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正常细胞的一生中可以产生活性氧基团 (ROS)。生理状态下 ,线粒体呼吸链是 ROS主要来源 ,其中不多于线粒体总氧耗的 5 %用于产生 ROS。研究已经表明 ,在剧烈有氧运动时骨骼肌 ROS生成增多 ,但是线粒体在 ROS生成增多中的量化作用仍不十分清楚。大强度运动可引起线粒体出现各种形式的氧化损伤 ,如脂质过氧化、蛋白质氧化、氧化还原状态紊乱及酶的失活等。这些生物化学的修饰作用将导致以呼吸链缺损和解偶联为标志的线粒体能量转换功能的下降。长期有氧训练可以通过抗氧化酶的适应性改变增加线粒体抗氧化应激的能力 ,而过度训练则因“氧化—抗氧化”的失衡损害于线粒体
Normal cells can produce reactive oxygen species (ROS) throughout their lives. Physiologically, the mitochondrial respiratory chain is the major source of ROS, with no more than 5% of the total mitochondrial oxygen consumption used to produce ROS. Studies have shown that there is an increase in skeletal muscle ROS production during intense aerobic exercise, but the quantitative role of mitochondria in ROS production is still not well understood. High-intensity exercise can cause various forms of mitochondrial oxidative damage, such as lipid peroxidation, protein oxidation, oxidation and reduction disorders and enzyme inactivation. These biochemical modifications will lead to a decrease in mitochondrial energy conversion function that is characterized by respiratory chain defects and uncoupling. Long-term aerobic training can alter the ability of mitochondria to increase oxidative stress through the adaptation of antioxidant enzymes, whereas over-training damages the mitochondria due to the imbalance of “oxidation-anti-oxidation”