Muscle Glycogen Supercompensation Research Articles

Enhanced skeletal muscle glycogen repletion after endurance exercise is associated with higher plasma insulin and skeletal muscle hexokinase 2 protein levels in mice: comparison of level running and downhill running model.

To identify factors that influence post-exercise muscle glycogen repletion, we compared the glycogen recovery after level running with downhill running, an experimental model of impaired post-exercise glycogen recovery. Male Institute of Cancer Research (ICR) mice performed endurance level running (no inclination) or downhill running (-5° inclination) on a treadmill. In Experiment 1, to determine whether these two types of exercise resulted in different post-exercise glycogen repletion patterns, tissues were harvested immediately post-exercise or 2 days post-exercise. Compared to the control (sedentary) group, level running induced significant glycogen supercompensation in the soleus muscle at 2 days post-exercise (p = 0.002). Downhill running did not induce glycogen supercompensation. In Experiment 2, mice were orally administered glucose 1 day post-exercise; this induced glycogen supercompensation in soleus and plantaris muscle only in the level running group (soleus: p = 0.005, plantaris: p = 0.003). There were significant positive main effects of level running compared to downhill running on the plasma insulin (p = 0.017) and C-peptide concentration (p = 0.011). There was no difference in the glucose transporter 4 level or the phosphorylated states of proteins related to insulin signaling and metabolism in skeletal muscle. The level running group showed significantly higher hexokinase 2 (HK2) protein content in both soleus (p = 0.046) and plantaris muscles (p =0.044) at 1 day after exercise compared to the downhill running group. Our findings suggest that post-exercise skeletal muscle glycogen repletion might be partly influenced by plasma insulin and skeletal muscle HK2 protein levels.

Carbohydrate Consumption and Periodization Strategies Applied to Elite Soccer Players.

During a soccer season, athletes tend to play intense and light matches such as decisive and qualifying games. The amount of muscle glycogen stores is a determining factor of performance during exercise, and manipulation of carbohydrate intake during the soccer season to enhance muscle glycogen stores can improve the performance of elite soccer players. The purpose of this review is to provide a holistic view of the periodization of carbohydrates and their effects on sports performance, based on what the literature recommends for the periodization of carbohydrates for endurance athletes, and of muscle glycogen recovery and compensation among professional soccer players. The ingestion of large amounts of carbohydrates (CHO;10g/kg of body weight (BW)/day) is important 36h before a match for the elite soccer player to ensure muscle glycogen supercompensation. In addition, elite soccer players should intake 1 to 1.5g/kg BW/h within the first 4h after a soccer game to maximize glycogen resynthesis. However, the season is comprised of away and home games that require different intensities; thus, soccer players need to periodize CHO intake based on evidence-based recommendations such as "train low," "train low, compete high," and/or "sleep low." The goal is to induce training adaptations by alternating with high or low CHO availability based on seasons, matches, and training intensities. The strategy can result in improved performance during games. Periodizing the consumption of carbohydrates, based on the intensity of training and matches, should include more carbohydrates when the matches require higher intensity and fewer carbohydrates when they require lower intensity; this is a strategy that will improve the performance of elite soccer athletes.

Repeated muscle glycogen supercompensation with four days’ recovery between exhaustive exercise

