Muscle Glycogen Reserves Research Articles

Glycogen and its metabolism.

Glycogen is a branched polymer of glucose which serves as a reservoir of glucose units. The two largest deposits in mammals are in the liver and skeletal muscle but many cells are capable synthesizing glycogen. Its accumulation and utilization are under elaborate controls involving primarily covalent phosphorylation and allosteric ligand binding. Both muscle and liver glycogen reserves are important for whole body glucose metabolism and their replenishment is linked hormonally to nutritional status. Control differs between muscle and liver in part due to the existence of different tissue-specific isoforms at key steps. Control of synthesis is shared between transport into the muscle and the step catalyzed by glycogen synthase. Breakdown of liver glycogen, as part of blood glucose homeostasis, is also in response to nutritional cues. Muscle glycogen serves only to fuel muscular activity and its utilization is controlled by muscle contraction and by catecholamines. Though the number of enzymes directly involved in the metabolism of glycogen is quite small, many more proteins act indirectly in a regulatory capacity. Defects in the basic metabolizing enzymes lead to severe consequences whereas, with some exceptions, mutations in the regulatory proteins appear to cause a more subtle phenotypic change.

GLYCOGEN UTILIZATION PATTERN DURING PROLONGED RUNNING USING13 C-GLUCOSE LABELING IN THE DIET.

1406 This study was conducted to determine endogenous glucose oxidation during prolonged running following a carbohydrate (CHO) diet labeled with 13C. Six male runners (VO2max, 60.0±2.2 ml·kg-1·min-1) performed two 120-min treadmill exercises (65% maximal speed; 69±2 VO2max). A first exercise was performed following an overnight fast and a light breakfast, and was followed by a cycling bout of exercise to exhaustion (Trial A). Then, over the next 48 hrs, subjects ingested a high (CHO) diet (1250 g, 90% CHO) artifically labeled with 13C-glucose and then performed a second exercise (Trial B). The average VO2, energy cost, and protein oxidation were significantly(p<0.05) lower in trial B than A (2.85±0.10 vs. 2.93±0.10 L·min-1; 14.38±0.38 vs. 14.72±0.50 kcal·min-1 and 0.07±0.001 vs. 0.11±0.008 g·min-1 respectively). Results from indirect calorimetry (IC), show no differences for fat and total CHO oxidations between trials (fat, 0.52±0.08 vs. 0.49±0.07; CHO, 2.34±0.23 vs. 2.38±0.24 g·min-1 in trials A and B respectively). Calculations of CHO oxidation from expired 13VCO2 was similar to that derived from IC: 1st hr, 1.19±0.10 vs 1.26±0.10 g·min-1; 2nd hr, 1.03±0.21 vs 1.12±0.13 g·min-1 for 13VCO2 and IC respectively. These results indicate that hepatic and muscle glycogen reserves can be adequately labeled with 13C-CHO with an exercise-diet regimen.

Carbohydrate and lipid requirements of soccer

Soccer involves high-intensity, intermittent exercise and places a heavy demand on the body's liver and muscle glycogen reserves. Thus, carbohydrate depletion may contribute, in part, to fatigue and reduced performance during a soccer match. In addition, fatty acids derived from both adipose tissue and intramuscular triglyceride stores will be utilized. Soccer players engaged in strenuous competition and training should be encouraged to consume a diet that is relatively high in carbohydrate (at least 55% of total energy intake). Furthermore, the inclusion of carbohydrate in beverages consumed during and after a soccer match is likely to enhance performance and facilitate the recovery of liver and muscle glycogen reserves.

Update on carbohydrate: solid versus liquid.

Athletes often train or compete in athletic events that significantly reduce muscle and liver glycogen reserves. Carbohydrate ingestion before or during endurance exercise enhances performance by maintaining blood glucose levels and carbohydrate utilization. Also, an adequate intake of carbohydrate following endurance exercise helps to restore muscle and liver glycogen. This paper reviews the physiologic and performance benefits of solid versus liquid carbohydrate feedings before, during, and following endurance exercise. Solid and liquid carbohydrates are equally effective in raising blood glucose and enhancing performance when consumed during endurance exercise. Also, both forms of carbohydrate are similarly beneficial in promoting muscle glycogen synthesis after exercise. It is unclear whether solid and liquid carbohydrate feedings have the same effect on serum glucose and performance when consumed before exercise. Although limited research suggests that a low glycemic solid carbohydrate may represent the best preexercise meal choice, further research is needed to support this hypothesis.

