Anaerobic exercise reduces tumor growth, cancer cachexia and increases macrophage and lymphocyte response in Walker 256 tumor-bearing rats

Here, we investigated the effect of jump exercise on tumor growth, cancer cachexia, lymphocyte proliferation and macrophage function in Walker 256 tumor-bearing rats. Male Wistar rats (60 days) were divided into sedentary (C) and exercised (E) groups. Jump training consisted of six sets of 10 jumps in water with overload of 50% of body mass with 1 min of resting, four times per week for 8 weeks. After 6 weeks of training, half of each group was inoculated with 2 × 10⁷ cells of Walker 256 tumor. Sedentary tumor-bearing and exercised tumor-bearing are referred to as T and TE, respectively. Tumor weight in the T group was 25 g. These animals display loss of weight, hypertriacylglycerolemia, hyperlacticidemia, depletion of glycogen stores and increase in PIF expression. Jump exercise (TE) induced a significant lower tumor weight, preserves liver glycogen stores, partly prevented the hypertriacylglycerolemia, hyperlacticidemia and, prevented the fall in body weight and reduced PIF expression. Lymphocyte was increased by tumor burden (T) and was higher by including exercise (TE). The same was observed regarding phagocytosis and lysosomal volume. Anaerobic exercise decreases tumor growth, cancer cachexia and increases innate and adaptative immune function.     

The effect of high-intensity intermittent swimming on post-exercise glycogen supercompensation in rat skeletal muscle

A single bout of prolonged endurance exercise stimulates glucose transport in skeletal muscles, leading to post-exercise muscle glycogen supercompensation if sufficient carbohydrate is provided after the cessation of exercise. Although we recently found that short-term sprint interval exercise also stimulates muscle glucose transport, the effect of this type of exercise on glycogen supercompensation is uncertain. Therefore, we compared the extent of muscle glycogen accumulation in response to carbohydrate feeding following sprint interval exercise with that following endurance exercise. In this study, 16-h-fasted rats underwent a bout of high-intensity intermittent swimming (HIS) as a model of sprint interval exercise or low-intensity prolonged swimming (LIS) as a model of endurance exercise. During HIS, the rats swam for eight 20-s sessions while burdened with a weight equal to 18% of their body weight. The LIS rats swam with no load for 3 h. The exercised rats were then refed for 4, 8, 12, or 16 h. Glycogen levels were almost depleted in the epitrochlearis muscles of HIS- or LIS-exercised rats immediately after the cessation of exercise. A rapid increase in muscle glycogen levels occurred during 4 h of refeeding, and glycogen levels had peaked at the end of 8 h of refeeding in each group of exercised refed rats. The peak glycogen levels during refeeding were not different between HIS- and LIS-exercised refed rats. Furthermore, although a large accumulation of muscle glycogen in response to carbohydrate refeeding is known to be associated with decreased insulin responsiveness of glucose transport, and despite the fact that muscle glycogen supercompensation was observed in the muscles of our exercised rats at the end of 4 h of refeeding, insulin responsiveness was not decreased in the muscles of either HIS- or LIS-exercised refed rats compared with non-exercised fasted control rats at this time point. These results suggest that sprint interval exercise enhances muscle glycogen supercompensation in response to carbohydrate refeeding as well as prolonged endurance exercise does. Furthermore, in this study, both HIS and LIS exercise prevented insulin resistance of glucose transport in glycogen supercompensated muscle during the early phase of carbohydrate refeeding. This probably led to the enhanced muscle glycogen supercompensation after exercise.     

