Aerobic Exercise Training Prevents Heart Failure-Induced Skeletal Muscle Atrophy by Anti-Catabolic, but Not Anabolic Actions

Authors

Rodrigo W.A. Souza, Sao Paulo State University
Warlen P. Piedade, Sao Paulo State University
Luana C. Soares, Sao Paulo State University
Paula A. T. Souza, Sao Paulo State University
Andreo F. Aguiar, North University of Parana
Ivan Jose Vechetti Jr, University of Nebraska-LincolnFollow
Dijon H.S. Campos, Sao Paulo State University
Ana A. H. Fernandes, Sao Paulo State University
Katashi Okoshi, Sao Paulo State University
Robson F. Carvalho, Sao Paulo State University
Antonio C. Cicogna, Sao Paulo State University
Maeli Dal-Pai-Silva, Sao Paulo State University

Date of this Version

10-17-2014

Citation

Souza RWA, Piedade WP, Soares LC, Souza PAT, Aguiar AF, et al. (2014) Aerobic Exercise Training Prevents Heart Failure-Induced Skeletal Muscle Atrophy by Anti-Catabolic, but Not Anabolic Actions. PLoS ONE 9(10): e110020. doi:10.1371/journal.pone.0110020

Comments

OPEN ACCESS

Abstract

Background: Heart failure (HF) is associated with cachexia and consequent exercise intolerance. Given the beneficial effects of aerobic exercise training (ET) in HF, the aim of this study was to determine if the ET performed during the transition from cardiac dysfunction to HF would alter the expression of anabolic and catabolic factors, thus preventing skeletal muscle wasting. Methods and Results: We employed ascending aortic stenosis (AS) inducing HF in Wistar male rats. Controls were sham operated animals. At 18 weeks after surgery, rats with cardiac dysfunction were randomized to 10 weeks of aerobic ET (AS-ET) or to an untrained group (AS-UN). At 28 weeks, the AS-UN group presented HF signs in conjunction with high TNF-α serum levels; soleus and plantaris muscle atrophy; and an increase in the expression of TNF-α, NF_kB (p65), MAFbx, MuRF1, FoxO1, and myostatin catabolic factors. However, in the AS-ET group, the deterioration of cardiac function was prevented, as well as muscle wasting, and the atrophy promoters were decreased. Interestingly, changes in anabolic factor expression (IGF-I, AKT, and mTOR) were not observed. Nevertheless, in the plantaris muscle, ET maintained high PGC1α levels. Conclusions: Thus, the ET capability to attenuate cardiac function during the transition from cardiac dysfunction to HF was accompanied by a prevention of skeletal muscle atrophy that did not occur via an increase in anabolic factors, but through anti-catabolic activity, presumably caused by PGC1α action. These findings indicate the therapeutic potential of aerobic ET to block HF-induced muscle atrophy by counteracting the increased catabolic state.