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CELLULAR |
1 The Randall Division of Cell and Molecular Biophysics, Guy's Campus, King's College London, London SE1 1UL, UK
2 Department of Physiology, Monash University, Victoria 3800, Australia
Redevelopment of isometric force following shortening of skeletal muscle is thought to result from a redistribution of cross-bridge states. We varied the initial force and cross-bridge distribution by applying various length-change protocols to active skinned single fibres from rabbit psoas muscle, and observed the effect on the slowest phase of recovery (late recovery) that follows transient changes. In response to step releases that reduced force to near zero (
8 nm (half sarcomere)1) or prolonged shortening at high velocity, late recovery was well described by two exponentials of approximately equal amplitude and rate constants of
2 s1 and
9 s1 at 5°C. When a large restretch was applied at the end of rapid shortening, recovery was accelerated by (1) the introduction of a slow falling component that truncated the rise in force, and (2) a relative increase in the contribution of the fast exponential component. The rate of the slow fall was similar to that observed after a small isometric step stretch, with a rate of 0.40.8 s1, and its effects could be reversed by reducing force to near zero immediately after the stretch. Force at the start of late recovery was varied in a series of shortening steps or ramps in order to probe the effect of cross-bridge strain on force redevelopment. The rate constants of the two components fell by 4050% as initial force was raised to 7580% of steady isometric force. As initial force increased, the relative contribution of the fast component decreased, and this was associated with a length constant of about 2 nm. The results are consistent with a two-state strain-dependent cross-bridge model. In the model there is a continuous distribution of recovery rate constants, but two-exponential fits show that the fast component results from cross-bridges initially at moderate positive strain and the slow component from cross-bridges at high positive strain.
(Received 12 December 2005;
accepted after revision 16 February 2006;
first published online 23 February 2006)
Corresponding author John Sleep: The Randall Division of Cell & Molecular Biophysics, New Hunt's House, Guy's Campus, King's College London, London SE1 1UL, UK. Email: john.sleep{at}kcl.ac.uk
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