ObjectivesTo determine if a 4 d period of high carbohydrate intake can supercompensate muscle glycogen and exercise work capacity on back-to-back occasions. DesignSeven trained cyclists (6 male, VO2peak: 57 ± 4 mL kg−1 min−1) completed a 9-d experimental period, consisting of three intermittent exhaustive cycling trials on days 1 (trial 1), 5 (trial 2) and 9 (trial 3). Following trial 1 cyclists were fed a high carbohydrate diet (˜10 g kg−1 day−1) for eight days to assess their capacity to repeatedly supercompensate muscle glycogen with 4 d recovery. MethodsA resting muscle biopsy was obtained prior to each trial consisting of 2 min work intervals (90–60% peak power output) interspersed with 2 min recovery (40% peak power output) repeated until exhaustion. Each 72-h period between trial days included two days of low volume cycling and a rest day. Resting muscle glycogen and total work completed was determined for each trial day. ResultsBaseline muscle glycogen on day 1 (583.6 ± 111.0 mmol kg−1 dry mass) was supercompensated on day 5 (835.1 ± 112.8 mmol kg−1 dry mass; p = 0.04, d = 2.25) and again on day 9 (848.3 ± 111.4 mmol kg−1 dry mass; p = 0.01, d = 2.38). Total cycling work capacity increased from trial 1 to trial 2 (+8.7 ± 5.4 kJ kg−1; p = 0.01; d = 1.41); a large effect was observed in trial 3 compared to trial 1 (+6.4 ± 6.8 kJ kg−1; p = 0.10; d = 1.10). ConclusionsA 4 d high carbohydrate feeding strategy is sufficient to repeatedly supercompensate muscle glycogen content following exhaustive exercise and results in enhanced work capacity.

Exercise-induced molecular mechanisms promoting glycogen supercompensation in human skeletal muscle

ObjectiveA single bout of exercise followed by intake of carbohydrates leads to glycogen supercompensation in prior exercised muscle. Our objective was to illuminate molecular mechanisms underlying this phenomenon in skeletal muscle of man. MethodsWe studied the temporal regulation of glycogen supercompensation in human skeletal muscle during a 5 day recovery period following a single bout of exercise. Nine healthy men depleted (day 1), normalized (day 2) and supercompensated (day 5) muscle glycogen in one leg while the contralateral leg served as a resting control. Euglycemic hyperinsulinemic clamps in combination with leg balance technique allowed for investigating insulin-stimulated leg glucose uptake under these 3 experimental conditions. Cellular signaling in muscle biopsies was investigated by global proteomic analyses and immunoblotting. We strengthened the validity of proposed molecular effectors by follow-up studies in muscle of transgenic mice. ResultsSustained activation of glycogen synthase (GS) and AMPK in combination with elevated expression of proteins determining glucose uptake capacity were evident in the prior exercised muscle. We hypothesize that these alterations offset the otherwise tight feedback inhibition of glycogen synthesis and glucose uptake by glycogen. In line with key roles of AMPK and GS seen in the human experiments we observed abrogated ability for glycogen supercompensation in muscle with inducible AMPK deletion and in muscle carrying a G6P-insensitive form of GS in muscle. ConclusionOur study demonstrates that both AMPK and GS are key regulators of glycogen supercompensation following a single bout of glycogen-depleting exercise in skeletal muscle of both man and mouse.

Hyper-hippocampal glycogen induced by glycogen loading with exhaustive exercise

Glycogen loading (GL), a well-known type of sports conditioning, in combination with exercise and a high carbohydrate diet (HCD) for 1 week enhances individual endurance capacity through muscle glycogen supercompensation. This exercise-diet combination is necessary for successful GL. Glycogen in the brain contributes to hippocampus-related memory functions and endurance capacity. Although the effect of HCD on the brain remains unknown, brain supercompensation occurs following exhaustive exercise (EE), a component of GL. We thus employed a rat model of GL and examined whether GL increases glycogen levels in the brain as well as in muscle, and found that GL increased glycogen levels in the hippocampus and hypothalamus, as well as in muscle. We further explored the essential components of GL (exercise and/or diet conditions) to establish a minimal model of GL focusing on the brain. Exercise, rather than a HCD, was found to be crucial for GL-induced hyper-glycogen in muscle, the hippocampus and the hypothalamus. Moreover, EE was essential for hyper-glycogen only in the hippocampus even without HCD. Here we propose the EE component of GL without HCD as a condition that enhances brain glycogen stores especially in the hippocampus, implicating a physiological strategy to enhance hippocampal functions.

