Nutrition and fuel utilization in the athletic horse.

Clinical Nutrition

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Nutrition and Fuel Utilization in the Athletic Horse Laurie M. Lawrence, PhD*

FUEL USE DURING EXERCISE The primary goal of performance nutrition is to meet an individual's nutrient requirements. However, it may also be possible to manipulate fuel utilization during exercise in order to delay substrate depletion and end product accumulation, two factors involved in fatigue and poor performance. In order to formulate an appropriate diet and to develop an appropriate feeding pattern, it is necessary to consider the ramifications of exercise on energy production and fuel utilization. The primary fuels are carbohydrate, fat, and protein. The extent to which each fuel is utilized by contracting muscle depends on several factors, including the intensity and duration of the exercise, the availability of carbohydrate or alternate fuels, and the influence of hormones. The respiratory exchange ratio, or respiratory quotient (R or RQ), can be used to evaluate the contribution of the major substrates to energy production. The R-value is the ratio of oxygen consumed to carbon dioxide produced. An R-value of 1.0 is indicative of carbohydrate as the primary fuel source, whereas an R-value approaching 0.7 indicates that fat is providing the majority of fuel. At rest, muscle metabolism is fueled primarily by fat, with less than half of total oxygen consumption attributed to carbohydrate oxidation. However, during exercise the proportion of energy provided by carbohy drate or fat will change. As exercise becomes more intense, increased carbohydrate utilization will cause an increased R-value. During very high intensity work, such as sprinting, carbohydrate utilization will account for essentially all of the oxygen consumed by the active muscles.118 By com parison, during submaximal work of long duration, the contribution of carbohydrate generally decreases and the contribution of fat increases.26 Carbohydrate is available to the muscle from either muscle glycogen or blood glucose. Blood glucose can be derived from hepatic release via *Associate Professor, Department of Animal Sciences, University of Illinois, Urbana, Illinois Veterinary Clinics of North America: Equine Practice-Vol. 6, No. 2, August 1990

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glycogenolysis or gluconeogenesis, or from dietary absorption. The contri bution of each fuel source to energy metabolism in the horse has not been well studied, but data from humans and laboratory animals indicate that muscle glycogen is the primary source of carbohydrate utilized during most types of exercise. However, as muscle glycogen stores become depleted during long-term exercise, the contribution of blood glucose may increase. At rest, blood glucose accounts for about 10% of the oxygen utilized by muscle. During prolonged steady-state submaximal exercise, blood glucose will account for up to 75% of the carbohydrate utilized.31 In the postab sorptive state, hepatic glucose release during exercise arises primarily from hepatic glycogenolysis, with gluconeogenesis starting to play an important role only as liver glycogen levels decrease and the substrates for gluconeo genesis (glycerol, lactate, pyruvate, and alanine) begin to increase in the later stages of exercise. At rest, approximately 25% of hepatic glucose output results from gluconeogenesis.9 During the initial stages of submaxi mal cycling exercise, hepatic glucose output increases, with most of the increase resulting from glycogenolysis. After an extended period of exercise, an increasing portion (45%) is derived from gluconeogenesis. The regulation of gluconeogenesis occurs through hormonal changes as well as substrate availability.141 Although lactate may be the primary precursor during early exercise, glycerol and amino acids (primarily alanine) become increasingly important as an exercise bout continues. In addition to influencing the proportion of energy derived from carbohydrate, exercise intensity influences the selection of the metabolic pathways used for carbohydrate metabolism. During rest and low intensity exercise, most carbohydrate used by skeletal muscle is completely oxidized to carbon dioxide and water. During high intensity exercise, the oxidation of some glucose will be incomplete and lactate will be formed. The conversion of glucose to lactic acid is relatively inefficient, producing less adenosine triphosphate (ATP) per glucosyl unit, but has advantages in that ATP production is relatively rapid and can occur in the absence of oxygen. As the intensity of exercise increases, the ATP needs of the muscle can exceed its ability to produce energy through the oxidative catabolism of fats and carbohydrates. This may occur as a result of inadequate oxygen at the muscle site, or as a result of inadequate oxidative capacity of the muscle (or both). Consequently, as exercise intensity increases, the production of lactic acid increases. Although the conversion of glucose to lactic acid has a number of advantages, it cannot continue indefinitely at a high rate. Under physiologic conditions, lactic acid actually exists as lactate and hydrogen ions. At low rates of production, the diffusion of lactate and H + out of the muscle and into blood will occur readily enough to prevent accumulation in muscle. Similarly, at low rates of production, lactate removal by liver and the buffering action of the blood bicarbonate will be sufficient to prevent H + accumulation in the blood. However, as the rate of production increases beyond the rate of removal, both ions will begin to accumulate. This point is often referred to as the lactate threshold (LT) or the onset of blood lactate accumulation (OBLA). Beyond this work intensity, blood lactate levels will rise rapidly and blood pH will begin to fall. Since lactate and H + also

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accumulate in the muscle at this time, muscle pH will decline. From a normal pH of 7. 0, maximal exercise may cause intramuscular pH to fall to 6. 5 or below. 58• 117 The consequence of intramuscular acidosis is believed to be a reduction in the flux through the glycolytic pathway, diminished ATP production, and decreased force output by the muscle fibers. Thus, the accumulation of "lactic acid" in muscle can be a cause of muscle fatigue during high intensity exercise. It has been hypothesized that reduced muscle pH exerts a regulatory effect on glycolysis by inhibiting phospho fructokinase (PFK), one of the rate limiting enzymes in the conversion of glucose to pyruvate. However, it has been pointed out that in vivo, flux through the glycolytic pathway and lactate production can continue even when muscle pH is low 118 and that the effect of pH on muscle may be exerted through a different mechanism. In vitro evidence also suggests that reduced muscle pH will alter tension development in muscle fibers. 23• 30 The accumulation of lactate and H + and the associated drop in muscle pH is recognized as a cause of fatigue only during very high intensity exercise. During submaximal exercises, fatigue most commonly results from carbohydrate depletion. As mentioned previously, carbohydrate utilization increases as the intensity of exercise increases; in contrast, during low intensity exercise of long duration, the contribution of carbohydrate to energy production gradually decreases and the contribution of fat increases. However, oxidation of fat decreases in the absence of carbohydrate. Consequently, as carbohydrate becomes limiting, muscle contraction must be reduced. The carbohydrate used in muscle contraction may be derived from several sources, with the most important contributor being muscle glycogen. Many studies have utilized muscle biopsies before and after exercise to estimate the degree of depletion caused by different types of exercise. Nimmo and Snow 103 examined the effect of speed and distance on the rate of glycogen utilization as well as on the total amount of glycogen used by galloping horses. The horses galloped 506, 1025, 1600, and 3650 m at 14. 5, 14. 1, 12. 6, and 11. 4 m/sec, respectively. The rate of glycogen utilization was highest during the shortest and fastest gallop (506 m), which lasted about 35 sec (Fig. 1). The rate of glycogen utilization decreased as the length of the gallop increased and the speed of the gallop decreased. Total glycogen utilization was lowest in the shortest, fastest gallop, with less than 15% of the initial glycogen being utilized. The amount of glycogen utilized was slightly, but not significantly, higher when the horses were galloped the longest distance at the slowest speed. More glycogen was utilized (about 30% of the total) during the two intermediate distances. Similarly, Harris et al59 found that approximately 28% and 32% of the total glycogen available was used during maximal galloping at 800 and 2000 m, respec tively. It is important to recognize that at these distances, which correspond to the distances raced by Thoroughbreds, more than half of the total glycogen available remains within the muscle at the end of the gallop. By comparison, Snow and Baxter 121 found that glycogen content of the middle gluteal muscle was depleted approximately 60% by an endurance ride. In a subsequent study, Snow et al 125 reported that after the first 40 km of an 80-km ride, muscle glycogen was depleted by about 64%, and that by the end of the 80 km, glycogen depletion was almost complete.