Effect of treadmill exercise on food intake and body weight in lean and obese rats

Body weight and food intake of lean and obese, male and female Osborne-Mendel rats following treadmill exercise were compared. Rats were assigned, separately by sex, to one of three diet groups; Group 1 was fed a low fat (10%) diet throughout the study, Group 2 was fed a high fat (55%) diet for 16 weeks and then switched to the low fat diet 1 week prior to exercise, and Group 3 was fed the high fat diet throughout the study. To control for differences in work output between the leanest and heaviest animals, exercise intensity was adjusted across groups such that all exercised rats had equivalent energy expenditure. After a 3 day training period, the exercise was successively increased over 8 days until a work output of 374.9J was reached. Relative to their respective controls, obese exercised males showed a reduction in body weight but no change in food intake. In contrast, exercised females showed no change in body weight or food intake, regardless of dietary condition.     

Exercise training prevents hyperinsulinemia, muscular glycogen loss and muscle atrophy induced by dexamethasone treatment

This study investigated whether exercise training could prevent the negative side effects of dexamethasone. Rats underwent a training period and were either submitted to a running protocol (60% physical capacity, 5 days/week for 8 weeks) or kept sedentary. After this training period, the animals underwent dexamethasone treatment (1 mg/kg per day, i.p., 10 days). Glycemia, insulinemia, muscular weight and muscular glycogen were measured from blood and skeletal muscle. Vascular endothelial growth factor (VEGF) protein was analyzed in skeletal muscles. Dexamethasone treatment evoked body weight loss (?24%), followed by muscular atrophy in the tibialis anterior (?25%) and the extensor digitorum longus (EDL, ?15%). Dexamethasone also increased serum insulin levels by 5.7-fold and glucose levels by 2.5-fold compared to control. The exercise protocol prevented atrophy of the EDL and insulin resistance. Also, dexamethasone-treated rats showed decreased muscular glycogen (?41%), which was further attenuated by the exercise protocol. The VEGF protein expression decreased in the skeletal muscles of dexamethasone-treated rats and was unaltered by the exercise protocol. These data suggest that exercise attenuates hyperglycemia and may also prevent insulin resistance, muscular glycogen loss and muscular atrophy, thus suggesting that exercise may have some benefits during glucocorticoid treatment.     

Effects of supranormal liver glycogen content on hyperglucagonemia-induced liver glycogen breakdown

The purpose of the present study was to test the hypothesis that a higher hepatic glycogen level is associated with higher glucagon-induced hepatic glycogen depletion. Four groups of anesthetized rats received three injections (at times 0, 30, and 60 min) of glucagon (intravenously, 20 [microg/kg). Among these groups, hepatic glycogen levels had previously been manipulated either by an overloading diet (Fast-refed), a reduction in food intake (1/2-fast), or exercise (75 min of running, 26 m/ min, 0% grade). A fourth group had normal hepatic glycogen levels. A fifth group of rats was injected only with saline (0.9% NaCl). Liver glycogen concentrations were measured every 30 min during the course of the 90-min experiment, using liver samples obtained from the open liver biopsy technique. Plasma glucagon concentrations were significantly higher (P < 0.05) in the glucagon-injected groups than in the saline-injected group. As expected, liver glycogen levels were significantly higher (P < 0.01; 1.6-fold) in the Fast-refed group than in all other groups. Glucagon-induced decreases in liver glycogen concentrations were similar in Fast-refed than in normally fed and exercised rats when the overall 90-min period was considered. However, during the course of the last 30-min period, liver glycogen was significantly (P < 0.01) decreased only in the Fast-refed group. The Fast-refed, normally fed, and exercised groups had a similar glucagon-induced hyperglycemia that was significantly more elevated (P < 0.01) than glucose levels measured in the saline-injected group. Glucagon-induced reactive hyperinsulinemia was observed only in the Fast-refed and normally fed rats, and not in the exercised and 1/2-fast rats. It is concluded that supranormal levels of liver glycogen may be associated with a larger hyperglucagonemia-induced liver glycogen breakdown.     

