Effects of physical training on throphism and myostatin/follistatin pathway in skeletal and cardiac muscle of spontaneously hypertensive rats with heart failure

Abstract

During heart failure, skeletal muscle atrophy and abnormalities play an important role on physical capacity impairment. Myostatin/follistatin pathway modulates muscle trophism. Studies have shown a negative correlation between myostatin expression and muscle mass suggesting that myostatin can induce skeletal muscle atrophy. Physical exercise is considered an essential component of heart failure treatment. However, mechanisms involved in modulation of muscle trophism and cardiac remodeling by physical exercise have not been completely definid. The spontaneously hypertensive rat (SHR) is widely used for experimental heart failure studies. Rats develop early arterial hypertension and left ventricular hypertrophy which evolves to heart failure during maturity and senescence. In this study we hypothesized that, during heart failure, skeletal muscle atrophy is related to myostatin/follistatin pathway changes which can be prevented or attenuated by physical training. Study aim: to determine whether physical training attenuates both skeletal muscle atrophy and cardiac remodeling and modulates gene and protein expression of myostatin/follistatin pathway in soleus and gastrocnemius muscle and in cardiac muscle of heart failure SHR. Sixteen-month-old SHR will be trained five times/week for four months. Normotensive Wistar-Kyoto rats will be used as Controls. Cardiac evaluation will be performed at beggining and at the end of experimental period by transthoracic echocardiogram. Muscle morphology will be analysed in histological sections. Gene and protein expression will be assessed by real time PCR and Western blot, respectively. Statistical analyse: two-way ANOVA; significance level: 5%. (AU)