The relative roles of augmented hemodynamic performance and direct stimulation of oxidative metabolism in mediating the increase of myocardial oxygen uptake (MVo2) produced by catecholamines have been examined in an isolated canine heart preparation. The responses of MVo2 to graded doses of isoproterenol, norepinephrine, or epinephrine were determined before and after the induction of cardiac arrest with potassium. Although increases of MVo2 occurred in the arrested state with the larger doses of the amines, they constituted only a small fraction, generally between 5 and 20%, of the increases produced by the same doses of amines when the hearts were beating. It is concluded that while large doses of catecholamines can increase oxidative metabolism of the nonbeating heart by a small amount, the increases of MVo2 produced by catecholamines in the beating heart are due in large part to the hemodynamic alterations which the amines induce.