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Physical activity in the form of exercise requires the metabolism of bodily fuel reserves to provide energy for muscle contraction. Under normal circumstances, very little protein is metabolized to provide the energy for muscle contraction. At rest and at low exercise intensities, the metabolism of fat provides a considerable proportion of the energy for resting metabolic processes and muscle contraction. However, at exercise intensities at which athletes train and compete, the metabolism of bodily carbohydrate reserves (eg, blood glucose and liver and muscle glycogen) provides the predominant fuel for muscle contraction. Furthermore, when these substrates reach critically low amounts or are decreased by some amount, fatigue occurs. There is a significant body of literature examining the effects of ingestion of various types of sugars at various times during exercise and during recovery from exercise on carbohydrate fuel reserves and on physical performance.

The effects of moderate- or high-carbohydrate diets on muscle glycogen and performance in runners and cyclists over 7 consecutive days of training were determined. Muscle biopsies were performed on 4 separate days before exercise for 1 h at 75% peak oxygen consumption (VO2) followed by five, 1-min sprints. After the training session on day 7, subjects ran or cycled to exhaustion at 80% peak VO2. Muscle glycogen for cyclists and runners was maintained with the high-carbohydrate diet but was reduced 30-36% (P < 0.05) with the moderate-carbohydrate diet. All subjects completed all training sessions, and there were no differences in times to exhaustion on day 7. For cyclists and runners, consuming a moderate-carbohydrate diet over 7 d of intense training reduces muscle glycogen but has no apparent deleterious effect on training capability or high-intensity exercise performance. A high-carbohydrate diet maintains muscle glycogen, but this has no apparent benefit on training capability or high-intensity exercise performance.

The effects of consuming two different amounts of liquid carbohydrate 1 h before exercise on the metabolic responses during exercise and on exercise performance were determined. Subjects consumed either 1.1 g (LC) or 2.2 g (HC) carbohydrate/kg body mass or a placebo (P). Subjects cycled at 70% of maximal oxygen consumption (VO2max) for 90 min and then underwent a performance trial. Blood glucose and insulin responses during exercise were different among the three trials. Total carbohydrate oxidation was greater for the carbohydrate trials compared with P. Time-trial performance was significantly improved by LC and HC. Despite elevated insulin concentrations at the start of and during exercise, and despite an initial drop in blood glucose, consumption of between 1.1 and 2.2 g liquid carbohydrate/kg body mass 60 min before moderately intense prolonged exercise can improve performance, presumably via enhanced carbohydrate oxidation.

We tested the effects of 9 d of a high-carbohydrate diet (80% of calories as CHO, 80% CHO diet) vs. a moderate-CHO diet (43% of calories as CHO, 43% CHO diet) on the abilities of collegiate swimmers to maintain a high intensity of interval swim training. Interval swim times and other physiological indices were recorded the last 5 d of each diet. Swim-interval distances ranged from 50-m interval sets to continuous 3000-m swims. There were no diet effects on mean swim velocities for any interval distance, and mean (+/- SEM) velocities for all swims were identical for both diets. There were no diet effects on the physiological indices; however, postswim blood lactate concentrations were higher after the 80% CHO diet. When mean +/- SEM daily caloric intake is 19.56 +/- 2.16 MJ (4675 +/- 516 kcal) for swimmers undertaking swim training to develop aerobic capacity, an 80% CHO diet provides no advantage over a 43% CHO diet for maintaining interval-swim-training intensity.

This study examined the effect of the type, amount, and the frequency of feeding of carbohydrates on muscle glycogen resynthesis after running. Trained male runners performed a 16.1 km run at 80% VO2 max to decrease gastrocnemius glycogen levels. A complex or simple carbohydrate diet (approximately 3000 kcal) resulted in similar muscle glycogen levels 24 h after exercise. Forty-eight hours after exercise the complex carbohydrate diet resulted in significantly higher (p less than 0.05) muscle glycogen levels. Consuming increasing amounts of carbohydrate, between 88 to 648 g carbohydrate/day, resulted in increasingly larger amounts of muscle glycogen resynthesis (24 h) after exercise. Frequent feedings of a high carbohydrate diet did not enhance muscle glycogen synthesis when compared to equal amounts of carbohydrates in two meals. It appears that muscle glycogen can be normalized between daily strenuous running activity.