Fermented Grain Beverage Supplementation Following Exercise Promotes Glycogen Supercompensation in Rodent Skeletal Muscle and Liver

The purpose of this study was to investigate the effects of post-endurance exercise fermented grain beverage (FGB) supplementation on glycogen reaccumulation in rat skeletal muscle and liver. Twelve-hour fasted male Wistar rats, 10-week-old, performed five 30-min bouts of swimming separated by 5-min rest periods in order to deplete tissue glycogen storage. The rats were orally administrated either water, glucose, or FGB in 30, 60, 90, and 120 min after the exercise. Immediately and/or 240 min after the exercise, soleus and gastrocnemius muscles and liver were removed and analyzed. A large glycogen reaccumulation was observed in skeletal muscles and liver at 240 min after the exercise when either glucose or FGB were ingested. This response tended to be greater in FGB-treated than in glucose-treated animals, particularly in liver and gastrocnemius muscle. These results suggest that post-endurance exercise FGB supplementation enhances glycogen restoration in both skeletal muscle and liver.

Postexercise muscle glycogen resynthesis in humans.

Since the pioneering studies conducted in the 1960s in which glycogen status was investigated using the muscle biopsy technique, sports scientists have developed a sophisticated appreciation of the role of glycogen in cellular adaptation and exercise performance, as well as sites of storage of this important metabolic fuel. While sports nutrition guidelines have evolved during the past decade to incorporate sport-specific and periodized manipulation of carbohydrate (CHO) availability, athletes attempt to maximize muscle glycogen synthesis between important workouts or competitive events so that fuel stores closely match the demands of the prescribed exercise. Therefore, it is important to understand the factors that enhance or impair this biphasic process. In the early postexercise period (0-4 h), glycogen depletion provides a strong drive for its own resynthesis, with the provision of CHO (~1 g/kg body mass) optimizing this process. During the later phase of recovery (4-24 h), CHO intake should meet the anticipated fuel needs of the training/competition, with the type, form, and pattern of intake being less important than total intake. Dietary strategies that can enhance glycogen synthesis from suboptimal amounts of CHO or energy intake are of practical interest to many athletes; in this scenario, the coingestion of protein with CHO can assist glycogen storage. Future research should identify other factors that enhance the rate of synthesis of glycogen storage in a limited time frame, improve glycogen storage from a limited CHO intake, or increase muscle glycogen supercompensation.

London 2012: The biomedical basis of elite performance

London 2012: The biomedical basis of elite performance

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 3h. The exercised rats were then refed for 4, 8, 12, or 16h. 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 4h of refeeding, and glycogen levels had peaked at the end of 8h 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 4h 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.

Insulin-assisted Glycogen Supercompensation Abolished The Exercise-induced Increase In Glut4 Protein

PURPOSE: The purpose of the study was to investigate the interactive effect of exogenous insulin on post-exercise glycogen supercompensation in skeletal muscle. METHODS: Forty eight rats were weight-matched and divided into following 6 groups: control (C), insulin treated (INS), immediately after exercise with previous glycogen supercompensation by exercise (EX0), immediately after exercise with previous glycogen supercompensation by exercise and insulin injection (EX0+INS), exercise followed a 16-hr recovery (EX16), and exercise followed a 16-hr recovery with insulin injection (EX16+INS). RESULTS: Glucose intubation with insulin treatment (INS groups) significantly elevated glycogen storage in various skeletal muscles. Insulin treatment further elevated exercise-induced glycogen supercompensation level (EX16+INS). We also found that residual glycogen content in EX0+INS group was significantly greater than EX0 group after exercise. In addition, we also observed that exercise-increased GLUT4 protein expression was attenuated by insulin-assisted glycogen supercompensated muscle during recovery. CONCLUSIONS: We demonstrated that our glycogen supercompensation protocol by exogenous insulin treatment further elevated glycogen supercompensation in exercised rats. This result has ensured a greater residual muscle glycogen when they performed the same exercise protocol. Furthermore, the amount of intramuscular glycogen storage appears to be a feedback signal that regulates GLUT4 protein expression in skeletal muscle.

