![]() Although we will discuss a broad range of issues related to exercise-induced oxidative stress, it is impossible for a brief review to address all aspects of this expansive field of study. The article will end with a discussion of redox control and skeletal muscle adaptation to exercise training. We will also discuss the redox modulation of muscle force production/fatigue and address redox sensitive targets within skeletal muscle. This will be followed with a historical synopsis of research in the field of exercise-induced oxidative stress and a discussion of cellular sources of oxidants during exercise. We will begin with an overview of radical species, the concept of oxidative stress and a discussion of cellular antioxidant systems. Our approach will be to provide a synopsis of major principles rather than a detailed analysis of individual investigations. This article will discuss the role that free radicals play in skeletal muscle function and adaptation to exercise. Although high levels of free radicals can damage cellular components, physiological levels of radicals and other oxidants play an important role in cells including the control of gene expression, regulation of cell signaling pathways, and modulation of skeletal muscle force production ( 111, 310, 325, 326, 375). ![]() It is clear that contracting skeletal muscles generate free radicals and that prolonged and intense exercise can promote oxidative damage to active myofibers ( 11, 96, 108, 115, 183, 329, 333). Ongoing research continues to explore the redox-sensitive targets in muscle that are responsible for both redox-regulation of muscle adaptation and oxidant-mediated muscle fatigue. Interestingly, low and physiological levels of reactive oxygen species are required for normal force production in skeletal muscle, but high levels of reactive oxygen species result in contractile dysfunction and fatigue. Furthermore, numerous products associated with oxidant-modulated genes have been identified and include antioxidant enzymes, stress proteins, and mitochondrial electron transport proteins. This oxidant-mediated change in gene expression involves changes at transcriptional, mRNA stability, and signal transduction levels. Further, oxidants regulate numerous cell signaling pathways and modulate the expression of many genes. Regardless of the sources of oxidants in contracting muscles, intense and prolonged exercise can result in oxidative damage to both proteins and lipids in the contracting myocytes. Although the sources of oxidant production during exercise continue to be debated, growing evidence suggests that mitochondria are not the dominant source. It is well established that contracting muscles produce both reactive oxygen and nitrogen species.
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