Serial total creatine kinase (CK) and CK MB activities were determined in the serum of seven runners following a marathon race and compared to enzyme activities in the sera from five patients following acute myocardial infarction (AMI). In the runner's sera, total CK and CK MB activities were significantly elevated at 1, 24, 48 and 72 hours post marathon race when compared to the 1 hour pre-marathon samples (p less than 0.01). Serum CK MB activities peaked at 24 hours in both groups of subjects. The MB activities 24 hours following the marathon were substantially higher (91 +/- 30 U/l; mean +/- SD) than the MB activities 24 hours following AMI (46 +/- 38 U/l). However, the percentages of CK MB 24 hours following the marathon and AMI were almost identical (7.0 +/- 2.4% and 7.2 +/- 2.3%, respectively). Furthermore, CK and CK MB clearances were significantly prolonged (p less than 0.02 and p less than 0.001, respectively) following the marathon race (T 1/2 CK, 49 hours; T 1/2 CK MB, 29 hours) as compared to following AMI (T 1/2 CK, 27 hours; T 1/2 CK MB, 12 hours). These results suggest release of CK MB from the skeletal muscle of marathon runners. Therefore, we recommend that elevation of CK MB in the range indicative of myocardial damage be interpreted with caution in long-distance runners.

This study describes the events occurring in exercise-induced muscular necrosis. Biopsies of the gastrocnemius muscles of volunteer human marathon runners were extracted prior to and at intervals for 7 days following a marathon, and investigated ultrastructurally. Most of the preparations, including the pre-marathon samples, showed evidence of muscle fiber necrosis and inflammation. These preparations had many mitochondria, erythrocytes, leukocytes and other phagocytic cells within the extracellular and extravascular spaces. Less frequently observed were Z-line streaming and degeneration, contracture knots, disrupted sarcolemma, presence of erythrocytes within the muscle fibers, and empty basal lamina tubes in which the contents of the fibers and the sarcolemma had broken down to leave only the basal lamina outlining the former fiber. These abnormal conditions were most prevalent at 1 and 3 days after the marathon. These ultrastructural changes are compared and correlated with the reports of clinical manifestations of rhabdomyolysis and myoglobinuria. Because the abnormalities persist for the 7 day duration of these observations, and because many of these were observed in the pre-marathon biopsies, we conclude that both the intensive training for, and the marathon itself, induce inflammation and fiber necrosis which are manifested in the clinical symptoms for rhabdomyolysis and myoglobinuria. The inflammatory reaction that accompanies these activities may be a major factor in post-exercise soreness. The combined influences of training and necrosis are discussed in relation to muscle fiber type compositions of endurance athletes.

The effect of altering the percent of dietary carbohydrate on the rate of skeletal muscle glucose uptake was studied using the perfused rat hindlimb preparation. The rats received either a high carbohydrate (HC; 65%), mixed (M; 35%) or low carbohydrate (LC; 10%) isocaloric diet for 7 days. With 0.1 mU/ml of insulin in the perfusate, the muscle of rats on the HC diet had a 33% increase in the rate of glucose uptake and the muscle of rats fed the LC diet a 23% decrease in the rate of glucose uptake when compared to the muscle of rats fed the M diet (3.34 mumol/g/30 min). With 10.0 mU/ml of insulin in the perfusate, ie maximal insulin stimulation, the rate of glucose uptake showed a similar dietary effect as that obtained with 0.1 mU/ml insulin. Compared to the M diet (8.67 mumol/g/30 min), the rate of glucose uptake increased 26% in muscle of rats from the HC group and decreased by 20% in muscle of rats from the LC group. Diet had no effect on the rate of muscle glucose uptake in the absence of insulin. Under both maximal and submaximal insulin stimulation, glycogen accumulation was greatest in muscle from HC fed rats and least in muscle from LC fed rats. During perfusion muscle intracellular free glucose and glucose-6-phosphate accumulation for the three dietary groups was negligible. The groups did not differ significantly in their muscle hexokinase or beta-hydroxyl acyl CoA dehydrogenase activities.(ABSTRACT TRUNCATED AT 250 WORDS)