APStracts 3:0394H, 1996.

Maximum oxidative phosphorylation capacity of the mammalian heart. Mootha, Vamsi K., Andrew E. Arai, and Robert S. Balaban. Laboratory of Cardiac Energetics, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892 USA

APStracts 3:0394H, 1996.

It is difficult to estimate the maximum, in vivo, aerobic ATP production of the intact heart independent of limitations imposed by blood flow, oxygen delivery, and maximum mechanical power. This value is critical for establishing the kinetic parameters which control oxidative phosphorylation as well as for providing insights into the limits of myocardial performance. In this study, the maximum ADP-Pi driven heart mitochondrial respiratory rate was determined with saturating levels of oxygen, substrates and co-factors at 37oC. These rates were normalized to cytochrome oxidase (cyt a) content. To extrapolate this rate to the intact heart, the cyt a content of the myocardium (nmol cyt a/g wet wt myocardium) was determined in the same hearts. The maximum, ADP-Pi driven mitochondrial respiratory rates were 676+/-31 and 665+/-65 nmol O2/min/ nmol cyt a in the dog and pig, respectively. The cyt a content in the two species was 43.6+/-2.4 and 36.6+/-3.1 nmol cyt a/g wet wt, respectively. Using these values, the MVO2mito was calculated to be 29.5 (dog) and 24.3 (pig) umol O2/min/ g wet wt myocardium. Comparison with in vivo studies shows that the exercising heart can utilize 80-90% of its maximum oxidative capacity, implying there is little aerobic ATP production reserve in the mammalian heart.

Received 16 July 1996; accepted in final form 4 September 1996.
APS Manuscript Number H636-6.
Article publication pending Am. J. Physiol. (Heart Circ. Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 7 October 1996