Recovery from endurance exercise

1) During training for and competition in endurance exercise athletes often significantly reduce both liver and muscle glycogen reserves. 2) Replenishment of muscle glycogen probably occurs preferentially over the replenishment of liver glycogen after exercise. 3) Muscle and liver glycogen can be replenished within 24 h after exercise provided adequate carbohydrate is consumed. 4) To replenish muscle glycogen within 24 h, 8-10 g carbohydrate.kg-1 body weight should be consumed. 5) To optimize muscle glycogen synthesis during the 4-6 h after exercise, carbohydrate must be consumed immediately after exercise and at frequent intervals thereafter. 6) While normal muscle and/or liver glycogen levels can be normalized 24 h after exercise, muscle function may or may not be fully recovered.

Overtraining in Athletes

Overtraining appears to be caused by too much high intensity training and/or too little regeneration (recovery) time often combined with other training and nontraining stressors. There are a multitude of symptoms of overtraining, the expression of which vary depending upon the athlete's physical and physiological makeup, type of exercise undertaken and other factors. The aetiology of overtraining may therefore be different in different people suggesting the need to be aware of a wide variety of parameters as markers of overtraining. At present there is no one single diagnostic test that can define overtraining. The recognition of overtraining requires the identification of stress indicators which do not return to baseline following a period of regeneration. Possible indicators include an imbalance of the neuroendocrine system, suppression of the immune system, indicators of muscle damage, depressed muscle glycogen reserves, deteriorating aerobic, ventilatory and cardiac efficiency, a depressed psychological profile, and poor performance in sport specific tests, e.g. time trials. Screening for changes in parameters indicative of overtraining needs to be a routine component of the training programme and must be incorporated into the programme in such a way that the short term fatigue associated with overload training is not confused with the chronic fatigue characteristic of overtraining. An in-depth knowledge of periodisation of training theory may be necessary to promote optimal performance improvements, prevent overtraining, and develop a system for incorporating a screening system into the training programme. Screening for overtraining and performance improvements must occur at the culmination of regeneration periods.

The effect of social interactions on calling energetics in the gray treefrog (Hyla versicolor)

The vocal behavior of Hyla versicolor was studied in the field by means of behavioral observations and playback experiments, and these data were coupled with measurements of oxygen consumption in calling frogs to estimate the effect of social interactions on calling energetics. Male gray treefrogs have intense calls (median peak SPL=109 dB, fast RMS SPL=100 dB at 50 cm). At an air temperature of 23° C, males produced an average of 1,200–1,300 calls/h for 2–4 h per night. Calling rates and call durations differed among individuals, but were relatively constant for each male during periods of sustained calling. Males in dense choruses gave calls about twice as long as isolated males, but produced calls at about half the rate. Consequently, total calling effort and estimated aerobic costs were largely independent of chorus density. Playbacks of recorded calls to males in the field elicited increases in call duration and decreases in calling rate, regardless of the rate or duration of the stimulus. Males gave longer calls in response to long calls or to stimuli presented at high rates, but they did not precisely match either stimulus rate or duration. Calling effort and estimated oxygen consumption changed only slightly during stimulus playbacks. These results indicate that male-male competition elicits pro-found changes in the vocal behavior of calling males, but these changes have little effect on energy expenditure. We estimated that most calling males had metabolic rates of about 1.7–1.8 ml O2/(g\h), or about 280 J/h for an average size (8.6 g) male at 20° C. Although changes in call duration and calling rate did not affect aerobic costs of calling, males producing long calls at slow rates called for fewer hours per night than males producing shorter calls at higher rates. This suggests that calling time may be limited by the rate at which muscle glycogen reserves are depleted.

Glucose ingestion before and during intense exercise.

Glucose and insulin responses were compared in glycogen depleted subjects when glucose (1.5 g/kg) was ingested 15 min before (n = 7) or during (min 3-5) intense exercise (80% VO2 max; n = 8). A nonexercise group (n = 8) and a no-glucose group (n = 8) were also included for comparisons. A 36- to 44-h fast, combined with exhaustive exercise to deplete muscle glycogen, (congruent to 80% in pilot studies) suggested that the subjects initiated exercise with substantially depleted hepatic and muscle glycogen reserves. With no glucose ingestion, blood glucose decreased during exercise (P less than 0.05) and blood lactate (HLa congruent to 3.8 mM) and the respiratory exchange ratio (R) remained low (0.83); with glucose ingestion before or during exercise, HLa concentrations were doubled (7.3 mM) and R was greater (0.90-0.92; P less than 0.05). Although insulin concentrations decreased rapidly to basal levels within 10 min after the onset of exercise in the preexercise glucose group (P less than 0.05), blood glucose continued to decrease throughout exercise. No such decrease occurred in the subjects who ingested glucose during exercise, nor did insulin concentrations change markedly in this group (P greater than 0.05). The HLa and R data indicated that a considerable portion of glucose was metabolized during exercise. Differences in the preexercise insulin environment appear to exert a persistent effect on glucose uptake throughout exercise.

