ABSTRACT
90We investigated how changes in ventricular contractility and hemodynamics associated with exercise influence the mechanical energy transmission from the left ventricle to the arterial system. Using five chronically instrumented dogs preconditioned to run on a treadmill, we imposed exercise loads of various degrees by altering the speed and slope of the treadmill (up to 7 km/h and a 20% slope). We evaluated ventricular contractility by end-systolic elastance (Ees) and arterial properties in terms of the effective arterial elastance (Ea). Ea was estimated by the ratio of mean aortic pressure to stroke volume. With exercise, Ees increased from 7.4 to 11 mmHg/ml (p<0.001) and Ea tended to increase from 5.2 to 7.1 mmHg/ml, while the ratio of Ea to Ees remained fairly constant (from 0.75 ± 0.24 to 0.65 ± 0.21, NS). The estimated ratio of stroke work (SW) to the maximal SW theoretically derived was 0.95 ± 0.06 at rest and was 0.93 ± 0.10 during exercise. Similarly, the ratio of SW to cardiac oxygen consumption estimated from the pressure-volume area was 0.97 ± 0.02 at rest and was 0.99 ± 0.01 during exercise of its theoretical maximal value.
We concluded that external work of the left ventricle of dogs was adjusted to nearly maximal during exercise as well as at rest, without compromising the conversion efficiency of metabolic energy to SW. Needless to say, however, whether the maximization of external work is the optimization criterion of the cardiovascular regulation remains to be seen.
