A couple of points to confuse the issue:
The amount of force developed by a striated muscle at any given point is a
function of the number of cross-bridges that are formed, as well as the
energy being returned from the series and parallel elastic elements; what
Mel referred to earlier as a composite of active and passive components.
Therefore, although there is certainly a relationship between the amount
of overlap between the actin and myosin, the real crux of the biscuit is
how many cross bridges are being formed.
In skeletal muscle, the primary factors involved in force production by a
single motor unit (and by extrapolation, to the entire muscle) are the
number of cross-bridges and the rate of action potential generation. The
dogma seems to be that at some magic length at or just beyond the "resting
length", the number of potential cross-bridges is optimal, so the force is
dependent upon the rate of formation of the cross-bridges.
In cardiac muscle, the essence of the Frank-Starling Law of the heart is
that the heart pumps what you give it, at least up to a point. When Frank
and Starling were describing this phenomenon, they explained it using
skeletal muscle physiology, which was appropriate for the time. That is,
the cardiac muscle cells created more cross-bridges with a stretch, but at
some point, the myosin heads nearest the H-zone were not opposed by an
active site on the myosin, thus fewer cross-bridges were possible, and
less force was generated, and less blood was ejected. There is evidence,
however, that in cardiac muscle, stretching the sarcomere creates a
situation where troponin-C has a higher affinity for calcium; thus, for a
given level of intracellular calcium, more troponin-C-Ca complex is
formed, more active sites on the actin are uncovered, and more cross
bridges are formed. It is likely that the stretch on the troponin-C
"uncovers" the calcium binding site, setting up the length-dependent
calcium affinity of troponin-C. The reasons for the descending limb of
the Starling curve are less apparent, but may be related to a loss of
overlap (the fewer cross-bridge possible thing), or a decrease in calcium
affinity of troponin-C (the stretch makes the calcium binding site less
accessible).
I think the bottom line is that invoking skeletal muscle physiological
principles to explain the behavior of intact cardiac muscle is a mistake,
even though both are striated muscle. Much of the early information we
have on cardiac muscle was obtained from the study of cardiac papillary
muscle, which resembles skeletal muscle in form and function much more
than does a ventricular myocyte.
Still haven't heard from any Pilates disciples.
Frank Underwood
Evansville, Indiana
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