Some features of glycogen metabolism in human skeletal muscle.

The higher the exercise intensity, the greater the relative proportion of energy output derived from carbohydrate metabolism. Muscle glycogen stores are the most important source of carbohydrate during heavy exercise and in normal dietary conditions. At the same relative energy output, a muscle rich in type II fibers obtains a relatively larger energy contribution from carbohydrates, in terms of local muscle glycogen utilization, than one rich in type I fibers. This pattern can be modified by different dietary means.     

Carbohydrate loading--a review.

The purpose of carbohydrate loading is to supersaturate with glycogen the muscles to be used in competition. The competition should be longer than 30 to 60 min. to fully utilize the glycogen stores. An exhausting exercise is first performed to deplete the glycogen stores, and a high-fat, high-protein diet is followed for three days to keep the glycogen stores low. After depletion of the muscles, a high-carbohydrate diet is followed for two to three days to restore and supersaturate the muscles with glycogen. The most important point to impress on the athlete is the nutritional adequacy of the entire diet. Though the technique of carbohydrate loading is a dietary manipulation emphasizing the intake of carbohydrate, the diet can be adequate with sound dietary planning.     

Carbohydrate and exercise

Total body carbohydrate stores are limited, and are often less than the carbohydrate requirements of athletic training and competition. However, the availability of carbohydrate as a substrate for muscle metabolism is a critical factor in the performance of both high-intensity intermittent work and prolonged aerobic exercise. The rate of carbohydrate oxidation during exercise is tightly regulated, with glucose availability closely matching the needs of the working muscles. Both the absolute and relative work rate play important roles in the regulation of substrate metabolism: carbohydrate-based fuels predominate at moderate to high power outputs, with muscle glycogen and glucose utilization scaling exponentially to the relative work rate. As such, strategies to maintain or enhance carbohydrate availability, such as the ingestion of carbohydrate before, during and after exercise, are critical to the performance of a variety of sports events, and are a key recommendation in current sports nutrition guidelines.     

Hemochromatosis and Iron Needs

Although iron is an essential dietary requirement, the amount absorbed by the body is well regulated and depends on body iron stores and on dietary iron availability. There is very little iron excreted under normal conditions. Iron deficiency is a worldwide problem but iron overload, as seen in the inherited disease, hemochromatosis, is a major cause of morbidity in some Caucasian populations. This is a problem particularly where there is an adequate dietary iron intake and especially in males. A mutation has recently been described in an MHC Class I-like gene (HFE) that encodes for a protein (HFE) of 343 amino acids. The molecule contains a signal sequence peptide-binding region, α₁ and α₂ domains, and an immunoglobulin-like α₃ domain, in addition to a transmembrane region and a small cytoplasmic tail. It is a candidate gene for hemochromatosis. Several possibilities as to the function of this gene and the corresponding protein have been suggested but none has yet been confirmed. The mutation has been detected by several different groups in 80%–100% of subjects with the disease. However, in one study, 18%–20% of patients with the mutation did not exhibit significant iron overload. The discovery of this gene has important implications for both clinical studies and the elucidation of the pathways of iron metabolism.     

Sucres,métabolisme musculaire et exercice physique

Muscles mainly draw their energy from lipids and carbohydrates. During physical exercice, glucose consumption by muscle considerably increases. Glucose, oxidized during physical activity, comes from glycogen stores from liver and muscles, and/or from ingested carbohydrates. Performance could be enhanced by the increase of intracellular glycogen stores and by carbohydrate ingestion before and during exercice. Several mechanisms may be involved: maintaining blood glucose and high levels of CHO oxidation, sparing endogenous glycogen, delaying time to exhaustion. However, short-term exercices (< 1 hour) do not require changes in food intake. Beyond, it seems important to make sufficient glycogen stores before exercise, using suitable diets. Glycogen stores replenishment after exercise should be done as soon as possible after the end of exercise. Based on this knowledge, nutrition recommendations can be made to sportmen and women, according to the type of exercise and of studied subjects.     

