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J Appl Physiol (November 1, 2007). doi:10.1152/japplphysiol.00493.2007
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Submitted on May 7, 2007
Accepted on October 30, 2007

Exercise Training Delays Cardiac Dysfunction and Prevents Calcium Handling Abnormalities in Sympathetic Hyperactivity-Induced Heart Failure Mice

Alessandra Medeiros1, Natale P.L. Rolim1, Rodrigo S.F. Oliveira1, Kaleizu Teodoro Rosa2, Katt C. Mattos3, Dulce Elena Casarini4, Maria Claudia Irigoyen2, Eduardo M. Krieger2, Jose E. Krieger2, Carlos Eduardo Negrao5, and Patricia Chakur Brum1*

1 School of Physical Education and Sport, University of Sao Paulo, Sao Paulo, Sao Paulo, Brazil
2 Heart Institute (InCor), School of Medicine, University of Sao Paulo, Sao Paulo, Sao Paulo, Brazil
3 Sao Paulo, Sao Paulo, Brazil; School of Physical Education and Sport, University of Sao Paulo, Sao Paulo, Sao Paulo, Brazil
4 MEDICINE - NEPHROLOGY, Federal University of Sao Paulo, Sao Paulo, Brazil
5 School of Physical Education and Sport, University of Sao Paulo, Sao Paulo, Sao Paulo, Brazil; Heart Institute (InCor), School of Medicine, University of Sao Paulo, Sao Paulo, Sao Paulo, Brazil

* To whom correspondence should be addressed. E-mail: pcbrum{at}usp.br.

Exercise training (ET) is a coadjuvant therapy in preventive cardiology. It delays cardiac dysfunction and exercise intolerance in heart failure (HF), however the molecular mechanisms underlying its cardioprotection are poorly understood. We tested the hypothesis that ET would prevent Ca2+ handling abnormalities and ventricular dysfunction in sympathetic hyperactivity-induced HF mice. A cohort of male wild type (WT) and congenic {alpha}2A/{alpha}2CARKO mice with C57BL6/J genetic background (3 to 5 months of age) were randomly assigned into untrained and exercise-trained groups. ET consisted of 8-wk swimming session, 60min, 5 days/wk. Fractional shortening (FS) was assessed by two-dimensional guided M-mode echocardiography. The protein expression of ryanodine receptor (RyR), phospho-Ser2809-RyR, sarcoplasmic reticulum Ca2+ ATPase (SERCA2), Na+-Ca2+ exchanger (NCX), phospholamban (PLN), phospho-Ser16-PLN, and phospho-Thr17-PLN were analyzed by Western blotting. At 3 months of age, no significant difference in FS and exercise tolerance were observed between WT and {alpha}2A/{alpha}2CARKO mice. At 5 months, when cardiac dysfunction is associated with lung edema and increased plasma noradrenaline levels, {alpha}2A/{alpha}2CARKO mice presented reduced FS paralleled by decreased SERCA2 (26%) and NCX (34%). Conversely, {alpha}2A/{alpha}2CARKO mice displayed increased phospho-Ser16-PLN (76%) and phospho-Ser2809-RyR (49%). ET in {alpha}2A/{alpha}2CARKO mice prevented exercise intolerance, ventricular dysfunction and decreased plasma noradrenaline. ET significantly increased the expression of SERCA2 (58%) and phospho-Ser16-PLN (30%) while it restored the expression of phospho-Ser2809-RyR to WT levels. Collectively, we provide evidence that improved net balance of Ca2+ handling proteins paralleled by a decreased sympathetic activity upon ET are, at least in part, compensatory mechanisms against deteriorating ventricular function in HF.




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