Hormesis and Exercise: How the Cell Copes with Oxidative Stress
- 1 University of Wisconsin-Madison, United States
- 2 Semerweis University, Hungary
- 3 Tokyo Metropolitan Gerontology Research Institute, Japan
Contraction-induced production of reactive oxygen and nitrogen species has been shown to cause oxidative stress to skeletal muscle, heart and other organs. As an adaptive response, muscle antioxidant defense systems are upregulated in response to exercise to restore intracellular prooxidantantioxidant homeostasis. Thus, both young and old animals and humans involved in regular exercise have shown reduced oxidative damage during acute physical exertion at accustomed or excessive intensity, or under oxidative challenges otherwise deemed detrimental. The current article provides a brief review of this exercise-induced hormesis with the emphasis on the role of redox sensitive signal transduction pathways (mainly nuclear factor κB and mitogen-activated protein kinase) that can activate the gene expression of antioxidant enzymes and proteins. Molecular mechanisms and gene targets for these signaling pathways, as well as the biological significance of the adaptations, are discussed.
Copyright: © 2008 Li Li Ji, Zsolt Radak and Sataro Goto. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
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- oxidative stress
- reactive oxygen species