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These findings in horses are comparable to results from human studies. Saltin and Karlsson119 presented data from several sources to demonstrate that maximal bicycle exercise produced a very rapid rate of glycogen utilization but that total muscle glycogen declined by less than 30%. During intense but submaximal exercise (75% V0 2 max), the rate of glycogen utilization was reduced, but at fatigue, approximately 80% of the total glycogen was depleted. At lower work intensities (30% to 60% V0 2 max), the rate of glycogen depletion was relatively low, and depletion was not attained during a 2-hour work bout. These authors concluded that at work intensities between 65% and 89% of V0 2 max, where fatigue occurs in 45 to 200 min, glycogen depletion can be the limiting factor. At work loads not in this range, glycogen availability may not be limiting. Muscle glycogen is the most important source of carbohydrate for exercising muscle, but as muscle stores are depleted, carbohydrate from other sources must be used as well. The contribution of amino acids to gluconeogenesis will be discussed later. Of greater pertinence is the contribution of blood glucose to energy production during exercise, which increases as muscle glycogen stores decline. The contribution of blood glucose to energy production in working muscle during submaximal exercise has been estimated to increase from about 10% at 10 min of exercise to between 35% and 40% at 90 to 120 min of exercise.9 During the initial periods of submaximal exercise, the increase in glucose uptake does not create a lowering of blood glucose levels because hepatic glucose release

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Figure 1. The effect of exercise intensity on the rate of muscle glycogen utilization in horses. (Data from Nimmo MA, Snow DH: Changes in muscle glycogen, lactate, and pyruvate concentrations in the Thoroughbred horse following maximal exercise. In Snow D, Persson S, Rose R (eds): Equine Exercise Physiology. Cambridge, England, Granta, 1983, p 237.)


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keeps pace with muscle utilization. Blood glucose levels are maintained primarily at the expense of hepatic glycogenolysis. At rest in the postab sorptive state, glycogen contributes 65% to 75% of the total glucose released by the liver. The contribution of gluconeogenesis to glucose release remains relatively constant during short-term mild exercise, but becomes increas ingly important as liver glycogen stores become depleted and as the availability of glucogenic precursors (alanine, lactate, pyruvate, and glycerol) increases. Unfortunately, the ability of gluconeogenesis to maintain blood glucose levels beyond hepatic glycogen depletion is limited, and after prolonged moderate exercise blood glucose levels will decline. In horses, Lindholm et al84 found that 4 hours of trotting depleted liver glycogen by about 90% and that there was a concomitant decrease in blood glucose. The uptake of blood glucose is related to the intensity of exercise as well as the duration of exercise. During short-term maximal exercise the uptake of blood glucose may occur, but the total amount of blood glucose utilized is relatively low as a result of the brief work time. Consequently, blood glucose levels may not decrease. In fact, short-term maximal exercise can be associated with elevated blood glucose levels. Glucosuria occurs in Thoroughbred horses sampled after racing. 15 The presence of glucose in the urine was believed to be the result of blood glucose· concentration during or after racing exceeding the renal glucose threshold. Blood glucose levels at or near the proposed threshold have been reported in sprinting horses. 122 The elevation in blood glucose in response to maximal effort may be the result of excessive liver glycogenolysis or increased gluconeogenesis in response to increased availability of glucogenic precursors (especially lactate). The actual importance of blood glucose uptake to energy production during maximal exercise is not clear. At very high rates of glycogen utilization in humans, a net release of free glucose from muscle was attributed to the glucose released from the branch points of the glycogen molecule. 135 More recently, Katz et aF0 reported that at 95% to 100% V02 max, there was an accumulation of free glucose in muscle as well as elevated glucose-6-phosphate. These findings were interpreted to indicate that the contribution of blood glucose to maximal exercise is minor compared with the contribution of muscle glycogen. While the changes that occur in carbohydrate metabolism during exercise are fairly well understood, the changes in protein and amino acid metabolism are not. There is a general perception that exercise increases muscle mass and therefore stimulates protein synthesis. However, it appears that the result of most exercise is actually decreased protein synthesis. Particularly during endurance exercise, protein synthesis in both muscle and liver has been reported to be decreased, 22 with the extent of the decrease being related to intensity and duration of exercise. Following exercise, protein synthesis may remain depressed immediately after the work bout, but usually returns to normal or increases during the recovery period. 45 In contrast to the decreased protein synthesis found during endurance-type exercise, isometric exercise that causes muscle hypertrophy results in increased protein synthesis. 42 Since net protein accumulation or loss is a balance between synthesis and degradation, several studies have attempted to quantify the effects of exercise on protein degradation. The

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conflict in results (some support increased degradation, others support decreased degradation, others indicate no change) can be attributed to differences in exercise type or duration and to variability in the methods employed to quantitate degradation. 22• 45 The overall effect of exercise on protein turnover during exercise appears to be a net increase in the free amino acid pool, either from muscle or liver. Thus, amino acids are made available for conversion to citric acid cycle intermediates or glucose, or for oxidation. As mentioned previously, in an absence of carbohydrate, fat oxidation is inhibited because of a reduced availability of citric acid cycle intermediates. Several amino acids including arginine, histidine, glutamate, proline, isoleucine, methionine, valine, tyrosine, phenylalanine, and aspartate-may be converted to citric acid cycle intermediates, thus sparing carbohydrate stores. Similarly, the carbon skeletons of several amino acids-including alanine, cystine, glycine, hydroxyproline, serine, threonine, and tryptophan-can be used to form pyruvate, which would be available for oxidation. The extent to which most amino acids contribute to energy production in muscle is unknown. Carbon skeleton availability results from deamination or transamination of the amino groups. These reactions occur predominantly in liver as opposed to muscle for most amino acids, the exception being the branched-chain amino acids, particularly leucine. Several studies with humans have supported the concept that leucine oxidation is increased during exercise.55• 142 During 2 hours of submaximal exercise at 55% VO 2 max, leucine incorporation in protein was decreased, and oxidation increased. 55 The overall contribution of amino acid oxidation to energy production during exercise is relatively minor compared with carbohydrate or fat, with estimates as low as 1% or as high as 15%. 45 Based on urea excretion, it was estimated that the contribution of protein to energy production in exercised rats was about 4%. When the leucine oxidation rates from other researchers were used to estimate the potential contribution of protein to the energy used, the estimate was 20% to 25%. 22 In order for leucine to be oxidized in muscle, the amino group must be removed. This occurs primarily by transamination, with the eventual formation of alanine and glutamine. During some types of exercise, alanine release from muscle increases, and in humans the extent of the increase appears to be related to exercise intensity and duration.46 When horses were worked at a mild intensity, no increase in plasma alanine was noted, 116 but during a more intense bout plasma alanine concentrations increased.98 The increase in plasma alanine level is almost certainly a result of increased release, since hepatic uptake increases or stays constant in humans. Both total splanchnic alanine uptake and fractional uptake increase during mild exercise. During heavy exercise, the increase in fractional extraction rate compensates for the decrease in splanchnic blood flow, resulting in a total alanine uptake not different from that at rest. 32 The alanine released by muscle acts as an important glucogenic precursor in the liver and thus contributes to the maintenance of the blood glucose level during exercise. Since most of the pyruvate used to form alanine is derived from blood glucose or muscle glycogen, the entire process has been referred to as the glucose-alanine cycle.


