Sullivan L
Ann Clin Res. 1982;14 Suppl 34:51-62.
The demand of the untrained skeletal muscle to produce additional mechanical work by utilizing more nutrients is the origin of the structural and metabolic adaptation of the muscle. The expanding capillary surface, in response to a lower vascular resistance during repeated contraction, enables the different fibre types to increase their oxygen extraction, and to adapt their uptake of substrates (glucose, FFA). The muscle fibre types in humans are selectively recruited for differing work intensity but the oxidative potential (SDH) increases in all types with long-term physical training. Details of the mechanism by which insulin promotes glucose uptake are unclear but there is some evidence that the hormonal stimulation involves cellular uptake of the insulin-receptor complex of the membrane. Hypoxia and raised cytoplasmic levels of calcium in muscle cells after work exert an insulin-like action on glucose uptake, which may be ascribed to the intracellular acidity.--The interrelationship between glucose and FFA oxidation is in part regulated by known key enzymes of the contracting muscle, but the exact extramuscular substrate mobilization appears to require both hormonal and supplementary feed-back control in storage organs.--During prolonged muscular exercise, the successive utilization of carbohydrate and fat from endogenous and exogenous stores can, however, in principle be attributed to known hormonal regulation.--Oral intake of glucose solution before and during work evokes a prolonged glucose utilization with relative hyperinsulinemia and hypoglucagonemia, preventing hepatic glycogenolysis. A prerequisite for successful endurance training is the improved capacity to use FFA as substrate. The necessary lipolysis in adipocytes is mainly mediated by an increased cellular exposure and sensitivity to catecholamines, but the delayed adaptation of the fat cells to their hormonal environment, especially insulin, in relation to the progress of the training is likely to modify the lipolytic response.
未经训练的骨骼肌通过利用更多营养物质来产生额外机械功的需求，是肌肉结构和代谢适应的起源。反复收缩期间，血管阻力降低，毛细血管表面积随之扩大，这使得不同纤维类型能够增加其氧气摄取量，并调整其底物（葡萄糖、游离脂肪酸）的摄取。人类的肌肉纤维类型会根据不同的工作强度被选择性地募集，但长期体育训练会使所有类型的肌肉纤维氧化潜力（琥珀酸脱氢酶）增加。胰岛素促进葡萄糖摄取的机制细节尚不清楚，但有证据表明，激素刺激涉及细胞膜胰岛素受体复合物的细胞摄取。工作后肌肉细胞中的缺氧和细胞质钙水平升高，对葡萄糖摄取具有胰岛素样作用，这可能归因于细胞内酸度。——葡萄糖和游离脂肪酸氧化之间的相互关系部分受收缩肌肉中已知关键酶的调节，但确切的肌肉外底物动员似乎需要储存器官中的激素和补充反馈控制。——然而，在长时间肌肉运动期间，内源性和外源性储存中碳水化合物和脂肪的相继利用原则上可归因于已知的激素调节。——在工作前和工作期间口服葡萄糖溶液会引起葡萄糖的长时间利用，并伴有相对高胰岛素血症和低胰高血糖素血症，从而防止肝糖原分解。成功进行耐力训练的一个先决条件是提高将游离脂肪酸用作底物的能力。脂肪细胞中必要的脂肪分解主要由细胞对儿茶酚胺的暴露增加和敏感性提高介导，但脂肪细胞相对于训练进展对其激素环境（尤其是胰岛素）的延迟适应可能会改变脂肪分解反应。
