Pernow, B.Essén, E.Jannson, and B.Saltin 1981 Availability of glycogen and plasma FFA for substrate utilization in leg muscle of man during exercise. Clin. Physiol. 1:27–42.
González-Alonso, J., C.L.Heaps, and E.F.Coyle 1992 Rehydration after exercise with common beverages and water. Int. J. Sports Med. 13:399–406.
Graham, T.E., and L.L.Spriet 1991 Performance and metabolic responses to a high caffeine dose during prolonged exercise. J. Appl. Physiol. 71:2292–2298.
Greenberger, N.J., J.B.Rodgers, and K.J.Isselbacher 1966 Absorption of medium and long-chain triglycerides: Factors influencing their hydrolysis and transport. J. Clin. Invest. 45:217–222.
Heigenhauser, G.J.F., and N.L.Jones 1991 Bicarbonate loading. Pp. 183–212 in Ergogenics, Enhancement of Performance in Exercise and Sport, D.R.Lamb and M.H.Williams, eds. Ann Arbor, Mich.: William C.Brown.
Hickson, R.C., M.J.Rennie, R.K.Conlee, W.W.Winder, and J.O.Holloszy 1977 Effects of increased plasma fatty acids on glycogen utilization and endurance. J. Appl. Physiol. 43:829–833.
Hirche, H., V.Hombach, H.D.Langohr, U.Wacher, and J.Busse 1975 Lactic acid permeation rate in working gastrocnemii of dogs during metabolic alkalosis and acidosis. Pflüegers Arch. 356:209–222.
Ivy, J.L., D.L.Costill, W.J.Fink, and R.W.Lower 1979 Influence of caffeine and carbohydrate feedings on endurance performance. Med. Sci. Sports 11:6–11.
Ivy, J.L., D.L.Costill, W.J.Fink, and E.Maglischo 1980 Contribution of medium and long chain triglyceride intake to energy metabolism during prolonged exercise. Int. J. Sports Med. 1:15–20.
Ivy, J.L., W.Miller, V.Dover, L.G.Goodyear, W.H.Sherman, S.Farrell, and H.Williams 1983 Endurance improved by ingestion of a glucose polymer supplement. Med. Sci. Sports Exerc. 15:466–471.
Ivy, J.L., A.L.Katz, C.L.Cuttler, W.M.Sherman, and E.F.Coyle 1988a Muscle glycogen synthesis after exercise: Effect of time of carbohydrate ingestion. J. Appl. Physiol. 64:1480–1485.
Ivy, J.L., M.C.Lee, J.T.Brozinick, and M.J.Reed 1988b Muscle glycogen storage after different amounts of carbohydrate ingestion. J. Appl. Physiol. 65:2018–2023.
Johnson, W.R., and D.H.Black 1953 Comparison of effects of certain blood alkalinizers and glucose upon competitive endurance performance. J. Appl. Physiol. 5:577–78.
Jones, N.L., J.R.Sutton, R.Taylor, and C.J.Toews 1977 Effect of pH on cardiorespiratory and metabolic responses to exercise. J. Appl. Physiol. 43:959–964.
Kreider, R.B., G.W.Miller, M.H.Williams, C.T.Samma, and T.A.Nasser 1990 Effects of phosphate loading on oxygen uptake, ventilatory anaerobic threshold, and run performance. Med. Sci. Sports Exerc. 22:250–256.
Morimoto, T., K.Miki, H.Nose, S.Yamada, K.Hirakawa, and C.Matsubara 1981 Changes in body fluid and its composition during heavy sweating and effect of fluid and electrolyte replacement. Jpn. J. Physiol. 18:31–39.
Nakamura, Y., and A.Schwartz 1972 The influence of hydrogen ion concentration on calcium binding and release by skeletal muscle sarcoplasmic reticulum. J. Gen. Physiol. 59:22–32.
Newsholme, E.A., and A.R.Leech 1983 Pp. 784–787 in Biochemistry for the Medical Sciences. Chicester, United Kingdom: Wiley.
