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.     

Regulation of glycogen metabolism in rat respiratory muscles during exercise

Summary The effect of prolonged exercise on the glycogen level in the respiratory muscles (diaphragm — D, external intercostal — IE and internal — II) has been studied in four groups of rats: 1-control, 2-fasted for 24 h, 3-treated with nicotinic acid and 4-treated with propranolol. There was a sharp reduction in glycogen level in each muscle after 30 min exercise in the control and fasted groups. Exercise till exhaustion further lowered the glycogen level in D in the control group and in IE and II in the fasted group. In the fasted group, the level of glycogen in each muscle, at rest, and after 30 min exercise, and in IE and II muscles after exercise till exhaustion was lower than in the control group. Nicotinic acid did not affect the glycogen level either at rest or during exercise as compared with the control group. Propranolol increased the glycogen level in the muscles at rest and during 30 min exercise. It partially prevented glycogen mobilization in D and IE and fully in II during exercise till exhaustion. In the control group, 24 and 48 h after exercise till exhaustion, the level of glycogen in each muscle exceeded the resting control value.It is concluded that exercise-induced glycogen metabolism in the respiratory muscles differs in some respects from that in the limb or heart muscles.     

The effect of increased respiratory resistance on glycogen and triglyceride levels in the respiratory muscles of the rat

Summary The effect of increased respiratory resistance (stenosis of the trachea) on glycogen and triglyceride levels in the diaphragm (D) and intercostal (external-IE, internal-II) muscles was studied in the rat. Tracheal stenosis resulted in a reduction of glycogen level in the muscles. For the fed rats the reductions were: D-45 and 79%, IE-14 and 30%, II-14 and 35%, 0.5 and 3 h after stenosis, respectively. For rats fasted for 24 h the reductions were: D-64 and 86%, IE-33 and 71%, II-40 and 82%, after 0.5 and 3 h respectively. The level of triglycerides in the muscles was stable during stenosis in the fed group, whereas in the fasted group it were reduced in the diaphragm by 50% after 0.5 h, and by 52% after 3 h. It is concluded that both endogenous and blood-born energy fuels are utilized by the respiratory muscles during increased resistance breathing. The work was supported by Polish Academy of Sciences (10.4.)     

Effect of substrate supply and beta-adrenergic blockade on heart glycogen and triglyceride utilization during exercise in the rat

Summary Exercise-induced heart glycogen and triglyceride mobilization was studied in control rats, in rats with reduced blood glucose supply (fasted rats), in rats with reduced plasma free fatty acids (FFA) supply (nicotinic acid-treated rats), and in rats with blockade of beta-adrenergic receptors (propranolol-treated rats). It was found in the fed control rats that both the heart glycogen and triglyceride levels were reduced at the beginning of the exercise and thereafter they returned to the control level despite the exercise being continued. The triglyceride level was reduced again during the exhaustive exercise. Reduced blood glucose supply increased the heart glycogen and triglyceride utilization during exercise. Partial prevention of the plasma FFA elevation during exercise increased the heart glycogen utilization and had no effect on utilization of the heart triglycerides. Blockade of the beta-adrenergic receptors fully prevented both the heart glycogen and triglyceride mobilization during exercise.This work was supported by the Polish Academy of Sciences, project No. 10.4.2.01.3.2.     

Effect of prolonged exercise on the level of triglycerides in the rat liver

Summary This study examined the effect of prolonged exercise on the level of triglycerides (TG) in rat liver. The rats were divided into groups: 1-control, 2-treated with nicotinic acid, 3-fed with glucose during exercise, 4-fasted, 5-adrenalectomized, 6-adrenalectomized and fed with oil. In the control group, there was gradual accumulation of TG in the liver and their level was doubled at exhaustion as compared to the resting value. Nicotinic acid lowered the resting level of TG and prevented their accumulation during exercise. Administration of glucose during exercise partially prevented the increase in TG level in the liver. In rats fasted for 24 h before exercise, the net increase in liver TG level during exercise was similar to that in the controls. Adrenalectomy, like nicotinic acid, lowered TG level at rest and prevented its increase during exercise. Feeding the adrenalectomized rats with oil elevated the plasma free fatty acid level but did not result in accumulation of TG in the liver, either at rest or during exercise. It is concluded that prolonged exercise results in accumulation of TG in the liver and that the process depends on the supply of free fatty acids and glucose and requires the presence of glucocorticoids.This work was supported by the Polish Central Programme for Basic Research 06-02.     

