We hypothesized that myocardial contractile function and coronary arterial function are greater after ischemia and reperfusion in high-intensity treadmill-trained vs sedentary rats. Rats performed 10 x 4 min bouts of treadmill-running consisting of 2 min@13 m/min + 2 min@45-60 m/min (ETR) or were sedentary (SED) for 12 weeks. Animals then were instrumented to measure left ventricular (LV) contractility in response to three 15-min coronary occlusion (O) and 5-min reperfusion (R) cycles (ISC) or a sham-operation (SHAM). Following the ISC and SHAM protocols, hearts were excised and coronary arterial (~105 µm, i.d.)function was evaluated using isometric techniques. LV developed pressure, LV dP/dt at a developed pressure of 40 mmHg, and systolic blood pressure were not different between ETR (n=14) and SED (n=7) rats before or after the SHAM protocol. Further, hemodynamic variables were similar in ETR (n=14) and SED (n=13) animals before the ISC protocol, and were depressed to the same degree by the three O/R cycles. Therefore, ETR did not alter myocardial contractile function in rats that were (i.e., ISC) or were not (i.e., SHAM) exposed to ischemia and reperfusion. Acetylcholine-evoked relaxation (10^-8 - 3 x 10^-5 M) was greater (p<0.05) in coronary arteries from SHAM-ETR vs SHAM-SED animals (5 of 8 doses tested) and ISC-ETR vs ISC-SED rats (3 of 8 doses tested). Maximal relaxation produced by sodium-nitroprusside (10^-4 M) was similar among groups. Vasocontractile responses produced by potassium-chloride (10-100 mM) and endothelin-1 (10^-11-10^-4M) were greater (p<0.05) in the presence vs the absence of nitric oxide synthase inhibition (10^-6M, N^G-monomethyl-L-arginine) in vessels from SHAM-ETR but not SHAM-SED rats, and ISC-ETR but not ISC-SED rats. These findings suggest that ETR-evoked improvements in coronary function are maintained in small arteries even when exposed to ischemia and reperfusion.