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Cited by 172Exercise and Physiological ResponsesCardiovascular and exercise physiologyRedox biology and oxidative stress

The DOI matches its Crossref record; 126 of the 126 references it cites were found in a registry or an index.

Redox modulation of mitochondriogenesis in exercise. Does antioxidant supplementation blunt the benefits of exercise training?

Gomez-Cabrera, Mari Carmen, Salvador-Pascual, Andrea, Cabo, Helena, Ferrando, Beatriz, Viña, Jose·2015·Free Radical Biology and Medicine
DOI 10.1016/j.freeradbiomed.2015.04.006
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Abstract

Physical exercise increases the cellular production of reactive oxygen species (ROS) in muscle, liver, and other organs. This is unlikely due to increased mitochondrial production but rather to extramitochondrial sources such as NADPH oxidase or xanthine oxidase. We have reported a xanthine oxidase-mediated increase in ROS production in many experimental models from isolated cells to humans. Originally, ROS were considered as detrimental and thus as a likely cause of cell damage associated with exhaustion. In the past decade, evidence showing that ROS act as signals has been gathered and thus the idea that antioxidant supplementation in exercise is always recommendable has proved incorrect. In fact, we proposed that exercise itself can be considered as an antioxidant because training increases the expression of classical antioxidant enzymes such as superoxide dismutase and glutathione peroxidase and, in general, lowering the endogenous antioxidant enzymes by administration of antioxidant supplements may not be a good strategy when training. Antioxidant enzymes are not the only ones to be activated by training. Mitochondriogenesis is an important process activated in exercise. Many redox-sensitive enzymes are involved in this process. Important signaling molecules like MAP kinases, NF-κB, PGC-1α, p53, heat shock factor, and others modulate muscle adaptation to exercise. Interventions aimed at modifying the production of ROS in exercise must be performed with care as they may be detrimental in that they may lower useful adaptations to exercise.

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Research works printed but not linked: 3

  1. Koren, 1980, EPR measurements of free radicals during tetanic contractions of frog skeletal muscle, Period. Biol., 82, 399
  2. Reid, 1994, N-Acetylcysteine inhibits muscle fatigue in humans, J. Clin. Invest., 94, 2468, 10.1172/JCI117615 · DOI
  3. Silveira, 1763, Biochim. Biophys. Acta, 969-976, 2006

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Metadata

Authors
Gomez-Cabrera, M. C., Salvador-Pascual, A., Cabo, H., Ferrando, B., & Viña, J.
Affiliations
Universitat de València (ES)
ORCID
Ferrando, Beatriz
Venue
Free Radical Biology and Medicine
Publisher
Elsevier BV
Published
2015-09
Volume
86
Pages
37-46
ISSN
0891-5849 (ISSN-L)
DOI
10.1016/j.freeradbiomed.2015.04.006
OpenAlex
W2084308966
Cited by
172
References
126
Citations by year
2026: 7 · 2025: 8 · 2024: 11 · 2023: 10 · 2022: 16 · 2021: 15 · 2020: 31 · 2019: 16 · 2018: 17 · 2017: 19 · 2016: 18 · 2015: 4
FWCI
2.68
Type
journal article
Language
en
Open access
closed
Licence
Locations
  • Free Radical Biology and Medicine (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • Ministerio de Educación, Cultura y Deporte (ISCIII2012-RED-43-029, PROMETEO2014/056)
  • Generalitat Valenciana (RS2012-609)
  • European Regional Development Fund
  • INCLIVA Instituto de Investigación Sanitaria
  • European Commission (CM1001)
Topics
  • Health Sciences › Medicine › Physiology (medical) › Exercise and Physiological Responses
  • Health Sciences › Medicine › Physiology (medical) › Cardiovascular and exercise physiology
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
Keywords
mitochondrial biogenesis, exercise training, reactive oxygen species, antioxidant supplementation, xanthine oxidase, NADPH oxidase, redox signaling, superoxide dismutase, glutathione peroxidase, PGC-1α, heat shock transcription factor, p53, NF-κB, mitogen-activated protein kinase, muscle adaptation, exercise fatigue
MeSH terms
Adaptation, Physiological, Animals, Antioxidants, Organelle Biogenesis, Humans, Mitochondria, Muscle, Oxidation-Reduction, Exercise, Oxidative Stress, Muscle, Skeletal, Dietary Supplements

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