title: Aerobic exercise training prevents heart failure-induced skeletal muscle atrophy by anti-catabolic, but not anabolic actions.
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.
  
  
  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, NFκB (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.
authors.affiliation: Department of Morphology, São Paulo State University, Botucatu, São Paulo, Brazil.
authors.forename: Rodrigo W A
authors.initials: RW
authors.lastname: Souza
authors.affiliation: Department of Morphology, São Paulo State University, Botucatu, São Paulo, Brazil.
authors.forename: Warlen P
authors.initials: WP
authors.lastname: Piedade
authors.affiliation: Department of Morphology, São Paulo State University, Botucatu, São Paulo, Brazil.
authors.forename: Luana C
authors.initials: LC
authors.lastname: Soares
authors.affiliation: Department of Morphology, São Paulo State University, Botucatu, São Paulo, Brazil.
authors.forename: Paula A T
authors.initials: PA
authors.lastname: Souza
authors.affiliation: Centre of Biological and Health Sciences, North University of Paraná, Londrina, Paraná, Brazil.
authors.forename: Andreo F
authors.initials: AF
authors.lastname: Aguiar
authors.affiliation: Department of Morphology, São Paulo State University, Botucatu, São Paulo, Brazil.
authors.forename: Ivan J
authors.initials: IJ
authors.lastname: Vechetti-Júnior
authors.affiliation: Department of Internal Medicine, São Paulo State University, Botucatu, São Paulo, Brazil.
authors.forename: Dijon H S
authors.initials: DH
authors.lastname: Campos
authors.affiliation: Department of Biochemistry, São Paulo State University, Botucatu, São Paulo, Brazil.
authors.forename: Ana A H
authors.initials: AA
authors.lastname: Fernandes
authors.affiliation: Department of Internal Medicine, São Paulo State University, Botucatu, São Paulo, Brazil.
authors.forename: Katashi
authors.initials: K
authors.lastname: Okoshi
authors.affiliation: Department of Morphology, São Paulo State University, Botucatu, São Paulo, Brazil.
authors.forename: Robson F
authors.initials: RF
authors.lastname: Carvalho
authors.affiliation: Department of Biochemistry, São Paulo State University, Botucatu, São Paulo, Brazil.
authors.forename: Antonio C
authors.initials: AC
authors.lastname: Cicogna
authors.affiliation: Department of Morphology, São Paulo State University, Botucatu, São Paulo, Brazil.
authors.forename: Maeli
authors.initials: M
authors.lastname: Dal-Pai-Silva
mesh_terms: D000818:Animals; D051858:Forkhead Transcription Factors / Q000235:genetics / Q000378:metabolism; D006333:Heart Failure / Q000150:complications*; D008297:Male; D009124:Muscle Proteins / Q000235:genetics / Q000378:metabolism; D018482:Muscle, Skeletal / Q000378:metabolism*; D009133:Muscular Atrophy / Q000209:etiology / Q000517:prevention & control*; D016328:NF-kappa B / Q000235:genetics / Q000378:metabolism; D009419:Nerve Tissue Proteins / Q000235:genetics / Q000378:metabolism; D005082:Physical Exertion; D051381:Rats; D017208:Rats, Wistar; D044843:SKP Cullin F-Box Protein Ligases / Q000235:genetics / Q000378:metabolism; D000070584:Tripartite Motif Proteins; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics / Q000378:metabolism; D044767:Ubiquitin-Protein Ligases / Q000235:genetics / Q000378:metabolism; D000071161:Forkhead Box Protein O1
chemical_list: D051858:Forkhead Transcription Factors; D009124:Muscle Proteins; D016328:NF-kappa B; D009419:Nerve Tissue Proteins; D044843:SKP Cullin F-Box Protein Ligases; D000070584:Tripartite Motif Proteins; D014409:Tumor Necrosis Factor-alpha; D044767:Ubiquitin-Protein Ligases; C074639:Foxo1 protein, rat; D000071161:Forkhead Box Protein O1; C486692:Fbxo32 protein, rat; C499086:Trim63 protein, rat