Effects of succinate dimethyl ester on the metabolic and hormonal response to exercise in fed and starved rats

This study aims at investigating the possible beneficial effect of succinic acid dimethyl ester (SAD), injected intraperitoneally (5.0 micromol/g body wt.), upon the metabolic and hormonal response to a 60 min exercise in both fed and overnight starved rats. In fed rats, the injection of SAD minimized the fall in plasma D-glucose concentration, and the increase in plasma lactate, beta-hydroxybutyrate, free fatty acid and glycerol concentrations, otherwise provoked by exercise. SAD, however, failed to prevent the decrease in plasma insulin concentration and liver glycogen content caused by exercise. Starved rats displayed lower plasma D-glucose and insulin concentrations and higher plasma beta-hydroxybutyrate and free fatty acid concentrations than fed rats. The body weight, liver weight and paraovarian fat weight, as well as the glycogen content of both liver and heart were also decreased in the starved rats. In the latter animals, the injection of SAD again opposed the exercise-induced increase in plasma beta-hydroxybutyrate, free fatty acid and glycerol concentrations, and again failed to prevent the more modest decreases in plasma insulin concentration and liver glycogen content caused by exercise in the starved, as distinct from fed rats. These findings suggest that, independently of any obvious change in plasma insulin concentration, SAD minimizes the exercise-induced mobilization and enhanced utilization of endogenous nutrients, especially fatty acids and glycerol produced by hydrolysis of triglycerides in adipose tissue, presumably through its capacity to act as an oxidizable nutrient in various cell types and as a gluconeogenic precursor in hepatocytes.     

Effect of short-term exercise training on muscle glycogen in resting conditions in rats fed a high fat diet

Summary It has been reported that exercise training increases muscle glycogen storage in rats fed a high carbohydrate (CHO) diet in resting conditions. The purpose of this study was to examine whether a 3-week swimming training programme would increase muscle glycogen stores in rats fed a high-fat (FAT) diet in resting conditions. Rats were fed either the FAT or CHO diet for 7 days ad libitum, and then were fed regularly twice a day (between 0800 and 0830 hours and 1800 and 1830 hours) for 32 days. During this period of regular feeding, half of the rats in both dietary groups had swimming training for 3 weeks and the other half were sedentary. The rats were not exercised for 48 h before sacrifice. All rats were killed 2 h after their final meal (2030 hours). The glycogen contents in red gastrocnemius muscle, heart and liver were significantly higher in sedentary rats fed the CHO diet than in those fed the FAT diet. Exercise training clearly increased glycogen content in soleus, red gastrocnemius and heart muscle in rats fed the CHO diet. In rats fed the FAT diet, however, training did not increase glycogen content in these muscles or the heart. Exercise training resulted in an 87% increase of total glycogen synthase activity in the gastrocnemius muscle of rats fed the CHO diet. However, this was not observed in rats fed the FAT diet. The total glycogen phosphorylase activity in the gastrocnemius muscle of the rats of both dietary groups was increased approximately twofold by training. These results suggested that muscle glycogen was enhanced in rats fed the CHO diet and that the glycogen content of the muscle of rats fed the FAT diet was not increased by exercise training.     

Glycogen depletion and resynthesis in the rat after downhill running

Summary to study the effect of downhill running on glycogen metabolism, 94 rats were exercised by running for 3 h on the level or down an 18° incline. Muscle and liver glycogen concentrations were measured before exercise and 0, 48 and 52 h postexercise. Rats were not fed during the first 48 h of recovery but ingested a glucose solution 48 h postexercise. Downhill running depleted glycogen in the soleus muscle and liver significantly more than level running (P<0.01). The amount of glycogen resynthesized in the soleus muscle and liver in fasting or nonfasting rats was not altered significantly by downhill running (P>0.05). On every day of recovery the rats were injected with dexamethasone, which induced similar increases in glycogen concentration in the soleus muscle and liver after the 52nd h of the postexercise period in the case of downhill and level running. The glycogen depletion and repletion results indicated that, under our experimental conditions, downhill running in the rat, a known model of eccentric exercise, affected muscle glycogen metabolism differently from eccentric cycling in humans.     

Evidence that a decrease in liver glycogen content stimulates FFA mobilization during exercise.

