Exercise-induced oxidative stress in humans: Cause and consequences

被引:319
作者
Powers, Scott K. [1 ]
Nelson, W. Bradley [1 ]
Hudson, Matthew B. [1 ]
机构
[1] Univ Florida, Dept Appl Physiol & Kinesiol, Gainesville, FL 32611 USA
关键词
Skeletal muscle; Mitochondria; Reactive oxygen species; Muscle fatigue; Free radicals; SARCOPLASMIC-RETICULUM CA2+-ATPASE; MUSCLE MITOCHONDRIAL BIOGENESIS; N-ACETYLCYSTEINE INFUSION; VITAMIN-E SUPPLEMENTATION; FREE-RADICAL PRODUCTION; NADPH OXIDASE ACTIVITY; MOUSE SKELETAL-MUSCLE; CA2+ RELEASE CHANNEL; REACTIVE OXYGEN; HYDROGEN-PEROXIDE;
D O I
10.1016/j.freeradbiomed.2010.12.009
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
The observation that muscular exercise is associated with oxidative stress in humans was first reported over 30 years ago. Since this initial report, numerous studies have confirmed that prolonged or high-intensity exercise results in oxidative damage to macromolecules in both blood and skeletal muscle. Although the primary tissue(s) responsible for reactive oxygen species (ROS) production during exercise remains a topic of debate, compelling evidence indicates that muscular activity promotes oxidant production in contracting skeletal muscle fibers. Mitochondria, NADPH oxidase, PLA(2)-dependent processes, and xanthine oxidase have all been postulated to contribute to contraction-induced ROS production in muscle but the primary site of contraction-induced ROS production in muscle fibers remains unclear. Nonetheless, contraction-induced ROS generation has been shown to play an important physiological function in the regulation of both muscle force production and contraction-induced adaptive responses of muscle fibers to exercise training. Although knowledge in the field of exercise and oxidative stress has grown markedly during the past 30 years, this area continues to expand and there is much more to be learned about the role of ROS as signaling molecules in skeletal muscle. (C) 2010 Elsevier Inc. All rights reserved.
引用
收藏
页码:942 / 950
页数:9
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