Cross-bridge cycling theories cannot explain high-speed lengthening behavior in frog muscle
نویسندگان
چکیده
منابع مشابه
Resting myosin cross-bridge configuration in frog muscle thick filaments
Clear images of myosin filaments have been seen in shadowed freeze-fracture replicas of single fibers of relaxed frog semitendinosus muscles rapidly frozen using a dual propane jet freezing device. These images have been analyzed by optical diffraction and computer averaging and have been modelled to reveal details of the myosin head configuration on the right-handed, three-stranded helix of cr...
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A mathematical formula was derived from an active cross-bridge model to express the changes in the active myocardial force which occurred during systole. Using the formula and the assumption that the energy expenditure for cross-bridge cycling (Um) was a linear function of the force-time integral (FTI), we developed formulae describing the left ventricular Um versus FTI relation, the Um versus ...
متن کاملCharacterization of cross-bridge elasticity and kinetics of cross-bridge cycling during force development in single smooth muscle cells
Force development in smooth muscle, as in skeletal muscle, is believed to reflect recruitment of force-generating myosin cross-bridges. However, little is known about the events underlying cross-bridge recruitment as the muscle cell approaches peak isometric force and then enters a period of tension maintenance. In the present studies on single smooth muscle cells isolated from the toad (Bufo m...
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. Abstract. Despite the great success of the Huxley sliding filament model proposed half a century ago for actin-myosin linkages (cross-bridges), it fails to explain the force-velocity behavior of stretching skeletal muscles. Huxley’s two-state kinetic equation for cross-bridge proportions is therefore reconsidered and a new solution to the problem of steady muscle eccentric and concentric cont...
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Nemaline myopathy, the most common non-dystrophic congenital myopathy, is caused by mutations in six genes, all of which encode thin-filament proteins, including NEB (nebulin) and TPM3 (α tropomyosin). In contrast to the mechanisms underlying weakness in NEB-based myopathy, which are related to loss of thin-filament functions normally exerted by nebulin, the pathogenesis of muscle weakness in p...
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ژورنال
عنوان ژورنال: Biophysical Journal
سال: 1990
ISSN: 0006-3495
DOI: 10.1016/s0006-3495(90)82523-6