Modulation of glycogen metabolism of rat skeletal muscles by endurance training and testosterone treatment

The effects of training and/or testosterone treatment on glycogen content and the activities of glycogen synthase, glycogen phosphorylase, and fructose-6-phosphate kinase were studied in extensor digitorum longus (EDL) and soleus muscles of intact adult female rats. One group of rats remained sedentary, whereas another group was trained for 7 weeks. Thereafter, both the sedentary and trained rats were subdivided into two control and four testosterone-treated subgroups. Testosterone was administered by a silastic implant. Training was continued for 2 weeks. On the final day of the experiment rats from one trained control and one trained testosterone-treated subgroup ran for 60 min submaximally. Upon testosterone treatment of sedentary rats the glycogen concentration was not changed. However, in the soleus, but not in the EDL, the glycogen content was increased by training (P<0.05) which could, at least partly, be explained by a decrease in activity of active glycogen phosphorylase (P < 0.05). In the EDL of trained rats testosterone treatment increased glycogen content significantly by both an increase in activity of active glycogen synthase and a decrease in activity of active glycogen phosphorylase (P<0.05). In the EDL and soleus of testosterone-treated animals from the exercised subgroup a significant sparing of glycogen was observed, which could be explained by an increase in activity of active glycogen synthase and, in the soleus, could also be explained by a concerted decrease in active glycogen phosphorylase (P<0.05). In the two muscles studied, we also found that testosterone treatment in trained animals shifted the fibre type distribution towards more oxidative fibres in both types of muscle in comparison with the control animals. We conclude that testosterone, at a pharmacological dose, potentiates the training-induced increase in glycogen content of skeletal muscle and induces a glycogen-sparing effect after submaximal exercise.An Established Investigator of the Netherlands Heart Foundation     

Variable resistance versus constant resistance strength training in adult males

Summary Intramuscular triglycerides mobilization during prolonged physical exercise was examined in rats fed ad libitum, in rats fasted for 24 h and in rats treated with nicotinic acid. It has been found that during exercise the intramuscular triglyceride level was markedly reduced only in the red muscle but not in the white and intermediate muscles. Fasting significantly augmented the utilization of triglycerides in the red muscle during exercise. The post-exercise triglyceride level in the red muscle of the rats treated with nicotinic acid was similar to that in the control group whereas blood FFA level, in the nicotinic acid-treated group was much lower than in the control group. Nicotinic acid increased glycogen utilization in the liver and in the skeletal muscles during exercise.It may be concluded that the major cause of the reduction of the triglyceride level in the red muscle during exercise is a developing shortage of available carbohydrates. The greatly elevated blood FFA level during exercise does not seem to have a sparing effect on the intramuscular triglyceride level during exercise. However, it does spare glycogen content in the liver and the skeletal muscles.This work was supported by the Polish Academy of Sciences. project 10.4.2.01.3.2     

Carbohydrate feeding and glycogen synthesis during exercise in man

In 7 male cyclists glycogen synthesis during exercise and rest was studied. Each subject did two exercise trials (A and B), in random order. In both trials, after determining the maximal workload (W _max), intermittent exercise was given to exhaustion. After the exhaustive exercise and taking a muscle biopsy the subjects either exercised at 40%W _max for 3 h (trial A) or rested for 3 h (trial B), during which they consumed approximately 21 of a 25% malto-dextrine drink in both trials. After 3 h rest (trial A) or 3 h of mild exercise (trial B) a second muscle biopsy was taken for total glycogen and histochemistry (ATPase and PAS). Blood glucose and insulin levels were elevated during the first 2 h of exercise (p<0.05). Glycogen depletion was most pronounced in type I and to a less extent in type IIA fibers. In trial A muscle glycogen increased from 136±66 to 199±71 mmol/kg DW, and in trial B from 145±56 to 257±79 mmol/kg DW. During exercise glycogen repletion was restricted to type IIA and IIB fibers, whereas during rest glycogen synthesis occurred both in type I and type II fibers. The present study demonstrates that oral carbohydrate administered during exercise may not only provide substrate for energy metabolism, but can also be utilized for glycogen synthesis in the non-active muscle fibers.     

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.     

