Exercise Training and Skeletal Muscle Antioxidant Enzymes: An Update

Abstract

The pivotal observation that muscular exercise is associated with oxidative stress in humans was first reported over 45 years ago. Soon after this landmark finding, it was discovered that contracting skeletal muscles produce oxygen radicals and other reactive species capable of oxidizing cellular biomolecules. Importantly, the failure to eliminate these oxidant molecules during exercise results in oxidation of cellular proteins and lipids. Fortuitously, muscle fibers and other cells contain endogenous antioxidant enzymes capable of eliminating oxidants. Moreover, it is now established that several modes of exercise training (e.g., resistance exercise and endurance exercise) increase the expression of numerous antioxidant enzymes that protect myocytes against exercise-induced oxidative damage. This review concisely summarizes the impact of endurance, high-intensity interval, and resistance exercise training on the activities of enzymatic antioxidants within skeletal muscles in humans and other mammals. We also discuss the evidence that exercise-induced up-regulation of cellular antioxidants reduces contraction-induced oxidative damage in skeletal muscles and has the potential to delay muscle fatigue and improve exercise performance. Finally, in hopes of stimulating further research, we also discuss gaps in our knowledge of exercise-induced changes in muscle antioxidant capacity.

Hormonal, immune, and oxidative stress responses to blood flow‐restricted exercise

“…However, where GP is active during low levels of radicals, catalase seems only to be activated when higher concentrations of H 2 O 2 are present in the cell. 180 For catalase, postexercise increases were greater with LL-FFRE compared to LL-BFRRE and HL-FFRE, and there was a significant reduction from pre-to post-exercise following LL-FFRE with no changes with LL-BFRRE and HL-FFRE. Nitric oxide (NO) is produced by the oxidation of one of the terminal guanidino nitrogen atoms of Larginine and through the nitrate-nitrite-nitric oxide pathway, 190 and is catalyzed by NOS.…”

“…This could indicate that LL-BFRRE induces higher metabolic demands and is a potential cause for hypertrophy associated with LL-BFRRE, as ROS is a regulator for muscle cell signaling pathways. 180,205 In mammals, three distinct isoforms exist: nNOS (type I), iNOS (type II), and eNOS (type III). nNOS is also an isoform of NOS located in skeletal muscles and nNOS is more predominant in fast-twitch fibers than slow-twitch fibers.…”

Muscle p62 stimulates the expression of antioxidant proteins alleviating cancer cachexia

“…Increased muscle contractile activity, as observed with regular exercise, prevents oxidative stress-induced muscle atrophy, at least partially, by improving the antioxidant defense system. 49,[51][52][53] We have previously reported that regular exercise increases antioxidant proteins, nuclear Nrf2 protein, and Nrf2 DNA-binding activity in association with increased p62 phosphorylation (Ser351) in mouse muscle 22 thereby demonstrating an effective strategy to stimulate the p62-Nrf2 pathway. However, future studies examining if the beneficial effects of exercise in cancer cachexia are dependent on the p62-Nrf2 pathway are still required.…”

Influence of Isolated Resistance Exercise on Cardiac Remodeling, Myocardial Oxidative Stress, and Metabolism in Infarcted Rats

“…Therefore, exercise reduced oxidative stress with no influence on antioxidant enzyme activity. In skeletal muscles, regular resistance training increases the abundance/activity of antioxidant enzymes, therefore increasing resistance to oxidative stress [ 52 ]. Our data suggest that the effects of resistance exercise on myocardium could differ from those on skeletal muscles.…”