Isotonic force modulates the rate of force redevelopment in frog muscle fibers independent of changes in unloaded shortening velocity, suggesting cooperative cross-bridge activation of thin filaments.
Advances sarcomere mechanics insight in amphibian muscle; leaves open translation to cardiac force generation in mammals.
We tested the hypothesis that force-velocity history modulates thin filament activation, as assessed by the rate of force redevelopment after shortening (+dF/dt(R)). The influence of isotonic force on +dF/dt(R) was assessed by imposing uniform amplitude (2.55 to 2.15 microm sarcomere(-1)) but different speed releases to intact frog muscle fibres during fused tetani. Each release consisted of a contiguous ramp- and step-change in length. Ramp speed was changed from release to release to vary fibre shortening speed from 1.00 (2.76 +/- 0.11 microm half-sarcomere(-1) s(-1)) to 0.30 of maximum unloaded shortening velocity (V(u)), thereby modulating isotonic force from 0 to 0.34 F(o), respectively. The step zeroed force and allowed the fibre to shorten unloaded for a brief period of time prior to force redevelopment. Although peak force redevelopment after different releases was similar, +dF/dt(R) increased by 81 +/- 6 % (P < 0.05) as fibre shortening speed was reduced from 1.00 V(u). The +dF/dt(R) after different releases was strongly correlated with the preceding isotonic force (r = 0.99, P < 0.001). Results from additional experiments showed that the slope of slack test plots produced by systematically increasing the step size that followed each ramp were similar. Thus, isotonic force did not influence V(u) (mean: 2.84 +/- 0.10 microm half-sarcomere(-1) s(-1), P < 0.05). We conclude that isotonic force modulates +dF/dt(R) independent of change in V(u), an outcome consistent with a cooperative influence of attached cross-bridges on thin filament activation that increases cross-bridge attachment rate without alteration to cross-bridge detachment rate.
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Vandenboom et al. (2002) studied this question.
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