Muscle Glycogen Sparing Research Articles

Carbohydrate Supplementation during Exercise

Muscle glycogen and plasma glucose are oxidized by skeletal muscle to supply the carbohydrate energy needed to exercise strenuously for several hours (i.e., 70% maximal O2 consumption). With increasing exercise duration there is a progressive shift from muscle glycogen to blood glucose. Blood glucose concentration declines to hypoglycemic levels (i.e., 2.5 mmol/L) in well-trained cyclists after ∼3 h of exercise and this appears to cause muscle fatigue by reducing the contribution of blood glucose to oxidative metabolism. Carbohydrate feeding throughout exercise delays fatigue by 30–60 min, apparently by maintaining blood glucose concentration and the rate of carbohydrate oxidation necessary to exercise strenuously. Carbohydrate feedings do not spare muscle glycogen utilization. Very little muscle glycogen is used for energy during the 3–4-h period of prolonged exercise when fed carbohydrate, suggesting that blood glucose is the predominant carbohydrate source. At this time, exogenous glucose disposal exceeds 1 g/min (i.e., 16 mg · kg-1 · min-1) as evidenced by the observation that intravenous glucose infusion at this rate is required to maintain blood glucose at 5 mmol/L. However, at this time these cyclist cannot exercise more intensely than 74% of maximal O2 consumption, suggesting a limit to the rate at which blood glucose can be used for energy. It is important to realize that carbohydrate supplementation during exercise delays fatigue by 30–60 min, but does not prevent fatigue. In conclusion, fatigue during prolonged strenuous exercise is often due to inadequate carbohydrate oxidation. This is partly a result of hypoglycemia, which limits carbohydrate oxidation and causes muscle fatigue. Carbohydrate feedings during strenuous exercise maintain blood glucose oxidation and delay fatigue by 30–60 min, but do not prevent fatigue, which eventually results from other yet unknown factors.

Substrate Metabolism under Cold Stress in Seasonally Acclimatized Dark-Eyed Juncos

Seasonally acclimatized dark-eyed juncos were exposed to one of three temperature regimes: 30° C (thermoneutrality), - 12° C (moderate cold), or 2° C in a 20.9% oxygen/79.1% helium gas mixture (severe cold), for 2 h or until they became hypothermic. Plasma glucose and free fatty acids (FFA), pectoralis muscle and liver glycogen, and pectoralis lactate were measured after exposure. Pectoralis muscle mass increased by 28% in winter. This increased muscle mass may assist in improving cold tolerance by increasing capacity for shivering thermogenesis in winter birds. Plasma glucose was signiicantly reduced and plasma FFA were significantly elevated under severe cold in winter No differences in plasma metabolites with temperature were detected in summer. Pectoralis muscle glycogen decreased with increasing severity of cold stress at both seasons, but winter levels were significantly greater than summer levels under severe cold. No temperature-induced differences in liver glycogen were apparent, but pooled winter values significantly exceeded summer values. Pectoralis lactate was significantly lower under severe cold at both seasons. In addition, mean lactate values for birds becoming hypothermic in both summer (n = 7) and winter (n = 1) were markedly lower than for normothermic birds at the same test temperatures. These data are consistent with a pattern of augmentedpreferential use of FFA to support shivering, coupled with sparing of muscle glycogen, in winter birds relative to summer birds. Furthermore, the decrement of pectoralis lactate with hypothermia may suggest a link between a reduced ability to mobilize muscle glycogen and the onset of hypothermia.

