Muscle glycogen repletion and pre-exercise glycogen content: effect of carbohydrate loading in rats previously fed a high fat diet

We have recently reported that rates of muscle glycogen repletion during the early period of recovery were increased by carbohydrate (CHO) loading in rats previously fed a high fat diet. However, the reason for this remained unanswered. The purpose of this study was to examine whether an increase of glycogen utilization due to an elevated pre-exercise glycogen store would enhance rates of glycogen repletion in muscle. Despite an equal degree of glycogen depletion, the rates of glycogen repletion of soleus, red and white gastrocnemius muscles by postexercise administration of glucose (3.0 g · kg^–1 body mass) and citrate (0.5 g · kg^–1 body mass) were faster in the CHO loaded (3 days) rats than in the nonloaded rats, as a result of elevated pre-exercise glycogen content and consequently the greater glycogen utilization. The higher rate of muscle glycogen repletion may in part be explained by increased postexercise glycogen synthase activity.     

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.     

The effect of exercise training on glycogen,glycogen synthase and phosphorylase in muscle and liver

Summary It is thought that exercise training in both man and the rat results in a protective effect against the depletion of carbohydrate stores during exercise (glycogen-sparing). However there has been no comprehensive study of the effects of training on glycogen anabolic and catabolic enzymes with liver or muscle. The aim of this study was to examine whether changes in these enzymes occur and whether these changes may provide an explanation for the glycogen-sparing which results from exercise training.Male rats were trained by a treadmill running program at three different workloads. In addition, there were three control groups: free eating (SF), food restricted (SR), and one SF with a single bout of exercise prior to sacrifice.Exercise training was associated with a 60–150% increase in glycogen synthase and phosphorylase and a 50–70% increase in glycogen content in soleus, an intermediate muscle, but not in extensor digitorum longus (EDL), a white muscle nor in liver. The increase in glycogen synthase and phosphorylase in intermediate muscle was proportional to the degree of training and there was a significant correlation between glycogen content, glycogen synthase, and phosphorylase activity in intermediate muscle. Cytochrome c oxidase activity, an indicator of respiratory capacity, increased 50% in gastrocnemius of trained rats and was significantly correlated with glycogen synthase and phosphorylase in soleus.These results indicate a significant effect of exercise training on glycogen anabolic and catabolic enzymes in intermediate muscle, with no significant effects in white muscle or liver. The changes do not provide an explanation for glycogen-sparing, but are consistent with improved capacity of intermediate muscle for rapid glycogen mobilisation and repletion.     

Muscle strength and fatigue after selective glycogen depletion in human skeletal muscle fibers

Summary Two groups of male subjects were studied to examine the effects of different exercise protocols on performance of an isokinetic, short-time strength test, the performance of which is related to fast twitch (FT) muscle fiber recruitment. The laboratory group (LG) (n=10) cycled (30 min, 70% VO₂ max), ran (75 min), and performed repeated bouts of sprint cycling and rapid, maximal contractions of the quadriceps. The marathon group (MG) (n=7) participated in and completed Stockholm's Marathon 1979. A strength test was performed before and within 1–2 h after completion of the group exercise protocol. The m. vastus lateralis was biopsied and muscle fibers classified as slow twitch (ST) or FT. After periodic acid-Schiff staining fibers were qualitatively classified as to glycogen content. In LG significant glycogen depletion occurred in both fiber types and in MG predominantly ST fibers were exhausted of glycogen after the exercise protocol. The glycogen exhaustion from both fiber types in LG was associated with impaired maximal muscular strength produced during a single dynamic contraction, as well as with reduced muscle fatigue patterns. When glycogen exhaustion was induced in ST muscle fibers only in the MG, no impairment was observed for maximal muscular strength but fatigue during 50 consecutive contractions was significantly increased.This study was supported in part by Coca-Cola Export Corporation, Sweden     

Effect of exercise on glycogen metabolism in muscles of triiodothyronine-treated rats

