EXERCISE-INDUCED OXIDATIVE STRESS AND ANTIOXIDANT DEFENSE IN ATHLETES: MECHANISMS, BIOMARKERS, AND IMPLICATIONS FOR PERFORMANCE AND RECOVERY: A NARRATIVE REVIEW

Abstract

Background: Muscular contraction increases the production of reactive oxygen and nitrogen species (ROS/RNS). Since the first reports in the late 1970s, exercise-induced oxidative stress has been reconceptualized from an unavoidable by-product of aerobic metabolism to a regulated signalling process that is required for training adaptation, while excessive or prolonged oxidant exposure remains capable of damaging lipids, proteins and DNA. Objective: To synthesize mechanistic, biomarker and applied evidence on exercise-induced oxidative stress and antioxidant defense in athletes, with particular emphasis on how exercise type and intensity shape redox responses, how these responses relate to muscle damage, recovery and performance, and what this implies for antioxidant supplementation and recovery strategies. Main content: Contracting skeletal muscle generates ROS through NADPH oxidases, mitochondria, xanthine oxidase and infiltrating phagocytes. Endogenous enzymatic (superoxide dismutase, catalase, glutathione peroxidase, peroxiredoxins) and non-enzymatic (glutathione, vitamins C and E, urate) systems keep these oxidants within a physiological range. Acute exercise transiently increases circulating markers of lipid, protein and DNA oxidation in proportion to the combined intensity and volume of the bout, whereas regular training up-regulates antioxidant enzymes and attenuates subsequent oxidative responses. Endurance, resistance, high-intensity interval and team-sport activities produce distinct time-courses of oxidative stress and muscle damage, typically peaking within 24–72 h. Redox-sensitive pathways—particularly the Nrf2–Keap1 axis and PGC-1α—link exercise-induced ROS to mitochondrial biogenesis and antioxidant gene expression, and randomized trials show that chronic high-dose vitamin C and E supplementation can blunt these adaptations. Biomarker interpretation is complicated by assay specificity, sampling time and large inter-individual (“redox individuality”) variation. Conclusion: Exercise-induced oxidative stress is best understood as a dose-dependent hormetic stimulus. Physiological ROS levels drive adaptation and are required for optimal muscle function, whereas excessive or insufficiently recovered training loads shift the balance toward oxidative damage, delayed recovery and impaired performance. Indiscriminate high-dose antioxidant supplementation is not supported; a food-first approach, targeting of documented antioxidant deficiencies, and periodization of any supplementation around adaptation-critical training phases are recommended.