The post-exercise recovery of triglycerides in rat tissues

Summary Triglycerides (TG) recovery after exhaustive muscular exertion was investigated in tissues of fed rats and rats fasted for 24 h before exercise. In both groups the exercise caused reduction of TG level in the fast-twitch-oxidative-glycolytic (FOG) muscle, in heart muscle, and in plasma and accumulation of TG in liver.In the fed group the level of TG in FOG muscle, in liver, and in plasma normalized after 1 h of recovery, but only after 3 h in heart muscle. Treatment with glucose somewhat slowed down this process in FOG muscle. In the fasted group, the level of TG in each tissue returned to the pre-exercise value after 3 h of recovery.The work was supported by Polish Academy of Sciences, project 10.4.2.01.3.2.     

The influence of free fatty acids on glycogen recovery in rat heart after exercise

Summary Glycogen supercompensation is the term used to denote the abnormally high levels of glycogen found in the heart shortly after an exercise-induced reduction of the substrate. Using rats, we tested whether this condition was linked to the use of plasma free fatty acids (FFA), which normally rise with exercise. Before a 1-h swim, animals received an injection of either saline (S) or nicotinic acid (NA). The nicotinic acid treatment dramatically suppressed the rise in plasma FFA observed in the S-group. Exercise caused a significant but similar reduction (35–38%) of the myocardial glycogen content in both groups. After 1 h of recovery in the S-group, myocardial glycogen reached a value of 30.3±1.7 Μmol·g⁻¹ or 113% of that measured before the exercise began. In contrast, the value for hearts from the NA-group with reduced FFA levels was 24.0±1.9 Μmol·g⁻¹ or only 91% of that measured before exercise. After 2 h the values were 33.8±1.4 and 29.0±1.9 Μmol·g⁻¹ respectively. These data indicate that glycogen repletion in rat heart after exercise is related to the amount of FFA present in the plasma. We suggest that carbohydrate metabolism is diverted towards synthesis and storage as a result of the glycolytic inhibition exerted by the increased use of fat as an energy source as previously observed in hearts from fasted or diabetic animals. This work was supported by a grant from the Utah Heart Association and the Deseret Gym Corporation     

Inspiratory muscles do not limit maximal incremental exercise performance in healthy subjects

We investigated whether the inspiratory muscles affect maximal incremental exercise performance using a placebo-controlled, crossover design. Six cyclists each performed six incremental exercise tests. For three trials, subjects exercised with proportional assist ventilation (PAV). For the remaining three trials, subjects underwent sham respiratory muscle unloading (placebo). Inspiratory muscle pressure (P(mus)) was reduced with PAV (-35.9+/-2.3% versus placebo; P<0.05). Furthermore, V(O2) and perceptions of dyspnea and limb discomfort at submaximal exercise intensities were significantly reduced with PAV. Peak power output, however, was not different between placebo and PAV (324+/-4W versus 326+/-4W; P>0.05). Diaphragm fatigue (bilateral phrenic nerve stimulation) did not occur in placebo. In conclusion, substantially unloading the inspiratory muscles did not affect maximal incremental exercise performance. Therefore, our data do not support a role for either inspiratory muscle work or fatigue per se in the limitation of maximal incremental exercise.     

Respiratory and leg muscles perceived exertion during exercise at altitude

We compared the rate of perceived exertion for respiratory (RPE,resp) and leg (RPE,legs) muscles, using a 10-point Borg scale, to their specific power outputs in 10 healthy male subjects during incremental cycle exercise at sea level (SL) and high altitude (HA, 4559 m). Respiratory power output was calculated from breath-by-breath esophageal pressure and chest wall volume changes. At HA ventilation was increased at any leg power output by ～ 54%. However, for any given ventilation, breathing pattern was unchanged in terms of tidal volume, respiratory rate and operational volumes of the different chest wall compartments. RPE,resp scaled uniquely with total respiratory power output, irrespectively of SL or HA, while RPE,legs for any leg power output was exacerbated at HA. With increasing respective power outputs, the rate of change of RPE,resp exponentially decreased, while that of RPE,legs increased. We conclude that RPE,resp uniquely relates to respiratory power output, while RPE,legs varies depending on muscle metabolic conditions.     