This study evaluated a liver glycogen content decrease before exercise on the metabolic responses during exercise. Rats injected with glucagon (20 microg x kg(-1)) were compared to rats with a 50% food restriction (1/2-fast) and normally fed rats. All were studied at rest and during exercise (26 m/min, 0% grade). Resting liver glycogen concentrations were twice as high (P<.01) in normally fed rats, with no significant differences between 1/2-fast and glucagon-injected rats. During exercise, liver glycogen content was significantly reduced in normally fed rats. After exercise, plasma insulin levels were decreased (P<.01) in all groups, and beta-hydroxybutyrate concentrations were similar in normally fed and glucagon-injected rats and significantly (P<.01) lower in 1/2-fast rats. Exercise caused a significant increase in FFA concentrations in all groups (P<.01). No significant differences in FFA concentrations were found between 1/2-fast and glucagon-injected groups (P>0.05).     

Effects of supranormal liver glycogen content on hyperglucagonemia-induced liver glycogen breakdown

The purpose of the present study was to test the hypothesis that a higher hepatic glycogen level is associated with higher glucagon-induced hepatic glycogen depletion. Four groups of anesthetized rats received three injections (at times 0, 30, and 60 min) of glucagon (intravenously, 20?μg/kg). Among these groups, hepatic glycogen levels had previously been manipulated either by an overloading diet (Fast-refed), a reduction in food intake (1/2-fast), or exercise (75?min of running, 26?m/min, 0% grade). A fourth group had normal hepatic glycogen levels. A fifth group of rats was injected only with saline (0.9% NaCl). Liver glycogen concentrations were measured every 30?min during the course of the 90-min experiment, using liver samples obtained from the open liver biopsy technique. Plasma glucagon concentrations were significantly higher (P?<?0.05) in the glucagon-injected groups than in the saline-injected group. As expected, liver glycogen levels were significantly higher (P?<?0.01; 1.6-fold) in the Fast-refed group than in all other groups. Glucagon-induced decreases in liver glycogen concentrations were similar in Fast-refed than in normally fed and exercised rats when the overall 90-min period was considered. However, during the course of the last 30-min period, liver glycogen was significantly (P?<?0.01) decreased only in the Fast-refed group. The Fast-refed, normally fed, and exercised groups had a similar glucagon-induced hyperglycemia that was significantly more elevated (P?<?0.01) than glucose levels measured in the saline-injected group. Glucagon-induced reactive hyperinsulinemia was observed only in the Fast-refed and normally fed rats, and not in the exercised and 1/2-fast rats. It is concluded that supranormal levels of liver glycogen may be associated with a larger hyperglucagonemia-induced liver glycogen breakdown.     

The influence of glucagon on hepatic glycogen mobilization in exercising rats

Summary The significance of glucagon for the alterations in carbohydrate and fat metabolism during swimming has been evaluated. Fed, male rats were used. Blood was drawn by cardiac puncture for glucose analysis and either rabbit-antiglucagonserum (A-rats) or normal rabbitserum (N-rats) injected. Twentynine rats were then forced to swim (S-rats) with a tail weight for 60 min, while 16 rats were resting controls (C-rats). Subsequently blood was drawn and samples of liver and muscle tissue collected. In SN-rats glucagon concentrations increased from 152±18 (S.E.) pg/ml (CN-rats) to 332±61 (P<0.05), while liver glycogen decreased (P<0.001) and blood glucose increased (P<0.05). In SA-rats, however, the changes in liver glycogen and blood glucose were halved indicating that increased glucagon secretion enhances hepatic glycogen depletion during prolonged exercise. NEFA rose in SA-rats (P<0.005) as well as in SN-rats (P<0.05). Glycerol concentrations, however, only increased in SA-rats (P<0.05) indicating a shift towards lipid combustion in antibody treated rats. Muscle glycogen and plasma insulin diminished and blood lactate increased uniformly in exercised rats.     

Moderate exercise in young female S5B/P1 rats does not reduce body fat.

