Myocardial reperfusion occurs in a number of clinical conditions which include unstable angina, thrombolytic therapy or percutaneous transluminal angioplasty during evolving myocardial infarction and cardioplegic arrest during cardiac surgery. The transition from the ischemic to the postischemic state of the myocyte is associated with a number of functional, morphological, ionic and metabolic alterations. This article reviews available information on metabolism of glucose and palmitate in postischemic myocardium. Overall oxidative metabolic rate recovers rapidly after the onset of reperfusion. In some studies myocardial oxygen consumption during early reperfusion has been disproportionately high compared to contractile function. Oxygen consumption may recover transiently even in myocardium that undergoes irreversible injury. There exists some evidence indicating that cytoplasmic calcium overload may lead to increased energy expenditure during reperfusion. The relative contribution of fatty acids and glucose to oxidative metabolism during the first hour of reperfusion has been found either to be unchanged or to exhibit a shift toward increased glucose oxidation. Several observations suggest that glucose utilization may be essential during reperfusion for the survival of the myocardium.