Exercise-induced oxidative stress in humans: cause and consequences

Powers, Scott K.; Nelson, W. Bradley; Hudson, Matthew B.

doi:10.1016/j.freeradbiomed.2010.12.009

Cited by 441Exercise and Physiological ResponsesCardiovascular and exercise physiologyAntioxidant Activity and Oxidative Stress

Exercise-induced oxidative stress in humans: cause and consequences

Powers, Scott K., Nelson, W. Bradley, Hudson, Matthew B.·2011·Free Radical Biology and Medicine

DOI 10.1016/j.freeradbiomed.2010.12.009

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Abstract

The observation that muscular exercise is associated with oxidative stress in humans was first reported over 30 years ago. Since this initial report, numerous studies have confirmed that prolonged or high-intensity exercise results in oxidative damage to macromolecules in both blood and skeletal muscle. Although the primary tissue(s) responsible for reactive oxygen species (ROS) production during exercise remains a topic of debate, compelling evidence indicates that muscular activity promotes oxidant production in contracting skeletal muscle fibers. Mitochondria, NADPH oxidase, PLA₂-dependent processes, and xanthine oxidase have all been postulated to contribute to contraction-induced ROS production in muscle but the primary site of contraction-induced ROS production in muscle fibers remains unclear. Nonetheless, contraction-induced ROS generation has been shown to play an important physiological function in the regulation of both muscle force production and contraction-induced adaptive responses of muscle fibers to exercise training. Although knowledge in the field of exercise and oxidative stress has grown markedly during the past 30 years, this area continues to expand and there is much more to be learned about the role of ROS as signaling molecules in skeletal muscle.

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Exercise acutely activates ROS production, which is essential for force generation within skeletal muscle, signaling to distal tissues and activating antioxidants.
“Exercise acutely activates ROS production, which is essential for force generation within skeletal muscle, signaling to distal tissues and activating antioxidants. This adaptation ensures homeostasis and prevention of excess oxidative stress (25).”
From Exercise Counters the Age-Related Accumulation of Senescent Cells (2022) · cites this paper as [25]

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Authors: Powers, S. K., Nelson, W. B., & Hudson, M. B.
Affiliations: University of Florida (US)
Corresponding author: Powers, Scott K.
ORCID: Nelson, W. Bradley
Hudson, Matthew B.
Venue: Free Radical Biology and Medicine
Publisher: Elsevier BV
Published: 2011-09
Volume: 51
Issue: 5
Pages: 942-950
ISSN: 0891-5849 (ISSN-L)
DOI: 10.1016/j.freeradbiomed.2010.12.009
OpenAlex: W2076659633
Cited by: 441
References: 162
Citations by year: 2026: 21 · 2025: 14 · 2024: 25 · 2023: 21 · 2022: 31 · 2021: 34 · 2020: 43 · 2019: 35 · 2018: 32 · 2017: 28 · 2016: 27 · 2015: 33 · 2014: 43 · 2013: 19 · 2012: 23
FWCI: 2.81
Type: journal article
Language: en
Open access: closed
Licence: www.elsevier.com/tdm/userlicense/1.0/ (tdm)
www.elsevier.com/legal/tdmrep-license (tdm)
Locations: Free Radical Biology and Medicine (publishedVersion)
PubMed (publishedVersion)
Funders: National Heart, Lung, and Blood Institute (R01HL072789)
Topics: Health Sciences › Medicine › Rehabilitation › Exercise and Physiological Responses
Health Sciences › Medicine › Complementary and alternative medicine › Cardiovascular and exercise physiology
Health Sciences › Medicine › Biochemistry › Antioxidant Activity and Oxidative Stress
Keywords: exercise-induced oxidative stress, reactive oxygen species, skeletal muscle, muscle contraction, mitochondria, NADPH oxidase, phospholipase A2, xanthine oxidase, training effects, muscle force production, ROS signaling
MeSH terms: Adaptation, Physiological, Animals, Humans, Muscle Contraction, Oxidation-Reduction, Exercise, Reactive Oxygen Species, Oxidative Stress, Muscle, Skeletal

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Exercise-induced oxidative stress in humans: cause and consequences

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