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In addition to serving as a mechanism for glucose cycling, alanine is important for transporting amino nitrogen from muscle to liver. Glutamine may also serve to transport nitrogen out of muscle and has been reported to increase in plasma during exercise in horses.98 In humans, the accumu lation of alanine and glutamine seems to be related to leucine oxidation.5 In the liver, alanine and glutamine give up their amino groups to glutamate, which is then catabolized in the formation of urea. Thus, the nitrogen removed from amino acids during exercise (primarily leucine) in muscle is ultimately excreted as urea. The combustion of protein is not energetically efficient because the synthesis and excretion of urea is an energy-requiring process. Thus, protein yields 5.6 kcal/g in a bomb calorimeter, but only about 4 kcal/g are available physiologically. Another aspect of nitrogen metabolism during exercise is the generation of ammonia. Plasma ammonia levels have been reported to increase as a result of high intensity exercise in several species, including horses.29• 97• 98 Although it is convenient to speculate that the increase in ammonia is derived from amino acid catabolism, Babij5 found little support for this hypothesis. The increase probably results from the catabolism of adenosine monophosphate (AMP) to inosine monophosphate (IMP). Since ammonia is a neurotoxin and may alter aspects of oxidative· metabolism, it may be involved in fatigue.29• 97 Quantitatively, fat constitutes the largest energy store in the body. The amount of energy stored as fat exceeds the energy stored as carbohy drate by 30- to 60-fold. In some animals, such as migrating birds, fat is the predominant energy source for muscle contraction.44 As has been mentioned previously, declining R-values during submaximal exercise demonstrate that the contribution of fat to energy production increases with the duration of exercise.26 Figure 2 illustrates the increasing contribution of fat to energy production during long-term submaximal exercise in a human subject. By comparison, fat use tends to decrease as the intensity of exercise increases so that at 100% V0 2 max, the contribution of fat oxidation to energy production is very small. Three major sources of fat are available for oxidation by muscle. The plasma free fatty acids (FFA) constitute the most important source. FFA are released from adipose, transported in the blood bound to albumin, and taken up by muscle for oxidation. Lipolysis in adipose tissue is inhibited by insulin and is increased by catecholamines, glucagon, and cortisol. Consequently, it has been well documented that long-term exercise causes an increase in plasma FFA concentrations. Havel and coworkers60 reported that FFA levels in submaximally exercising men increased during the first 30 min of exercise and then leveled off during the subsequent 90 min. Another study reported an increase in FFA levels during long-term exercise but not during short-term exercise.u 3 Increased FFA levels in horses after endurance tests have been noted by several studies.88· 89• 122• 126 The elevation in plasma FFA concentration during submaximal exercise is important because it appears to be the availability of substrate that regulates the contribution of fat to energy production during exercise. u3 Costill et al 19 found that the contribution of fat oxidation to energy production in exercising men was increased when plasma FFA were elevated prior to a

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work bout at 68% V0 2 max. The elevated FFA levels were produced by consumption of a high-fat meal and subsequent treatment with heparin to induce lipoprotein lipase activation. The effect of this treatment was compared with a control (5- to 6-hour fast) or a glucose ingestion treatment that produced much lower plasma FFA concentrations. When FFA were elevated before the 30-min work bout, there was a lower respiratory exchange ratio, lower lactate production, and lower glycogen utilization compared with the control condition. During high intensity exercise, the increase in R-value, high rate of glycogen use, and the high level of lactate accumulation support the contention that fat metabolism is limited. In addition, the fractional uptake of FFA has been reported to decrease during intense exercise when compared with moderate exercise.54 Nontheless, Snow et al 122 found a change in the composition of the circulating FFA pool in response to racing in horses, even though total FFA concentration remained constant. In a second group of horses, total FFA concentration increased during a 15-min walk to the track and then decreased after galloping. The authors suggested that although the relative contribution of FFA to total energy production might be decreased during maximal exercise, FFA uptake and utilization are still increased over the resting rate. These authors also pointed out that since the horse has such high aerobic capacity compared with other species,

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Minutes of Exercise Figure 2. The contribution of fat and carbohydrate to energy production during long term submaximal exercise in a human subject. (Data from Edwards HT, Margaria R, Dill DB: Metabolic rate, blood sugar, and the utilization of carbohydrate. Am J Physiol 108:203, 1934.)


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its ability to use fat during high intensity exercise might be greater than that of other animals. In one study with humans, essentially all of the FFA taken up by muscle during low intensity work was accounted for in CO2 production, suggesting that at low work intensities most of the FFA taken up is oxidized. By comparison, at the higher work intensity, CO2 production accounted for only 60% of the FFA taken up by the muscle. 54 The incomplete oxidation of fatty acids could lead to an increase in ketone synthesis, a possibility that has been investigated in only a few studies. After long distance exercise in horses, an increase in ketone bodies has been reported by Lucke and Hall, 88 but Snow and MacKenzie126 reported a slight decrease in 13hydroxybutyrate. Askew et al4 found an increase in 13-hydroxybutyrate following exhausting endurance exercise in rats. Koeslag74 suggests that the development of ketosis subsequent to exercise is related to the carbohydrate status of the individual. An alternative fate for nonoxidized acetate may be the formation of acylcarnitine. 81 Carnitine is best known for its role in fatty acid transport across the mitochondrial membrane. Long-chain acyl coenzyme A (CoA) molecules must be transported to the mitochondrion for oxidation but are not able to pass through the mitochondrial membrane. To facilitate transport they react with carnitine at the outer mitochondrial membrane to form long-chain fatty acylcarnitine esters and are transported through the mem brane and then separated from the carnitine. Thus, the transport of fatty acids into the mitochondria for oxidation during exercise is dependent upon the availability of carnitine. It has also been proposed that carnitine may function to buffer cells against the build up of excess acetyl groups during periods when these compounds are produced more rapidly than they can be oxidized. Harris et al57 found that in resting muscle, approximately 77% of the total carnitine existed as free carnitine and 19% as acetylcarnitine. Following intense muscular contraction, the amount found as free carnitine decreased with a reciprocal increase in the amount found as acetylcarnitine. After 4 min of intense bicycle exercise in one individual, 99. 4% of the total carnitine was found as acetylcarnitine. Foster and Harris34 reported similar findings in maximally exercised horses. However, these authors suggested that because of the brevity and intensity of the exercise, the increase in acetylcarnitine can be attributed primarily to acetyl CoA derived from pyruvate decarbox ylation rather than fatty acids. The formation of acetylcarnitine may be useful during exercise, as it allows CoA to be regenerated for use in the citric acid cycle. In addition, during high intensity short duration exercise, the decrease in free carnitine may limit the ability to transport fatty acids into the mitochondrion where they could flood it with acyl CoA esters. Finally, during high intensity exercise, temporarily diverting excess pyruvate to acetylcarnitine will eliminate pyruvate as a potential lactate precursor. Foster and Harris34 and Harris et al57 did not find an increase in acylcarnitine in maximally exercising horses, suggesting that during short term high intensity exercise carnitine is not acting as a deterrent against the build up of long-chain acyl CoA esters. The response during endurance type exercise may be different. 81

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The extent to which plasma free fatty acids contribute to the total amount of fat oxidized during exercise seems to be somewhat controversial. Several reports have suggested that the total amount of fat oxidized cannot be accounted for by FFA oxidation alone. 28• 67 Other potential sources of fat for energy production include the intramuscular triglyceride stores and the circulating triglycerides. Figure 3 diagrams the potential sources of fat for exercising muscle. Barclay and Stainsby8 found decreased muscle triglyc eride levels when muscle was stimulated to twitch at 5/sec but not at a lower rate or when tetanic contraction was stimulated. A suggestion was made that at the lower twitch rates FFA uptake was sufficient to meet energy use, but that at the higher twitch rate, which corresponded to a higher oxygen utilization, intramuscular triglyceride stores were used. Other studies have also appeared to support the concept that intramuscular triglycerides are an important energy source during endurance-type work. 28• 39• 40 • 1 06 Conversely, some studies have failed to show a reduction in muscle triglyceride levels. 68 Gollnick and Saltin44 point out that in many cases the discrepancy in results may depend on the methodology used for obtaining the muscle sample. The third possible source of fat for oxidation during exercise is the circulating triglyceride pool. Circulating triglycerides are predominantly of dietary or hepatic origin. The contribution of circulating triglycerides to energy metabolism in exercising horses has not been studied, but estimates in other species range from 5% to 15% of energy production. 129 Some studies have shown an enhanced uptake of triglyceride by exercising muscle. Terjung et al 128 studied chylomicron triglyceride metabolism in exercising, fed dogs. At rest, adipose tissue uptake was greater than muscle tissue

