Efeito do treinamento físico na expressão de proteínas que transportam Ca2+  e participam do sistema proteolítico dependente de Ca2+ na  musculatura esquelética em modelo experimental de insuficiência cardíaca

Carlos Roberto Bueno Junior

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Author(s):	Carlos Roberto Bueno Junior Total Authors: 1
Document type:	Master's Dissertation
Press:	São Paulo.
Institution:	Universidade de São Paulo (USP). Escola de Educação Física e Esportes (EEFE/BT)
Defense date:	2009-03-20
Examining board members:	Patricia Chakur Brum; Marcelo Saldanha Aoki; Martha Meriwether Sorenson
Advisor:	Patricia Chakur Brum
Abstract
Heart failure (HF) is a clinical syndrome with poor prognosis characterized by exercise intolerance, early fatigue and skeletal muscle myopathy, which has been considered an independent predictor of mortality. Conversely, aerobic exercise training prevents skeletal muscle dysfunction, which might be related to altered intracellular Ca2+ handling. Therefore, we tested whether HF would lead to alterations in skeletal musculature function related to changes in Ca2+ handling proteins expression (DHPRα1, DHPR α2, DHPR β1, RYR, NCX, SERCA 1, SERCA 2, parvalbumin) and activity of the Ca2+-dependent proteolysis (calpain and calpastatin) in soleus and plantaris muscles. The potential role of exercise training in preventing Ca2+ handling alterations was also studied. Male wild type and α2A e α2C adrenoceptor knockout (KO) mice on a C56BL/6J genetic background were studied at 7 months of age, when KO mice display HF and skeletal muscle myopathy associated with sympathetic hyperactivity and 50% of mortality. KO mice displayed skeletal muscle dysfunction paralleled by altered Ca2+ handling protein expression and Ca2+- induced proteolysis in both soleus and plantaris. Interestingly, exercise training prevented skeletal muscle dysfunction and Ca2+-induced proteolysis in both soleus and plantaris. Collectively, we provide evidence that improved net balance of Ca2+ handling proteins and decreased Ca2+-induced proteolysis upon exercise training is, at least in part, a compensatory mechanism against skeletal muscle myopathy of sympathetic hyperactivity-induced HF (AU)

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