Higuchi M, Cartier L J, Chen M, Holloszy J O
J Gerontol. 1985 May;40(3):281-6. doi: 10.1093/geronj/40.3.281.
Cellular damage caused by free radical reactions may play a role in the aging process. A bout of exercise can increase free radical concentration with damage to mitochondria in muscle (Davies et al., 1982). This study was undertaken to determine if muscle adapts to exercise training with an enhancement of enzymatic defenses against free radical damage. A program of running that induced two-fold increases in mitochondrial enzymes in leg muscles of rats resulted in no increase in catalase or cytoplasmic superoxide dismutase (SOD) activities. Mitochondrial SOD activity was increased 37% in fast-twitch red and slow-twitch red types of muscle and 14% in white muscle. Thus, despite an increase in mitochondrial SOD, the ratio of SOD to mitochondrial citrate cycle and respiratory chain enzymes was decreased. It seems unlikely that increased capacity for enzymatic scavenging of superoxide radical is a major protective adaptation against free radical damage in exercise-trained muscle.
自由基反应引起的细胞损伤可能在衰老过程中起作用。一次运动可增加自由基浓度,并对肌肉中的线粒体造成损伤(戴维斯等人,1982年)。本研究旨在确定肌肉是否通过增强针对自由基损伤的酶防御能力来适应运动训练。一项使大鼠腿部肌肉线粒体酶增加两倍的跑步计划,并未使过氧化氢酶或细胞质超氧化物歧化酶(SOD)活性增加。快速收缩红色和慢速收缩红色类型肌肉中的线粒体SOD活性增加了37%,白色肌肉中增加了14%。因此,尽管线粒体SOD增加,但SOD与线粒体柠檬酸循环及呼吸链酶的比率却降低了。看来,超氧化物自由基酶清除能力的增强不太可能是运动训练肌肉中针对自由基损伤的主要保护性适应机制。