Dietary Fat

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Figure 3 . Potential sources of fatty acids fo r oxidation in exercising muscle. TC triglyceride, FA = fatty acid, LPL = lipoprotein lipase, VLDL = very low density lipoprotein,


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uptake. During exercise, an increase in muscle uptake was accompanied by a large (but nonsignificant) decrease in adipose uptake. Whether animals are in a fed or fasted · state influences the rate at which triglycerides are cleared from the blood and also the site of uptake. 90 Circulating triglyceride uptake is regulated by lipoprotein lipase (LPL). In fed animals, elevated insulin increases LPL activity in adipose, resulting in increased triglyceride storage. Consequently, during long-term exercise, when insulin levels fall, the uptake of triglycerides by adipose would be decreased. Increased LPL activity has been reported in the muscle of rats, dogs, and humans following exercise. 13• 86• 106 In addition, LPL activity in muscle fibers appears to be correlated with oxidative capacity. 83• 90 Mackie et al90 reported that triglyc eride uptake was greatest in contracting slow-twitch red fibers and lowest in contracting fast-twitch white fibers. These authors point out that although the contribution of circulating triglycerides to total energy production might be minor, the contribution to certain types of fibers might be important. In particular, it was suggested that the increased uptake of exogenous triglycerides might help to maintain or replete endogenous stores.

CHANGES IN SUBSTRATE UTILIZATION WITH TRAINING For most types of activities, competitive individuals undergo rigorous physical training that produces several marked adjustments in the response to exercise. In addition to an increased time to fatigue, there is a reduced rate of glycogen use and lactate formation. This appears to occur as a result of increased fat oxidation because the R-values for the whole body and across trained muscle are reduced during a standard work bout. 63 Training has been reported to increase the capacity to oxidize pyruvate and fatty acids. 62 Lennon et al81 reported that the accumulation of long chain acylcarnitine derivatives was less in well trained athletes compared to moderately trained athletes. Postexercise ketone levels are also lower in trained individuals, 74 and the level of ketone oxidizing enzymes have been reported to increase with training. 4 Increased activities of citric acid cycle enzymes such as citrate synthase and succinate dehydrogenase have been reported to occur with training in several species. 62• 8.5 Enhanced activity of the respiratory chain components has also been reported. 62• 108 A number of enzymes involved in fatty acid oxidation or transport are increased by training. 7• 85 These adaptations explain how the muscle can use more fat at a given exercise level, and also how glycogen can be more efficiently metabolized with a resulting reduction in lactate production. The source of the fat used by trained muscle has not been clearly determined. Since FFA availability has been proposed as a limiting factor in fat use during submaximal exercise, it has been suggested that training might effect FFA availability. Bukowiecki et al1 4 reported that training increased the lipolytic response of adipocytes to epinephrine. This effect could be interpreted to indicate that during exercise that elevates cate cholamine levels, training will enhance the lipolytic response of adipose and increase FFA release. However, training also appears to reduce the catecholamine response to exercise. 63 Oscai et al1°7 studied the effect of

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training on rats and concluded that the capacity for intracellular triglyceride hydrolysis in adipose tissue is not enhanced by training. Plasma FFA concentrations actually tend to be lower in trained individuals, 66 although this could be a consequence of increased uptake by muscle rather than altered release from adipose. Since glycerol levels are also lower in trained individuals, plasma FFA probably do not account for the increased fat used by trained muscle during exercise. 66 Muscle triglyceride use in humans before and after a 12-week training program was essentially doubled in one study. 66 Training has been reported to result in increased activity of LPL. 6• 106 It is possible that the contribution of plasma triglyceride may also be increased by training. 101 The adaptations discussed thus far pertain only to responses to repeated bouts of submaximal endurance-type exercise. The magnitude and the time course of these changes relate to the type of exercise undertaken. 24 Sprint training induces changes of a different nature than endurance training. Roberts et al 115 reported that in response to a 16-week program of sprint training significant increases occurred in the activities of phosphofructoki nase, phosphorylase, glyceraldehyde phosphate dehydrogenase, lactate dehydrogenase, and malate dehydrogenase. In addition, Wilmore and Costill 140 suggest that increases in creatine phosphokinase and myokinase, as well as increases in strength, are important adaptations to sprint training. Except for the very short distance sprinting performed by Quarter Horses, most training programs for race horses will include some submaximal exercise training to improve oxidative capacity. Since lactate generation and muscle acidosis are factors in racing fatigue, adaptations that decrease lactate generation may enhance performance. Additionally, adaptations that allow rapid lactic acid production without a concomitant drop in muscle pH will permit the horse to perform at a high intensity for a longer duration. Muscle buffering capacity tends to be higher in athletes adapted to strength or sprint work compared with endurance work. 1 12 Increases in muscle buffering capacity have also been reported to occur in horses with race type training. 35• 95 EXERCISE AND NUTRITION Clearly, one of the most profound effects of exercise on nutrition is the increased demand for energy. This is particularly evident in human athletes in intensive training. Grandjean47 reports that average energy consumption by athletes in different sports may be 50% to 75% above the energy consumption of sex-matched nonathletes. Even higher intakes are suggested by other reports. 27• 78 In the horse, Pagan and Hintz1 10 estimated the energy consumed by submaximal exercise using indirect respiration calorimetry and derived an equation based on speed of exercise, weight of the horse, rider, and tack, and the duration of exercise. This method accurately predicts the amount of additional energy that will be used in a work bout but does not necessarily account for residual effects of the work bout in recovery. In 1935, Edwards et al27 reported that only a portion of the apparent increased energy


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requirement of football players could be accounted for by the actual work performed. These authors presented data that suggested that the effects of individual work bouts are long lasting and may elevate basal metabolic rate for a time period beyond the cessation of exercise. As a result, basing energy requirements only on the amount of work performed may under estimate the true requirement. Anderson et al 1 estimated energy require ments of exercising horses by determining the amount of digestible energy required to maintain body weight. With this method any residual effects of exercise are accounted for. However, there is no consideration as to whether the initial body weight and composition are ideal. An important component that can be considered in the nutrition of the performance athlete is the attainment of a desirable body composition. Profiles of elite human athletes in different sports have revealed differences in percent of body fat and lean body mass compared with nonathletic controls. Endurance runners tend to have lower percentages of body fat and greater aerobic power per kilogram of body weight than weight lifters.m Attaining a lower body fat percentage is advantageous because there is a negative relationship between percent of body fat and performance of any sport in which the body must be moved horizon.tally or vertically. 139 In nonathletic humans, body fat averages 15% for men and 25% for women. In sports that may be affected by excess fat, the body fat range is 4% to 10% for men and 13% to 18% for women.87 Although reducing body fat may be useful, there still appears to be an absolute need for some body fat, with minimums of 3% to 7% suggested for men and 10% to 20% for women. Body fat is not the only body component of interest. Of equal or more important consideration for many events is lean body mass. Both percent of body fat and lean body mass tend to be affected more rapidly by under or overnutrition than by exercise. During caloric restriction there is a loss in both body fat and lean body mass. In obese animals on low calorie diets, up to one-fourth of the weight loss may be lean body mass, and the degree of loss of each tissue depends upon the initial condition of the animal and the degree of restriction.33 When weight loss is accomplished by increasing energy expenditure through exercise and with diet control, rather than just diet alone, the decline in lean body mass may be abated. Little is known about optimal body composition in horses performing different tasks. One of the ramifications of drastically increased energy requirements is the need for a relatively high daily feed intake. In fact, maintaining food intake in athletes is a practical problem. Frape36 discusses the conflict between increasing energy requirement and intake limitation in horses. Typically, this is handled by increasing the energy density of the diet, usually through increased reliance on concentrate. The NRC104 suggests that horses in light work might consume a diet containing 80% roughage and 20% concentrate, whereas horses in heavy work might consume 33% roughage and 67% concentrate. Since horses are susceptible to laminitis as a result of grain overload, exceedingly high concentrate intakes are usually avoided. Energy intake can be elevated by using highly digestible roughage sources, maximizing total intake with the use of palatable feeds, or including fat in the diet as a means to increase energy density.25• 6 1• 109

