Muscle Structure and Theories of Contraction

Huxley, Andrew

doi:10.1016/s0096-4174(18)30128-8

Cited by 3,012 publications

(2,690 citation statements)

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“…Clearly the phenomenon ofexcess tension cannot be explained in terms of actin-myosin overlap as in the sliding filament hypothesis (Gordon et al, 1966a and1966b;Huxley, 1957). Sugi (1972) suggested that, during the process of stretch, some of the cross bridges are so displaced that they are brought into a "lockedon" situation.…”

Section: Discussionmentioning

confidence: 99%

“…Investigations carried out on skeletal muscle over the last 20 years have led to the now generally accepted fact that contraction is brought about by the sliding of thin filaments between thick filaments caused by tension exerted by cross-bridges which link the two sorts of filament together (Hansen and Huxley, 1955;Huxley, 1953Huxley, , 1957Huxley, , 1960Huxley, , 1969Huxley, , 1971Huxley, , and 1974Huxley and Niedergerke, 1954;Huxley and Hansen, 1954).…”

Section: Introductionmentioning

confidence: 99%

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Active tension changes in frog skeletal muscle during and after mechanical extension

Atteveldt

Crowe

1980

Journal of Biomechanics

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-Isolated frog sartorious muscle at 4°C has been used to study the phenomenon whereby tetanically stimulated muscle, subjected to a mechanical extension, yields an active tension which is greater than that obtained during an isometric contraction in which the muscle is stretched prior to stimulation. The excess tension magnitude and decay with time depend upon the total muscle length. After stimulation ceases the excess tension does not persist over a time appreciably longer than that needed for the normal isometric tension to disappear. No persistent excess tension could be seen from stretches applied after stimulation had ceased but before the active tension had fully decayed.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Active tension changes in frog skeletal muscle during and after mechanical extension

Atteveldt

Crowe

1980

Journal of Biomechanics

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“…Figure 3 shows an example of a fitted curve. The data were thus completely described in terms of the three parameters A,b and g. As these parameters are difficult to interpret physiologically, the fitted functions were extrapolated to yield an estimate of the parameter H, the intercept of the function on the horizontal axis, which is the amplitude of the quick release necessary to reduce the active force to exactly zero (Huxley, 1957). Using this parameter, the curves measured at different stretched strip lengths were normalized, i.e.…”

Section: Methodsmentioning

confidence: 99%

The length dependence of the series elasticity of pig bladder smooth muscle

Mastrigt

1988

J Muscle Res Cell Motil

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SummaryStrips of urinary bladder smooth muscle were sul~jected to a series of quick release measurements. Each measurement consisted of several releases and resets to the original length, made during one contraction. The complete length-force characteristic of series elasticity was quantified by estimating H, the amplitude of quick release necessary to reduce the active force to exactly zero, and Db, a measure for the deviation of the characteristic from a straight line. By measuring a series of contractions at increasing stretched strip lengths, the length dependence of these parameters was studied. It was found that H depends linearly on stretched strip length. On average Hflength amounted to 0.04. Db decreased when strips were stretched, i.e. a straight line was more closely approximated. Both parameter dependencies support the concept of two separate elastic mechanisms, a linear true passive elasticity in series with a non-linear elasticity in the cross-bridges. For the latter, H amounts to 3.8% of the initial strip length.

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“…8), that it is tempting to interpret it in terms of physiologic functioning of myocardial muscle. The way to do so would be through the construction of a detailed ventricular model, based on actin-myosin filament interaction (36,42,49,56,78), and ventricular geometry (17,30,41,46,54,65,66,79,81), as well as anatomy (4,81,90,92,104), and electrophysiology (10). However, such studies seldom attempt to quantitatively predict ventricular performance in terms of compressed data models as the present three-compartment model.…”

Section: Co T a + Ementioning

confidence: 99%