Force, not sarcomere length, correlates with prolongation of
isosarcometric contraction.
Janssen, Paul M. L., and William C. Hunter.
Department of Biomedical Engineering, The Johns Hopkins School of
Medicine, Baltimore, Maryland, 21205, USA.
APStracts 2:0100H, 1995.
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 9 excised rat trabeculae contracting
isosarcometrically. By varying both sarcomere length (SL) and
extracellular calcium concentration ( [Ca2+]o ) we determined which
of these factors, or the developed peak twitch force correlated
better with the prolongation of contraction. We focussed 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
calcium binding to troponin-C, and/or (2) attached cross-bridges act
cooperatively to oppose the inhibiting effects of tropomyosin as
calcium is lost from the thin filaments.
Received 19 January 1994; accepted in final form 5 February 1995.
APS Manuscript Number H41-4.
Article publication pending Am. J. Physiol. (Heart Circ. Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 28 March 1995.