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Considerable interest has been directed toward determining the most desirable source of dietary calories for human athletes. Grandjean47 suggests a diet in which total calories are derived 30% to 35% from fat, 50% to 60% from carbohydrate, and 10% to 15% from protein, with the qualification that athletes involved in extensive endurance training should increase the contribution of carbohydrate to 60% to 70% of total calories. Leaf and Frisa78 recommend a caloric intake composed of 55% to 65% carbohydrate, 12% to 15% protein, and 20% to 30% fat. These recommendations appear to be derived from studies on the effect of diet on substrate utilization, with adjustments made for practical considerations such as total intake and palatability.

HIGH CARBOHYDRATE DIETS Since the availability of carbohydrate during submaximal exercise can limit performance, diets that influence carbohydrate availability can alter exercise performance as well. There is a vast body of scientific literature supporting the use of high carbohydrate diets by humans for endurance exercise. The literature has been reviewed recently.1 7• 65 In the initial studies, the effect of glycogen depletion/repletion programs on glycogen use and endurance in long-term exercise were investigated. From these studies it was apparent that endurance performance was reduced when exercise was undertaken in a glycogen-depleted state and that nutritional manipulation could elevate glycogen levels and positively affect perform ance. Nutritional manipulation included a period of intense training accom panied by the consumption of a low carbohydrate diet, followed by a period of reduced activity and consumption of a very high carbohydrate diet. Since this traditional approach to glycogen loading apparently has some negative side effects and is not always well tolerated by athletes, the more current practice is to consume a normal diet until a few days before competition and then to combine a program of decreased activity with increased carbohydrate consumption, the goal being 500 to 600 g of carbohydrate or 60% to 70% of the total calories.47 • 138 The effect of glycogen loading on horses competing in endurance activities has not been investigated. While the benefits of high carbohydrate diets and elevated glycogen levels for human endurance athletes are reasonably well documented, there is some question as to the benefit of this practice for intense short-term work. Maughan and Poole94 reported that a high carbohydrate diet pro longed fatigue time during high intensity exercise over a normal or low carbohydrate diet. However, in subsequent experiments, exhaustion time at 100% V02 max was not different between normal and high carbohydrate diets.49 • 51 • 52 Similarly, Topliff et al 130· 132 accomplished glycogen loading in horses, but were unable to demonstrate any benefit in work performance over the normal diet at relatively intense workloads. Although the con sumption of higher than normal carbohydrate diets prior to intense work does not appear to be preferred to normal diets, it is clear that low carbohydrate diets are not of benefit. The combination of low carbohydrate diets and regular exercise causes a reduction in glycogen stores and decreased performance in horses.130• 132 Although muscle glycogen stores


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were not measured in the studies of Greenhaff et al, 4 9• 5 2 work performance was reduced on a low carbohydrate diet compared with the normal or high carbohydrate diets. A common finding of studies comparing carbohydrate use given high and low carbohydrate diets is a lower postexercise lactate level in response to the low carbohydrate diet.48• 50 · 5 1• 52 This finding would be consistent with decreased availability and use of glycogen, which could explain the reduced performance on the low carbohydrate diet. By com parison, differences between lactate levels on high carbohydrate diets compared with normal diets are only occasionally reported, 50 which would support the lack of benefit of high carbohydrate diets over normal diets for this type of exercise.

CARBOHYDRATE SUPPLEMENTATION BEFORE OR DURING EXERCISE Since carbohydrate utilization is an important concern during both long-term and short-term exercise, a number of studies with human athletes have investigated the usefulness of carbohydrate supplementation prior to or during exercise. When glucose is ingested prior to exercise (30 to 90 min), there is an increase in insulin that results in enhanced glucose uptake and glycogen synthesis, enhanced lipogenesis, and decreased lipolysis. During exercise there will be increased use of blood glucose and decreased use of fat as a result of low FFA availability. The net result during submaximal exercise is a reduction in work performance.19• 93 It has been suggested that fructose could be superior to glucose because it causes a smaller insulin response, which would permit greater fat use.92 An area of horse nutrition that requires investigation is the timing of pre-event feeding. Arana et aP demonstrated that when horses were exercised 2 hours after a meal or during a fast, blood glucose levels in the fed horses decreased, but remained constant in the fasted horses. Ralston114 reported that of the 54 horses surveyed in a 160-km endurance ride, 18 had no change in their feeding program prior to the start, 32 received reduced amounts of hay or grain, three were fasted, and two received extra grain. Schils and Jordan120 interviewed 22 race horse trainers and found that 96% reduced hay intake on race day and 50% reduced grain intake. A practical advantage of reduced intake on race day may be the decrease in weight that will occur. Considering that horses are "handicapped" by a few pounds of lead, one wonders what the effect of adding or subtracting 10 lb of digesta are. While a carbohydrate supplement taken an hour or so before exercise does not appear to convey any benefit to endurance performance, a supplement taken during an exercise bout may be useful.18 Since fatigue during endurance exercise appears to be related to the decline in plasma glucose that results from the inability of hepatic glucose release to keep pace with muscle uptake, the use of an oral glucose supplement to maintain plasma glucose levels in late exercise could delay fatigue. Coggan and Coyle16 administered a placebo or a drink containing glucose polymers to cyclists after 135 min of exercise and significantly prolonged the time to exhaustion with the glucose treatment. Whether or not this practice has

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any application to endurance horses or horses involved in other types of work in which glycogen stores might be depleted is unknown. Ralston114 observed that 52 of 54 horses in two 160-km endurance rides were allowed free-choice roughage at rest stops, whereas 36 were given some grain.

FAT SUPPLEMENTATION As mentioned previously, fat can be added to horse diets to increase energy density. However, it has been suggested that since fat is an efficient fuel source for exercising muscle, there might be additional benefits to supplementing horse diets with fat. However, much controversy exists on this subject, and definitive studies have not been conducted. The effects of adding fat to normal rations on metabolic changes have been studied in horses performing a variety of activities. A number of studies involving feeding "high fat" diets to horses are summarized in Table 1. When evaluating these studies, comparisons are made difficult by differences in the condition of the horses, the length of the adaptation periods to the diets, the type of fat used as the supplement, and the level of fat supplemented. For example, in the last case, some experiments describe the level of fat as a percentage of the total calories, 25 others describe the level of fat as a percentage of the total feed, 56• 6 1 and others as a percentage of the concentrate portion of the feed. 96• 105• 109• 1 36 Only one study53 clearly lists the analyzed percentage of fat (as ether extract). To assist in making comparisons, the levels of fat used in the various studies cited in Table 1 have been expressed as a percentage of the total diet. Since some studies were less specific about exact amounts of feed provided, there is some inaccuracy involved. Across the studies, the level of supplemented fat ranged from about 1. 5% to 14%. Most diets were 6% to 12% fat (percentage of total diet), which corresponds to approximately 20% to 40% of the total calories as fat. Although these diets are frequently referred to as "high fat, " they are actually much closer to the "normal" (and in some cases, the "high carbohydrate") diets used in experiments with other species (rats and Table 1. Effect of Feeding High Fat Diets on Carbohydrate Utilization During Different Types of Exercise* EXERCISE TYPE (REFERENCE)

Endurance (56) Endurance (61) Endurance (109) Moderate (53) Moderate (96) Moderate (109) Moderate (136) Intense (25) Intense ( 105) Intense (109) Intense (136)

PERCENT OF DIETARY FAT

GLYCOGEN UTILIZATION

4, 8, 12, 16 8 12 10. 5 3.5, 7 12 6 1. 5, 3, 6 6 12 6

nd nd nd dee nd inc dee

BLOOD LACTATE

nd nd nd nd nd nd nd nd dee nd

BLOOD GLUCOSE

inc inc nd nd dee inc inc nd nd nd

*Comparison between fat-supplemented diet and control diet; nd = no difference, inc = higher on fat diet, dee = lower on fat diet, - = not measured.