The Effects of a Ketogenic Diet on Exercise Metabolism and Physical Performance in Off-Road Cyclists

The main objective of this research was to determine the effects of a long-term ketogenic diet, rich in polyunsaturated fatty acids, on aerobic performance and exercise metabolism in off-road cyclists. Additionally, the effects of this diet on body mass and body composition were evaluated, as well as those that occurred in the lipid and lipoprotein profiles due to the dietary intervention. The research material included eight male subjects, aged 28.3 ± 3.9 years, with at least five years of training experience that competed in off-road cycling. Each cyclist performed a continuous exercise protocol on a cycloergometer with varied intensity, after a mixed and ketogenic diet in a crossover design. The ketogenic diet stimulated favorable changes in body mass and body composition, as well as in the lipid and lipoprotein profiles. Important findings of the present study include a significant increase in the relative values of maximal oxygen uptake (VO_2max) and oxygen uptake at lactate threshold (VO₂ LT) after the ketogenic diet, which can be explained by reductions in body mass and fat mass and/or the greater oxygen uptake necessary to obtain the same energy yield as on a mixed diet, due to increased fat oxidation or by enhanced sympathetic activation. The max work load and the work load at lactate threshold were significantly higher after the mixed diet. The values of the respiratory exchange ratio (RER) were significantly lower at rest and during particular stages of the exercise protocol following the ketogenic diet. The heart rate (HR) and oxygen uptake were significantly higher at rest and during the first three stages of exercise after the ketogenic diet, while the reverse was true during the last stage of the exercise protocol conducted with maximal intensity. Creatine kinase (CK) and lactate dehydrogenase (LDH) activity were significantly lower at rest and during particular stages of the 105-min exercise protocol following the low carbohydrate ketogenic diet. The alterations in insulin and cortisol concentrations due to the dietary intervention confirm the concept that the glucostatic mechanism controls the hormonal and metabolic responses to exercise.     

What Is the Evidence That Dietary Macronutrient Composition Influences Exercise Performance? A Narrative Review

The introduction of the needle muscle biopsy technique in the 1960s allowed muscle tissue to be sampled from exercising humans for the first time. The finding that muscle glycogen content reached low levels at exhaustion suggested that the metabolic cause of fatigue during prolonged exercise had been discovered. A special pre-exercise diet that maximized pre-exercise muscle glycogen storage also increased time to fatigue during prolonged exercise. The logical conclusion was that the athlete’s pre-exercise muscle glycogen content is the single most important acutely modifiable determinant of endurance capacity. Muscle biochemists proposed that skeletal muscle has an obligatory dependence on high rates of muscle glycogen/carbohydrate oxidation, especially during high intensity or prolonged exercise. Without this obligatory carbohydrate oxidation from muscle glycogen, optimum muscle metabolism cannot be sustained; fatigue develops and exercise performance is impaired. As plausible as this explanation may appear, it has never been proven. Here, I propose an alternate explanation. All the original studies overlooked one crucial finding, specifically that not only were muscle glycogen concentrations low at exhaustion in all trials, but hypoglycemia was also always present. Here, I provide the historical and modern evidence showing that the blood glucose concentration—reflecting the liver glycogen rather than the muscle glycogen content—is the homeostatically-regulated (protected) variable that drives the metabolic response to prolonged exercise. If this is so, nutritional interventions that enhance exercise performance, especially during prolonged exercise, will be those that assist the body in its efforts to maintain the blood glucose concentration within the normal range.     

Carbohydrate-loading during the follicular phase of the menstrual cycle: effects on muscle glycogen and exercise performance

The effects of employing a high-carbohydrate diet (carbohydrate-loading) to increase glycogen storage in skeletal muscle are not well established in female athletes. On 4 occasions--2 familiarization trials and 2 experimental trials--6 well-trained female subjects completed 6 x 15-min continuous intervals of cycling (12 min at 72% VO2max, 1 min at maximal effort, and 2 min at 50% VO2max), followed by a time trial 15 min later. The women consumed their habitual diets (HD; 6-7 g carbohydrate/kg lean body mass) for 3 days after the second familiarization trial and before the first experimental trial. During the 3 days following the first experimental trial, the subjects consumed a high-carbohydrate diet (CD; 9-10 g carbohydrate/kg lean body mass) prior to the second experimental trial. Mean (+/-SEM) pre-exercise muscle glycogen concentrations were greater after CD versus HD (171.9+/-8.7 vs. 131.4+/-10.3 mmol/kg wet weight, P < 0.003). Although 4 of the 6 subjects improved their time-trial performance after CD, mean performance for the time trial was not significantly different between diets (HD: 763.9+/-35.6 s; CD: 752.9+/-30.1 s). Thus, female cyclists can increase their muscle glycogen stores after a carbohydrate-loading diet during the follicular phase of the menstrual cycle, but we found no compelling evidence of a dietary effect on performance of a cycling time trial performed after 90 min of moderate-intensity exercise.     

