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1 University of São Paulo, School of Physical Education and Sport, São Paulo, São Paulo, Brazil
2 University of São Paulo, Heart Institute (InCor), Medical School, São Paulo, São Paulo, Brazil
3 University of São Paulo, Heart Institute (InCor), Medical School, São paulo, São Paulo, Brazil
4 University of São Paulo, School of Physical Education and Sport, Heart Institute (InCor), Sao Paulo, Sao Paulo, Brazil
* To whom correspondence should be addressed. E-mail: pcbrum{at}usp.br.
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 C57Bl6/J genetic background (5 to 7 months of age) were 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. ET significantly increased the expression of SERCA2 (20%) and phospho-Ser16-PLN (63%), phospho-Thr17-PLN (211%) in 2A/2CARKO. Furthermore, ET restored NCX and PP1 expression in untrained 2A/2CARKO to 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.
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