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humans). This point is important to keep in mind when studies with horses are compared with studies with rats or humans. It has been proposed that feeding an increased level of fat will cause metabolic adaptations that permit horses to preferentially utilize fat and spare glycogen during exercise.96· 105 Thus, feeding fat might have an effect similar to training. In fact, a number of studies in other species have examined whether feeding high fat diets can induce changes in the metabolic machinery involved in fat utilization. A high fat diet induced changes in ketone metabolizing enzymes, but not in the capacity of the electron transport chain or in fatty acid oxidation.4 Miller et al00 compared citrate synthase activity and 3-hydroxyacyl CoA dehydrogenase (3-HAD) activity in rats adapted to a high fat diet and found that 3-HAD activity was enhanced after 1 week and 5 weeks. Citrate synthase activity was higher in the red vastus lateralis muscle after 1 week on the high fat diet but not after 5 weeks. An interesting finding in this study was an enhanced endurance ability of the rats on the high fat diet. The rats in this study received no forced exercise during the experiment, which makes compari sons to trained animals somewhat difficult. Feeding high fat diets to rats also increases LPL activity in some muscles, and decreases adipose LPL activity.10• 11 Duren et al25 reported that the horses receiving the highest level of fat had the lowest level of circulating triglycerides, suggesting that increased LPL might be responsible. In each of the studies with rats, the fat diet contained enough fat to provide about 70% of the total calories, whereas the control or low fat diets usually contained enough fat to provide less than 15% of the calories. Whether the levels of fat used in horse diets could be expected to elicit similar changes is unknown. In studies with horses, changes in glycogen, glucose, and lactate during exercise have been the focus because of the concept that feeding fat can increase lipid oxidation and spare glycogen stores. Unfortunately, there is little consistency in the results of the various studies (see Table 1). If feeding fat increases the proportion of energy derived from fat, the respiratory exchange ratio should decrease. R-values have been measured in only two studies. In one study the R-value decreased, 109 in the other, there was no change as a result of a high fat diet.96 Similarly, if high fat feeding spares glycogen, a reduction in muscle glycogen utilization would be expected during an exercise test. In three studies with endurance-type work bouts, glycogen utilization was unaffected by diet.56· 6 1 • 109 In one study with moderate exercise, glycogen utilization was unchanged.109 In another, it was decreased53 with a high fat diet. In one high speed test, glycogen utilization was higher on the high fat diet 105 ; in another test it was lower.109 During intense exercise, lactate accumulation can be an indicator of carbohydrate utilization, with lower levels reflecting an increased depend ance on fat. In the studies that used exercise bouts that were described as being intense enough to elicit marked lactate production, four reported no significant effect of diet25• 96 • 105• 1 36 and one reported lower lactate levels. 109 During long-term exercise, diminishing muscle and liver glycogen stores result in a decline in blood glucose. Four studies have reported a positive effect of supplemental fat on blood glucose levels during exercise.25• 56• 6 1 • 1 36 To date the information supporting a positive effect of supplemental fat on

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fuel metabolism is inconclusive. Factors that could contribute to contradic tory results include differences in time of feeding prior to the exercise testing, the degree of training during the adaptation period, the length of the adaptation period, and the type of fat used in the diet. An interesting suggestion has been made that dietary unsaturated fats are more likely to be oxidized and saturated fats are more easily stored. 2 PROTEIN SUPPLEMENTS Protein is not a major fuel during most types of exercise, and providing calories as protein is not particularly efficient, energetically or financially. However, there does appear to be some oxidation of amino acids, primarily leucine, during exercise. Protein oxidation may become increasingly im portant as muscle glycogen stores are depleted. 80 Consequently, protein repletion may be necessary after long-term severe exercise. In addition, changes in lean body mass would suggest that some additional protein might be required above maintenance levels. In horses, apparent nitrogen retention was increased by work, although nitrogen loss in the sweat was not accounted for. 38 Adequate levels of protein intake for human athletes have been estimated at 1 to 1. 5 g/kg, although some activities such as strength training might require an intake as high as 2 g/kg. 78 This level would translate to a requirement of no more than 1000 g per 500-kg horse. The NRC104 recommendation for a 500-kg horse in intense work is 1312 g, which was calculated by keeping the same protein/digestible energy ratio as for maintenance and estimating the energy requirement for work. One important comparison between human and equine protein re quirements would be in the area of protein quality. While the NRC recommendation appears somewhat high compared with a level predicted by human research, it reflects the use of lower quality and less digestible protein sources. Excessive levels of protein intake are often fed to perform ance horses. 41 Studies demonstrating that protein supplementation improves equine exercise performance are not available. In addition, studies evalu ating the effect of high protein diets on exercising horses have failed to suggest a mechanism through which this might occur. In a submaximal exercise test, RQ, glycogen utilization, and lactate accumulation were lower in horses fed a high protein (18%) diet compared with a normal protein high carbohydrate diet (12% CP). 109 Miller and Lawrence98 found that diet and exercise interacted to result in lower lactate levels during submaximal exercise. In addition, alanine and glutamine levels were lower on the high protein diets. These studies support the concept that protein is not an efficient energy source and may suggest a detrimental effect on glycogen availability. Some interest has arisen in the area of specific amino acid supplementation, especially leucine. If the branched chain amino acids are the primary amino acids being oxidized, then their requirement might be elevated. VITAMIN SUPPLEMENTS Although vitamin supplementation may be the most commercially promoted area of nutritional supplementation for horses, it is also the least


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studied. Very few investigations have examined the effects of vitamin supplementation on exercising horses. The NRC104 suggests that horses grazing high quality pastures probably receive adequate levels of most vitamins. Most performance horses receive rations of hay and grain, which may contain lower levels of certain vitamins. Vitamin losses in hay during storage or as a result of rain or sun damage may be significant. 104 Although frank deficiencies are rarely reported, it is possible that some horses receive marginal vitamin intakes. However, it is even more possible given the high incidence of vitamin supplementation within the horse industry that many horses receive excessive levels of vitamins, 1 0 , 1 4 The effectiveness of vitamin supplementation above required levels has not been supported by studies in human athletes. 1 • 75 In exercising individuals, the B vitamins are of particular importance because of their roles in energy metabolism. An increase in the requirement for these vitamins as a result of increased physical activity would not be unexpected. In addition, a deficiency might be expected to alter perform ance. When human athletes were restricted to less than 50% of their requirement for vitamins B 1 , B , B6 , and C for 4 weeks, a significant decrease in performance occurred. 133 In another experiment, the restriction of only vitamin C did not affect performance. 134 In the horse, dietary B vitamin levels are augmented by bacterially synthesized B vitamins in the hindgut. In ruminants, synthesis of some B vitamins, most notably thiamin, is reduced when low fiber, high concentrate diets are fed. In order to meet the energy requirements of hard working horses, concentrate is usually increased and roughage decreased, which could lead to decreased synthesis. Topliff et al 131 investigated the effect of adding thiamin to a normal diet to produce levels of 2, 4, and 28 mg/kg of feed. After exercise, blood lactate levels were lowest on the highest thiamin level. Other parameters were improved by the 4 mg/kg level with no further benefit at the highest level. The current NRC104 recommendation is for 5 mg/kg feed. There is very little information on the requirement for other B vitamins, and the NRC 104 does not even include recommendations for niacin, pantothenic acid, pyridoxine, folacin, or B12 • Similarly, there is no recommendation for vitamin C. Snow and Frigg123 reported low plasma ascorbic acid levels in Thoroughbred horses training in Great Britain, which has been interpreted to suggest that vitamin C supplementation might be useful. 1 4 2

