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Reactive Oxygen Species: Impact on Skeletal Muscle

  1. Scott K. Powers1,
  2. Li Li Ji2,
  3. Andreas N. Kavazis1,
  4. Malcolm J. Jackson3

Published Online: 1 APR 2011

DOI: 10.1002/cphy.c100054

Comprehensive Physiology

Comprehensive Physiology

How to Cite

Powers, S. K., Ji, L. L., Kavazis, A. N. and Jackson, M. J. 2011. Reactive Oxygen Species: Impact on Skeletal Muscle. Comprehensive Physiology. 1:941–969.

Author Information

  1. 1

    Department of Applied Physiology and Kinesiology, University of Florida, Gainesville, Florida

  2. 2

    Department of Kinesiology, University of Wisconsin, Madison, Wisconsin

  3. 3

    Institute of Ageing and Chronic Disease, University of Liverpool, Liverpool, United Kingdom

Publication History

  1. Published Online: 1 APR 2011


It is well established that contracting muscles produce both reactive oxygen and nitrogen species. Although the sources of oxidant production during exercise continue to be debated, growing evidence suggests that mitochondria are not the dominant source. 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. Further, oxidants regulate numerous cell signaling pathways and modulate the expression of many genes. This oxidant-mediated change in gene expression involves changes at transcriptional, mRNA stability, and signal transduction levels. Furthermore, numerous products associated with oxidant-modulated genes have been identified and include antioxidant enzymes, stress proteins, and mitochondrial electron transport proteins. 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. 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. © 2011 American Physiological Society. Compr Physiol 1:941-969, 2011.