Influence of length changes on myocardial metabolism in the cat papillary muscle.

Myocardial oxygen consumption (MVOi) increases in proportion to the cumulative product of active tension and time throughout the normal isometric contraction. However, rapid shortening at any time during a contraction prevents further tension generation and oxygen consumption during the remainder of that contraction. My hypothesis is that, under physiological conditions, shortening produces this effect by reducing the extent and duration of the energy-dependent events subserving contraction. I tested this hypothesis by minimizing the potential reduction of metabolism via muscle shortening during contraction; this was done by lowering temperature (23C), reducing shortening rate (0.8 muscle length/sec) and increasing myoplasmic calcium (7.5 mM Ca I+ + 10 mM caffeine). Twelve right ventricular cat papillary muscles were released from that length at which maximum active force is developed to a slack length at increasing intervals after stimulation. Under these conditions, absolute MVOj increased significantly, but the relative increase with progressively longer stimulus-release intervals was greatly attenuated. At a 0-miec stimulus-release interval under the present conditions, MVOi was 8.26 nl/mg dry wt per contraction; for a full contraction MVOa was only 27% greater. Under the more physiological conditions employed in a prior study, this increase, from 0.41 to 2.97 nl/mg dry wt per contraction, wa 824%. The addition of 10"' M norepinephrine under otherwise physiological conditions increased MVOi at all times during contraction, but the relationship between MVOi and length was not altered. These data suggest that, both under normal conditions and after inotropic augmentation, shortening of cardiac muscle during contraction decreases the level of the energydependent events supporting contraction; this may be the mechanism by which MVO, is regulated by length-dependent changes in metabolism throughout contraction.