Impact of Reactive Oxygen Species and the Interplay of Antioxidants during Physical Exercise in Skeletal Muscles

Review Article

Impact of Reactive Oxygen Species and the Interplay of Antioxidants during Physical Exercise in Skeletal Muscles

Freya Scott*

Department of Biochemistry, University of Southampton, Southampton, UK

Published: 12 September 2018

Abstract

Skeletal muscle, a dynamic and metabolically active tissue, is profoundly influenced by redox homeostasis an essential equilibrium between reactive oxygen species (ROS) production and antioxidant defenses. Physical exercise, while beneficial, imposes oxidative stress on muscle fibers by increasing ROS generation. Historically viewed primarily as detrimental, ROS are now understood to play a dual role in skeletal muscle physiology. At elevated levels, ROS can cause cellular damage, contributing to fatigue, inflammation, and even muscle atrophy under chronic exposure. However, at physiological concentrations, ROS function as essential signaling molecules, regulating key adaptive processes such as mitochondrial biogenesis, glucose metabolism, and muscle hypertrophy. Central to managing exercise-induced ROS are endogenous antioxidants molecular and enzymatic defense systems that neutralize oxidative agents and maintain redox balance. Enzymes such as superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) form the first line of defense, rapidly detoxifying superoxide and hydrogen peroxide. These antioxidants are not static; rather, their expression and activity are modulated by exercise, particularly through redox-sensitive transcription factors like nuclear factor erythroid 2-related factor 2 (Nrf2). This regulatory mechanism underscores how ROS themselves can stimulate adaptive upregulation of antioxidant capacity, fostering resilience against future oxidative insults.

This review builds upon foundational insights, to present a current perspective on the sources and signaling roles of ROS in skeletal muscle during exercise. Special emphasis is placed on the dynamic interplay between ROS and endogenous antioxidants, highlighting how this balance determines whether oxidative signals yield beneficial adaptations or pathological consequences. Understanding these processes is crucial for developing targeted interventions that harness the benefits of ROS signaling while minimizing oxidative stress, particularly in clinical populations or athletes exposed to high training loads.

Keywords: HIV; Liver dysfunction; HAART; Hepatotoxicity; Liver biomarkers; Co-infection; Hepatic fibrosis; Antiretroviral therapy