Enhancement of Athletic Performance with Drugs

Drug use among athletes has become a recognised problem in sports. Athletes may use drugs for therapeutic indications, for recreational or social reasons, as ergogenic aids or to mask the presence of other drugs during drug testing. Stimulants were some of the first drugs used and studied as ergogenic aids. Amphetamines may increase time to exhaustion by masking the physiological response to fatigue. Caffeine may improve utilisation of fatty acids as a fuel source thereby sparing muscle glycogen. Cocaine and other sympathomimetic drugs have little or no effect on athletic performance. Anabolic steroids appear to have the potential to increase lean muscle mass and strength under certain conditions. Human growth hormone may also be used for an anabolic effect, but data on this effect are lacking. Erythropoietin may represent a pharmacological alternative to blood doping by increasing red blood cell mass. The use of narcotic analgesics is not necessarily ergogenic but can be harmful if used to allow participation of an athlete with a severe injury. According to the American College of Sports Medicine alcohol does not possess an ergogenic effect. However, it may be used to reduce anxiety or tremor prior to competition. Marijuana does not increase strength. Tobacco products may produce psychomotor effects or control appetite which may be beneficial to some athletes. Other drugs used by athletes include beta-blocking agents, diuretics, and a variety of nutritional supplements. In addition, diuretics and probenecid may be taken to mask drug contents in the urine. Whether the ergogenic effects are real or perceived, the potential for adverse effects exists for all of these drugs. Potential health complications represent a serious risk to an otherwise healthy population. Further research on the long term health risks in athletes taking ergogenic drugs is needed.

Physiological responses to caffeine during endurance running in habitual caffeine users

Several studies have found that caffeine improved endurance exercise performance, but the factors which are responsible for this are not fully understood. Possibilities include an increased free fatty acid (FFA) oxidation and a resultant sparing of muscle glycogen as well as an enhancement of neuromuscular function during exercise. In order to further examine these factors, six varsity level runners (VO2max = 63.3 ml.kg-1.min-1) were studied over 90 min of treadmill running (70% VO2max) in a thermoneutral environment in order to determine the metabolic and neuromuscular effects of caffeine (6 mg.kg-1) administered in a randomized, crossover, double-blind manner. Subjects were habitual caffeine consumers (200 mg.d-1) and were given identical diets during each 3-d testing period. Caffeine administration, 60 min prior to exercise, significantly (P less than 0.05) increased plasma FFA levels both prior to and during exercise. Caffeine administration did not alter any of the other variables examined: VO2, HR, RER, rating of perceived exertion; plasma levels of glucose, lactate, epinephrine, and norepinephrine; or neuromuscular function (maximal voluntary strength, peak twitch torque, and motor unit activation). We conclude that caffeine administration (6 mg.kg-1) in athletic, habitual caffeine consumers increased plasma FFA levels but had neither metabolic nor neuromuscular effects that would be of potential ergogenic benefit in endurance running.

Effect of caffeine on glycogenolysis during exercise in endurance trained rats

Caffeine has been reported to enhance performance by increasing lipid oxidation and sparing liver and muscle glycogen in human subjects during prolonged endurance exercise. In the present study, the effects of intravenous caffeine on the liver and muscle glycogenolysis during exercise in endurance trained rats were investigated. Male endurance trained rats (2 h.d-1 for 6-7 wk) were given injections of 5 mg.kg-1 caffeine (5 CAF), 25 mg.kg-1 caffeine (25 CAF), or 0.9% sodium chloride (SAL) and were run on the treadmill for 45 min, 90 min, or until exhaustion at 26 m.min-1 up a 15% grade. Intravenous caffeine did not enhance the endurance run time: 5 CAF = 149 +/- 14 min, 25 CAF = 152 +/- 10 min, and SAL = 176 +/- 10 min. Caffeine did not influence the rate of liver glycogenolysis during exercise [liver glycogen (mmol glucose units.g-1) after 90 min: 5 CAF = 139 +/- 26, 25 CAF = 133 +/- 25, and SAL = 120 +/- 32]. Liver cAMP, muscle glycogen, plasma free fatty acids, blood glucose, and lactate were likewise not affected by caffeine [plasma free fatty acids (mM) after 90 min: 5 CAF = 0.42 +/- 0.04, 25 CAF = 0.45 +/- 0.07, and SAL = 0.41 +/- 0.05]. These data indicate that intravenous caffeine does not enhance the endurance run time or alter the plasma free fatty acids or liver and muscle glycogen utilization in endurance trained rats.

