Tepmanas Bupha-IntrJitanan LaosiripisanJonggonnee WattanapermpoolMahidol University2018-09-132018-09-132009-10-01Journal of Applied Physiology. Vol.107, No.4 (2009), 1105-111215221601875075872-s2.0-70350169220https://repository.li.mahidol.ac.th/handle/20.500.14594/27134The impact of regular exercise in protecting cardiac deteriorating results of female sex hormone deprivation was evaluated by measuring changes in intracellular Ca2+removal activity of sarcoplasmic reticulum (SR) in ovariectomized rats following 9-wk treadmill running exercise at moderate intensity. Despite induction of cardiac hypertrophy in exercised groups of both sham-operated and ovariectomized rats, exercise training had no effect on SR Ca2+uptake and SR Ca2+-ATPase (SERCA) in hormone intact rat heart. However, exercise training normalized the suppressed maximum SR Ca2+uptake and SERCA activity in ovariectomized rat heart. While exercise training normalized the leftward shift in pCa (-log[Ca2+])-SR Ca2+uptake relation in ovariectomized rats, no effect was detected in exercised sham-operated rats. Similar phenomena were also observed on SERCA and on phospholamban (PLB) phosphorylation levels; exercise training in ovariectomized rats enhanced SERCA expression to reach the level as that in sham-operated rats, in which there were no differences in SERCA and phospho-PLB levels between sedentary and exercised groups. In addition, the reduction in phospho-Thr17PLB in myocardium of ovariectomized rats was abolished by exercise training. These results showed that regular exercise maintains the molecular activation of cardiac SR Ca2+uptake under normal physiological conditions and is able to induce a protective impact on cardiac SR Ca2+uptake in ovarian sex hormone-deprived status. © 2009 the American Physiological Society.Mahidol UniversityBiochemistry, Genetics and Molecular BiologyMedicineArticleSCOPUS10.1152/japplphysiol.00407.2009