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Biophys J, December 1998, p. 2971-2983, Vol. 75, No. 6
*Department of Biochemistry and Biophysics, and the Cardiovascular Research Institute, University of California, San Francisco, California 94143; #UCSF/UCB Bioengineering Graduate Group, University of California, San Francisco, California 94143, and Berkeley, California 94720; and §Department of Integrative Biology, University of California, Berkeley, California 94720 USA
Active glycerinated rabbit psoas fibers were stretched at
constant velocity (0.1-3.0 lengths/s) under sarcomere length control. As observed by previous investigators, force rose in two phases: an
initial rapid increase over a small stretch (phase I), and a slower,
more modest rise over the remainder of the stretch (phase II). The
transition between the two phases occurred at a critical stretch
(LC) of 7.7 ± 0.1 nm/half-sarcomere
that is independent of velocity. The force at critical stretch
(PC) increased with velocity up to 1 length/s, then was constant at 3.26 ± 0.06 times isometric force.
The decay of the force response to a small step stretch was much faster
during stretch than in isometric fibers. The addition of 3 mM vanadate
reduced isometric tension to 0.08 ± 0.01 times control isometric
tension (P0), but only reduced PC to 0.82 ± 0.06 times
P0, demonstrating that prepowerstroke states
contribute to force rise during stretch. The data can be explained by a
model in which actin-attached cross-bridges in a prepowerstroke state
are stretched into regions of high force and detach very rapidly when
stretched beyond this region. The prepowerstroke state acts as a
mechanical rectifier, producing large forces during stretch but small
forces during shortening.
Biophys J, December 1998, p. 2971-2983, Vol. 75, No. 6
© 1998 by the Biophysical Society 0006-3495/98/12/2971/13 $2.00
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