Background: Degenerative mitral regurgitation (MR) is often accompanied by hypertension(pressure overload) with aging. This study determined the contribution of volume overload and cardiac fibrosis on left ventricular (LV) remodeling and exercise capacity in rats with pressure overloaded rats. Method: Pressure overloaded and left ventricular hypertrophy (LVH) were created by suprarenal aortic constriction (SAC) in SD rats. Serial echocardiographic studies and exercise tests were performed at 2-week intervals and invasive hemodynamic examination by a pressure-volume catheter system was done at 14 weeks after SAC. The rats were divided into 4 groups [SAC, SAC+MR =SAC followed by MR operation, MR=laparotomy followed by MR operation, Control]. MR was created by introducing a needle through LV apex and making a hole on anterior mitral leaflet. SAC was done at 2 weeks before MR formation in SAC+MR group. Results: LV wall thickness increased in SAC group compared to control group whereas LV ejection fraction (EF) and E/E' did not change. LV end diastolic pressure and the EDPVR slope were greater in SAC group than in control group. LV dilatation and exercise intolerance were developed first in SAC+MR group. However, MR group showed a catch-up of remodeling and exercise intolerance at 10 weeks after MR formation (LV ESD at 10 weeks after MR formation, 4.33짹0.26 vs. 6.50짹0.40 vs. 6.59짹1.38 mm for control vs. MR vs. SAC+MR, P<0.05; LV EDD, 7.68짹0.15 vs. 10.48짹0.46 vs. 10.20짹1.26 mm, P<0.05 exercise duration, 765.3짹130.1 vs. 487.8짹49.0 vs. 434.0짹80.3 seconds, P<0.05 no statistical differences between SAC+MR and MR). Myocardial fibrosis was greatest in SAC and greater in SAC+MR compared with MR and control. Conclusion: Induction of volume overload before cardiac fibrosis in pressure overloaded rats affected LV compliance and improved exercise capacity over time in rats. Cardiac fibrosis was correlated with EDPVR and was higher in pressure overloaded rats compared with MR.