Available online 7 May 2024

Contracting skeletal muscles generate reactive oxygen species (ROS) from several locations with the cell

Although numerous ROS exist, hydrogen peroxide is recognized as a key ROS player in redox control of biological signaling

Contraction-induced ROS production triggers signaling pathways regulating mitochondrial biogenesis and the expression of numerous genes expressing mitochondrial proteins and antioxidant enzymes

Growing data indicate that exercise-induced ROS production is essential to achieve the full benefit of exercise-induced adaptation in skeletal muscles

The discovery that contracting skeletal muscle generates reactive oxygen species (ROS) was first reported over 40 years ago. The prevailing view in the 1980s was that exercise-induced ROS production promotes oxidation of proteins and lipids resulting in muscle damage. However, a paradigm shift occurred in the 1990s as growing research revealed that ROS are signaling molecules, capable of activating transcriptional activators/coactivators and promoting exercise-induced muscle adaptation. Growing evidence supports the notion that reduction-oxidation (redox) signaling pathways play an important role in the muscle remodeling that occurs in response to endurance exercise training. This review examines the specific role that redox signaling plays in this endurance exercise-induced skeletal muscle adaptation. We begin with a discussion of the primary sites of ROS production in contracting muscle fibers followed by a summary of the antioxidant enzymes involved in the regulation of ROS levels in the cell. We then discuss which redox-sensitive signaling pathways promote endurance exercise-induced muscle adaptation and debate the strength of the evidence supporting the notion that redox signaling plays an essential role in muscle adaptation to endurance exercise training. In hopes of stimulating future research, we highlight several important unanswered questions in this field.

Antioxidants

Mitochondrial biogenesis

Radicals

Redox signaling

© 2024 Published by Elsevier B.V. on behalf of Shanghai University of Sport.