This study investigated the influence of beta-blockade on the resting heat production of myocardial tissue by microcalorimetry. During one week, propranolol (beta(1) beta(2)-adrenoceptor antagonist) was orally given to 14 rats - 5 mg kg(-1) once daily, and carvedilol (beta(1) beta(2)- and alpha(1)-antagonist) to eight rats -3 mg kg(-1) once daily; 36 rats were controls. Thin slices of cardiac tissue, approximate to 10 mg, were removed from the apex. Carbogen-saturated Krebs-Ringer bicarbonate buffer with glucose as substrate was pumped through the microcalorimetric ampoule during the measurement at 37 degrees C. Unexpectedly, the mean resting heat production was higher after both propranolol, 1.25 mW g(-1) wet tissue (p < 0.01, ANOVA) and carvedilol, 1.19 mW g(-1) (p < 0.05) treatments, than in the control group, 1.01 mW g(-1). The same applied to oxygen consumption. The calculated anaerobic fractions were 16, 8 and 24% in the respective groups, but differences were not significant. Also, when added in vitro, propranolol caused an enhanced myocardial resting heat production by an average of 23%. As resting myocardial metabolism contributes to the overall cardiac energetics to a relatively minor extent, the net result of treatment will probably be of only marginal physiological importance. The experimental outcome is indicative of a stimulation of resting myocardial metabolic activity after propranolol and carvedilol, rather than a predicted decrease. We hypothesize that the absence of anything to depress in the non-beating heart tissue, reveals a small degree of partial beta-agonist activity, possibly via the newly discovered beta(3)-adrenoceptor.