The purpose of this study was to examine whether exercise training, superimposed on compensated-concentric hypertrophy, could increase myocardial hypoperfusion-reperfusion (H/R) tolerance. Female Wistar-Kyoto (WKY) and spontaneously hypertensive rats (SHR) (age:4 months; N=40), were placed into a sedentary (SED) or exercise training (TRD) group (treadmill running; 25 m/min, 1 hr/d, 5 d/wk for 16 wks). Four groups were studied: (WKY-SED, n=10), (WKY-TRD, n=10), (SHR-SED, n=10), (SHR-TRD, n=10). Blood pressure and heart rate were determined and in vitro isolated heart performance was measured with a retrogradely perfused, Langendorff, isovolumic preparation. The H/R protocol consisted of a 75% reduction in coronary flow for 17 min followed by 30 min of reperfusion. Although the rate-pressure product (RPP) was significantly elevated in SHR relative to WKY, training-induced bradycardia with TRD reduced the RPP in SHR-TRD (P<0.05) without an attenuation in systolic blood pressure. Heart/body weight ratio was greater in both groups of SHR vs. WKY-SED (P<0.001). Absolute and relative myocardial tolerance to H/R was greater in WKY-TRD and both groups of SHR relative to WKY-SED (P<0.05). Endurance training superimposed on hypertension-induced compensated hypertrophy conferred no further cardioprotection to H/R. Post-reperfusion HSP72 abundance was enhanced in WKY-TRD and both groups of SHR relative to WKY-SED (P<0.05) and was highly correlated with absolute LV functional recovery during reperfusion (R²=0.86, P<0.0001). These data suggest both compensated hypertrophy associated with short-term hypertension and endurance training individually improved H/R and that increased post-reperfusion HSP72 abundance was, in part, associated with the cardioprotective phenotype observed in this study.