Effect of intravenous caffeine on muscle glycogenolysis in fasted exercising rats

Caffeine has been reported to enhance performance by increasing fat utilization and by sparing liver and muscle glycogen. The lipolytic effect of caffeine has been reported to be diminished in response to previous carbohydrate loading of the subjects. The present study was designed to investigate the effects of caffeine during submaximal exercise in rats where the influence of dietary carbohydrate was removed by fasting. Rats were fasted overnight and given injection of 25 mg.kg-1 caffeine (CAF) or 0.9% NaCl (SAL) 60 min before exercise. They were run for 15, 30, and 60 min on a rodent treadmill up a 15% grade at 21 m.min-1. Plasma free fatty acids (FFA) were significantly elevated to 0.72 +/- 0.04 mM in CAF as compared to 0.45 +/- 0.03 mM in SAL at the beginning of exercise. During exercise, however, a significant difference in FFA levels between CAF and SAL was seen only at 30 min and not at other time points. No significant decrease in muscle glycogenolysis was observed in the CAF as compared to SAL rats, and the liver cyclic AMP remained the same in both CAF and SAL. Blood lactate (mM) showed an increase due to caffeine only at 15 min of exercise (CAF = 2.4 +/- 0.2; SAL = 1.7 +/- 0.3). Intravenous caffeine during exercise did not alter plasma glucagon or blood glucose. We conclude that caffeine has no effect on muscle glycogen utilization in fasted rats during exercise even though there was an increased FFA in CAF rats at the beginning of exercise.

Effects of Carbohydrate Intake before and during an Ice Hockey Game on Blood and Muscle Energy Substrates

Abstract This study was performed to determine whether carbohydrate (CHO) intake before and during an ice hockey game could spare muscle glycogen and improve performance. The effect of the CHO supplementation on blood glucose, lactate, triglycerides, and glycerol was also investigated. Seven elite collegiate ice hockey players were tested during two regular competitive league matches. The CHO supplement consisted of 100 g of glucose ingested during the 75–210 min period prior to the match and a total of 20 g glucose during the match. A lower blood glucose level before the game and higher glucose concentration after the game were measured in the experimental group. Muscle glycogen content was lowered in both groups. When the glycogen decrease was corrected for the distance skated, a greater sparing of this substrate was observed following the CHO-feeding. These data demonstrate that CHO intake can result in less glycogen usage per distance skated. This finding is of particular relevance for hockey tournaments during which players may participate in more than one match per day.

Glucose, glycogen, and insulin responses in the hypothermic rat

The rat appears to be unable to utilize glucose during hypothermia. The objective of this study was to examine carbohydrate homeostasis during induction, hypothermia, and rewarming phases. Groups of normothermic animals were euthanized to serve as time controls for comparison. Hypothermia (15 °C) was produced by exposure to helox (80% helium:20% oxygen) at 0 ± 1 °C. Hyperglycemia was noted during the induction process (169 ± 8 in control vs 326 ± 49 mg/dl). Serum glucose increased further during 4 hr of hypothermia, but following rewarming ( T re of 33 ± 1 ° C) was reduced (153 ± 16 mg/dl) significantly ( P < 0.05). Serum insulin was depressed during hypothermic induction (from 48 ± 4 in controls to 19 ± 3 μU/ml in hypothermic rats) and increased only slightly during the arousal process, remaining significantly lower than in normothermic subjects. Initial hepatic, skeletal muscle, and cardiac glycogen concentrations were reduced 34, 68, and 75%, respectively, during hypothermic induction. While liver glycogen decreased further during 4 hr of hypothermia, skeletal and cardiac stores increased markedly. During rewarming, hepatic glycogen was markedly decreased, while skeletal and cardiac stores were maintained. These data suggest that hyperglycemia in the hypothermic rat can be accounted for by glycogenolysis and hypoinsulinemia. In addition, this study indicates repletion of skeletal and cardiac muscle glycogen during maintained hypothermia and sparing of muscle glycogen during rewarming.

