脂质过氧化
内质网
线粒体生物发生
线粒体
耐力训练
内科学
内分泌学
衰老自由基理论
激进的
化学
维生素E
生物化学
抗氧化剂
生物
医学
作者
Kelvin J.A. Davies,Alexandre Quintanilha,George A. Brooks,Lester Packer
标识
DOI:10.1016/s0006-291x(82)80124-1
摘要
We report a two- to three-fold increase in free radical (R•) concentrations of muscle and liver following exercise to exhaustion. Exhaustive exercise also resulted in decreased mitochondrial respiratory control, loss of sarcoplasmic reticulum (SR) and endoplasmic reticulum (ER) integrity, and increased levels of lipid peroxidation products. Free radical concentrations, lipid peroxidation, and SR, ER, and mitochondrial damage were similar in exercise exhausted control animals and non-exercised vitamin E deficient animals, suggesting the possibility of a common R• dependent damage process. In agreement with previous work showing that exercise endurance capacity is largely determined by the functional mitochondrial content of muscle (1–4), vitamin E deficient animals endurance was 40% lower than that of controls. The results suggest that R• induced damage may provide a stimulus to the mitochondrial biogenesis which results from endurance training.
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