During the continuous and simultaneous recording of left ventricular diastolic pressures and changes in the length of a segment of left ventricular myocardium it was demonstrated that neither cardiac sympathetic nor vagal efferent nerve stimulation produces a change in ventricular myocardial extensibility. It was further shown that, at the heart rates studied, autonomic nerve stimulation does not modify the end-diastolic pressurelength curve. These data indicate that, during cardiac sympathetic stimulation, the augmented ventricular stroke work from any given end-diastolic Pressure is accomplished without a change in end-diastolic fiber length.Evidence was obtained, however, which suggests that the abbreviation of diastole at high imposed heart rates or large stroke volumes may leave an inadequate time for ventricular relaxation to take place and for inertial and viscous factors to be dissipated. Under these circumstances, sympathetic stimulation, by shortening systole and thereby lengthening diastole, permits the ventricle to remain on its “normal” pressure-length curve. This component of cardiac sympathetic efferent activity is peculiarly appropriate to the tachycardia that occurs with increased sympathetic outflow to the heart.