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 voluntary respiratory efforts on breath-holding time

INTRODUCTION: Near the end of a maximal voluntary breath-hold, re-inhalation of the expired gas allows an additional period of breath-holding, indicating that the breaking point does not depend solely on chemical drive. We hypothesized that afferents from respiratory muscle and/or chest wall are significant in breath-holding. METHODS: Nineteen normal adults breathed room air through a mouthpiece connected to a pneumotachograph and were instructed to breath-hold with and without voluntary regular respiratory efforts against an occluded airway. RESULTS: Fifty one trials with and 53 without respiratory efforts were analyzed. The mean number of efforts per minute was 19+/-2.3 and the mean lowest airway pressure (P(aw)) -16.6+/-5.4 cmH(2)O. Breath-holding time (BHT) did not differ without (33.0+/-18.2 s) and with (29.3+/-12.3 s) efforts. In five patients arterial blood gasses were measured before and at the end of breath-holding and they did not differ between trials without and with efforts, indicating similar chemical drive. Our results suggest that afferents from respiratory muscle and/or chest wall are not the major determinants of BHT.     

Collagen metabolism of mouse skeletal muscle during the repair of exercise injuries

The activities of prolyl 4-hydroxylase and -glucuronidase, the concentration of hydroxyproline as well as reticulin and collagen type III, IV and V stainings were followed in skeletal muscle during a 20-day period after a 9-h treadmill running in untrained and trained male mice, aged 4–6 months. The prolonged 9-h running of untrained mice temporarily increased prolyl 4-hydroxylase activity 2, 5 and 10 days after exercise, more prominently in the red than in the white part of quadriceps femoris-muscle, and in analogical manner as -glucuronidase activity in tibialis anterior-muscle. Twenty days after exercise these enzymatic activities were back to the control level. The hydroxyproline content of red muscle was increased for 10 and that of white muscle for 20 days after the exertion. Training for 45 days did not affect hydroxyproline content and prolyl 4-hydroxylase activity was at the control level after the training. A 9-h exercise increased prolyl 4-hydroxylase activity much less in trained muscle than in the untrained muscle and did not affect muscle collagen content.Histological observations showed fiber necrosis 2 days and signs of fiber regeneration 5 days after the exertion in untrained mice. Twenty days afterwards the regeneration was nearly completed. Reticulin staining was increased in injured muscle areas 10–20 days after the exertion. In immunohistochemical staining, antibodies to all studied collagen types (type III, IV and V) showed increased staining 5–20 days after the exertion in the areas of muscle injuries and regeneration. It is concluded that collagen metabolism is stimulated during the regeneration of muscle fibers and that preceeding endurance training is able to alleviate exrcise induced injuries.     

Effect of airway inflammation on short-latency reflex inhibition to inspiratory loading in human scalene muscles

The short-latency reflex inhibition of human inspiratory muscles produced by loading is prolonged in asthma and obstructive sleep apnoea, both diseases involving airway and systemic inflammation. Both diseases also involve repetitive inspiratory loading. Although airway mucosal afferents are not critical components of the normal reflex arc, during airway inflammation, prolongation of the reflex may be caused by altered mucosal afferent sensitivity, or altered central processing of their inputs. We hypothesised that acute viral airway inflammation would replicate the reflex abnormality. The reflex was tested in 9 subjects with a "common cold" during both the acute infection and when well. Surface electrodes recorded electromyographic (EMG) activity bilaterally from scalene muscles. Latencies of the inhibitory response (IR) did not differ significantly (IR peak 67 vs 70 ms (p=0.12), and IR offset 87 vs 90 ms (p=0.23), between the inflamed and well conditions, respectively). There was no difference in any measure of the size of the reflex inhibition.     

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     

Fat and carbohydrate metabolism during low intensity exercise: Effects of the availability of muscle glycogen

Summary Four subjects were studied during exercise at 50% of maximum oxygen uptake after a normal diet, after a low carbohydrate (CHO) diet following exercise-induced glycogen depletion, and after a high CHO diet. This regime has previously been shown to cause changes in the amount of glycogen stored in the exercising muscles. Metabolic and respiratory parameters were measured during the exercise. The respiratory exchange ratio, blood lactate, blood pyruvate, blood glucose and plasma triglycerides were lower than normal following the low CHO diet and higher than normal following the high CHO diet. Plasma free fatty acids and plasma glycerol were higher than normal after the low CHO diet and lower than normal after the high CHO diet. The contribution of CHO to metabolism was less than normal after the low CHO diet and greater than normal after the high CHO diet. The altered availability of FFA does not appear to be a result of the variations in the blood lactate content. R. J. M. is in receipt of a Science Research Council Postgraduate Studentship award     

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.