Exercise training decreases NADPH oxidase activity and restores skeletal muscle mass in heart failure rats
Abstract
We have recently demonstrated that NADPH oxidase hyperactivity, NF-κB activation, and increased p38 phosphorylation lead to atrophy of glycolytic muscle in heart failure (HF). Aerobic exercise training (AET) is an efficient strategy to counteract skeletal muscle atrophy in this syndrome. Therefore, we tested whether AET would regulate muscle redox balance and protein degradation by decreasing NADPH oxidase hyperactivity and reestablishing NF-κB signaling, p38 phosphorylation, and proteasome activity in plantaris muscle of myocardial infarcted-induced HF (MI) rats. Thirty-two male Wistar rats underwent MI or fictitious surgery (SHAM) and were randomly assigned into untrained (UNT) and trained (T; 8 wk of AET on treadmill) groups. AET prevented HF signals and skeletal muscle atrophy in MI-T, which showed an improved exercise tolerance, attenuated cardiac dysfunction and increased plantaris fiber cross-sectional area. To verify the role of inflammation and redox imbalance in triggering protein degradation, circulating TNF-α levels, NADPH oxidase profile, NF-κB signaling, p38 protein levels, and proteasome activity were assessed. MI-T showed a reduced TNF-α levels, NADPH oxidase activity, and Nox2 mRNA expression toward SHAM-UNT levels. The rescue of NADPH oxidase activity induced by AET in MI rats was paralleled by reducing nuclear binding activity of the NF-κB, p38 phosphorylation, atrogin-1, mRNA levels, and 26S chymotrypsin-like proteasome activity. Taken together our data provide evidence for AET improving plantaris redox homeostasis in HF associated with a decreased NADPH oxidase, redox-sensitive proteins activation, and proteasome hyperactivity further preventing atrophy. These data reinforce the role of AET as an efficient therapy for muscle wasting in HF. NEW & NOTEWORTHY This study demonstrates, for the first time, the contribution of aerobic exercise training (AET) in decreasing muscle NADPH oxidase activity associated with reduced reactive oxygen species production and systemic inflammation, which diminish NF-κB overactivation, p38 phosphorylation, and ubiquitin proteasome system hyperactivity. These molecular changes counteract plantaris atrophy in trained myocardial infarction-induced heart failure rats. Our data provide new evidence into how AET may regulate protein degradation and thus prevent skeletal muscle atrophy.
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Exercise reactivates mitophagy, reduces accumulation of ROS, improves mitochondrial health, and delays the loss of muscle mass that accompanies various pathologies, including aging sarcopenia, heart failure, and neurogenic myopathy.
“Moreover, exercise is the best non-pharmacological strategy to reactivate mitophagy, which reduces the accumulation of ROS and thus, improves mitochondrial health and delays the loss of muscle mass that accompanies various pathologies, including aging sarcopenia, heart failure and neurogenic myopathy [224, 238–240].”
From The connection between the dynamic remodeling of the mitochondrial network and the regulation of muscle mass (2021) · cites this paper as [240]
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- Authors
- Cunha, T. F., Bechara, L. R. G., Bacurau, A. V. N., Jannig, P. R., Voltarelli, V. A., Dourado, P. M., Vasconcelos, A. R., Scavone, C., Ferreira, J. C. B., & Brum, P. C.
- Affiliations
- Universidade de São Paulo (BR)
- Department of Pharmacology, Institute of Biomedical Science, University of São Paulo, São Paulo, Brazil; and
- Department of Anatomy, Institute of Biomedical Sciences, São Paulo, Brazil
- School of Physical Education and Sport, University of São Paulo, São Paulo, Brazil;
- ORCID
- Venue
- Journal of Applied Physiology
- Publisher
- American Physiological Society
- Published
- 2017-04-01
- Volume
- 122
- Issue
- 4
- Pages
- 817-827
- ISSN
- 0161-7567 (ISSN-L)
- 8750-7587
- 1522-1601
- OpenAlex
- W2577619280
- Cited by
- 51
- References
- 66
- Citations by year
- 2026: 1 · 2025: 6 · 2024: 5 · 2023: 4 · 2022: 6 · 2021: 6 · 2020: 11 · 2019: 4 · 2018: 5 · 2017: 3
- FWCI
- 2.57
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Journal of Applied Physiology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Ministry of Science, Technology and Innovation | Conselho Nacional de Desenvolvimento Científico e Tecnológico (474365/2012-3)
- Fundação de Amprao à Pesquisa do Estado de São Paulo (2011/00728-9)
- Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP) (2012/05765-2, 2014/23703-0)
- Ministry of Science, Technology and Innovation | Conselho Nacional de Desenvolvimento Científico e Tecnológico (National Council for Scientific and Technological Development) (301105/2012-0, 302201/2011-4, 454560/2014-1)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Muscle Physiology and Disorders
- Health Sciences › Medicine › Complementary and alternative medicine › Cardiovascular and exercise physiology
- Health Sciences › Medicine › Rehabilitation › Exercise and Physiological Responses
- Keywords
- aerobic exercise training, heart failure, skeletal muscle atrophy, NADPH oxidase, NOX2, NF-κB signaling, p38 phosphorylation, proteasome activity, ubiquitin-proteasome system, atrogin-1, TNF-α, reactive oxygen species, redox homeostasis, myocardial infarction, plantaris muscle, protein degradation, inflammation
- MeSH terms
- Animals, Disease Models, Animal, Exercise Test, Heart, Heart Failure, Male, Muscular Atrophy, Myocardial Infarction, Oxidation-Reduction, Phosphorylation, Physical Conditioning, Animal, Tumor Necrosis Factor-alpha, Signal Transduction, NF-kappa B, Rats, Wistar, Muscle, Skeletal, Muscle Fibers, Skeletal, NADPH Oxidases, Proteasome Endopeptidase Complex, p38 Mitogen-Activated Protein Kinases, Rats, Proteolysis
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