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(Reference retrieved automatically from Web of Science through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

Exercise training decreases NADPH oxidase activity and restores skeletal muscle mass in heart failure rats

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Author(s):
Cunha, Telma F. ; Bechara, Luiz R. G. ; Bacurau, Aline V. N. ; Jannig, Paulo R. ; Voltarelli, Vanessa A. ; Dourado, Paulo M. ; Vasconcelos, Andrea R. ; Scavone, Cristoforo ; Ferreira, Julio C. B. ; Brum, Patricia C.
Total Authors: 10
Document type: Journal article
Source: Journal of Applied Physiology; v. 122, n. 4, p. 817-827, APR 2017.
Web of Science Citations: 6
Abstract

We have recently demonstrated that NADPH oxidase hyperactivity, NF-kappa B 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-kappa B 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-alpha levels, NADPH oxidase profile, NF-kappa B signaling, p38 protein levels, and proteasome activity were assessed. MI-T showed a reduced TNF-alpha 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-kappa B, 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-kappa B 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. (AU)

FAPESP's process: 14/23703-0 - The role myogenic precursor cells in skeletal myopathy-induced heart failure: effect of exercise training
Grantee:Patricia Chakur Brum
Support type: Regular Research Grants
FAPESP's process: 11/00728-9 - Oxidative stress contribution to NF-kB, FOXO and MAPK pathways signaling activation in skeletal muscle atrophy associated to heart failure: effect of aerobic training and N-acetylcysteine treatment
Grantee:Telma Fátima da Cunha Moraes
Support type: Scholarships in Brazil - Doctorate
FAPESP's process: 12/05765-2 - Contribution of aldehyde dehydrogenase 2 to heart failure development
Grantee:Julio Cesar Batista Ferreira
Support type: Research Grants - Young Investigators Grants