An acute bout of high-intensity intermittent swimming induces glycogen supercompensation in rat skeletal muscle

High-intensity intermittent exercise substantially increases muscle glucose transport, which is thought to be the rate-limiting step for glycogen synthesis. In the present study, we compared muscle glycogen supercompensation after high-intensity intermittent exercise with that observed after low-intensity continuous exercise in rats. Four- to five-week-old male Sprague-Dawley rats performed either low-intensity swimming (240 min of swimming exercise with a weight equivalent to 1% of their body mass; LOW) or high-intensity swimming (twenty 30-s swimming bouts with 30 s rest between bouts with a weight equivalent to 16% of their body mass; HIGH) to deplete muscle glycogen. After the glycogen-depleting exercise, rats were given a rodent chow diet plus 5% glucose solution for 6 h or 24 h. Immediately after the two types of exercise, glycogen concentration in rat epitrochlearis muscle was similarly depleted. After the 6-h and 24-h recovery periods, muscle glycogen concentrations in both the HIGH and LOW groups were restored well above the normally fed state. Furthermore, muscle glycogen accumulation in the HIGH group for the 6-h and 24-h recovery periods was not significantly different from that observed in the LOW group. The high-intensity intermittent swimming exercise also induced muscle glycogen supercompensation in well-trained rats that had performed 7 days of endurance swimming training (6 h per day). Our results indicate that high-intensity intermittent exercise as well as low-intensity continuous exercise could induce glycogen supercompensation in rat skeletal muscle.

Possible Involvement of Protein Synthesis in the Regulation of Glycogen Supercompensation in Rat Skeletal Muscle

Possible Involvement of Protein Synthesis in the Regulation of Glycogen Supercompensation in Rat Skeletal Muscle

Effects of an Ad Libitum, High Carbohydrate Diet and Aerobic Exercise Training on Insulin Action and Muscle Metabolism in Older Men and Women

Previous studies have demonstrated that aerobic exercise training and weight loss have independent effects on insulin-stimulated glucose disposal (ISGD). We hypothesized that ad libitum consumption of a high-carbohydrate diet would result in weight loss and improved ISGD, and that aerobic exercise training would facilitate greater improvements in ISGD compared with diet alone. Older participants (13 women, 9 men; age = 66 +/- 1 year) with impaired glucose tolerance were randomly assigned to an ad libitum diet alone (18% fat, 19% protein, 63% carbohydrate) or this diet plus aerobic exercise training (4 d/wk, 45 min/d, 80% VO(2peak)) for 12 weeks. ISGD, abdominal fat distribution, muscle glycogen, and glycogen synthase activity were assessed pre- and postintervention. Consumption of the diet resulted in significant weight loss and an improvement in ISGD. Consumption of the diet plus exercise training also resulted in weight loss and increased ISGD, but results were not significantly different from those in the diet-alone group. Mean abdominal visceral and subcutaneous adipose tissue cross-sectional areas were smaller postintervention compared to baseline with no difference between groups. Exercise training and consumption of the diet increased muscle glycogen content (344.7 +/- 21.3 to 616.7 +/- 34.4 micromol.g(-1)) and decreased glycogen synthase activity (0.21 +/- 0.02 to 0.13 +/- 0.01) compared to the diet alone. These results demonstrate that consumption of an ad libitum, high-carbohydrate diet alone or in combination with aerobic exercise training results in weight loss and improved insulin sensitivity. Furthermore, exercise combined with this diet appears to limit additional increases in insulin sensitivity due to muscle glycogen supercompensation with a concomitant adaptive response of glycogen synthase.

