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运动时 ,钙离子 (由PKC介导 )的前馈调节和细胞内代谢变化的反馈调节 (由AMPK介导 )是骨骼肌葡萄糖摄取的细胞内机制 ,一氧化氮、糖原和缺氧可能也参与其中。在恢复期 ,胰岛素敏感性提高似乎与胰岛素信号增强无关 ,而依赖于糖原水平。肌糖原含量是骨骼肌葡萄糖摄取的重要调节因素 ,它既能影响胰岛素信号瀑布 ,也能影响收缩介导的或AICAR诱导的AMPK活化 ,还影响糖原合成酶的亚细胞定位和活性。骨骼肌葡萄糖代谢的运动适应与MAPK信号瀑布有关。
During exercise, feedback regulation of calcium (mediated by PKC) and feedback regulation of intracellular metabolic changes (mediated by AMPK) are intracellular mechanisms of skeletal muscle glucose uptake, and nitric oxide, glycogen and hypoxia may also participate. During convalescence, the increase in insulin sensitivity appears to be independent of the increase in insulin signaling and is dependent on glycogen levels. Muscular glycogen content is an important regulator of skeletal muscle glucose uptake, affecting not only the insulin signaling cascade but also contraction-mediated or AICAR-induced AMPK activation and the subcellular localization and activity of glycogen synthase. Skeletal muscle glucose metabolism and exercise adaptation MAPK signal falls.