Suppression of glycogen consumption during acute exercise by dietary branched-chain amino acids in rats

The effects of a diet supplemented with branched-chain amino acids (BCAA; 4.8% or 6.2%) on BCAA catabolism and glycogen metabolism in rats were examined. Rats were fed a BCAA diet or control diet for 4 wk and part of the rats were subjected to exercise training during the experimental period. Feeding the BCAA diet increased serum BCAA concentrations and activity of the hepatic branched-chain alpha-keto acid dehydrogenase complex, the rate-limiting enzyme in the catabolism of BCAA, suggesting that dietary BCAA promotes BCAA catabolism. Although the serum glucose concentration and glycogen contents in the liver and gastrocnemius muscle of rested rats were not significantly affected by feeding of the BCAA diet, those in rats exhausted by acute exercise were 2-4-fold higher in rats fed the BCAA diet than in rats fed the control diet. The activity of pyruvate dehydrogenase complex in the liver and gastrocnemius muscle after acute exercise showed reverse trends; the complex activities (especially in liver) tended to be less in the BCAA diet group than in the control diet group. These results suggest that dietary BCAA spares glycogen stores in liver and skeletal muscle during exercise and that the decrease in pyruvate dehydrogenase complex activity in these tissues by dietary BCAA is involved in the mechanisms.     

Oral hydroxycitrate supplementation enhances glycogen synthesis in exercised human skeletal muscle

Glycogen stored in skeletal muscle is the main fuel for endurance exercise. The present study examined the effects of oral hydroxycitrate (HCA) supplementation on post-meal glycogen synthesis in exercised human skeletal muscle. Eight healthy male volunteers (aged 22·0 (se 0·3) years) completed a 60-min cycling exercise at 70-75 % VO?max and received HCA or placebo in a crossover design repeated after a 7 d washout period. They consumed 500 mg HCA or placebo with a high-carbohydrate meal (2 g carbohydrate/kg body weight, 80 % carbohydrate, 8 % fat, 12 % protein) for a 3-h post-exercise recovery. Muscle biopsy samples were obtained from vastus lateralis immediately and 3 h after the exercise. We found that HCA supplementation significantly lowered post-meal insulin response with similar glucose level compared to placebo. The rate of glycogen synthesis with the HCA meal was approximately onefold higher than that with the placebo meal. In contrast, GLUT4 protein level after HCA supplementation was significantly decreased below the placebo level, whereas expression of fatty acid translocase (FAT)/CD36 mRNA was significantly increased above the placebo level. Furthermore, HCA supplementation significantly increased energy reliance on fat oxidation, estimated by the gaseous exchange method. However, no differences were found in circulating NEFA and glycerol levels with the HCA meal compared with the placebo meal. The present study reports the first evidence that HCA supplementation enhanced glycogen synthesis rate in exercised human skeletal muscle and improved post-meal insulin sensitivity.     

High-fat diet versus habitual diet prior to carbohydrate loading: effects of exercise metabolism and cycling performance

We examined the effects of a high-fat diet (HFD-CHO) versus a habitual diet, prior to carbohydrate (CHO)-loading on fuel metabolism and cycling time-trial (TT) performance. Five endurance-trained cyclists participated in two 14-day randomized cross-over trials during which subjects consumed either a HFD (> 65% MJ from fat) or their habitual diet (CTL) (30 +/- 5% MJ from fat) for 10 day, before ingesting a high-CHO diet (CHO-loading, CHO > 70% MJ) for 3 days. Trials consisted of a 150-min cycle at 70% of peak oxygen uptake (VáO2peak), followed immediately by a 20-km TT. One hour before each trial, cyclists ingested 400 ml of a 3.44% medium-chain triacylglycerol (MCT) solution, and during the trial, ingested 600 ml/hour of a 10% 14C-glucose + 3.44% MCT solution. The dietary treatments did not alter the subjects' weight, body fat, or lipid profile. There were also no changes in circulating glucose, lactate, free fatty acid (FFA), and b-hydroxybutyrate concentrations during exercise. However, mean serum glycerol concentrations were significantly higher (p < .01) in the HFD-CHO trial. The HFD-CHO diet increased total fat oxidation and reduced total CHO oxidation but did not alter plasma glucose oxidation during exercise. By contrast, the estimated rates of muscle glycogen and lactate oxidation were lower after the HFD-CHO diet. The HFD-CHO treatment was also associated with improved TT times (29.5 +/- 2.9 min vs. 30.9 +/- 3.4 min for HFD-CHO and CTL-CHO, p <.05). High-fat feeding for 10 days prior to CHO-loading was associated with an increased reliance on fat, a decreased reliance on muscle glycogen, and improved time trial performance after prolonged exercise.     

Effect of diet on glucose tolerance 36 hours after glycogen-depleting exercise.

