Abstract
Unaccustomed and/or exhaustive exercise generates excessive free radicals and reactive oxygen and nitrogen species leading to muscle oxidative stress-related damage and impaired contractility. Conversely, a moderate level of free radicals induces the body’s adaptive responses. Thus, a low oxidant level in resting muscle is essential for normal force production, and the production of oxidants during each session of physical training increases the body’s antioxidant defenses. Mitochondria, NADPH oxidases and xanthine oxidases have been identified as sources of free radicals during muscle contraction, but the exact mechanisms underlying exercise-induced harmful or beneficial effects yet remain elusive. However, it is clear that redox signaling influences numerous transcriptional activators, which regulate the expression of genes involved in changes in muscle phenotype. The mitogen-activated protein kinase family is one of the main links between cellular oxidant levels and skeletal muscle adaptation. The family components phosphorylate and modulate the activities of hundreds of substrates, including transcription factors involved in cell response to oxidative stress elicited by exercise in skeletal muscle. To elucidate the complex role of ROS in exercise, here we reviewed the literature dealing on sources of ROS production and concerning the most important redox signaling pathways, including MAPKs that are involved in the responses to acute and chronic exercise in the muscle, particularly those involved in the induction of antioxidant enzymes.
Highlights
For several years the practice of physical activity has expanded in scope from competitive sports to disease prevention and health promotion
The idea is widely shared that the utilization of oxygen by aerobic organisms exposes them to the attack of reactive oxygen and nitrogen species, which can initiate chain reactions leading to oxidative damage of important biological molecules
Aerobic organisms are provided with an efficient antioxidant defense system that allows them to neutralize the oxidative effects of reactive metabolites of oxygen and nitrogen
Summary
For several years the practice of physical activity has expanded in scope from competitive sports to disease prevention and health promotion. The results of numerous studies have shown that regular physical activity reduces risk of several diseases including cardiovascular diseases, type 2 diabetes (T2DM), some types of cancer, osteoporosis, fall-related injuries, depression, and obesity [1,2,3] Despite these clear benefits, little is known about the adaptive mechanisms involved in the protection offered by exercise even though to date accumulating evidence has allowed establishing that the production of free radicals represents a potential link between exercise and protection against diseases. Aerobic physical activity induces skeletal muscle adaptive responses [1] able to determine an increased resistance to conditions, among which prolonged or strenuous exercise, in which ROS production increase [7,8,9]. This review, after examining the link between physical activity and ROS production, focuses on signaling pathways, such as MAPKS and transcription factors and cofactors, through which ROS produced in the regular physical activity elicit the adaptive responses implicated in increased antioxidant defenses effectiveness and mitochondrial content of skeletal muscle
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