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Cardioprotective effects of exercise training on myofilament calcium activation in ovariectomized rats

Department of Physiology, Faculty of Science, Mahidol University, Bangkok 10400, Thailand

Submitted 17 November 2003 ; accepted in final form 11 December 2003

The risks associated with hormone replacement therapy, especially cardiac diseases in postmenopausal women, have prompted extensive studies for other preventive or therapeutic alternatives. We investigated the cardioprotective effects of exercise training on the changes in cardiac myofilament Ca²⁺ activation in 10-wk-old ovariectomized rats. The exercise groups were subjected to a 9-wk running program on a motor-driven treadmill 1 wk after surgery. The relationship 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 toward -MHC in ovariectomized hearts. The upregulation of ₁-adrenergic receptors in the left ventricular membranes of ovariectomized rat hearts, as measured by receptor binding and immunoblot analyses, was no longer observed in exercise-ovariectomized hearts. Immunoblot 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 cardioprotective 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 cardioprotective effects.

myofilament calcium activation; ovarian sex hormones; myosin heavy chain; ₁-adrenergic receptors; heat shock protein

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