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Biophys J, November 2000, p. 2667-2681, Vol. 79, No. 5
Harvard School of Public Health, Boston, Massachusetts 02115 USA
We carried out a detailed mathematical analysis of the
effects of length fluctuations on the dynamically evolving cross-bridge distributions, simulating those that occur in airway smooth muscle during breathing. We used the latch regulation scheme of Hai and Murphy
(Am. J. Physiol. Cell Physiol. 255:C86-C94, 1988)
integrated with Huxley's sliding filament theory of muscle
contraction. This analysis showed that imposed length fluctuations
decrease the mean number of attached bridges, depress muscle force and
stiffness, and increase force-length hysteresis. At frequencies >0.1
Hz, the bond-length distribution of slowly cycling latch bridges
changed little over the stretch cycle and contributed almost
elastically to muscle force, but the rapidly cycling cross-bridge
distribution changed substantially and dominated the hysteresis. By
contrast, at frequencies <0.033 Hz this behavior was reversed: the
rapid cycling cross-bridge distribution changed little, effectively functioning as a constant force generator, while the latch bridge bond
distribution changed substantially and dominated the stiffness and
hysteresis. The analysis showed the dissociation of force/length hysteresis and cross-bridge cycling rates when strain amplitude exceeds
3%; that is, there is only a weak coupling between net external
mechanical work and the ATP consumption required for cycling
cross-bridges during the oscillatory steady state. Although these
results are specific to airway smooth muscle, the approach generalizes
to other smooth muscles subjected to cyclic length fluctuations.
Biophys J, November 2000, p. 2667-2681, Vol. 79, No. 5
© 2000 by the Biophysical Society 0006-3495/00/11/2667/15 $2.00
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