Muscle and Blood Redox Status after Exercise Training in Severe COPD Patients
Abstract
Beneficial effects of exercise training in patients with chronic obstructive pulmonary disease (COPD) are acknowledged. However, high-intensity exercise may enhance muscle oxidative stress in severe COPD patients. We hypothesized that high-intensity exercise training of long duration does not deteriorate muscle redox status. In the vastus lateralis and blood of 18 severe COPD patients and 12 controls, before and after an 8-week training program, protein oxidation and nitration, antioxidant systems, and inflammatory cytokines were examined. At baseline, COPD patients showed greater muscle oxidative stress and superoxide dismutase activity and circulating inflammatory cytokines than controls. Among COPD patients, muscle and blood protein carbonylation levels were correlated. Both groups showed training-induced increase in VO(2) peak and decreased blood lactate levels. After training, among the COPD patients, blood protein nitration levels were significantly reduced and muscle protein oxidation and nitration levels did not cause impairment. Muscle and blood levels of inflammatory cytokines were not modified by training in either patients or controls. We conclude that in severe COPD patients, high-intensity exercise training of long duration improves exercise capacity while preventing the enhancement of systemic and muscle oxidative stress. In addition, in these patients, resting protein oxidation levels correlate between skeletal muscle and blood compartments.
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Unchanged glutathione and catalase quadriceps levels have been reported in COPD.
“Unchanged glutathione and catalase quadriceps levels have been reported [118,122].”
From Main Pathogenic Mechanisms and Recent Advances in COPD Peripheral Skeletal Muscle Wasting (2023) · cites this paper as [122]
In COPD, the protective mechanism of increasing antioxidants in response to oxidative stress seems defective, although contradictory data have been reported.
“Skeletal muscle tissue usually compensates the excessive oxidative stress (induced for example by exercise training) by increasing the levels of antioxidants [122,127], but in COPD, this protective mechanism seems to be defective, although contradictory data have been reported.”
From Main Pathogenic Mechanisms and Recent Advances in COPD Peripheral Skeletal Muscle Wasting (2023) · cites this paper as [122]
Increased Mn-superoxide dismutase (SOD) and Cu-Zn-SOD protein levels have been demonstrated in COPD quadriceps, whereas unchanged SOD content and decreased SOD activity have been reported in another study, and unchanged MnSOD, Cu/ZnSOD, and catalase expressions have been found in cultured COPD myoblasts and myotubes.
“For example, increased Mn-superoxide dismutase (SOD) and Cu-Zn-SOD protein levels have been demonstrated in the quadriceps [118,127], whereas unchanged SOD content and decreased SOD activity have been reported in another study [122], and unchanged MnSOD, Cu/ZnSOD, and catalase expressions in cultured COPD myoblasts and myotubes have been found [128].”
From Main Pathogenic Mechanisms and Recent Advances in COPD Peripheral Skeletal Muscle Wasting (2023) · cites this paper as [122]
Multiple studies point towards increased protein carbonylation in COPD quadriceps compared to healthy controls, including total protein content and specific proteins such as glycolytic enzymes, antioxidant enzymes, and myosin heavy chain.
“Multiple studies point towards an increased protein carbonylation in COPD quadriceps compared to healthy controls, including total protein content but also specific proteins such as glycolytic enzymes (creatine kinase), antioxidant enzymes (glutathione peroxidase), and myosin heavy chain [118,120,121,122].”
From Main Pathogenic Mechanisms and Recent Advances in COPD Peripheral Skeletal Muscle Wasting (2023) · cites this paper as [122]
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Main Pathogenic Mechanisms and Recent Advances in COPD Peripheral Skeletal Muscle Wasting
Henrot, P., Dupin, I., Schilfarth, P., Esteves, P., Blervaque, L., Zysman, M., Gouzi, F., Hayot, M., Pomiès, P., & Berger, P. (2023) · International Journal of Molecular Sciences · doi:10.3390/ijms24076454 · Cited by 85 · see citing works
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- Authors
- Rodriguez, D. A., Kalko, S., Puig-Vilanova, E., Perez-Olabarría, M., Falciani, F., Gea, J., Cascante, M., Barreiro, E., & Roca, J.
- Affiliations
- Instituto de Salud Carlos III (ES)
- Hospital Clínic de Barcelona (ES)
- Universitat Pompeu Fabra (ES)
- Institut de Biomedicina de la Universitat de Barcelona (ES)
- Corresponding author
- Barreiro, Esther
- Venue
- Free Radical Biology and Medicine
- Publisher
- Elsevier BV
- Published
- 2012-01
- Volume
- 52
- Issue
- 1
- Pages
- 88-94
- ISSN
- 0891-5849 (ISSN-L)
- OpenAlex
- W2057304386
- Cited by
- 102
- References
- 4
- Citations by year
- 2026: 2 · 2025: 1 · 2024: 2 · 2023: 6 · 2022: 5 · 2021: 3 · 2020: 6 · 2019: 7 · 2018: 8 · 2017: 4 · 2016: 17 · 2015: 7 · 2014: 14 · 2013: 15 · 2012: 5
- FWCI
- 11.02
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Free Radical Biology and Medicine (publishedVersion)
- PubMed (publishedVersion)
- University of Birmingham Research Portal (University of Birmingham) (submittedVersion)
- Funders
- European Commission
- Topics
- Health Sciences › Medicine › Rehabilitation › Exercise and Physiological Responses
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Chronic Obstructive Pulmonary Disease (COPD) Research
- Health Sciences › Medicine › Biochemistry › Antioxidant Activity and Oxidative Stress
- Keywords
- chronic obstructive pulmonary disease, exercise training, oxidative stress, protein oxidation, protein nitration, protein carbonylation, superoxide dismutase, inflammatory cytokines, antioxidant defense, high-intensity exercise, exercise capacity, vastus lateralis, blood lactate, peak oxygen uptake
- MeSH terms
- Aged, Catalase, Female, Glutathione, Humans, Inflammation, Male, Middle Aged, Nitrates, Oxidation-Reduction, Severity of Illness Index, Superoxide Dismutase, Exercise, Case-Control Studies, Cytokines, Oxidative Stress, Muscle, Skeletal, Lactic Acid, Pulmonary Disease, Chronic Obstructive, Protein Carbonylation
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