2

2

2

2

ERGOGENIC AIDS In addition to nutritional supplements, a number of ergogenic aids have been promoted in the horse industry. These include, but are not confined to, sodium bicarbonate, dimethyl glycine (DMG), and carnitine. Numerous studies in humans have demonstrated a positive effect of sodium bicarbonate ingestion on performance and acid-base balance during exercise. 0, 69 • 91 • 1 7· 137 A number of studies have also found that performance may be unaffected by rndium bicarbonate. 64 • 7 1 • 73 Sodium bicarbonate administration is beneficial only in specific situations. It has been proposed that sodium bicarbonate enhances performance by increasing blood pH and 2

2

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enhancing the movement of lactate and H + out of the muscle, thus delaying the onset of exercise-induced intramuscular acidosis. 69 Sodium bicarbonate is most effective when the exercise bout lasts at least 2 min and is of sufficient intensity to produce a significant acidosis. Sodium bicarbonate is ineffective during very short maximal work bouts and during long-term exercise. The limited studies on horses suggest that sodium bicarbonate may influence lactate and H + ion movement from muscle into blood and may improve performance of Standardbreds racing a mile, but not Thor oughbreds. 72 · 76• 77 It is possible that a I-mile race for Thoroughbreds is too brief to be affected by sodium bicarbonate. No evidence suggests that sodium bicarbonate can be useful during endurance exercise. In fact, this practice should be avoided, as the alkalosis resulting from the sodium bicarbonate would only exacerbate the respiratory alkalosis and electrolyte imbalances that can occur in endurance horses. Another compound that has been promoted as a means to control the fatigue produced by intramuscular acidosis is DMG. In a study in which DMG was added to the diets of racing Standardbreds, lactate levels after training exercising were lower than in controls not given supplements. 82 However, even the lactate levels in the controls were fairly low and were not representative of lactate levels after racing. Similarly, although Moffit et al 100 reported a small reduction in lactate levels following D MG supple mentation, lactate concentrations were relatively low. Thus, the effects of DMG during intense exercise have not been adequately examined, and there are no results of performance testing studies. Adaptations that enhance fat utilization and spare glycogen can improve endurance time. Newsholm 102 has hypothesized that it is the rate of uptake that limits fat oxidation. The role of carnitine in fatty acid transport raises the question of whether carnitine supplementation might enhance utiliza tion and improve performance. Decombaz et al21 did not find any effect of carnitine supplementation on fuel utilization in exercised rats. The effect of carnitine supplementation on horses has not been studied. Snow and Harris124 indicate that the use of DL-carnitine should be avoided because the unnatural D isomer might be harmful to mitochondrial function. S UMMARY Substrate depletion and end product accumulation are two important factors in exercise fatigue. Fatigue during long-term exercise results from a depletion of muscle and liver glycogen and coincides with an inability to maintain blood glucose levels. During high intensity exercise, the rapid catabolism of carbohydrate and the resultant production of lactate and hydrogen ions cause a reduction in muscle pH that inhibits maximum force generation. Dietary manipulations that can influence carbohydrate status or lactate accumulation may be beneficial to performance. In human athletes, carbohydrate loading and carbohydrate supplementation can en hance endurance time during long-term exercise. These practices have not been explored extensively in the equine athlete, although glycogen loading does not enhance the performance of horses during short-term intense


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work. Short-term work can be detrimentally affected if glycogen levels are inadequate. The most marked effect of exercise on nutrient requirements is in the energy requirement. Horses in heavy training may require more energy than they can consume on a conventional diet. Fat has been added to horse diets to increase energy density, usually at levels between 6% and 12% of the total diet. Although protein requirements may be slightly increased in the working horse, supplementing protein as a means of adding calories is not an efficient practice. In addition, although studies with horses are not available, human studies indicate that there are no benefits to vitamin supplementation above required levels . At this point, more is unknown than is known about feeding perform ance horses . Most information on fuel utilization is extrapolated from studies with rats and humans . Areas that have received little attention but are critical to optimizing feeding practices are the timing of pre-event feeding and the determination of ideal body composition in equine athletes of different types.

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16. Coggan AR, Coyle EF: Metabolism and performance following carbohydrate ingestion in exercise. Med Sci Sport Exerc 21:59, 1989 17. Conlee RK: Muscle glycogen and exercise endurance: A 20-year perspective. In Pandolf KB (ed): Exercise and Sport Science Reviews, vol 15. New York, Macmillan, 1987, p 1 18. Costill DL: Carbohydrate nutrition before, during, and after exercise. Fed Proc 44:364, 1985 19. Costill DL, Coyle E, Dalsky D, et al: Effects of elevated plasma FFA and insulin on muscle glycogen usage during exercise. J Appl Physiol 43:695, 1977 20. Costill DL, Verstappen DF, Kuipers H, et al: Acid-base balance during repeated bouts of exercise: Influence of HCO3 • Int J Sports Med 5:228, 1984 21. Decombaz J, Sartori D, Fournier N: DL-Carnitine supplementation during exercise training in the rat. Proc Nutr Soc 44:29A, 1985 22. Dohm CL, Kasperek G, Tapscott EB, et al: Protein metabolism during endurance exercise. Fed Proc 44:348, 1985 23. Donaldson SK, Hermansen L: Differential, direct effects of H + on Ca2 + activated force of skinned fibers from the soleus, cardiac and adductor magnus muscles of rabbits. Pflugers Arch 376:55, 1978 24. Dudley GA, Abraham WM, Terjung RL: Influence of exercise intensity and duration on biochemical adaptations in skeletal muscle. J Appl Physiol 53:844, 1982 25. Duren SE, Jackson SC, Baker JP, et al: Effect of dietary fat on blood parameters in exercised Thoroughbred horses. In Gillespie J, Robinson NE (eds): Equine Exercise Physiology, vol 2. Davis, CA, ICEEP Publications, 1987, p 674 26. Edwards HT, Margaria R, Dill DB: Metabolic rate, blood sugar and the utilization of carbohydrate. Am J Physiol 108:203, 1934 27. Edwards HT, Thorndike A, Dill DB: The energy requirement in strenuous muscular exercise. N Engl J Med 213:532, 1935 28. Essen B, Hagenfeldt L, Kaijser J: Utilization of blood-borne and intramuscular substrates during continuous and intermittent exercise in man. J Physiol (Lond) 265:489, 1977 29. Essen-Gustavsson B, Valberg S: Blood ammonia concentrations in horses during treadmill work and after racing. In Gillespie J, Robinson N (eds): Equine Exercise Physiology, vol 2. Davis, CA, ICEEP Publications, 1987, p 456 30. Fabiato A, Fabiato F: Effects of pH on the myofilaments and the sarcoplasmic reticulum of skinned cells from cardiac and skeletal muscles. J Physiol (Lond) 267:233, 1978 31. Felig P, Wahren J: Fuel homeostasis in exercise. N Engl J Med 293:1078, 1975 32. Felig P, Wahren J: Interrelationship between amino acid and carbohydrate metabolism during exercise: The glucose alanine cycle. In Pernow B, Saltin B (eds): Muscle Metabolism During Exercise. New York, Plenum Press, 1977, p 205 33. Forbes GB: Body composition as affected by physical activity and nutrition. Fed Proc 44:343, 1985 34. Foster CV, Harris RC: Changes in free and bound carnitine in muscle with maximal sprint exercise in the Thoroughbred horse. In Gillespie J, Robinson N (eds): Equine Exercise Physiology, vol 2. Davis, CA, ICEEP Publications, 1987, p 341 35. Fox G, Henckel P, Jeul C, et al: Skeletal muscle buffer capacity changes in Standardbred horses: Effects of growth and training. In Gillespie J, Robinson N (eds): Equine Exercise Physiology, vol 2. Davis, CA, ICEEP Publications, 1987, p 341 36. Frape DL: Dietary requirements and athletic performance of horses. Equine Vet J 20:163, 1988 37. Frape DL: Nutrition and the growth and racing performance of Thoroughbred horses. Proc Nutr Soc 48:141, 1989 38. Freeman DW, Potter GD, Schelling GT, et al: Nitrogen metabolism in mature horses at varying levels of work. J Anim Sci 66:407, 1988 39. Froberg SO, Mossfeldt F: Effect of prolonged strenuous exercise on the concentration of triglycerides, phospholipid and glycogen in muscle of man. Acta Physiol Scand 82:167, 1971 40. Froberg SO, Ostman I, Sjostrand NO: Effect of training on esterified fatty acids and carnitine in muscle and on lipolysis in adipose tissue in vitro. Acta Physiol Scand 86:166, 1972 41. Glade MJ: Nutrition and performance of racing Thoroughbreds. Equine Vet J 15:31, 1983