Weanling S5B/P1 female rats were divided into four groups as follows: high fat diet, exercised (FE); high fat diet, unexercised (FU); high carbohydrate diet, exercised (CE); and high carbohydrate diet, unexercised (CU). After 25 days of progressive training, exercised rats ran on a motor-driven treadmill for 30 days at 25 m/min per 1 h at 0 degree grade for 6 days a week. Rats were weighed weekly throughout the experiment and food intakes were recorded for the last 3 weeks of the experiment. After euthanasia at 15 weeks of age, three muscles, liver, heart, kidney, 3 fat depots, and tibia-fibula were dissected out and weighted. The carcass, including weighted organs and fat depots, was analyzed for body fat. Exercised rats, regardless of diet, weighed slightly but significantly more than unexercised rats. They also tended to eat more food and to have a higher quantity of fat-free body mass than unexercised rats. Percent body fat was similar for exercised and unexercised rats. The tibia weighed significantly more (p less than 0.05) in CU than in FU rats but the weight was similar in CE and FE rats. The density of the tibia was significantly higher (p less than 0.01) in exercised than in unexercised rats.     

The effects of a high carbohydrate diet on postprandial energy expenditure during exercise in rats

Summary Whether or not a high intake of carbohydrate increases postprandial energy expenditure during exercise was studied in rats. The rats were meal-fed regularly twice a day (0800–0900 hours and 1800–1900 hours) on either a high carbohydrate (CHO) (carbohydrate/fat/protein = 70/5/25, % of energy) or high fat (FAT) (35/40/25) diet for 12 days. On the final day of the experiment, all of the rats in each dietary group were fed an evening meal containing equal amounts of energy (420 kJ · kg^–1 body mass). After the meal, they were divided into three subgroups: pre-exercise control (PC), exercise (EX), and resting control (RC). The PC-CHO and PC-FAT groups were sacrificed at 2030 hours. The EX-CHO and EX-FAT groups were given a period of 3-h swimming, and then sacrificed at 2330 hours. The RC-CHO and RC-FAT groups rested after the meal and were sacrificed at 2330 hours. Total energy expenditure during the period 1.5 h from the commencement of exercise was higher in EX-CHO than in EX-FAT. The respiratory exchange ratio was also higher in EX-CHO than in EX-FAT, suggesting enhanced carbohydrate oxidation in the former. Compared with both PC-FAT and RC-FAT, the liver glycogen content of EX-FAT rats was significantly decreased by exercise. On the other hand, the liver glycogen content of both EX-CHO and RC-CHO was higher than that of PC-CHO rats. The glycogen content of soleus muscle of EX-FAT was slightly decreased during exercise, however, that of EX-CHO increased significantly. Thus postprandial energy expenditure during exercise was higher in the rats fed the CHO diet than in those fed the FAT diet, which could have been related to the increase of both liver and muscle glycogen storage during exercise in the former.     

Effects of intensive aerobic exercise on stress reactivity and myocardial morphology in rats

The effects of intensive aerobic exercise, weight control, and no treatment on (1) stress reactivity (measured by weight loss, glucocorticoid elevation, and incidence of gastric lesions) and (2) myocardial morphology were compared in male Sprague-Dawley ulcer susceptible rats. Animals were allocated to a free-feeding exercise group aerobically conditioned by a 26 week treadmill-running program; a sedentary group whose mean body weight was made to parallel that of the exercise group; and a free-feeding sedentary group. In week 27 animals were stressed for five days with daily presentation of escape trials on a variable interval schedule. Differences were found between the heart tissues of the exercised and the sedentary animals: both sedentary groups evidenced adverse morphological changes in ventricular tissue and microcirculation, while the myocardia of the exercise group were completely free of such changes. In response to the stress procedure significant differentiation between groups was obtained only on the weight index. After an initial loss, the exercise group commenced to gain weight on the fourth stress day, while the control groups continued to lose weight.     

PNMT inhibition decreases exercise performance in the rat.

