HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via ISI Web of Science (1) Citing Articles via Google Scholar Google Scholar Articles by Powers, S. K. Articles by Jackson, M. J. Search for Related Content PubMed PubMed Citation Articles by Powers, S. K. Articles by Jackson, M. J.

Exercise-Induced Oxidative Stress: Cellular Mechanisms and Impact on Muscle Force Production

Department of Applied Physiology and Kinesiology, University of Florida, Gainesville, Florida; and Division of Metabolic and Cellular Medicine, University of Liverpool, Liverpool, United Kingdom

The first suggestion that physical exercise results in free radical-mediated damage to tissues appeared in 1978, and the past three decades have resulted in a large growth of knowledge regarding exercise and oxidative stress. Although the sources of oxidant production during exercise continue to be debated, it is now well established that both resting and contracting skeletal muscles produce reactive oxygen species and reactive nitrogen species. Importantly, intense and prolonged exercise can result in oxidative damage to both proteins and lipids in the contracting myocytes. Furthermore, oxidants can modulate a number of cell signaling pathways and regulate the expression of multiple genes in eukaryotic cells. 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, DNA repair 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 promote contractile dysfunction resulting in muscle weakness and fatigue. Ongoing research continues to probe the mechanisms by which oxidants influence skeletal muscle contractile properties and to explore interventions capable of protecting muscle from oxidant-mediated dysfunction.

This article has been cited by other articles:

				N. Eynon, M. Sagiv, Y. Meckel, J. A. Duarte, A. J. Alves, C. Yamin, M. Sagiv, E. Goldhammer, and J. Oliveira NRF2 intron 3 A/G polymorphism is associated with endurance athletes' status J Appl Physiol, July 1, 2009; 107(1): 76 - 79. [Abstract] [Full Text] [PDF]

				M. Ristow, K. Zarse, A. Oberbach, N. Kloting, M. Birringer, M. Kiehntopf, M. Stumvoll, C. R. Kahn, and M. Bluher Antioxidants prevent health-promoting effects of physical exercise in humans PNAS, May 26, 2009; 106(21): 8665 - 8670. [Abstract] [Full Text] [PDF]

				R. A. Jacobs, E. L. Donovan, and M. M. Robinson Parallels of snipe hunting and ROS research: the challenges of studying ROS and redox signalling in response to exercise J. Physiol., March 1, 2009; 587(5): 927 - 928. [Full Text] [PDF]