Glycogen overload by postexercise insulin administration abolished the exercise-induced increase in GLUT4 protein

To elucidate the role of muscle glycogen storage on regulation of GLUT4 protein expression and whole-body glucose tolerance, muscle glycogen level was manipulated by exercise and insulin administration. Sixty Sprague-Dawley rats were evenly separated into three groups: control (CON), immediately after exercise (EX0), and 16 h after exercise (EX16). Rats from each group were further divided into two groups: saline- and insulin-injected. The 2-day exercise protocol consisted of 2 bouts of 3-h swimming with 45-min rest for each day, which effectively depleted glycogen in both red gastrocnemius (RG) and plantaris muscles. EX0 rats were sacrificed immediately after the last bout of exercise on second day. CON and EX16 rats were intubated with 1 g/kg glucose solution following exercise and recovery for 16 h before muscle tissue collection. Insulin (0.5 microU/kg) or saline was injected daily at the time when glucose was intubated. Insulin injection elevated muscle glycogen levels substantially in both muscles above saline-injected group at CON and EX16. With previous day insulin injection, EX0 preserved greater amount of postexercise glycogen above their saline-injected control. In the saline-injected rats, EX16 significantly increased GLUT4 protein level above CON, concurrent with muscle glycogen supercompensation. Insulin injection for EX16 rats significantly enhanced muscle glycogen level above their saline-injected control, but the increases in muscle GLUT4 protein and whole-body glucose tolerance were attenuated. In conclusion, the new finding of the study was that glycogen overload by postexercise insulin administration significantly abolished the exercise-induced increases in GLUT4 protein and glucose tolerance.

Effect of Different Types of Carbohydrate Supplementation on Glycogen Supercompensation in Rat Skeletal Muscle

The purpose of this study was to examine the effects of glucose and sucrose supplement on glycogen accumulation in rat skeletal muscle and liver after exhaustive endurance exercise. Four- to five-week-old male Sprague-Dawley rats with an initial body weight ranging from 90 to 110 g were used for this study. All rats were trained by using a 7-day-long swimming exercise program, during which rats swam 6 h/day in two 3-h bouts separated by 45 min of rest. On the next day of the last training, all trained animals performed 240 min of swimming exercise with a weight equivalent to 3 % of their body weight to deplete muscle and liver glycogen. After glycogen-depleting exercise, rats were given a rodent chow diet plus either 5 % sucrose (SUC), 5 % glucose (GLU) or water (CON) for 6 h or 24 h. Despite equal amount of carbohydrate intake, glycogen concentration in rat epitrochlearis muscle of the GLU group rats was significantly higher compared with those observed in the CON (p<0.001) and the SUC groups (p<0.01). No significant difference in liver glycogen was observed among three groups. These results indicate that glucose supplementation rather than sucrose supplementation efficiently promotes glycogen supercompensation in rat skeletal muscle.

Effect of Different Types of Carbohydrate Supplementation on Glycogen Supercompensation in Rat Skeletal Muscle

0154 Nakatani et al. (J Appl Physiol. 1997) reported that exercise training that induces an increase in muscle GLUT-4 content results in a large increase in the muscle glycogen supercompensation level after a glycogen-depleting bout of exercise in rats. In their study, rats were given not only Purina chow but also 5 % sucrose in their drinking water ad libitum after glycogen depleting swimming exercise. The rationale for supplementation of sucrose was to ensure an adequate carbohydrate intake. However, to our knowledge, there have been few studies that examined the influence of the different types of carbohydrate consumed on glycogen supercompensation. PURPOSE: To examine effect of different types of carbohydrate on glycogen accumulation in rat skeletal muscle and liver after endurance exercise. METHODS: Four- to five-week-old male Sprague-Dawley rats with an initial body weight ranging from 90 to 110 g were used for this study. All rats were trained by using a 7-daylong swimming exercise program, during which rats swam 6 h/day in two 3-h bouts separated by 45 min of rest. On the last training day, swimming training was finished before 9:00 PM, and food was restricted to 8 g/rat after 10:00 PM the night before the glycogen depletion exercise bout. Between 3:00 PM and 4:00 PM on the next day of the last training, the rats performed 240 min of swimming exercise with a weight equivalent to 3 % of their body weight to deplete muscle and liver glycogen. After glycogen-depleting exercise, rats were given a ad libitum rodent chow diet plus either 5 % sucrose (S), 5 % glucose (G), 5 % fructose (F) or water (C) for 6 h or 24 h. Immediately after two repletion periods, rat epitrochlearis muscle and liver were dissected out. Glycogen concentrations in epitrochlearis muscle and liver were determined by enzymatic methods after acid hydrolysis. At the same point, plasma glucose concentration was also measured. RESULTS: Glycogen concentration in epitrochlearis muscle of G group rats after 6-h and 24-h repletion periods was significantly higher compared with that observed in F and C groups (p<0.01; 6 h, p<0.01; 24 h, respectively). There was no significant difference in the muscle glycogen among S, F and C groups or between S and G groups. No significant difference in liver glycogen and plasma glucose concentration was observed among the four groups after both recovery periods. CONCLUSIONS: The present investigation may suggest that glucose supplementation efficiently promotes glycogen supercompensation in rat skeletal muscle.

