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Mechanisms of muscle fatigue in intense exercise.
  • H. Green
  • Chemistry, Medicine
  • Journal of sports sciences
  • 1 June 1997
Increased fatigue resistance would appear to depend on carefully planned programmes designed to adapt the excitation and contraction processes, the cytoskeleton and the metabolic systems, not only to tolerate but also to minimize the changes in the intracellular environment that are caused by the intense activity. Expand
Effects of training duration on substrate turnover and oxidation during exercise.
It is concluded that long-term training induces a progressive increase in fat utilization mediated by a greater oxidation of fats from intramuscular sources and a reduction in glucose oxidation. Expand
Progressive effect of endurance training on metabolic adaptations in working skeletal muscle.
The results show that a period of short-term training results in many characteristic training adaptations but that these adaptations occurred before increases in mitochondrial potential, which were linked to the increase in muscle mitochondrial capacity. Expand
Skeletal muscle biochemistry and histology in ambulatory patients with long-term heart failure.
Major alterations in skeletal muscle histology and biochemistry in patients with long-term heart failure are demonstrated, including fiber atrophy, a decrease in percentage of composition of type I fibers, and an increase in type IIb fibers accompanied by a decreases in oxidative enzyme capacity. Expand
Human neuromuscular fatigue is associated with altered Na+-K+-ATPase activity following isometric exercise.
It is demonstrated that Na+-K+- ATPase activity is reduced by sustained isometric exercise in humans from that in a matched Con leg and that this reduction in Na-K-ATPases activity is associated with loss of excitability as indicated by M-wave alterations. Expand
Operation Everest II: structural adaptations in skeletal muscle in response to extreme simulated altitude.
The data indicate that chronic, severe hypoxia on its own does not result in an increase in absolute muscle capillary number or a de novo synthesis of mitochondria. Expand
Increases in submaximal cycling efficiency mediated by altitude acclimatization.
It is concluded that, because resting VO(2) was unchanged, net efficiency is enhanced during submaximal exercise after a mountaineering expedition when the exercise is performed soon after return to sea level conditions. Expand
Increases in human skeletal muscle Na(+)-K(+)-ATPase concentration with short-term training.
Not only is training capable of inducing an upregulation in sarcolemmal Na(+-K(+)-ATPase concentration in humans, but provided that the exercise is of sufficient intensity and duration, the upregulation can occur within the first week of training. Expand
Operation Everest II: adaptations in human skeletal muscle.
The hypothesis, at least in humans, that, at the level of the muscle cell, extreme hypobaric hypoxia elicits adaptations directed toward maximizing oxidative function is not supported. Expand
Capillary density of skeletal muscle: a contributing mechanism for exercise intolerance in class II-III chronic heart failure independent of other peripheral alterations.
The inverse relationship with peak oxygen consumption seen in the CHF group suggests that a reduction in microvascular density of skeletal muscle may precede other skeletal muscle alterations and play a critical role in the exercise intolerance characteristic of patients with CHF. Expand