The aim of the present study was to examine the rate of glycogen mobilization during exercise and the rate of the postexercise glycogen replenishment in different muscle types [white (WG), and red (RG) gastrocnemius, soleus (S) and diaphragm (D)] in rats treated with triiodothyronine (T₃, group T). Rats of the control group (C) were treated with saline. The animals were made to run on a treadmill set at 0° gradient and at a speed of 1200 m·h^–1. The time taken to reach exhaustion in group C was 188 (SD 23) min, whereas in group T, it was only 63 (SD 12) min. The content of glycogen in all muscles of the rats from group T at rest and during exercise was significantly lower than in group C at each corresponding time. At exhaustion, the glycogen content was in WG(C) 34.79 (SD 4.65), (T) 20.10 (SD 4.10); in RG(C) 22.82 (SD 4.66), (T) 16.50 (SD 2.00); in S(C) 14.85 (SD 2.48), (T) 11.90 (SD 2.93); in D(C) 18.18 (SD 3.49), (T) 7.54 (SD 3.36) (mol of glucosyl units·g^–1). The amount of glycogen mobilized during exhausting exercise in RG, S and D was similar in both groups whereas in WG it was much higher in rats of group T than in group C. The concentration of glycogen returned to pre-exercise values in each muscle 3 h after exercise. The net amount of glycogen resynthetized during 3 h of recovery depended on the muscle type. It was in WG(C) 3.30, (T) 18.03; in RG(C) 21.34, (T) 25.88, in S(C) 34.00, (T) 17.68, and in D(C) 17.25, (T) 12.22 mol of glucosyl units·g^–1 (each number represents the difference between the means). It concluded that treatment with T₃ markedly affects this exercise-induced metabolism of glycogen in each muscle type.From our study it is suggested that low muscle glycogen content may contribute to a reduction in exercise performance in hyperthyroidism.     

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.     

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.     

Insulin-induced hyperphagia in alloxan-diabetic rats fed a high-fat diet.

Alloxan-diabetic rats fed a standard, low-fat diet lost body weight and were hyperphagic; those fed a high-fat diet lost comparable amounts of weight, but did not overeat compared to normal animals. When given injections of protamine-zinc insulin, all diabetic rats gained weight; however, while those fed the low-fat reduced food intake from elevated levels, diabetics fed the high-fat diet became hyperphagic. Diabetic rats maintained on a high-fat diet increased food intake during long-term insulin treatment sooner and to a greater extent than normal controls. These findings are interpreted in light of the effects of insulin on storage and supply of metabolic fuels.     

High energy phosphates and related compounds,glycogen levels and histology in the rat tibialis anterior muscle after forced lengthening and isometric exercise

Eccentric exercise may elicit damage to the contractile elements. This primary damage is followed by secondary changes, consisting of histological changes and changes in glycogen and energy metabolism. The mechanism underlying changes in glycogen homeostasis and energy metabolism is not well established. The aim of this study was to investigate the possible relationship between changes in adenine and guanine nucleotides, inosine monophosphate (IMP), creatine phosphate, glycogen content and histology in the rat tibialis anterior (TA) muscle after forced lengthening or isometric exercise. The right muscles were either forcibly lenghtened or isometrically exercised, while the contralateral muscles served as non-exercised controls. The exercised muscles were dissected 0, 6 and 24 h post-exercise and the contents of adenine and guanine nucleotides, IMP, creatine phosphate, and glycogen determined. In addition, histological changes were assessed. Immediately after both types of exercise increases in tissue IMP levels were found. Irrespective of the type of exercise, glycogen content was decreased immediately post-exercise, but restored 6 h postexercise. Twenty-four hours later a second decline in glycogen content was found after both types of exercise. In forcibly lengthened muscles ATP content was decreased 24 h post-exercise. In isometrically exercised muscles ATP was not decreased at any time. Gross structural changes were found in all forcibly lengthened muscles (9–12% of TA muscle volume). In isometrically exercised muscles structural changes were minor (up to 0.1 % of muscle volume), were found only immediately post-exercise and in only 4 out of 18 muscles. It is concluded that forced lengthening results in decreased ATP levels. Changes in glycogen homeostasis were found after both isometric exercise and forced lengthening, demonstrating that these changes are not strictly related to degenerative changes.     

Effects of pre-exercise carbohydrate feedings on muscle glycogen use during exercise in well-trained runners