Failure of Repeated Carbohydrate Loading to Supercompensate Muscle Glycogen Stores

0155 A number of different dietary/training interventions have been used to supercompensate muscle glycogen stores and enhance prolonged aerobic exercise performance. These studies have all evaluated the efficacy of such regimens on a single exercise bout. At present it is not known whether it is possible to repeatedly supercompensate muscle glycogen stores within several days. PURPOSE: To evaluate the effect of repeated carbohydrate (CHO) loading on muscle glycogen resynthesis and exercise performance. METHODS: Six well trained subjects completed a high-intensity intermittent exhaustive exercise protocol (EX) on four occasions, with the first trial serving as a familiarization trial. During a 5 d intervention period, subjects repeated EX on three occasions separated by 48 h (i.e. DAY 1, 3 and 5). Before the familiarisation trial and DAY 1, subjects consumed a moderate (6 g·kg−1) CHO diet. Throughout the 5 d intervention period, subjects consumed a high (12 g·kg·d−1) CHO diet. Subjects consumed 4 g·kg−1 CHO immediately after completing the EX. Muscle biopsies were taken before, immediately upon completing the EX, and after 3 h of recovery and analysed for glycogen and intramuscular triacylglycerol (IMTG) concentration. RESULTS: Compared to a moderate CHO diet, high CHO feeding resulted in elevated pre-exercise glycogen on DAY 3 (435 ± 57 vs 713 ± 60 mmol·kg−1 dw, P <0.001) but not DAY 5 (409 ± 40 mmol·kg−1 dw). Muscle glycogen utilization was higher on DAY 3 compared to both DAY 1 and 5 (600 ± 86 vs 340 ± 84 and 350 ± 51 mmol·kg−1 dw respectively, P <0.001). Neither pre-exercise IMTG concentration nor utilization was altered during the 5 d intervention period. Compared to DAY 1, performance was increased on DAY 3 and 5, (22 ± 1 vs 31 ± 2 and 35 ± 4 kJ·kg−1 respectively, P <0.05). CONCLUSIONS: Repeated muscle glycogen supercompensation is not possible, even when subjects consume a high CHO diet and maintain only light training. However, performance enhancement is maintained. Supported by a research grant from GlaxoSmithKline (United Kingdom)

Role of insulin on exercise-induced GLUT-4 protein expression and glycogen supercompensation in rat skeletal muscle.

