运动时骨骼肌糖、脂肪氧化的交互作用及机制

运动时骨骼肌两种重要能源底物，碳水化合物和脂肪在氧化供能时存在交互关系，且与G-FA循环理论以外的机制有关。运动中增加脂肪的可用性可降低骨骼肌PDH活性，减少肌糖原分解，可能是通过增加线粒体NADH可用性，进而缓解运动诱导的游离ADP，AMP和Pi累积增加；增加外源性CHO可用性能减少骨骼肌脂肪氧化，可能是通过血浆胰岛素水平增加和FFA可用性下降，也可能是通过减少脂肪转运进入肌肉和/或降低线粒体速率等机制；运动强度增加机体更依赖于CHO供能，可能通过肌肉内、外机制下调脂肪代谢。

Interaction and Mechanism of Carbohydrate and Lipid Oxidation in Skeletal Muscle

As the two important energy substrates of skeletal muscle, carbohydrate is reciprocally related to fat oxidation, and to the mechanism beyond the original G-FA cycle theory. Increased availability of fat can reduce the activity of PDH and down-regulate CHO oxidation, probably by increasing the mitochondrial NADH availability, and weakening exercise-induced the accumulation of ADP, AMP and Pi. The increase of the availability of exogenous CHO can down-regulate lipid oxidation, possibly through increased plasma insulin levels and decreased FFA availability. It is also possible that fat is transported into muscle and/or the rate of mitochondrial oxidation is reduced. In high intensity exercise, skeletal muscle is more dependent on the CHO energy supply, which may be responsible for the regulation of lipid metabolism through the internal and external mechanisms.