Skeletal myopathy in heart failure: effects of aerobic exercise training

Autor(es)

Brum, P. C. ^{[1, 2]} ; Bacurau, A. V. ^[1] ; Cunha, T. F. ^[1] ; Bechara, L. R. G. ^[1] ; Moreira, J. B. N. ^[2]

Afiliação do(s) autor(es)

^[1] Univ Sao Paulo, Sch Phys Educ & Sport, BR-05508900 Sao Paulo - Brazil

^[2] Norwegian Univ Sci & Technol, KG Jebsen Ctr Exercise Med, N-7034 Trondheim - Norway

• Tipo de documento: Artigo Científico
• Fonte: Experimental Physiology; v. 99, n. 4, p. 616-620, APR 1 2014.
• Citações Web of Science: 14

Resumo

New Findings What is the topic of this review?This symposium report addresses the effects of aerobic exercise training on skeletal muscle myopathy induced by heart failure (HF), with emphasis on the mechanisms involved in muscle atrophy. What advances does it highlight?It highlights the therapeutic effect of aerobic exercise training to combat skeletal myopathy in HF. Our results demonstrated that aerobic exercise training re-established normal redox balance and prevented increased protein degradation by the ubiquitin-proteasome system, thereby preserving skeletal muscle mass in experimental models of HF. Our findings contribute to a better understanding of the mechanisms involved in skeletal myopathy in HF and the effects of training. Reduced aerobic capacity, as measured by maximal oxygen uptake, is a hallmark in cardiovascular diseases and strongly predicts poor prognosis and higher mortality rates in heart failure patients. While exercise capacity is poorly correlated with cardiac function in this population, skeletal muscle abnormalities present a striking association with maximal oxygen uptake. This fact draws substantial attention to the clinical relevance of targeting skeletal myopathy in heart failure. Considering that skeletal muscle is highly responsive to aerobic exercise training, we addressed the benefits of aerobic exercise training to combat skeletal myopathy in heart failure, focusing on the mechanisms by which aerobic exercise training counteracts skeletal muscle atrophy. (AU)

• Processo FAPESP: 10/50048-1 - Bases celulares e funcionais do exercício físico na doença cardiovascular
• Beneficiário: Carlos Eduardo Negrão
• Modalidade de apoio: Auxílio à Pesquisa - Temático