In order to estimate the effect of muscle glycogen content on the glycaemic response, glucose tolerance and glucose oxidation were measured in eight healthy male subjects. Each subject followed three different treatments, consisting of either a physical exercise session followed by 36 h of a low-carbohydrate high-fat diet (glycogen depletion treatment); or a physical exercise followed by 36 h of a high carbohydrate diet (glycogen repletion treatment); or a low-carbohydrate high-fat diet alone (diet treatment). After both the glycogen depletion and the diet treatments, the subjects showed a high glycaemic response (443 +/- 57 and 419 +/- 63 mmol.min/l resp.), a high insulinaemic response (7158 +/- 671 and 7643 +/- 913 mU.min/l), and a low rate of glucose oxidation (27.5 +/- 2.4 and 31.0 +/- 5.8 g/3 h respiration). In contrast, after the glycogen repletion treatment, the subjects had a lower glycaemic response (197 +/- 21 mmol.min/l), a lower insulinaemic response (4645 +/- 327 mU.min/l) and a higher glucose oxidation level (47.4 +/- 2.0 g/3h). Fasting free fatty acids (FFA) were positively correlated with glucose area (P less than 0.001) and negatively with glucose oxidation (P less than 0.01). These results show a strong inhibitory effect of the low-carbohydrate high-fat diet on glucose tolerance despite prior strenuous exercise. Because of this, the effect of the muscle glycogen content could not be tested. However, the results suggest that the FFA/glucose interrelationship may override exercise-induced changes in insulin-stimulated glucose uptake.     

Further glycogen decrease during early recovery after eccentric exercise despite a high carbohydrate intake

BACKGROUND: Delayed onset muscle soreness (DOMS) is a well-known phenomenon of athletes. It has been reported from muscle biopsies that the rate of muscle glycogen resynthesis is reduced after eccentric compared to concentric exercise. AIM OF THE STUDY: Try to compensate by a carbohydrate (CHO)-rich diet the decelerated glycogen resynthesis after eccentric exercise, measured by magnetic resonance spectroscopy. METHODS: Glycogen, phosphocreatine, ATP, and Pi were measured in the human calf muscle. Twenty athletes divided into two groups (DOMS and CONTROL), reduced glycogen in M. gastrocnemius during two different running protocols. Additionally, 12 DOMS subjects performed an eccentric exercise while the CONTROL group rested. Subsequently, subjects consumed a CHO-rich diet (> 10 g/kg body mass/24 h). RESULTS: In both groups, glycogen has been reduced by about 50%. The first 2 h after exercise, glycogen dropped further (-15.6 +/- 15.7 mmol/ kg ww) in the DOMS but rose by +18.4 +/- 20.8 mmol/kg ww in the CONTROL group (P < 0.001). CONTROL subjects reached resting glycogen within 24 h (137 +/- 47 mmol/kg ww), while DOMS subjects needed more than one day (91 +/- 23 mmol/kg ww; P < 0.001). Pi and Pi/PCr, indicators of muscle injury, rose significantly in the DOMS but not in the CONTROL group. CONCLUSION: The diet rich in CHO's was not able to refill glycogen stores after eccentric exercise. Glycogen decreased even further during the beginning of recovery. This loss, which to our knowledge has not been measured before is probably the consequence of muscle cell damage and their reparation.     

ALTERED MEMBRANE LIPID COMPOSITION: A POSSIBLE MOLECULAR BASIS OF VITAMIN D ACTION

1,25(OH)₂D₃ may exert its effect on calcium absorption by altering intestinal mucosal membrane lipid composition. Essential fatty acid deficiency may block vitamin D action.     

Preexercise ingestion of carbohydrate plus whey protein hydrolysates attenuates skeletal muscle glycogen depletion during exercise in rats

ObjectiveDepletion of glycogen stores is associated with fatigue during both sprint and endurance exercises and therefore it is considered important to maintain adequate tissue stores of glycogen during exercise. The aims of the present study in rats were therefore to investigate the effects of preexercise supplementation with carbohydrate and whey protein hydrolysates (WPH) on glycogen content, and phosphorylated signaling molecules of key enzymes that regulate glucose uptake and glycogen synthesis during exercise.MethodsMale SD rats were used in the study (n = 7/group). Prior to exercise, one group of rats was sacrificed, whereas the other groups were given either water, glucose, or glucose plus WPH solutions. After ingestion of the test solutions, glycogen-depleting exercise was carried out for 60 min. The rats were then sacrificed and the triceps muscles excised quickly.ResultsCompared to water or glucose only, preexercise ingestion of glucose plus WPH caused a significant attenuation of muscle glycogen depletion during the postexercise period. Coingestion of glucose and WPH also significantly lowered phosphorylated glycogen synthase levels compared to ingestion of water only. In the glucose plus WPH group, the levels of phosphorylated Akt were increased significantly compared to the group ingesting water only, while the levels of phosphorylated PKC were significantly higher than in the groups ingesting only water or glucose.ConclusionTaken together, these results indicate that, compared to ingestion of glucose or water only, preexercise ingestion of carbohydrate plus WPH activates skeletal muscle proteins of key enzymes that regulate glucose uptake and glycogen synthesis during exercise, thereby attenuating exercise-induced glycogen depletion.     

