Efeitos do treinamento físico aeróbico sobre a expressão da miostatina e o trofismo de músculos esqueléticos e cardíaco de ratos espontaneamente hipertensos com insuficiência cardíaca

• Autor(a) principal: Damatto, Ricardo Luiz [UNESP]
• Data de Publicação: 2014
• Tipo de documento: Dissertação
• Idioma: por
• Título da fonte: Repositório Institucional da UNESP
• Texto Completo: http://hdl.handle.net/11449/113869
• topic: Exercicios fisicos - Aspectos fisiologicos; Sistema musculoesquelético; Folistatina; Miostatina; Atrofia muscular; Insuficiencia cardiaca; Rato como animal de laboratorio; Hipertensão; Musculoskeletal system

Heart failure is characterized by a reduced tolerance to physical activity with early development of fatigue and dyspnea. Besides cardiac and pulmonary dysfunction, skeletal muscle abnormalities can also be involved in the reduced physical capacity. Atrophy is a commonly found skeletal muscle alteration. Myostatin/follistatin pathway has an important role in skeletal muscle mass maintenance with myostatin being negatively correlated with muscle mass. In myocardium, myostatin levels increase during chronic overload and can contribute to the decreased peripheral muscle mass. Physical exercise has an important role in heart failure treatment. However, mechanisms involved in exercise-induced improvement of physical capacity are not completely understood. In this study, we hypothesized that spontaneously hypertensive rats (SHR) with heart failure present myostatin/follistatin pathway change in skeletal and cardiac muscle, which can be modulated by prolonged physical training. The aims of this study are: 1) to evaluate whether skeletal muscle atrophy is associated with changes in the myostatin/follistatin intracelular pathway in SHR with heart failure; 2) to determine whether aerobic physical training attenuates muscle atrophy and/or modulates mostatin/follistatin expression in soleus and gastrocnemius muscles; e 3) to evaluate myocardial myostatin/follistatin levels and to determine whether training attenuates cardiac remodeling and possible achanges in the myostatin/follistatin pathway. Methods: Male sixteen-month-old normotensive Wistar-Kyoto (WKY) rats and SHR were assigned to four groups: 1) control (WKYSed, n=20); 2) exercised control (WKY-Ex, n=20); 3) heart failure (SHR-Sed, n=25); and 4) exercised heart failure (SHR-Ex, n=25). Exercised groups were subjected to a treadmill exercise protocol, five days a week, for four months. Transthoracic echocardiogram was performed before and after ...