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Exercise training improves the net balance of cardiac Ca²⁺ handling protein expression in heart failure

¹ School of Physical Education and Sport
² Heart Institute (InCor), Medical School, University of São Paulo, São Paulo, Brazil

The molecular basis of the beneficial effects associated with exercise training (ET) on overall ventricular function (VF) in heart failure (HF) remains unclear. We investigated potential Ca²⁺ handling abnormalities and whether ET would improve VF of mice lacking _2A- and _2C-adrenoceptors (_2A/_2CARKO) that have sympathetic hyperactivity-induced HF. A cohort of male wild-type (WT) and congenic _2A/_2CARKO mice in a C57BL/J genetic background (5–7 mo of age) was randomly assigned into untrained and trained groups. VF was assessed by two-dimensional guided M-mode echocardiography. Cardiac myocyte width and ventricular fibrosis were evaluated with a computer-assisted morphometric system. Sarcoplasmic reticulum Ca²⁺ ATPase (SERCA2), phospholamban (PLN), phospho-Ser¹⁶-PLN, phospho-Thr¹⁷-PLN, phosphatase 1 (PP1), and Na⁺-Ca²⁺ exchanger (NCX) were analyzed by Western blotting. ET consisted of 8-wk running sessions of 60 min, 5 days/wk. _2A/_2CARKO mice displayed exercise intolerance, systolic dysfunction, increased cardiac myocyte width, and ventricular fibrosis paralleled by decreased SERCA2 and increased NCX expression levels. ET in _2A/_2CARKO mice improved exercise tolerance and systolic function. ET slightly reduced cardiac myocyte width, but unchanged ventricular fibrosis in _2A/_2CARKO mice. ET significantly increased the expression of SERCA2 (20%) and phospho-Ser¹⁶-PLN (63%), phospho-Thr¹⁷-PLN (211%) in _2A/_2CARKO mice. Furthermore, ET restored NCX and PP1 expression in _2A/_2CARKO to untrained WT mice levels. Thus, we provide evidence that Ca²⁺ handling is impaired in this HF model and that overall VF improved upon ET, which was associated to changes in the net balance of cardiac Ca²⁺ handling proteins.

calcium; hemodynamics

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