Nilsson, L.H., and E.Hultman 1974 Liver and muscle glycogen in man after glucose and fructose infusion. Scand. J. Clin. Lab. Invest. 33:5–10.
Nose, H., G.W.Mack, X.Shi, and E.R.Nadel 1988 Role of osmolality and plasma volume during rehydration in humans. J. Appl. Physiol. 65:325–331.
Pardridge, W.M., and W.M.Oldendorf 1975 Kinetic analysis of blood-brain barrier transport of amino acids. Biochim. Biophys. Acta 401:128–136.
Reed, M.J., J.T.Brozinick, M.C.Lee, and J.L.Ivy 1989 Muscle glycogen storage postexercise: Effect of mode of carbohydrate administration. J. Appl. Physiol. 66:720–726.
Saltin, B. 1964 Circulatory response to submaximal and maximal exercise after thermal dehydration. J. Appl. Physiol. 19:1125–1132.
Schneider, S.H., P.M.Komanicky, M.N.Goodman, and N.B.Ruderman 1981 Dichloroacetate: Effects on exercise endurance in untrained rats. Metabolism 30:590–595.
Schwabe, A.D., L.R.Bennett, and L.P.Bowman 1964 Octanoic acid absorption and oxidation in humans. J. Appl. Physiol. 19:335–337.
Sherman, W.M., D.L.Costill, W.J.Fink, and J.M.Miller 1981 The effect of exercise and diet manipulation on muscle glycogen and its subsequent utilization during performance. Int. J. Sports Med. 2:114–118.
Spriet, L.L. 1991 Blood doping and oxygen transport. Pp. 213–284 in Ergogenics, Enhancement of Performance in Exercise and Sport, D.R.Lamb and M.H.Williams, eds. Ann Arbor, Mich.: William C.Brown.
Spriet, L.L., D.A.MacLean, D.J.Dyck, E.Hultman, G.Cederblad, and T.E.Graham 1992 Caffeine ingestion and muscle metabolism during prolonged exercise in humans. Am. J. Physiol. 262:E891-E898.
Stanko, R.T., R.J.Robertson, R.J.Spina, J.J.Reilly, Jr., K.D.Greenawalt, and F.L.Goss 1990a Enhancement of arm exercise endurance capacity with dihydroxyacetone and pyruvate. J. Appl. Physiol. 68:119–124.
Stanko, R.T., R.J.Robertson, R.W.Galbreath, J.J.Reilly, Jr., K.D.Greenawalt, and F.L.Goss 1990b Enhanced leg exercise endurance with a high-carbohydrate diet and HRT dihydroxyacetone and pyruvate. J. Appl. Physiol. 69:1651–1656.2
Stewart, I., L.McNaughton, P.Davies, and S.Tristram 1990 Phosphate loading and the effects on in trained cyclists. Res. Q. Exerc. Sport 61:80–84.
Sutton, J.R., N.L.Jones, and C.J.Toews 1976 Growth hormone secretion in acid-base alterations at rest and during exercise. Clin. Sci. 50:241–247.
Trivedi, B., and W.H.Danforth 1966 Effect of pH on the kinetics of frog muscle phosphofructokinase. J. Biol. Chem. 241:4110–4112.
Whitehouse, S., R.H.Casper, and P.J.Randle 1974 Mechanism of activation of PDH by DCA and other halogenated carboxylic acids. Biochem. J. 141:761–774.
Yaspelkis, III, B.B., and J.L.Ivy 1991 Effect of carbohydrate supplements and water on exercise metabolism in the heat. J. Appl. Physiol. 71:680–687.
Yaspelkis, III, B.B., J.G.Patterson, P.A.Anderla, A.Ding, and J.L.Ivy 1993 Carbohydrate supplementation spares muscle glycogen press during variable intensity exercise. J. Appl. Physiol. 75:1477–1485.
Zawadzki, K.M., B.B.Yaspelkis III, and J.L.Ivy 1992 Carbohydrate-protein complex increases the rate of muscle glycogen storage after exercise. J. Appl. Physiol. 72:1854–1859.