The purpose of this investigation was to examine the effect of phenylethanolamine N-methyltransferase (PNMT) inhibition on the regulation of peripheral metabolic and hormonal responses during treadmill exercise in the rat. Changes in plasma catecholamine (epinephrine, norepinephrine, and dopamine), glucagon and glucose, and the glycogen content of the liver and two skeletal muscles were studied in four groups of rats. Two groups of rats were studied at rest: one group had been treated with LY134046, an inhibitor of PNMT, and the second group was treated with physiological saline. A third group treated with LY134046 was studied after treadmill exercise (28 m.min-1 and 8% slope). In this group of rats, exhaustion came after 37.5 +/- 7.9 minutes of exercise. In order to make appropriate comparisons, a fourth group of rats treated with physiological saline was exercised for 37.5 min. Running endurance during the treadmill exercise was thus reduced in LY134046-treated rats. Plasma epinephrine and glucagon concentrations and other metabolic (plasma glucose and gastrocnemius lateralis and superficial vastus lateralis muscles and liver glycogen contents) responses were similar between LY134046- and saline-treated rats at rest and after exercise. These results suggest that PNMT inhibition in epinephrine brain neurons might be the principal factor involved in the LY134046-induced reduction of exercise endurance.     

Changes in glycemia induced by exercise in rats: contribution of hepatic glycogenolysis and gluconeogenesis

The participation of hepatic glycogenolysis and gluconeogenesis to the glycemic changes promoted by exercise was investigated. For this purpose, we employed swimming rats (2.5% body weight extra load attached to the tail, at 24 degrees C) using a favorable condition to measure hepatic glycogenolysis (fed rats) and a favorable condition to measure hepatic gluconeogenesis (fasted rats). This experimental approach permits us to compare the contribution of hepatic glycogenolysis and gluconeogenesis to glucose changes for a specific schedule of exercise. The animals were investigated at rest, after 5 minutes of swimming and after swimming to exhaustion. Our results show that hepatic glycogen has a crucial role to determine hyperglycemia during exercise. In contrast, hypoglycemia developed during exercise when glycogen was depleted. However, the ability of the liver to produce glucose from L-lactate, glycerol and L-glutamine was increased during exercise. Taken together, these findings suggest that the hepatic capacity to produce glucose from gluconeogenic substrates (except for L-alanine) was increased when hepatic glycogen stores were depleted. Thus, the increased capacity to produce glucose shown by livers from exercising rats must to be an important metabolic adaptation to protect against severe hypoglycemia.     

Effects of intracerebroventricularly administered opioid peptide antagonists on tissue glycogen levels in rats after exercise

Background/aim Physical exercise is a state of physiological stress that requires adaptation of the organism to physical activity. Glycogen is an important and essential energy source for muscle contraction. Skeletal muscle and liver are two important glycogen stores, and the energy required to maintain exercise in rodents are provided by destruction of this glycogen depot. In this study, the effects of endogenous opioid peptide antagonism at the central nervous system level on tissue glycogen content after exhaustive exercise were investigated. Materials and methods Rats had intracerebroventricularly (icv) received nonspecific opioid peptide receptor antagonist, naloxone (50 μg/10 μL in saline) and δ-opioid receptor-selective antagonist naltrindole (50 μg/10 μL in saline) and then exercised till exhaustion. After exhaustion, skeletal muscle, heart, and liver were excised immediately. Results Both opioid peptide antagonists decreased glycogen levels in skeletal muscle. Although, in soleus muscle, this decrease was not statistically significant (p > 0.05), in gastrocnemius muscle, it was significant in the icv naloxone administered group compared with control (p < 0.05). Heart glycogen levels increased significantly in both naloxone and naltrindole groups compared to control and sham-operated groups (p < 0.05). Heart glycogen levels were higher in the naloxone group than naltrindole (p < 0.05). Liver glycogen levels were elevated significantly with icv naloxone administration compared with the control group (p < 0.05). Glycogen levels in the naloxone group was also significantly higher than the naltrindole group (p < 0.05). Conclusion Our findings indicate that icv administered opioid peptide antagonists may play a role in glycogen metabolism in peripheral tissues such as skeletal muscle, heart, and liver.     