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42. Goldberg AL, Etlinger JD, Goldspink J, et al: Mechanism of work induced hypertrophy of skeletal muscle. Med Sci Sport 7:248, 1975 43. Gollnick PD: Metabolism of substrates: Energy substrate metabolism during exercise and modified by training. Fed Proc 44:353, 1985 44. Gollnick PD, Saltin B: Fuel for muscular exercise: Role of fat. In Horton ES, Terjung RL (eds): Exercise, Nutrition and Energy Metabolism. New York, Macmillan, 1988, p 72 45. Goodman MN: Amino acid and protein metabolism. In Horton ES, Terjung RL (eds): Exercise, Nutrition and Energy Metabolism. New York, Macmillan, 1988, p 89 46. Goodman MN, Ruderman NB: Influence of muscle use on amino acid metabolism. In Terjung RL (ed): Exercise and Sport Science Reviews. Philadelphia, Franklin Institute Press, 1982, p 1 47. Grandjean AC: Micronutrient intake of US athletes compared with the general population and recommendations made for athletes. Am J Clin Nutr 49:1070, 1989 48. Greenhafl" PL, Gleeson M, Maughan RJ: The effects of dietary manipulation on blood acid-base status and the performance of high intensity exercise. Eur J Appl Physiol 56:331, 1987 49. Greenhafl" PL, Gleeson M, Whiting MH, et al: Dietary composition and acid-base status: Limiting factors in the performance of maximal exercise in man. Eur J Appl Physiol 56:444, 1987 50. Greenhafl" PL, Gleeson M, Maughan RJ: The effects of a glycogen loading regimen on acid-base status and blood lactate concentration before and after a fixed period of high intensity exercise in man. Eur J Appl Physiol 57:254, 1988 5 1. Greenhafl" PL, Gleeson M, Maughan RJ: The effects of diet on muscle pH and metabolism during high intensity exercise. Eur J Appl Physiol 57:532, 1988 52. Greenhafl" PL, Gleeson M, Maughan RJ: Diet-induced metabolism and the performance of high intensity exercise in man. Eur J Appl Physiol 57:583, 1988 53. Griewe KM, Meacham TN, Fregin CF, et al: Effect of added dietary fat on exercising horses. Proc Equine Nutr Physiol Symp, Stillwater, Oklahoma, 1989, p 101 54. Hagenfeldt L, Wahren J: Metabolism of free fatty acids and ketone bodies in skeletal muscle. In Saltin B, Pernow B (eds): Muscle Metabolism During Exercise. New York, Plenum Press, 1971, p 101 55. Hagg SA, Morse EL, Adibi S: Effect of exercise on rates of oxidation and plasma clearance of leucine in human subjects. Am J Physiol 50:E407, 1982 56. Hambleton PL, Slade LM, Hamar DW, et al: Dietary fat and exercise conditioning effect on metabolic parameters in the horse. J Anim Sci 51: 1330, 1980 57. Harris RC, Foster CV, Hultman E: Acetylcarnitine formation during intense muscular contraction in humans. J Appl Physiol 63:440, 1987 58. Harris RC, Katz A, Sahlin K, et al: Measurement of muscle pH in horse muscle and its relation to lactate content (abstr). J Physiol (Lond) 357: 119, 1984 59. Harris RC, Marlin DJ, Snow DH: Metabolic response to maximal exercise of 800 and 2000 m in the Thoroughbred horse. J Appl Physiol 63: 12, 1987 60. Havel RJ, Carlson LA, Ekelund L, et al: Turnover rate and oxidation of different free fatty acids in man during exercise. J Appl Physiol 19:613, 1964 61. Hintz HF, Ross M, Lesser F, et al: Dietary' fat for working horses. Cornell Nutrition Conference, Ithaca, NY, 1977, p 87 62. Holloszy JO: Biochemical adaptations in muscle: Effects of exercise on mitochondrial oxygen uptake and respiratory enzyme activity in skeletal muscle. J Biol Chem 242:2278, 1967 63. Holloszy JO: Metabolic Consequences of endurance exercise training. In Horton ES, Terjung RL (eds): Exercise, Nutrition and Energy Metabolism. New York, Macmillan, 1983, p 116 64. Hooker S, Morgan C, Wells C: Effect of sodium bicarbonate ingestion on time to exhaustion and blood lactate of 10 k runners (abstr). Med Sci Sports Exerc 19(suppl 2):s67, 1987 65. Hultman E: Nutritional effects on work performance. Am J Clin Nutr 49:949, 1989 66. Hurley BF, Nemeth PW, Martin WH, et al: Muscle triglyceride utilization during exercise: Effect of training. J Appl Physiol 60:562, 1986 67. Issekutz B, Paul P: Intramuscular energy sources in exercising normal and pancreatized dogs. Am J Physiol 215: 197, 1968

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[Diagnosis and therapy of tendinitis exemplified by the athletic horse].

Brown fat fuel utilization and thermogenesis.

Findings from the preparticipation athletic examination and athletic injuries.

Recent advances in canola meal utilization in swine nutrition.

Exercise endurance and fuel utilization: a reevaluation of the effects of fasting.

Effects of glucose on fuel utilization and glycerol turnover in normal and injured man.

Utilization of nutrition-focused physical assessment in identifying micronutrient deficiencies.

Utilization of a nutrition service in a neighborhood health center.

Effects of growth hormone on fuel utilization and muscle glycogen synthase activity in normal humans.

Abbreviated half-lives and impaired fuel utilization in carnitine palmitoyltransferase II variant fibroblasts.

AKT Pathway and Fuel Utilization During Primate Torpor in the Gray Mouse Lemur, Microcebus murinus.

Influence of high altitude on cerebral blood flow and fuel utilization during exercise and recovery.

The contribution of arterial blood gases in cerebral blood flow regulation and fuel utilization in man at high altitude.

Deconditioning the athletic heart.

The experiences of female athletic trainers in the role of the head athletic trainer.

Athletic Directors' Barriers to Hiring Athletic Trainers in High Schools.

Snakebite in the horse.

Pyæmia in the Horse.

The influence of different durations of aerobic exercise on fuel utilization, lactate level and antioxidant defense system in trained rats.

Motherhood and work-life balance in the national collegiate athletic association division I setting: mentors and the female athletic trainer.

Supervising athletic trainers' perceptions of professional socialization of graduate assistant athletic trainers in the collegiate setting.

Atrial fibrillation and the athletic heart.

Utilization of hydrolysate from lignocellulosic biomass pretreatment to generate electricity by enzymatic fuel cell system.

Chemical restraint and analgesia in the horse.