Studies Of Docosahexaenoic And Eicosapentaenoic Acids In Trout And Frogs

A prostaglandin (C₂₂-PGF_4α) is formed from docosahexaenoic acid by trout gill tissue. Trout fed a diet low in ώ-3 fatty acids for three months continue to maintain high levels of 22:6ώ-3 in serum lipoproteins.     

ANTAGONISTIC EFFECTS IN UNSATURATED FATTY ACID METABOLISM

The ability of linoleic and linolenic acids to reduce C₂₀-trienoic acid in fat deficiency can be explained by assuming a competitive inhibition between unsaturated C₁₈ fatty acids for conversion to C₂₀ fatty acids.     

Caffeine as a lipolytic food component increases endurance performance in rats and athletes

Caffeine is one of the famous ergogenic aids in the athletic field. Caffeine has been known to stimulate lipolysis that spares stored glycogen utilization during moderate intensity exercise. Therefore, we investigated the effects of caffeine ingestion on exercise performance in rats and athletes. Rats were administered the caffeine (6 mg/kg) 1 h prior to the exercise then were run on a treadmill at a speed of 20 m/min. They were decapitated at 0 min, 30 min, 60 min of exercise, and exhausted time point. Human subjects ingested the caffeine (5 mg/kg) 1 h prior to the exercise. They exercised on a cycle ergometer at 60% of their VO2max for 45 min, and then the exercise intensity was increased to 80% of their VO2max until exhaustion. Blood and breathing gas samples were collected and calculated every 10 min during exercise. Respiratory exchange ratio of the caffeine trial was significantly lower than that of the placebo trial in the athletes' study (p<0.05). Blood free fatty acid (FFA) levels in studies of both rats and athletes were increased by caffeine ingestion during exercise (p<0.05). Blood lactate levels were also increased during exercise in both rats and athletes (p<0.05). Increased FFA and glycerol concentrations reduced glycogen utilization during exercise compared with placebo group in rats. In addition, endurance time to exhaustion was significantly increased by the caffeine ingestion in both rats and athletes (p<0.05). These results suggest that the caffeine ingestion enhanced endurance performance resulting from spare stored glycogen with increasing lipolysis from adipose tissues and fat oxidation during exercise both in rats and in athletes.     

Postexercise muscle triacylglycerol and glycogen metabolism in obese insulin-resistant zucker rats

OBJECTIVE: To determine the impact of insulin resistance and obesity on muscle triacylglycerol (IMTG) and glycogen metabolism during and after prolonged exercise. RESEARCH METHODS AND PROCEDURES: Female lean (fa/?; N = 40, ZL) and obese insulin-resistant (fa/fa; N = 40, ZO) Zucker rats performed an acute bout of swimming exercise (8 times for 30 minutes) followed by 6 hours of carbohydrate supplementation (CHO) or fasting (FAST). IMTG and glycogen were measured in the extensor digitorum longus (EDL) and red vastus lateralis (RVL) muscles. RESULTS: Despite resting IMTG content being 4-fold higher in ZO compared with ZL rats, IMTG levels were unchanged in either EDL or RVL muscles immediately after exercise. Resting glycogen concentration in EDL and RVL muscles was similar between genotypes, with exercise resulting in glycogen use in both muscles from ZL rats (approximately 85%, p < 0.05). However, in ZO rats, there was a much smaller decrease in postexercise glycogen content in both EDL and RVL muscles (approximately 30%). During postexercise recovery, there was a decrease in EDL muscle levels of IMTG in ZL rats supplemented with CHO after 30 and 360 minutes (p < 0.05). In contrast, IMTG content was increased above resting levels in RVL muscles of ZO rats fasted for 360 minutes. Six hours of CHO refeeding restored glycogen content to resting levels in both muscles in ZL rats. However, after 6 hours of FAST in ZO animals, RVL muscle glycogen content was still lower than resting levels (p < 0.05). At this time, IMTG levels were elevated above basal (p < 0.05). DISCUSSION: In both healthy and insulin-resistant skeletal muscle, there was negligible net IMTG degradation after a single bout of prolonged exercise. However, during postexercise recovery, there was differential metabolism of IMTG between phenotypes.