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Review
. 2015 Apr 10;5(2):356-77.
doi: 10.3390/biom5020356.

Impact of oxidative stress on exercising skeletal muscle

Peter Steinbacher  1 , Peter Eckl  2
Affiliations
Review

Impact of oxidative stress on exercising skeletal muscle

Peter Steinbacher et al. Biomolecules. .

Abstract

It is well established that muscle contractions during exercise lead to elevated levels of reactive oxygen species (ROS) in skeletal muscle. These highly reactive molecules have many deleterious effects, such as a reduction of force generation and increased muscle atrophy. Since the discovery of exercise-induced oxidative stress several decades ago, evidence has accumulated that ROS produced during exercise also have positive effects by influencing cellular processes that lead to increased expression of antioxidants. These molecules are particularly elevated in regularly exercising muscle to prevent the negative effects of ROS by neutralizing the free radicals. In addition, ROS also seem to be involved in the exercise-induced adaptation of the muscle phenotype. This review provides an overview of the evidences to date on the effects of ROS in exercising muscle. These aspects include the sources of ROS, their positive and negative cellular effects, the role of antioxidants, and the present evidence on ROS-dependent adaptations of muscle cells in response to physical exercise.

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Figures

Figure 1
Figure 1
Sources of reactive oxygen species (ROS) and endogenous antioxidants in skeletal muscle fibers. Following exercise, ROS are produced endogenously by mitochondria, NOXs, PLA2 and XO. In addition, exercise increases ROS production also in activated neutrophils and macrophages, endothelia of blood vessels and by catecholamines. Regular exercise leads to an increase of endogenous antioxidants, which are able to neutralize free radicals. A, adrenaline; CAT, catalase; Cu, Zn-SOD, copper-zinc superoxide dismutase; DA, dopamine; GPX, glutathione peroxidase; GSH, glutathione; IFN, interferon γ; IL-1, interleukin-1; Mn-SOD, manganese superoxide dismutase; NA, noradrenaline; NOX, nicotinamide adenine dinucleotide phosphate oxidase; PLA2, phospholipase A2; SR, sarcoplasmic reticulum; TNF, tumor necrosis factor; TxnRd2, thioredoxin reductase 2; XO, xanthine oxidase.
Figure 2
Figure 2
Deleterious and beneficial effects of exercise-induced ROS increase. Exercise produces ROS and whether they are beneficial or detrimental to health is dependent upon the ROS concentration, duration of ROS exposure and training status of the individual. A single bout of exhaustive exercise leads to strong increases of ROS, which cannot be buffered by endogenous antioxidants, particularly in untrained individuals. This results in severe oxidative damage, including muscle weakness and fatigue, DNA mutations, lipid peroxidation, mitochondrial dysfunction and apoptosis/necrosis. Trained persons have a higher level of adaptation and less health risks. ROS produced during regular exercise continuously increase the level of adaptation by improving antioxidant capacity, mitochondrial biogenesis, insulin sensitivity, cytoprotection and aerobic capacity of skeletal muscle.
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