Studies of ventricular energetics using the relation between myocardial O2 consumption (MVO2) and pressure-volume area (PVA) have been performed extensively in the isolated heart, but not in the intact animal. We characterized the MVO2-PVA relation and its response to heart rate (HR) in eight closed-chest dogs instrumented with high-fidelity micromanometers, piezoelectric crystals, coronary flow probes, and coronary sinus oximetric catheters. The effect of dobutamine was studied in five dogs. MVO2 is linearly related to PVA with lower MVO2 required for the generation of smaller PVAs. Baseline contractile efficiency (EFF) was 25.6 +/- 2.8%. High pacing rates reduced EFF (25.7 +/- 3.2% at a HR of 107 +/- 3 beats/min vs. 16.3 +/- 2.4% at a HR of 194 +/- 5 beats/min, P < 0.0167) and load-independent MVO2 per beat (0.562 +/- 0.119 vs. 0.377 +/- 0.074 J.beat-1 x 100 g LV-1, P < 0.0167) while increasing end-systolic elastance (Ees) (9.4 +/- 1.3 vs. 18.6 +/- 3.1 mmHg/ml, P < 0.0167). Dobutamine administration increased load-independent MVO2 per beat (0.392 +/- 0.108 vs. 0.607 +/- 0.083 J.beat-1 x 100 g LV-1, P < 0.05) and contractility (Ees 10.1 +/- 1.5 vs. 32.0 +/- 7.6 mmHg/ml, P < 0.05) without changing EFF (28.8 +/- 3.8 vs. 30.3 +/- 3.8%, P = NS). Thus the intact animal displays loss of EFF at high heart rates but maintains EFF during dobutamine stimulation. Both interventions increased load-independent MVO2 per minute, indicating increased O2 requirements for excitation-contraction coupling.