Heart basal metabolism has been classically studied as the energy expenditure of those processes unrelated to mechanical activity and often measured by rendering the heart inactive using cardioplegic solutions (usually by increasing extracellular K concentration ([Kle]). In arterially perfused rat heart (at 25 degrees C), raising [K]e from 7 to 25 mM at a constant extracellular Ca concentration ([Ca]e) (0.5 mM), induced an increase in resting heat production (Hr) from 4.1 +/- 0.3 to 5.1 +/- 0.3 mol. wt g-1. Under 25 mM K additional increase in [Ca]e further increased Hr to 6.0 +/- 0.4, 7.0 +/- 0.4 and 8.3 +/- 0.9 mol. wt g-1 for 1, 2 and 4 mM Ca, respectively. While under 7 mM K perfusion Hr was not affected by 4 microM verapamil, under 25 mM K and 2 mM Ca 0.4 microM verapamil induced a decrease in Hr (-1.6 +/- 0.2 mol. wt g-1, n = 5, P < 0.001). Caffeine increased Hr under 0.5 mM Ca and 7 mM K perfusion (+0.32 +/- 0.06 and +1.19 +/- 0.25 mol. wt g-1 for 1 and 5 mM caffeine respectively), but under 25 mM K conditions Hr was not affected by caffeine 2 mM. Severe hypoxia decreased Hr under both 7 and 25 mM K (3.7 +/- 0.5 to 2.7 +/- 0.4 mol. wt g-1 and 7.0 +/- 0.4 to 2.2 +/- 0.5 mol. wt g-1, respectively) suggesting that the increased Hr associated with the verapamil sensitive fraction of heat released is associated to a mitochondrial mechanism. Therefore, the use of high [K]e overestimates basal values by increasing a verapamil sensitive fraction of the energy released. In addition, high [K]e modifies a caffeine sensitive energy component probably due to a depletion of caffeine-dependent Ca stores.