Summary The purpose of this study was to examine the effects of pre-exercise glucose and fructose feedings on muscle glycogen utilization during exercise in six well-trained runners ( =68.2±3.4 ml·kg^–1·min^–1). On three separate occasions, the runners performed a 30 min treadmill run at 70% . Thirty minutes prior to exercise each runner ingested 75 g of glucose (trial G), 75 g of fructose (trial F) or 150 ml of a sweetened placebo (trial C). During exercise, no differences were observed between any of the trials for oxygen uptake, heart rate or perceived exertion. Serum glucose levels were elevated as a result of the glucose feeding (P<0.05) reaching peak levels at 30 min post-feeding (7.90±0.24 mmol·l^–1). With the onset of exercise, glucose levels dropped to a low of 5.89±0.85 mmol·l^–1 at 15 min of exercise in trial G. Serum glucose levels in trials F and C averaged 6.21±0.31 mmol·l^–1 and 5.95±0.23 mmol·l^–1 respectively, and were not significantly different (P<0.05). There were also no differences in serum glucose levels between any of the trials at 15 and 30 min of exercise. Muscle glycogen utilization in the first 15 min of exercise was similar in trial C (18.8±8.3 mmol·kg^–1), trial F (16.3±3.8 mmol·kg^–1) and trial G (17.0±1.8 mmol·kg^–1), and total glycogen use was also similar in trial C (25.6±7.9 mmol·kg^–1), trial F (35.4±5.7 mmol·kg^–1) and trial G (24.6±3.2 mmol·kg^–1). In contrast to previous research, these results suggest that pre-exercise feedings of fructose or glucose do not affect the rate of muscle glycogen utilization during 30 min of treadmill running in trained runners.     

Effect of endurance and sprint exercise on the sensitivity of glucose metabolism to insulin in the epitrochlearis muscle of sedentary and trained rats

Summary The effects of two types of acute exercise (1 h treadmill running at 20 m· min^–1, or 6 × 10-s periods at 43 m · min^–1, 0° inclination), as well as two training regimes (endurance and sprint) on the sensitivity of epitrochlearis muscle [fast twitch (FT) fibres] to insulin were measured in vitro in rats. The hormone concentration in the incubation medium producing the half maximal stimulation of lactate (la) production and glycogen synthesis was determined and used as an index of the muscle insulin sensitivity. A single period of moderate endurance as well as the sprint-type exercise increased the sensitivity of la production to insulin although the rate of la production enhanced markedly only after sprint exercise at 10 and 100 U· ml^–1 of insulin. These effects persisted for up to 2 h after the termination of exercise. Both types of exercise significantly decreased the muscle glycogen content, causing a moderate enhancement in the insulin-stimulated rates of glycogen synthesis in vitro for up to 2 h after exercise. However, a significant increase in the sensitivity of this process to insulin was found only in the muscle removed 0.25 h after the sprint effort. Training of the sprint and endurance types increased insulin-stimulated rates of glycolysis 24 h after the last period of exercise. The sensitivity of this process to insulin was also increased at this instant. Both types of training increased the basal and maximal rates of glycogen snythesis, as well as the sensitivity of this process to insulin at the 24^th following the last training session. It was concluded that in the epitrochlearis muscle, containing mainly FT fibres, both moderate and intensive exercise (acute and repeated) were effective in increasing sensitivity of glucose utilization to insulin. Thus, the response in this muscle type to increased physical activity differs from that reported previously in the soleus muscle, representing the slow-twitch, oxidative fibres in which sprint exercise did not produce any changes in the muscle insulin sensitivity.     

Effect of infusing branched-chain amino acid during incremental exercise with reduced muscle glycogen content

Summary The aim of this study was to investigate whether, when muscle glycogen is reduced, a pre-exercise infusion of branched-chain amino acids (BCAA) modifies exercise performance or the metabolic and respiratory responses to incremental exercise. Six moderately trained volunteers took part in the following protocol on two occasions. On day 1, at 9 a.m. in the postabsorptive state, they performed a graded incremental exercise (increases of 35 W every 4 min) to exhaustion (Ex-1). A meal of 1,000 kcal (4,200 kJ; 60% protein, 40% fat) was consumed at 12 p.m. No food was then allowed until the end of the experiment (20–21 h later). A 90-min period of exercise at alternating high and moderate intensities, designed to deplete muscle glycogen, was performed between 6 p.m. and 7.30 p.m. The morning after (day 2), the subjects randomly received either a mixed solution of BCAA (260 mg × kg^–1 × h^–1 for 70 min), or saline. They then repeated the graded incremental exercise to exhaustion (Ex-2). Metabolic and respiratory measurements suggested a muscle glycogen-depleted state had been achieved. No significant differences were observed in total work performed, maximal oxygen uptake or plasma ammonia, alanine, and blood pyruvate concentrations in the two treatments. After BCAA infusion, higher blood lactate concentrations were observed at maximal power output in comparison with those during saline [BCAA 4.97 (SEM 0.41) mmol × l^–1, Saline 3.88 (SEM 0.47) mmol × l^–1,P < 0.05]. In summary, in conditions of reduced muscle glycogen content, after a short period of fasting, BCAA infusion had no significant effect on the total work that could be performed during a graded incremental exercise.     

