Oct 13 (Thursday) Sam Walcott (Theoretical and Applied Mechanics, Cornell)

Explaining history dependence in muscle with molecules.
(A pseudo history-dependent cross-bridge model).

Abstract:

To understand how people move, one must have an understanding of
biological  motors, muscle.  Understanding muscle, in turn, requires at
least an  appreciation of the molecules of contraction and their chemical
interactions.  Muscle contraction occurs through the sliding of two types
of proteins past each other - thin filaments (made primarily of the
protein  actin) and thick filaments (made primarily of the protein
myosin).  Projections from the thick filament, so-called "cross-bridges",
are thought to bind to the thin filament, and then change conformation
resulting in a force that causes the thick and thin filaments to slide
relative to each other and muscle contraction to occur.

A muscle or muscle fiber of a given length contracts more forcefully if it
is actively stretched prior to contraction.  This force-enhancement from
stretch is one aspect of the history-dependence of muscle
contraction.   How does the macroscopic history-dependence occur at the
molecular level?  Some people claim that classic models for the
cross-bridge theory cannot explain history-dependence.  I show that, in
fact, history-dependent force-enhancement can be explained within the
confines of cross-bridge theory, through two models: the stuck
cross-bridge  model and the pseudo history-dependent model.  Here I
consider only the  latter model.  In this model, when a cross-bridge is
sufficiently  stretched, it "pops" into a new configuration and cannot
return to its  original configuration until it is stretched again.  This
molecular  behavior seems very unlikely.  Thus, I argue that although
history-dependence can be explained by the cross-bridge theory, it is more
likely that the cross-bridge theory is incomplete, and that
history-dependence (and other properties of muscle) arise from this
incompleteness.