In 12 dogs on right-heart bypass with heart rate, stroke volume, and aortic pressure constant, the velocity of contraction was augmented comparably by three fundamentally distinct interventions in the same heart: 1) sustained postextrasystolic potentiation produced by paired, electrical stimulation; 2) norepinephrine infusion; and 3) calcium infusion. In each instance the correlation between velocity of contraction and MVo2 was striking. During paired stimulation, maximum rate of left ventricular ejection increased by an average of 50.3% ± 3.8% (se of mean) above control, MVo2 increased by 1.96 ± 0.10 ml/100 g per min (39.8% ± 1.6% above control), while the tension-time index (TTI) fell 12.4% ± 1.1%. With norepinephrine, and with calcium, left ventricular ejection rates were increased 52.9 ± 3.2% and 55.1 ± 3.2%, respectively, and MVo2 was augmented 2.03 ± 0.08 ml/100 g per min and 1.87 ± 0.04 ml/100 g per min, while the TTI decreased 15.9 ± 0.6% and 12.4 ± 2.4%. Since MVo2 always increased substantially while TTI fell, tension cannot be considered to be the sole determinant of MVo2. Since comparable increases in velocity of contraction produced by different interventions were associated with similar large augmentations of MVo2, it appears that the velocity of contraction is an important determinant of MVo2. Furthermore, it is likely that the so-called O2 wasting effect exerted by norepinephrine on myocardial metabolism may be explained largely by an increased velocity of contraction.