Using microcalorimetry and measuring oxygen consumption rate, we have studied metabolic activity in myocardial tissue from rats suffering from congestive heart failure (CHF) after ligation of the left coronary artery followed by myocardial infarction, comprising 30-40% of the endocardial circumference, known to be large enough to induce heart failure and neuroendocrine counter-regulation. The heat production in the preserved part of the left ventricle, harbouring the myocardial infarction, was 0.94 +/- 0.05 mW g(-1) (n = 10) and not different from the controls i.e g 0.94 +/- 0.05 mW g(-1), (n = 23). The oxygen consumption rate was 1.36 +/- 0.20 nmol O-2 s(-1) g(-1) in CHF myocardium and 1.55 +/- 0.24 nmol O-2 s(-1) g(-1) in the control rats, (n = 20), n.s. The calculated contribution from aerobic metabolism to total heat production was 71 +/- 9% in the CHF rats and 80 +/- 6% in the control group, n.s. In tissue samples taken from the region of the border of and into the macroscopically damaged area of the myocardial infarction (n = 5), the value for heat production was 1.15 +/- 0.13 mW g(-1) and oxygen uptake 1.79 +/- 0.23 nmol O-2 s(-1) g(-1). These results show that the contribution from aerobic metabolism to total energy expenditure in preserved left ventricular tissue is not higher than normal and suggest that the effects of left coronary occlusion are not limited to the generation of a myocardial infarction, but may also have a substantial impact on the ability of myocardial cells to increase metabolic activity in macro- and microscopically preserved regions of the left ventricle. In addition, the data demonstrate persistent metabolic activity within the region of ischemically damaged myocardium not different from that found in undamaged myocardium.