Muscle samples were obtained from the gastrocnemius of 17 female and 23 male track athletes, 10 untrained women, and 11 untrained men. Portions of the specimen were analyzed for total phosphorylase, lactic dehydrogenase (LDH), and succinate dehydrogenase (SDH) activities. Sections of the muscle were stained for myosin adenosine triphosphatase, NADH2 tetrazolium reductase, and alpha-glycerophosphate dehydrogenase. Maximal oxygen uptake (VO2max) was measured on a treadmill for 23 of the volunteers (6 female athletes, 11 male athletes, 10 untrained women, and 6 untrained men). These measurements confirm earlier reports which suggest that the athlete's preference for strength, speed, and/or endurance events is in part a matter of genetic endowment. Aside from differences in fiber composition and enzymes among middle-distance runners, the only distinction between the sexes was the larger fiber areas of the male athletes. SDH activity was found to correlate 0.79 with VO2max, while muscle LDH appeared to be a function of muscle fiber composition. While sprint- and endurance-trained athletes are characterized by distinct fiber compositions and enzyme activities, participants in strength events (e.g., shot-put) have relatively low muscle enzyme activities and a variety of fiber compositions.
Seven men were studied during 30 min of treadmill exercise (approximately 70% VO2 max) to determine the effects of increased availability of plasma free fatty acids (FFA) and elevated plasma insulin on the utilization of muscle glycogen. This elevation of plasma FFA (1.01 mmol/1) with heparin (2,000 units) decreased the rate of muscle glycogen depletion by 40% as compared to the control experiment (FFA = 0.21 mmol/1). The ingestion of 75 g of glucose 45 min before exercise produced a 3.3-fold increase in plasma insulin and a 38% rise in plasma glucose at 0 min of exercise. Subsequent exercise increased muscle glycogen utilization and total carbohydrate (CHO) oxidation 17 and 13%, respectively, when compared to the control trial. This elevation of plasma insulin produced hypoglycemia (less than 3.5 mmol/1) in most subjects throughout the exercise. These data illustrate the regulatory influence of both plasma insulin and FFA on the rate of CHO usage during prolonged severe muscular activity.
Creatine supplementation enhanced fat-free mass, physical performance, and muscle morphology in response to heavy resistance training, presumably mediated via higher quality training sessions.
This study examined the effect of three exercise-diet regimens on muscle glycogen supercompensation and subsequent performance during a 20.9-km run. A diet containing 15% carbohydrate (CHO,L), 50% CHO (M), or 70% (CHO (H) was arranged in three trials as follows: trial A = 3 days L, 3 days H; trial B = 3 days M, 3 days H; trial C = 6 days M. For each trial a 5-day depletion-taper exercise sequence was conducted on the treadmill at 73% VO2 max. The runs were 90, 40, 40, 20, and 20 min, respectively. A day of rest preceded the 20.9-km performance run. Muscle biopsies were obtained from the gastrocnemius on days 4 and 7 (both prior to and after the performance run). Trials A, B, and C elevated muscle glycogen to 207, 203, and 159 mmol glucosyl units/kg wet tissue (mmG), respectively. The performance run in both trials A and B utilized significantly more glycogen than in trial C: 5.0 and 5.1 mmG/km vs. 3.1 mmG/km. There were, however, no differences in either performance run times or post-performance run glycogen levels between the trials. These data demonstrate that (1) muscle glycogen can be elevated to high levels with a moderate exercise-diet regimen; (2) initial muscle glycogen levels influence the amount subsequently utilized during exercise; (3) carbohydrate loading is of no benefit to performance for trained runners during a 20.9-km run.
In an effort to assess the effects of dehydration on the content of water and electrolytes (Na+, K+, Cl-, and Mg2+) in plasma and muscle tissue, eight men exercised in the heat (39.5 degrees C, 25%). Blood urine, and muscle biopsy samples were obtained before exercise and after the subjects had reduced their body weight by 2.2, 4.1, and 5.8%. On the average, plasma and muscle water (H2Om) contents were found to decline 2.4 and 1.2% for each percent decrease in body weight. Muscle sodium (Na+m) and chloride (Cl-m) content remained unchanged with dehydration, while muscle magnesium (Mg2+m) declined 12% as a result of the 5.8% dehydration. In terms of intracellular concentrations, K+i increased 7.2 and 10.6% at the 2.2 and 4.1% dehydration levels, respectively. Calculations of the resting membrane potential suggest that the water and electrolyte losses observed in these studies do not significantly alter the excitability of the muscle cell membrane.
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.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.