Force, not sarcomere length, correlates with prolongation of isosarcometric contraction

Recent studies have emphasized the importance of the late systolic phase for understanding ventricular ejection. To examine the myocardial factors controlling this phase, we studied the timing of twitch contraction in nine excised rat trabeculae contracting isosarcometrically. By varying both sarcomere length (SL) and extracellular Ca²⁺ concentration ([Ca²⁺](o)) we determined which of these factors or the developed peak twitch force correlated better with the prolongation of contraction. We focused on the period from just before the peak of force to the time of half relaxation. SL was measured by laser diffraction and kept constant using adaptive control. Peak twitch force was the factor most tightly correlated with prolongation of contraction: as force rose from 10 to 100 mN/mm², duration tripled from 100 to 300 ms. When the trend with force was removed, however, no separate influence of SL remained. Increase in [Ca²⁺](o) abbreviated contraction equally at all force levels. Prolongation of late systolic contraction was also highly correlated with prolongation of the time constant for late relaxation, suggesting a common mechanism by which peak twitch force lengthens the entire subsequent time course of a twitch. We hypothesize that 1) increased force correlates with prolonged Ca²⁺ binding to troponin-C, and/or 2) attached cross bridges act cooperatively to oppose the inhibiting effects of tropomyosin as Ca²⁺ is lost from the thin filaments.