In the isolated cat papillary muscle, the time course of activation during isometric contraction was measured using instantaneous velocity of shortening after quick releases at constant contractile element length and controlled load. Activation rose and declined ahead of isometric force. This course of activation could be altered by the mode of the quick release. Undamped quick releases increasingly deactivated contraction with time. Deactivation was reduced by damping the rapid movement of the lever after the release and by increasing the afterloads to which the releases were made, thus lessening the extent of the releases. The curves of activation obtained from releases to different afterloads converged after the first half of the rising phase of the twitch. Deactivation from quick releases was eliminated by tetanizing the muscle. Hence, the instantaneous relation of force and velocity of shortening was not unique relative to time except when the muscle was tetanized. Deactivation was also reduced by lowering the temperature, by adding 10 mM caffeine, or by increasing the Ca 2+ concentration in the bathing medium in the presence of 10 mM caffeine. These results suggest that quick releases deactivate contraction by uncoupling crossbridges which can be reformed if the Ca 2+ available to activate contractile sites is not sequestered elsewhere. KEY WORDS activation of contraction heart muscle sarcoplasmic reticulum instantaneous force-velocity relation calcium• In A. V. Hill's model of contracting muscle (1), an active contractile element (CE) is arranged in series with a passive series elastic element (SE). During isometric contraction, the CE shortens and stretches the SE, leading to an increase in force. When the muscle is released to a small load, two phases of shortening are observed: (a) a very rapid shortening reflecting primarily the passive recoil of the SE and (b) a slower sustained shortening reflecting the subsequent active shortening of the CE with a load (l). Quick releases were originally used in skeletal muscle to discharge the SE and study the relation between velocity and load at known CE lengths and times during contraction (2). In cardiac muscle, the quick-release technique has been widely used to define the intensity and the

The time course of the ability to shorten during contraction was measured using velocity of shortening of the contractile element corrected for length after quick releases to constant loads, in isolated papillary muscles of the cat, rabbit, dog, and rat. The ratios of time-to-peak shortening ability at preload (TTPA), to time-to-peak active force (TPF), were 0.30, 0.36, 0.32, and 0.70 in the cat, dog, rat and rabbit, respectively. When the pacing rate was increased from 12 to 60/min, peak force was augmented in the cat (36%) and rabbit (108%), while TPF decreased in the cat (by 30%) but not in the rabbit. Various inotropic interventions did not alter the ratio of TTPA/TPF in any species. However, caffeine (10mM) increased this ratio to that normally found in the rabbit, in which it was not altered. Afterloaded force-peak velocity relations of the cat, dog, and rat were curvilinear, but in the rabbit in the control state, and in the cat and dog in the presence of caffeine, these relationships tended to be linear. The differences in the time course of the ability to shorten among these mammalian species may be related to differences in excitation-contraction coupling.

In isometrically contracting isolated cat papillary muscles, the mechanism determining the reduction in active tension (P) at lengths (L) below the optimal length (Lmax) for maximal tension development (Pmax) was studied. Increasing [Ca2+] from 1.25 to 5 mM, paired electrical stimulation and caffeine augmented P-O/max by 77,61 and 23% respectively, as well as the tension developed at any given length on the ascending limb of the length-active tension relation. To see whether below Lmax the degree of activation is dependent on length, these length-active tension relations were expressed as P/Pmax relative to L/Lmax where Pmax and Lmax in each inotropic state was 100%. These normalized length-active tension relations were not altered by different [Ca2+]o, but shifted upward and to the left by caffeine and paired stimulation. The effects of elevating [Ca2+] on the length-active tension relation suggests that restoring forces and fixed internal loads are not an important factor in decreasing active tension at short lengths. The effects of caffeine and paired stimulation support the view that in cardiac muscle inactivitation of contraction is a major factor determining the fall in active tension at decreasing length.

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