Effect of different types of high carbohydrate diets on glycogen metabolism in liver and skeletal muscle of endurance-trained rats

Male Wistar rats were fed ad libitum four different diets containing fructose, sucrose, maltodextrins or starch as the source of carbohydrate (CH). One group was subjected to moderate physical training on a motor-driven treadmill for 10 weeks (trained rats). A second group received no training and acted as a control (sedentary rats). Glycogen metabolism was studied in the liver and skeletal muscle of these animals. In the sedentary rats, liver glycogen concentrations increased by 60%–90% with the administration of simple CH diets compared with complex CH diets, whereas skeletal muscle glycogen stores were not significantly affected by the diet. Physical training induced a marked decrease in the glycogen content in liver (20%–30% of the sedentary rats) and skeletal muscle (50%–80% of the sedentary rats) in animals fed simple (but not complex) CH diets. In liver this was accompanied by a two-fold increase of triacylglycerol concentrations. Compared with simple CH diets, complex CH feeding increased by 50%–150% glycogen synthase (GS) activity in liver, whereas only a slight increase in GS activity was observed in skeletal muscle. In all the animal groups, a direct relationship existed between tissue glucose 6-phosphate concentration and glycogen content (r = 0.9911 in liver, r = 0.7177 in skeletal muscle). In contrast, no relationship was evident between glycogen concentrations and either glycogen phosphorylase activity or adenosine 5-monophosphate tissue concentration. The results from this study thus suggest that for trained rats diets containing complex CH (compared with diets containing simple CH) improve the glycogenic capacity of liver and skeletal muscle, thus enabling the adequate regeneration of glycogen stores in these two tissues.     

Effect of diet on human muscle weakness following prolonged exercise

Summary The effect of altering muscle glycogen on the ability of skeletal muscle to generate voluntary and electrically evoked isometric force following prolonged exercise has been investigated in five healthy male subjects. Measurements from the triceps surae were made at rest, and before and after prolonged exercise (uphill walking) at approximately 75% in low muscle glycogen (low CHO) and high muscle glycogen (high CHO) conditions.The results showed that before exercise there was no change in maximal twitch tension ( ), maximal tetanic tension at frequencies of 10 (P_o10), 20 (P_o20) and 50 Hz (P_o50), and maximal voluntary contraction (MVC) in low and high CHO compared with normal. The loss of force during a 2 min electrically evoked fatigue test at rest was found to be higher (p<0.05) in low CHO and lower (p<0.05) in high CHO than normal.Following the prolonged exercise, muscle weakness was produced in both low and high CHO conditions, but was found to be significantly greater in the low CHO condition for the measurements of P_o10 (p<0.01), P_o20 (p<0.05) and MVC (p<0.05).It is concluded that changes in muscle glycogen alone do not alter the isometric force generating capacity of human muscle, but when combined with prolonged exercise low muscle glycogen enhances exercise-induced muscle weakness.     

Effect of various types of acute exercise and exercise training on the insulin sensitivity of rat soleus muscle measured in vitro

Effects of acute exercise varying in duration and intensity, as well as of two training regimes (endurance and sprint training) on the sensitivity of the soleus muscle of rat to insulin was measured in vitro and compared in rats. As an index of the muscle insulin sensitivity the hormone concentration in the incubation medium which would produce half maximum stimulation of lactate production (LA) and glycogen synthesis was determined. A single bout of moderate endurance exercise (60 min treadmill running at 20 m×min^–1, 0° inclination) increased the rate of LA production at the hormone concentrations used and increased the sensitivity of the process to insulin at 0.25 and 2 h but not 24 h after termination of exercise. Similar though less pronounced effects were found after heavy endurance exercise (30 min at 25 m×min^–1, 10°), but sprint exercise (6×10 s bouts at 43 m×min^–1, 0°) had no influence on the insulin sensitivity of the soleus muscle. The rate of glycogen synthesis in vitro was accelerated after endurance exercise, but the sensitivity of this process to insulin was unaffected by the preceding exercise. Endurance training for 5 weeks caused marked enhancement of sensitivity of both LA production and glycogen synthesis to insulin, which persisted for at least 48 h after the last training session. No changes in the soleus muscle sensitivity to insulin were found after sprint training. It is concluded that the increased insulin sensitivity of glucose utilization by skeletal muscle which occurs after endurance exercise and particularly during endurance training can substantially contribute to improved carbohydrate tolerance. Sprint exercise does not produce any changes in muscle insulin sensitivity, at least in the soleus muscle of the rat.Dedicated to the late Professor Stanislaw Kozlowski     

