The mechanism which governs the duration and extent of ongoing contractile activity in intact cardiac muscle is to be studied using direct visualization, measurement, and control of sarcomere dynamics. New, infrared-light diffraction techniques which give better sarcomere length resolution have been developed for these experiments. First the effect of myofilament displacement upon subsequent contractile activity will be studied. Specifically, tension generated at a given degree of myofilament overlap will be used to quantify the "deactivation" caused by previous myofilament displacement. Positive and negative inotropic interventions will be employed to determine if the level of contractile activity alters the response to myofilament motion. Next, the maximum duration of contractile activity at constant sarcomere length will be studied after peak shortening. When sarcomere length is unchanging, the possible influence of length-dependent restoring forces will be negligible. Since the source of such restoring forces is unclear, the sarcomere and tissue length changes - the latter demarcated by the positions of microspheres lodged within the small vessels - will be compared to determine the influence of cardiac tissue distortion on sarcomere dynamics at these short lengths. Once the effect of preceding motion upon contractile activity and the influence of the surrounding tissue upon sarcomere dynamics have been identified, pharmacological interventions are planned to determine if the rate of calcium uptake influences the duration of contractile activity in the absence of myofilament motion. Cardiac muscles from rats and rabbits will be studied as distinct models which have postulated differences in contractile activation and control.