In the cross-circulated canine heart-lung preparation,the stroke volume(SV)or the end-systolic volume increased linearly with increasing end-diastolic volume(EDV)when the afterloading impedance was fixed.Exactly the same result was obtained in the relation between the initial length(I)and the amount of shortening(S)for the tetanic contraction of isolated frog ventricular muscle.The slope of the EDV-SV or I-S relation was less than 1.0,suggesting that a kind of depressive effect or a deactivation of contraction was working during the active shortening of cardiac muscle.The slope,which inversely reflects the degree of deactivation,slightly tended to 1.0 with decreasing load and markedly by inotropic intervention,but it was not changed by partial ischemia.The horizontal axis intercept of the EDV-SV or I-S relation, which reflects the ability of the cardiac muscle to shorten under a specified afterloaded condition,shifted to the right(the ability decreased)at a larger load or under partial ischemia but shifted to the left with inotropic intervention. The deactivation increased linearly with the amount of active shortening but no deactivation was observed when there was no active shortening or no load.The mechanism of the deactivation is not due to a shortage of active-state duration but probably due to a depressive effect on Ca2+ utilization of the contractile system during the sliding phase of myofilaments.With reference to the skeletal muscle,a discrepancy is reported between the tension-length diagram determined by isometric tetanic contractions and that determined by isotonic or afterloaded contractions (BUCHTHAL and KAISER,1951; DELEZE,1961;EDMAN,1975).A kind of depression of mechanical performance by active shortening will occur during twitch and tetanus of muscle fiber.According to EDMAN(1980),the depressive effects are consistent with a true deactivation of the contractile system.The depressive effect of myocardial mechanical performance by active shortening has also been reported.For example,