Although the kinetics of cardiac systolic force restitution have been well described, the restitution kinetics of left ventricular relaxation have not been examined. animals2'3 as well as in isolated hearts4-6 and isolated muscle preparations.7-10Weir and Yue10 have shown that the time constants of mechanical restitution and postextrasystolic potentiation are very similar and that contractile response has a linear correlation with intracellular Ca'+ concentration. Their studies with ryanodine, an inhibitor of the sarcoplasmic reticulum (SR) Ca2t release channel, have defined an essential role for the SR in the force-interval relation. These investigators concluded that the relation is a physiological expression of the availability of intracellular Ca2 , which is dependent on the SR. A phenomenological model of Ca2' flux among the SR, myoplasm, and extracellular space has been proposed to describe the kinetics of the force-interval relation.6'10Despite the large body of work performed delineating cardiac systolic restitution, very little has been done to define the pattern by which the heart's ability to relax rapidly returns after a stimulus, a phenomenon we term relaxation restitution. Relaxation, like myocardial contraction, is an energy-requiring process. Myocardial crossbridge separation and sarcomere force decay are dependent on active Ca21 uptake by the SR and resultant dissociation of Ca2' from troponin C. Although sarcolemmal Na+-Ca21 exchange participates in determining intracellular Ca2' levels, it is a low-affinity transport system and probably does not play a major role during isovolumic relaxation (see Reference 11 for review).