Effect of low glycogen on glycogen synthase in human muscle during and after exercise

Subjects cycled at a work load calculated to elicit 75% of maximal oxygen uptake on two occasions: the first to fatigue (34.5 ± 5.3 min; mean ± SE), and the second at the same workload and for the same duration as the first. Biopsies were obtained from the quadriceps femoris muscle before and immediately after exercise, and 5 min post-exercise. Before the first experiment, muscle glycogen was lowered by a combination of exercise and diet, and before the second, experiment muscle glycogen was elevated. In the low glycogen condition (LG), muscle glycogen decreased from 169 ± 15 mmol glucosyl units kg^-1dry wt at to rest to 13 ± 6 after exercise. In the high glycogen condition (HG) glycogen decreased from 706 ± 52 at rest to 405 ± 68 after exercise. Glycogen synthase fractional activity (GSF) was always higher during the LG treatment. During exercise in the HG condition, those subjects who cycled for < 35 min (n= 3) had GSF values in muscle which were lower than at rest, whereas those subjects who cycled for > 35 min (n= 4) had values which were similar to or higher than at rest. Thus the change in GSF in muscle during HG was positively related to the exercise duration (r= 0.94; y = 254–17x + 0.3x²; P < 0.001) and negatively related to the glycogen content at the end of exercise (r=–0.82; y= 516–2x + 0.001x²; P < 0.05). During LG exercise GSF remained constant. GSF increased markedly after 5 min post-exercise in both HG and LG conditions. cAMP dependent protein kinase activity increased similarly during both LG and HG exercise and reverted to the preexercise values 5 min post-exercise. It is concluded that muscle contraction decreases GSF, but low glycogen levels can attenuate or abolish the decrease in GSF. The rapid increase of GSF during recovery from exercise does not require glycogen depletion during the exercise.     

Effect of hyperglycaemia on muscle glycogen mobilization during muscle contractions in the rat

Summary In the rat, muscle glycogen is mobilized during the first stage of exercise, despite normoglycaemia. The aim of the present study was to examine if this process could be prevented or reduced by hyperglycaemia. Three experiments were carried out: in the first, rats were forced to run on a treadmill; in the second the gastrocnemius muscle group was made to contract by stimulation of the sciatic nerve and in the third adrenaline was administered subcutaneously. Each group was divided into two subgroups: control and enriched with glucose (hyperglycaemic). It was shown that hyperglycaemia has no effect on running-induced glycogen mobilization in hind-limb muscles of different fibre composition but prevented it totally in diaphragm muscle. Hyperglycaemia also did not affect the glycogen mobilization induced by stimulation of the sciatic nerve. However, it delayed and reduced markedly the glycogenolytic effect of adrenaline. It is concluded that increased glycogenolysis in muscles at the beginning of exercise may be a consequence of a delay in the activation of glucose transporting mechanisms in muscle cells.     

Effect of diet on muscle glycogen and blood glucose utilization during a short-term exercise in man

7 subjects were studied at rest and during a 6 min submaximal exercise (65% of Vo₂, max) on two occasions, the first preceded by a fat rich diet and the second by a carbohydrate rich diet. Oxygen uptake and respiratory exchange ratio (R) were measured at rest and heart rate both at rest and during exercise. Arterial-femoral venous differences for oxygen, glucose, lactate and β-hydroxybutyrate and arterial concentrations of free fatty acids were measured at rest and during exercise. Changes in muscle glycogen (in 6 subjects) and lactate concentration were determined by biopsies from m. quadriceps femoris taken before and immediately after exercise. Muscle glycogen decreased less during exercise after the fat than after the carbohydrate diet in 5 of the 6 subjects, whereas blood glucose extraction by the exercising legs did not change with diet. Muscle lactate accumulation and release were smaller after the fat diet. In conclusion, the muscle glycogen utilization during a short-term exercise appeared to be lower after the fat than after the carbohydrate diet, but not the concomitant blood glucose extraction. These differences between diets were similar to those observed after a more prolonged work at the same load.     

Effect of exercise on metabolism of glycogen and triglycerides in the respiratory muscles

It was shown that during muscular exertion the diaphragm muscle and the intercostal muscles utilize endogenous glycogen whereas only the diaphragm muscle utilizes endogenous triglycerides. The post-excercise glycogen repletion in the diaphragm muscle was much faster than in the intercostal muscles. In the diaphragm muscle, marked overshoot of the glycogen level occurred early after the exercise.The work was supported by Polish Academy of Sciences within the project 10.4.2.01.3.2.