Carbohydrate and fluid needs of the soccer player.

Soccer is a game that demands a combination of repeated maximal sprinting wit with 10 to 11km of moderate running, sometimes performed under extremely warm conditions. Over the course of a match, there is partial to near complete depletion of glycogen reserves in the leg muscles (depending on the extent of initial reserves and the level of competition), with a resultant decrease in physical performance. Blood glucose levels also fall, sometimes to values likely to cause a deterioration of both tactical thinking and cooperation between players (3.0 to 3.8 mmol/L), while in tropical climates, fluid losses can amount to 4 to 5kg of bodyweight. The effectiveness of glucose solutions in correcting these problems is limited for 2 main reasons: concentrations greater than 2.5% slow the rate of gastric emptying and thus fluid absorption, while provoking a secretion of insulin with a resultant hypoglycaemia. Fructose solutions are less liable to increase insulin secretion, but they have an equal propensity for slowing gastric emptying; moreover, the ingested fructose is largely metabolised in the liver, without boosting blood glucose. However, glucose polymer preparations have a low osmotic pressure per unit content of glucose equivalent, so that substantial amounts of carbohydrate can be administered in this fashion before gastric emptying is inhibited. If polymers are given before and during a soccer game, they sustain blood glucose, sparing muscle glycogen stores and increasing game performance. If the concentration of polymer is too high, one possible complication is a movement of water from the plasma into the gut; nevertheless, with an appropriate choice of concentration (for example, 7% polycose, 360 mOsm/L, plasma volume is increased rather than decreased relative to that seen with administration of water. Probably because the intergame interval for competitive soccer players is short, replenishment of glycogen reserves proceeds quite slowly. Moreover, this process does not seem to be helped by ingestion of either glucose polymers or a high carbohydrate diet.

Muscle metabolism during exercise in the heat in unacclimatized and acclimatized humans.

The effect of heat acclimatization on aerobic exercise tolerance in the heat and on subsequent sprint exercise performance was investigated. Before (UN) and after (ACC) 8 days of heat acclimatization, 10 male subjects performed a heat-exercise test (HET) consisting of 6 h of intermittent submaximal [50% of the maximal O2 uptake] exercise in the heat (39.7 degrees C dB, 31.0% relative humidity). A 45-s maximal cycle ride was performed before (sprint 1) and after (sprint 2) each HET. Mean muscle glycogen use during the HET was lower following acclimatization [ACC = 28.6 +/- 6.4 (SE) and UN = 57.4 +/- 5.1 mmol/kg; P less than 0.05]. No differences were noted between the UN and ACC trials with respect to blood glucose, lactate (LA), or respiratory exchange ratio. During the UN trial only, total work output during sprint 2 was reduced compared with sprint 1 (24.01 +/- 0.80 vs. 21.56 +/- 1.18 kJ; P less than 0.05). This reduction in sprint performance was associated with an attenuated fall in muscle pH following sprint 2 (6.86 vs. 6.67, P less than 0.05) and a reduced accumulation of LA in the blood. These data indicate that heat acclimatization produced a shift in fuel selection during submaximal exercise in the heat. The observed sparing of muscle glycogen may be associated with the enhanced ability to perform highly intense exercise following prolonged exertion in the heat.

Interactions between glucagon and other counterregulatory hormones during normoglycemic and hypoglycemic exercise in dogs.

