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1 Physiology, Faculty of Science, Mahidol University, Bangkok, Thailand
* To whom correspondence should be addressed. E-mail: tejwt{at}mahidol.ac.th.
The risks associated with hormone replacement therapy (HRT) especially cardiac diseases in postmenopausal women have prompted extensive studies for other preventive or therapeutic alternatives. We investigated the cardio-protective effects of exercise training on the changes in cardiac myofilament Ca2+ activation in 10-wk ovariectomized rats. The exercise groups were subjected to a nine-wk running program on a motor-driven treadmill one week after surgery. The relation between pCa (-log molar free Ca2+ concentration) and myofibrillar MgATPase activity of exercise-sham myofibrils or exercise-ovariectomized myofibrils was the same and could not be distinguished from that of sedentary-sham control hearts. In contrast, a significant suppression in maximum MgATPase activity and a leftward shift of pCa50 (half-maximally activating pCa) in the pCa-ATPase activity relationship were detected in sedentary-ovariectomized rats. Exercise training also prevented the shift in myosin heavy chain (MHC) isoforms towards 
-MHC in ovariectomized hearts. The upregulation of 1-adrenergic receptors in the left ventricular membranes of ovariectomized rat hearts, as measured using receptor binding and immunoblot analyses, was no longer observed in exercise-ovariectomized hearts. Immuno-blot analyses of heat shock protein (Hsp) 72, an inducible form of Hsp70, demonstrated a significant downregulation in ovariectomized hearts. Exercise training in ovariectomized rats completely reversed the expression of Hsp72 to the same level as sham controls. Our results clearly indicate the cardio-protective effects of exercise training on changes in cardiac myofilament Ca2+ activation in ovariectomized rats. Alterations in expression of 1-adrenergic receptors and Hsp72 may in part play a mechanistic role in the cardio-protective effects.
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