Although the heart has been considered primarily an aerobic organ, recent work (1) has reemphasized the possibility that measurement of oxygen consumption alone may not 1)e adequate to define the total energy utilization under all conditions. The role of anaerobic metabolism must be reviewed.Methods of defining as well as quantifying anaerobiosis are currently in dispute. When oxidation and glycolysis proceed at the same rate, carbohydrate is oxidized to CO2 and H20. Lactate arises whenever the rate of glycolysis exceeds the rate of oxidation. Net production of lactate by an organ, as evidenced for example by venous concentration greater than arterial, has been considered to represent anaerobic metabolism due to cellular hypoxia (2). More recent work (3) has demonstrated that large changes in lactate production can occur unassociated with hypoxia, but related instead to increased pyruvate production. Huckabee introduced the concept of "excess lactate" in order to distinguish between pyruvateinduced changes in lactate and those related solely to a shift in DPN: DPNH redox potential. This was inferred from alterations in arterial lactatepyruvate ratio and the relative arteriovenous differences of the two substrates. "Excess lactate," so defined, was considered an indicator of cellular oxygenation and was used quantitatively as a measure of anaerobic metabolic rate.Anaerobic metabolism in cardiac muscle has been considered to occur only under extreme conditions. Whereas earlier work (4-9) showed lactate production only sporadically with stresses of hypoxia, shock, or myocardial emboli, Huckabee (1) found that in dogs the stress of either 10 per cent oxygen breathing or leg exercise would result in myocardial excess lactate despite positive