Somatostatin (ST)-induced glucagon suppression results in hypoglycemia during rest and exercise. To further delineate the role of glucagon and interactions between glucagon and the catecholamines during exercise, we compensated for the counterregulatory responses to hypoglycemia with glucose replacement. Five dogs were run (100 m/min, 12 degrees) during exercise alone, exercise plus ST infusion (0.5 micrograms/kg-min), or exercise plus. ST plus glucose replacement (3.5 mg/kg-min) to maintain euglycemia. During exercise alone there was a maximum increase in immunoreactive glucagon (IRG), epinephrine (E), norepinephrine (NE), FFA, and lactate (L) of 306 +/- 147 pg/ml, 360 +/- 80 pg/ml, 443 +/- 140 pg/ml, 541 +/- 173 mu eq/liter, and 6.3 +/- 0.7 mg/dl, respectively. Immunoreactive insulin (IRI) decreased by 10.2 +/- 4 micro/ml and cortisol (C) increased only slightly (2.1 +/- 0.3 micrograms/dl). The rates of glucose production (Ra) and glucose uptake (Rd) rose markedly by 6.6 +/- 2.2 mg/kg-min and 6.2 +/- 1.5 mg/kg-min. In contrast, when ST was given during exercise, IRG fell transiently by 130 +/- 20 pg/ml, Ra rose by only 3.6 +/- 0.5 mg/kg-min, and plasma glucose decreased by 29 +/- 6 mg/dl. The decrease in IRI was no different than with exercise alone (10.2 +/- 2.0 microU/ml). As plasma glucose fell, C, FFA, and L rose excessively to peaks of 5.4 +/- 1.3 micrograms/dl, 1,166 +/- 182 mu eq/liter and 15.5 +/- 7.0 mg/dl. The peak increment in E (765 +/- 287 pg/ml) coincided with the nadir in plasma glucose and was four times greater than during normoglycemic exercise. Hypoglycemia did not affect the rise in NE. The increase in Rd was attenuated and reached a peak of only 3.7 +/- 0.8 mg/kg-min. During glucose replacement, IRG decreased by 109 +/- 30 pg/ml and the IRI response did not differ from the response to normal exercise. Ra rose minimally by 1.5 +/- 0.3 mg/kg-min. The changes in E, C, Rd, and L were restored to normal, whereas the FFA response remained excessive. In all protocols increments in Ra were directly correlated to the IRG/IRI molar ratio while no correlation could be demonstrated between epinephrine or norepinephrine and Ra. In conclusion, (a) glucagon controlled approximately 70% of the increase of Ra during exercise. This became evident when counterregulatory responses to hypoglycemia (E and C) were obviated by glucose replacement; (b) increments in Ra were strongly correlated to the IRG/IRI molar ratio but not the plasma catecholamine concentration; (c) the main role of E in hypoglycemia was to limit glucose uptake by the muscle; (d) with glucagon suppression, glucose production was deficient but a further decline of glucose was prevented through the peripheral effects of E, (e) the hypoglycemic stimulus for E secretion was facilitated by exercise; and (f) we hypothesize that an important role of glucagons during exercise could be to spare muscle glycogen by stimulating glucose production by the liver.

Catecholamine responses and their interactions with other glucoregulatory hormones.

