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PGC-1 alpha mediates a rapid, exercise-induced downregulation of glycogenolysis in rat skeletal muscle

机译:PGC-1α介导运动引起的大鼠骨骼肌糖原分解的快速下调

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Key points Long-term endurance exercise training results in a reduction in the rates of muscle glycogen depletion and lactic acid accumulation during submaximal exercise; this adaptation is mediated by an increase in muscle mitochondria. There is evidence suggesting that short-term training induces adaptations that downregulate glycogenolysis before there is an increase in functional mitochondria. We discovered that a single long bout of exercise induces decreases in expression of glycogenolytic and glycolytic enzymes in rat skeletal muscle; this adaptation results in slower rates of glycogenolysis and lactic acid accumulation in muscle during contractile activity. Two additional days of training amplified the adaptive response, which appears to be mediated by PGC-1; this adaptation is biologically significant, because glycogen depletion and lactic acid accumulation are major causes of muscle fatigue.
机译:要点长期耐力运动训练可减少次最大运动过程中肌肉糖原消耗和乳酸积累的速率;这种适应由肌肉线粒体的增加介导。有证据表明,在功能性线粒体增加之前,短期训练会诱导调节糖原分解的调节。我们发现,一次长时间的运动会诱导大鼠骨骼肌糖原分解酶和糖酵解酶的表达下降。这种适应导致收缩活动期间肌肉中糖原分解和乳酸积累的速率降低。另外两天的训练放大了适应性反应,这似乎是由PGC-1介导的。这种适应在生物学上很重要,因为糖原消耗和乳酸积累是肌肉疲劳的主要原因。

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