Abstract
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 prooxidant- antioxidant 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.
Highlights
Maintenance of oxidative -antioxidant homeostasis is critical for cell survival and normal function[1]
Bejma et al.[11,78] reported that free radical generation was significantly higher in skeletal muscle, heart and expression of thioredoxin reductase, the key enzyme to liver of old rats subjected to an acute bout of treadmill reduce oxidized TRX, was reportedly elevated in mouse running to exhaustion
Increased inducible NOS (iNOS) mRNA level after an acute bout of exercise in rat skeletal muscles has been reported by some authors [117,132], but not others[134]
Summary
Maintenance of oxidative -antioxidant homeostasis is critical for cell survival and normal function[1]. In the field of free radical biochemistry, one paradox continues to puzzle both researchers and the general public: physical activity demonstrates clear benefit to increase body fitness, prevent disease and improve quality of life, but heavy physical work has been shown to generate reactive oxygen and nitrogen species (RONS), which seriously threaten structural and functional integrity at the cellular, organic and systematic levels. RONS generated during exercise can cause oxidative stress and damage to skeletal muscle, heart and other organs, but research evidence demonstrates a critical role of RONS to serve as the chemical agents to maintain cellular milieu and to transfer message to vital cellular components to conduct physiological functions, such as contraction, bioenergetics, growth, proliferation and remodeling (adaptation). Skeletal muscle will be our primary concern, but heart and liver will be incorporated to enhance our understanding of how exercise affects the entire body homeostasis
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