We have investigated catecholamine-glucagon-insulin interactions using three stress models: 1) hypoglycemia; 2) exercise; and 3) epinephrine infusion. Phlorizin caused mild hypoglycemia with hypoinsulinemia. Plasma glucagon increased as did hepatic glucose production. Catecholamines did not increase. Insulin caused severe hypoglycemia. Metabolic counterregulation was due mainly to the 40-fold increase in epinephrine. Glucagon played a role only in the recovery from insulin-induced hypoglycemia, which could reflect increased hepatic sensitivity to glucagon with declining plasma insulin. Glucagon suppression during exercise caused transient hypoglycemia due to an inadequate rise in glucose production. Exaggerated epinephrine release during hypoglycemic exercise prevented severe hypoglycemia by inhibiting glucose utilization and stimulating glucose production, with an associated increase in lactate and free fatty acid levels. Hypoglycemic exercise also caused increased cortisol release. Counterregulation was prevented by a euglycemic clamp. We conclude that, during exercise, glucagon is directly responsible for 80% of the increment of glucose production and controls glucose uptake by the muscle indirectly; thus glucagon spares muscle glycogen by increasing hepatic glucose production. Epinephrine infusion in normal dogs caused a transient increase in glucose production and a sustained inhibition of glucose clearance, resulting in hyperglycemia. Insulin rose transiently, followed by a relative inhibition of secretion. Glucagon suppression did not modify the metabolic effects of epinephrine. In alloxan-diabetic dogs, the glucagon response to epinephrine was augmented, whereas in depancreatized dogs, during subbasal insulin infusion, the hepatic response to glucagon was excessive. Glucagon suppression diminished hepatic responsiveness to epinephrine in both models. Stress-induced diabetic instability could relate to exaggerated glucagon release or to increased hepatic sensitivity to glucagon. Thus, during hypoglycemia, exercise, or epinephrine infusion, prevailing plasma insulin levels govern the relative metabolic roles of epinephrine and glucagon.

Effectiveness of carbohydrate feeding in delaying fatigue during prolonged exercise.

Prolonged exercise in the fasted state frequently results in a lowering of blood glucose concentration, and when the intensity is moderate (i.e. 60-80% of VO2 max), muscle often becomes depleted of glycogen. The extent to which carbohydrate feedings contribute to energy production, and their effectiveness for improving endurance during prolonged exercise, are reviewed in this article. Prolonged exercise (i.e. greater than 2 hours) results in a failure of hepatic glucose output to keep pace with muscle glucose uptake. As a result, blood glucose concentration frequently declines below 2.5 mmol/L. Despite this hypoglycaemia, fewer than 25% of subjects display symptoms suggestive of central nervous system dysfunction. Since fatigue rarely results from hypoglycaemia alone, the effectiveness of carbohydrate feeding should be judged by its potential for muscle glycogen sparing. Carbohydrate feeding during moderate intensity exercise postpones the development of fatigue by approximately 15 to 30 minutes, yet it does not prevent fatigue. This observation agrees with data suggesting that carbohydrate supplementation reduces muscle glycogen depletion. It is not certain whether carbohydrate feeding increases muscle glucose uptake throughout moderate exercise or if glucose uptake is higher only during the latter stages of exercise. In contrast to moderate intensity exercise, carbohydrate feeding during low intensity exercise (i.e. less than 45% of VO2 max) results in hyperinsulinaemia. Consequently, muscle glucose uptake and total carbohydrate oxidation are increased by approximately the same amount. The amount of ingested glucose which is oxidised is greater than the increase in total carbohydrate oxidation and therefore endogenous carbohydrate is spared. The majority of sparing appears to occur in the liver, which is reasonable since muscle glycogen is not utilised to a large extent during mild exercise. Although carbohydrate feedings prevent hypoglycaemia and are readily used for energy during mild exercise, there is little data indicating that feedings improve endurance during low intensity exercise. When the reliance on carbohydrate for fuel is greater, as during moderate intensity exercise, carbohydrate feedings delay fatigue by apparently slowing the depletion of muscle glycogen.

Effect of glycerol feeding on endurance and metabolism during prolonged exercise in man

This study evaluated the effectiveness of pre-exercise glycerol feeding in protecting against development of hypoglycemia and sparing muscle glycogen during prolonged, intense exercise. Thirty minutes after ingesting either glycerol (1 gm X kg-1 body weight) or a placebo, 10 cyclists performed as much exercise on a cycle ergometer as they were able in 150 min. The average exercise intensity was 72% of VO2max during both trials. Glycerol ingestion increased blood glycerol concentration 100-fold, but did not alter the respiratory exchange ratio (R), plasma levels of insulin and free-fatty acids, or blood lactate and beta-hydroxybutyrate. The only significant effect of glycerol feeding was to postpone the decline in blood glucose by about 30 min. This suggests that glycerol served, to a limited extent, as a gluconeogenic substrate; however, glycerol ingestion did not spare muscle glycogen during 90 min of treadmill exercise at 71% VO2max. It appears that man cannot utilize glycerol as gluconeogenic substrate rapidly enough to serve as a major energy source during strenuous exercise.

