Obesity is known to confer an increased risk for developing cardiovascular disease and is related to vasomotor dysfunction in the peripheral and cerebral circulations. However, the impact of obesity on the function of the coronary microvascular circulation is less known, especially regarding the overall vasodilator capacity of this system. Our study aimed at evaluating the cardiac mechanical function and the coronary reactivity of Wistar rats after a short- (3 months) and a long-term (7 months) period of a high-fat (HF) or standard diet. The rats were anesthetized with an intraperitoneal injection of sodium pentobarbital (30mg/kg) and their hearts were immediately perfused according to the Langendorff mode. After vasoconstriction with continuous infusion of a thromboxane A2 analogue (U46619, 30nM), the endothelial-dependent (EDD) and endothelial-independent (EID) dilatations were determined in the beating heart by injections of increasing doses of acetylcholine (4, 10, 20, 40, 60, 80, 100 pmoles) and sodium nitroprusside (100, 200, 400, 600, 800, 1000 pmoles) respectively. The mitochondrial oxidative stress was then evaluated in the isolated cardiac mitochondria (rate of H2O2 production) and in the whole heart (aconitase-to-fumarase ratio). In our study, the high-fat diet induced a reduction of the cardiac mechanical function which was not affected by ageing. The EDD was also increased by the diet at the early phase (+23.5%) and remained always higher compared to the control rats even though it was progressively decreased by ageing (-21,9% for the control and -19,2% for the HF rats). However, the EID was not affected neither by the diet neither by the ageing and it remained at the same levels for all the rat groups. These results indicate a functional adaptation of the coronary system induced by high-fat diet which is probably due to an enhanced function of their endothelial cells. The increased mitochondrial stress found either in the whole heart by a reduction of the aconitase-to-fumarase ratio (-41,4% for the control and -41.6% for the HF rats) either in the isolated mitochondria (+53% for the control and -41.6% for the HF rats when glutamate/malate/succinate were used as substrates) of rats following a long-term diet can only explain the progressive reduction of the EDD by ageing and not the diet effect. Thus, these data suggest the development of a compensatory adaptation of the coronary system shortly after the beginning of a high-fat diet. This phenomenon helps the heart to maintain the EDD and consequently an adequate tissue perfusion meeting the higher metabolic requirements of the organism. Finally, it seems that the process of ageing is more important than diet in affecting negatively the vascular function via the presence of oxidative stress.