Aoi Wataru, Naito Yuji, Yoshikawa Toshikazu
Laboratory of Health Science, Graduate School of Life and Environmental Sciences, Kyoto Prefectural University, Kyoto 606-8522, Japan.
Department of Molecular Gastroenterology and Hepatology, Graduate School of Medical Science, Kyoto Prefectural University of Medicine, Kyoto 602-8566, Japan.
Free Radic Biol Med. 2013 Dec;65:1265-1272. doi: 10.1016/j.freeradbiomed.2013.09.014. Epub 2013 Sep 27.
Skeletal muscle is a major tissue that utilizes blood glucose. A single bout of exercise improves glucose uptake in skeletal muscle through insulin-dependent and insulin-independent signal transduction mechanisms. However, glucose utilization is decreased in muscle damage induced by acute, unaccustomed, or eccentric exercise. The decrease in glucose utilization is caused by decreased insulin-stimulated glucose uptake in damaged muscles with inhibition of the membrane translocation of glucose transporter 4 through phosphatidyl 3-kinase/Akt signaling. In addition to inflammatory cytokines, reactive oxygen species including 4-hydroxy-2-nonenal and peroxynitrate can induce degradation or inactivation of signaling proteins through posttranslational modification, thereby resulting in a disturbance in insulin signal transduction. In contrast, treatment with factors that attenuate oxidative stress in damaged muscle suppresses the impairment of insulin sensitivity. Muscle-damaging exercise may thus lead to decreased endurance capacity and muscle fatigue in exercise, and it may decrease the efficiency of exercise therapy for metabolic improvement.
骨骼肌是利用血糖的主要组织。单次运动通过胰岛素依赖和非胰岛素依赖信号转导机制改善骨骼肌中的葡萄糖摄取。然而，在急性、不习惯或离心运动引起的肌肉损伤中，葡萄糖利用率会降低。葡萄糖利用率的降低是由于受损肌肉中胰岛素刺激的葡萄糖摄取减少，通过磷脂酰3-激酶/蛋白激酶B信号传导抑制葡萄糖转运蛋白4的膜转位所致。除炎症细胞因子外，包括4-羟基-2-壬烯醛和过氧亚硝酸盐在内的活性氧可通过翻译后修饰诱导信号蛋白降解或失活，从而导致胰岛素信号转导紊乱。相反，用减轻受损肌肉氧化应激的因子进行治疗可抑制胰岛素敏感性的损害。因此，损伤肌肉的运动可能导致运动耐力和肌肉疲劳下降，并且可能降低改善代谢的运动疗法的效率。