Sparing effect of chronic high-altitude exposure on muscle glycogen utilization.

Substrate utilization during heavy [approximately 85% maximum O2 consumption (VO2max)] bicycle exercise was examined in eight low-altitude residents at sea level (SL) and after acute (2 h) and chronic (18 days) high-altitude (HA) exposure at 4,300 m. Mean VO2max was approximately 27% lower at acute HA than at SL and did not change significantly with continued HA exposure. Biopsies from the vastus lateralis muscle and venous blood samples were obtained before and after 30 min of exercise, whereas determinations of the respiratory exchange ratio (R) were made at 10-min intervals during each of the submaximal bouts. Resting levels of serum-free fatty acids at acute and chronic HA were, respectively, two and three times higher than SL but were unchanged with exercise. Exercise did not alter resting serum glycerol levels at SL or during acute HA, but during chronic HA resting glycerol levels were increased 11-fold. Although mean blood lactate concentrations following exercise at SL and acute HA were not significantly different, postexercise lactate concentrations were 87% lower after chronic HA. During exercise at SL and acute HA, muscle glycogen utilization and R were not different. At chronic HA, muscle glycogen utilization and R were 41 and 15% lower, respectively. These data suggest that after chronic HA exposure, increased mobilization and use of free fatty acids during exercise resulted in sparing of muscle glycogen.

Dichloroacetate: Effects on exercise endurance in untrained rats

The effect of dichloroacetate (DCA), an activator of pyruvate dehydrogenase, on the performance of fed, untrained rats was evaluated while swimming for different durations. DCA-treated rats were able to swim almost 40% longer than controls (354 ± 18 versus 255 ± 18 sec, p < .001). This was associated with lower levels of blood and muscle lactate at rest and after 210 and 240 sec of swimming. At exhaustion, blood lactate was the same in the two groups even though the DCA rats had worked for an additional 99 sec (16.9 ± 1.2 versus 15.8 ± 1.2 mM/L NS). Pretreatment with DCA did not alter the usual exercise-induced decreases in muscle ATP and creatine phosphate or liver glycogen. After 210 sec of exercise, plasma FFA and blood glucose and acetoacetate were also the same in the two groups; however, β-hydroxybutyrate was somewhat higher, and there was a small but significant sparing of muscle glycogen in the DCA group. The data indicate that DCA enhances the ability of rats to exercise at near maximal work loads. They are consistent with the notion that improved endurance is a consequence of a decreased rate of lactate accumulation; however, the possibility that it is secondary to some other action of DCA cannot be excluded.

Free fatty acid and glucose metabolism during increased energy expenditure and after training

The amount of fat available as substrate to provide the energy needed for submaximal exercise is almost unlimited; therefore, it stands to reason that the organism will adapt so that it uses fat as the major energy substrate during very prolonged exercise. Nevertheless, the quantitatively smaller body stores of carbohydrate, which contain only one to two percent as many calories as the fat stores, play a very important role during exercise, since depletion of either muscle or liver glycogen will force an individual to terminate strenuous muscular work. In normal dogs during long-lasting exercise, at energy expenditures ranging from the resting state of 0.73 kcal/m2 min to a work load of 4.66 kcal/m2 min, the FFA mobilization, and participation of FFA oxidation in total energy expenditure increases. During prolonged exercise in trained dogs, 50-90% of the energy may derive from plasma FFA, while plasma glucose contributes not more than 10% to the energy expenditure. However, there is an inverse relationship between the amount of glycogen stored inside the muscle, its rate of depletion, and muscular endurance during prolonged strenuous work. Oxidation of FFA spares muscle glycogen and in this way increases work endurance.