Dietary obesity and exercise in young rats

Food intake, body weight, body composition, resting metabolic rate (RMR) and the thermic effect of food (TEF) were measured in young rats, some of which were fed a high energy (HE) diet and some of which were forced to swim daily. In general, high energy feeding as compared to chow feeding, resulted in higher food intake, higher body weight, higher body fat, and a slightly lower TEF. In many cases, however, the specific effects varied with the age and sex of the animals. Animals forced to swim weighed less; were leaner; and had higher RMR and TEF than sedentary animals. The effects of exercise on energy balance were greatest in males, while the effects of the high energy diet on energy balance were greatest in females. All HE-fed rats were switched to lab chow at 104 days of age. Body weights of sedentary HE-fed rats returned to control levels but those of exercised HE-fed rats did not. Both HE-fed groups remained fatter than chow-fed controls, even two months after the diet switch.     

The effect of repeated muscle biopsy sampling on ATP and glycogen resynthesis following exercise in man

The present study investigated the effect of repeated biopsy sampling on muscle adenosine 5-triphosphate (ATP) and glycogen resynthesis following prolonged submaximal exercise. In one group of subjects (Ia, n = 7), biopsy specimens were obtained from the vastus lateralis immediately and 48 h after exhaustive one-legged cycling from both the non-exercised (control) and exercised legs. Additional samples were obtained from the exercised leg at 3, 10 and 24 h post-exercise. In a second group of subjects (Ib, n = 6), biopsy specimens were obtained immediately after exercise from both the control and exercised legs and at 48 h post-exercise from the exercised leg. All muscle biopsies were separated by a distance of 2.5 cm. In group Ia, ATP in the exercised leg was still lower after 48 h of recovery compared with the control leg (P < 0.05), but complete restoration had occurred in group Ib (P > 0.05). Glycogen super compensation was not observed in group Ia. However, at the end of recovery, in group Ib glycogen in the exercised leg was 42% greater than in the control leg (tP < 0.01) . Thus, following exhaustive dynamic exercise, repeated muscle biopsy sampling impaired ATP and glycogen resynthesis for several days, which may have been a result of the distance separating each biopsy site. The inhibition of ATP resynthesis appeared to be associated mainly with type II muscle fibres. The finding that, in contrast to muscle glycogen, ATP did not return to the basal level during the 48 h of recovery, suggests that the measurement of ATP may be a more sensitive measure of muscle damage than that of glycogen.     

Post-exercise ketosis and the glycogen content of liver and muscle in rats on a high carbohydrate diet

Summary Post-exercise ketosis is known to be suppressed by physical training and by a high carbohydrate diet. As a result it has often been presumed, but not proven, that the development of post-exercise ketosis is closely related to the glycogen content of the liver. We therefore studied the effect of 1 h of treadmill running on the blood 3-hydroxybutyrate and liver and muscle glycogen concentrations of carbohydrate-loaded trained (n=72) and untrained rats (n=72). Resting liver and muscle glycogen levels were 25%–30% higher in the trained than in the untrained animals. The resting 3-hydroxybutyrate concentrations of both groups of rats were very low: <0.08 mmol·1⁻¹. Exercise did not significantly influence the blood 3-hydroxybutyrate concentrations of trained rats, but caused a marked post-exercise ketosis (1.40±0.40 mmol·1⁻¹ 1 h after exercise) in the untrained animals, the time-course of which was the approximate inverse of the changes in liver glycogen concentration. Interpreting the results in the light of similar data obtained after a normal and low carbohydrate diet it has been concluded that trained animals probably owe their relative resistance to post-exercise ketosis to their higher liver glycogen concentrations as well as to greater peripheral stores of mobilizable carbohydrate.