Energy demand, supply, and utilization in hypoxia, and force recovery after reoxygenation in rabbit heart muscle.

Abstract

In rabbit papillary muscle contracting at 20 degrees C in nitrogen at 0.2 Hz, glycolytic ATP formation is just enough to support the diminished contractile activity. Basal metabolism, important to maintain cellular function and integrity, is strongly inhibited. In the present study, we address the question of whether the inhibition of basal processes in hypoxia determines redevelopment of force in reoxygenation. By not stimulating the muscle during hypoxia, we try to make more ATP available for basal processes. Isometric force of papillary muscles (0.2-Hz stimulation) is measured before, during, and after 40 minutes of hypoxia. ATP formation and utilization in hypoxia are estimated from lactate production and changes in nucleotides and creatine compounds. After reoxygenation, muscles stimulated during hypoxia produce a steady-state force of 78% of the aerobic control; resting muscles recover to 94%. In contrast to expectation, lactate production in hypoxic resting muscles is only 30% of that in contracting ones. The findings indicate that basal metabolic rate of hypoxic muscles at rest is 14% of that of quiescent, well-oxygenated myocardium. We conclude that in hypoxic myocardium little ATP is available for basal metabolism, irrespective of the energy demand of the contractile system. It is therefore unlikely that the lower force found after reoxygenation in muscles stimulated during hypoxia is related to the degree of inhibition of basal processes.