The purpose of this study was to investigate the role of insulin on skeletal muscle GLUT-4 protein expression and glycogen storage after postexercise carbohydrate supplementation. Male Sprague-Dawley rats were randomly assigned to one of six treatment groups: sedentary control (Con), Con with streptozocin (Stz/C), immediately postexercise (Ex0), Ex0 with Stz (Stz/Ex0), 5-h postexercise (Ex5), and Ex5 with Stz (Stz/Ex5). Rats were exercised by swimming (2 bouts of 3 h) and carbohydrate supplemented immediately after each exercise session by glucose intubation (1 ml of a 50% wt/vol). Stz was administered 72-h before exercise, which resulted in hyperglycemia and elimination of the insulin response to the carbohydrate supplement. GLUT-4 protein of Ex0 rats was 30% above Con in fast-twitch (FT) red and 21% above Con in FT white muscle. In Ex5, GLUT-4 protein was 52% above Con in FT red and 47% above Con in FT white muscle. Muscle glycogen in FT red and white muscle was also increased above Con in Ex5 rats. Neither GLUT-4 protein nor muscle glycogen was increased above Con in Stz/Ex0 or Stz/Ex5 rats. GLUT-4 mRNA in FT red muscle of Ex0 rats was 61% above Con but only 33% above Con in Ex5 rats. GLUT-4 mRNA in FT red muscle of Stz/C and Stz/Ex0 rats was similar but significantly elevated in Ex5/Stz rats. These results suggest that insulin is essential for the increase in GLUT-4 protein expression following postexercise carbohydrate supplementation.

Mechanisms underlying impaired GLUT-4 translocation in glycogen-supercompensated muscles of exercised rats.

Exercise training induces an increase in GLUT-4 in muscle. We previously found that feeding rats a high-carbohydrate diet after exercise, with muscle glycogen supercompensation, results in a decrease in insulin responsiveness so severe that it masks the effect of a training-induced twofold increase in GLUT-4 on insulin-stimulated muscle glucose transport. One purpose of this study was to determine whether insulin signaling is impaired. Maximally insulin-stimulated phosphatidylinositol (PI) 3-kinase activity was not significantly reduced, whereas protein kinase B (PKB) phosphorylation was approximately 50% lower (P < 0.01) in muscles of chow-fed, than in those of fasted, exercise-trained rats. Our second purpose was to determine whether contraction-stimulated glucose transport is also impaired. The stimulation of glucose transport and the increase in cell surface GLUT-4 induced by contractions were both decreased by approximately 65% in glycogen-supercompensated muscles of trained rats. The contraction-stimulated increase in AMP kinase activity, which has been implicated in the activation of glucose transport by contractions, was approximately 80% lower in the muscles of the fed compared with the fasted rats 18 h after exercise. These results show that both the insulin- and contraction-stimulated pathways for muscle glucose transport activation are impaired in glycogen-supercompensated muscles and provide insight regarding possible mechanisms.

Glycogen supercompensation masks the effect of a traininginduced increase in GLUT-4 on muscle glucose transport.

Endurance exercise training induces a rapid increase in the GLUT-4 isoform of the glucose transporter in muscle. In fasted rats, insulin-stimulated muscle glucose transport is increased in proportion to the increase in GLUT-4. There is evidence that high muscle glycogen may decrease insulin-stimulated glucose transport. This study was undertaken to determine whether glycogen supercompensation interferes with the increase in glucose transport associated with an exercise-induced increase in GLUT-4. Rats were trained by means of swimming for 6 h/day for 2 days. Rats fasted overnight after the last exercise bout had an approximately twofold increase in epitrochlearis muscle GLUT-4 and an associated approximately twofold increase in maximally insulin-stimulated glucose transport activity. Epitrochlearis muscles of rats fed rodent chow after exercise were glycogen supercompensated (86.4 +/- 4.8 micromol/g wet wt) and showed no significant increase in maximally insulin-stimulated glucose transport above the sedentary control value despite an approximately twofold increase in GLUT-4. Fasting resulted in higher basal muscle glucose transport rates in both sedentary and trained rats but did not significantly increase maximally insulin-stimulated transport in the sedentary group. We conclude that carbohydrate feeding that results in muscle glycogen supercompensation prevents the increase in maximally insulin-stimulated glucose transport associated with an exercise training-induced increase in muscle GLUT-4.