Stress and Chronic Effects of Untreated and Treated Bleached Kraft Pulpmill Effluent on the Biochemistry and Stamina of Juvenile Coho Salmon (Oncorhynchus kisutch)

Growth of juvenile coho salmon (Oncorhynchus kisutch) fed a limiting ration (70% of satiation) in experimental stream channels was not altered significantly by prolonged exposure to untreated or laboratory-treated (fermented) bleached kraft pulpmill effluent (BKME), although mean weights for control fish were consistently lower than those for all effluent-exposed groups from 100 to 200 d. Body protein, fat, and moisture content were unaffected by treatment at 30, 90, and 200 d. Fish exposed to all strengths of untreated or treated BKME (i.e. untreated concentrations equivalent by volume to 0.05, 0.1, 0.2, 0.3, and 0.5 of the untreated effluent's 96-h LC50 value; and treated concentrations equivalent by volume to 0.2 and 1.0 LC50) showed significant decreases in serum albumin levels at 30 d, whereas these recovered to control values at 90 and 200 d. The serum electrolytes Na+, K+, and Ca++ were unaffected by treatment at 200 d and not measured for other exposures. Liver and muscle glycogen reserves were decreased significantly by continuous exposure of fish to untreated or treated BKME concentrations for 30 d. These values recovered to control levels at 90 d and were unaffected or depressed at 200 d. Plasma glucose levels at 30 d were elevated significantly in all BKME-exposed groups except those held in the lowest concentration of untreated or treated effluent. Blood sugar values at 90 d were increased only by the highest strength of untreated or treated BKME; whereas at 200 d these values were elevated from control levels in all effluent-exposed groups. Levels of plasma lactic acid were unmeasured at 30 d, increased at 90 d in all BKME-exposed groups except the lowest strength of untreated effluent, and elevated at 200 d in all effluent-exposed groups. The stamina of these fish as determined by critical swimming speeds in freshwater was unaffected by exposure to pulpmill effluent for 90 d and unmeasured for other exposures. Based on the changes in intermediary metabolism for BKME-exposed fish at 30, 90, and 200 d, it was concluded that these fish remained in a state of chronic stress and did not acclimate to prolonged exposure to pulpmill effluent. Treatment of this waste reduced or removed its acute (lethal) toxicity but did not alter the biochemical effects caused by chronic exposure. Key words: stress, growth, proximate analyses, albumin, electrolyte, glycogen, glucose, lactate, critical swimming speed, acclimation

Glycogen Stores in Trout Tissues Before and After Stream Planting

Changes in the glycogen reserves of epaxial and heart muscle of trout were followed after stream planting. Muscle glycogen recovered quickly in large fish; more slowly in smaller ones, and was related to earlier reported changes in liver glycogen and blood lactic acid. Heart glycogen increased initially, but fell again shortly after feeding became stabilized. Muscle glycogen reserves of wild trout were lower in the presence of hatchery fish than in their absence. A depletion of some metabolite, such as glycogen, in conjunction with an increased body demand due to raised basal metabolism was suggested as a factor in delayed mortality.

The effect of hypoxia and ACTH on the carbohydrate reserve in tissues of the white rat

The author studied the effect of preliminary ACTH administration of glycogen and lactic acid concentrations in liver, skeletal muscle, and myocardium of male white rats during oxygen deficiency resulting from reduced barometric pressure and in the posthypoxic period. It was shown that preliminary administration of ACTH (with a total dose of 12 units) to rats later subjected to acute oxygen deficiency markedly reduces the fall in glycogen content in liver and skeletal muscle and simultaneously inhibits the accumulation of lactic acid in these organs. It also leads to more rapid restoration of liver and skeletal muscle glycogen reserves, and more complete elimination of excess lactic acid, during the posthypoxic period. Under conditions of hypoxia and posthypoxia, preliminary administration of ACTH has no significant effect on the cardiac glycogen reserve.