Cerebral Palsy

The cellular mechanisms of positive effects associated with aerobic exercise training on overall intrinsic skeletal muscle changes in heart failure (HF) remains unclear. We investigated potential Ca(2+) abnormalities in skeletal muscles comprised with different fiber composition and whether aerobic exercise training would improve muscle function in a genetic model of sympathetic hyperactivity-induced HF. A cohort of male 5 month-old wild type (WT) and congenic alpha(2A)/alpha(2C) ARKO mice in a C57Bl6/J genetic background were randomly assigned into untrained and trained groups. Exercise training consisted of 8 weeks running session of 60 min, 5 days/wk (from 5 to 7 months of age). After completion of exercise training protocol, exercise tolerance was determined by graded treadmill exercise test, muscle function by Rotarod, ambulation and resistance to inclination tests, cardiac function by echocardiography and Ca(2+) handling related protein expression by Western blot. alpha(2A)/alpha(2C) ARKO mice displayed decreased ventricular function, exercise intolerance and muscle weakness paralleled by decreased expression of sarcoplasmic Ca(2+) release-related proteins [alpha1, alpha2 and beta1 subunits of dihydropyridine receptor (DHPR) and ryanodine receptor (RyR)] and Ca(2+) reuptake-related proteins [sarco/endoplasmic reticulum Ca(2+)-ATPase (SERCA1/2), and Na(+)/Ca(2+) exchanger (NCX)] in soleus and plantaris. Aerobic exercise training significantly improved exercise tolerance, muscle function and re-established the expression of proteins involved in sarcoplasmic Ca(2+) handling toward WT levels. We provide evidence that Ca(2+) handling-related protein expression is decreased in this heart failure model and that exercise training improved skeletal muscle function associated to changes in the net balance of skeletal muscle Ca(2+) handling proteins.

Be Sociable, Share!

•