While most attention has been focused on mitochondrial ATP production and transfer in failing hearts, less interest has been on the non-failing hypertensive heart. Here energetic complications are less obvious yet may provide insight to disease ontogeny. We studied hearts from twelve-month old Spontaneously Hypertensive Rats (SHR) relative to normotensive Wistar-Kyoto (WKY) rats. The ex vivo working heart model SHR hearts showed reduced compliance and impaired responses to increasing preloads. High resolution respirometry, showed higher state 3 (with excess ADP) respiration rates in SHR left ventricle (LV) fibers using complex (C) 1 substrates, and maximal uncoupled respiration with combined CI and CII substrates. Respiration with ATP showed a 15% depression in SHR fibers relative to WKY fibers, suggesting impaired ATP hydrolysis. This was consistent with a 50% depression in actomyosin ATPase activities. Superoxide production from SHR fibers was similar to WKY fibers respiring with ADP, however increased by 15% with ATP. In addition the apparent Km for ADP was 54% higher for SHR fibers, and assays conducted following ex vivo work resulted in a 28% depression of CI in SHR fibers, but not in WKY fibers. TEM showed similar mitochondrial volumes yet decrease cristae number in SHR mitochondria. Tissue lipid peroxidation was also 15% greater in SHR LV. Overall these data suggest that while SHR cardiac mitochondria from non-failing hearts function marginally better than those of WKY rats, they show dysfunction following intense work. Impaired ATP turnover in hard-working SHR hearts may starve cardiac mitochondria of ADP and elevate superoxide.