scholarly journals Changes in sarcomere length during isometric tension development in frog skeletal muscle

1972 ◽  
Vol 227 (1) ◽  
pp. 1-17 ◽  
Author(s):  
D. R. Cleworth ◽  
K. A. P. Edman
1972 ◽  
Vol 50 (1) ◽  
pp. 37-44 ◽  
Author(s):  
E. C. Vos ◽  
G. B. Frank

A brief exposure (about 10–30 s) of a frog's toe muscle or a small bundle of fibers from the semi-tendinosus muscle to just subthreshold potassium concentrations potentiated contractures subsequently produced by exposing the muscles to a potassium concentration slightly above the threshold. The contractures thus potentiated had greater maximum tensions, and greater rates of tension development and relaxation than control contractures elicited by the same final potassium concentration. The resistance to stretch (R.T.S.) in the first few seconds of the potentiated contractures was about twice that of control contractures. Maximum potentiation occurred with preexposures of about 30 s; longer preexposures led to a decrease of potentiation and eventually to a depression of the contracture. The potentiation was not immediately abolished when the muscle was reexposed to Ringer solution but persisted for 2 min or longer (the 'washout effect'). It was concluded that exposing a muscle to low subcontracture threshold concentrations of potassium for a few seconds primes the intracellular contractile apparatus, probably by causing an increased sarcoplasmic concentration of Ca2+ ions, resulting in a potentiation of subsequently induced submaximal potassium contractures. The increase in metabolism (or 'Solandt effect') seen under these conditions is temporally related to the decline and eventual loss of the potentiation and is probably a reflection of active processes involved in reducing the sarcoplasmic concentration of Ca2+ ions.


1974 ◽  
Vol 52 (6) ◽  
pp. 1126-1135 ◽  
Author(s):  
D. J. Parry ◽  
A. Kover ◽  
G. B. Frank

Exposure of frog toe muscles to 1 mM La3+ results in a decrease in amplitude and rate of tension development of potassium contractures and twitches. At this concentration La3+ also inhibits the uptake of calcium, both in the resting condition and during stimulation. Caffeine contractures are unaffected even after a 5-min pre-exposure to La3+. The depolarization induced by various concentrations of K+ is reduced by about 10 mV as is the amplitude of the action potential. The rate of rise of the action potential is reduced by about 40% after 1 min in La3+ Ringer. Neither the decreased amplitude nor the reduced rate of depolarization is considered to be sufficient to explain the inhibition of tension development. It is suggested that La3+ partially uncouples excitation from contraction by preventing the release of a trigger-Ca2+ fraction from some site on the muscle membrane. This fraction normally plays a role in excitation–contraction coupling, although some tension may still be developed in the absence of a trigger-Ca2+ influx.


1993 ◽  
Vol 115 (1) ◽  
pp. 82-90 ◽  
Author(s):  
J. M. Guccione ◽  
L. K. Waldman ◽  
A. D. McCulloch

Models of contracting ventricular myocardium were used to study the effects of different assumptions concerning active tension development on the distributions of stress and strain in the equatorial region of the intact left ventricle during systole. Three models of cardiac muscle contraction were incorporated in a cylindrical model for passive left ventricular mechanics developed previously [Guccione et al. ASME Journal of Biomechanical Engineering, Vol. 113, pp. 42-55 (1991)]. Systolic sarcomere length and fiber stresses predicted by a general “deactivation” model of cardiac contraction [Guccione and McCulloch, ASME Journal of Biomechanical Engineering, Vol. 115, pp. 72-81 (1993)] were compared with those computed using two less complex models of active fiber stress: In a time-varying “elastance” model, isometric tension development was computed from a function of peak intracellular calcium concentration, time after contraction onset and sarcomere length; a “Hill” model was formulated by scaling this isometric tension using the force-velocity relation derived from the deactivation model. For the same calcium ion concentration, the sarcomeres in the deactivation model shortened approximately 0.1 μm less throughout the wall at end-systole than those in the other models. Thus, muscle fibers in the intact ventricle are subjected to rapid length changes that cause deactivation during the ejection phase of a normal cardiac cycle. The deactivation model predicted rather uniform transmural profiles of fiber stress and cross-fiber stress distributions that were almost identical to those of the radial component. These three components were indistinguishable from the principal stresses. Transmural strain distributions predicted at end-systole by the deactivation model agreed closely with experimental measurements from the anterior free wall of the canine left ventricle.


1981 ◽  
Vol 78 (4) ◽  
pp. 365-382 ◽  
Author(s):  
K A Edman ◽  
G Elzinga ◽  
M I Noble

29 single frog skeletal muscle fibers were stretched during fused tetanic contractions. The force increase during stretch exhibited a breakpoint at a critical length change (average: 16.6 nm per one-half sarcomere) that was independent of velocity of stretch and of sarcomere length between 1.8 and 2.8 microns. After stretch there was an early decaying force component with a force-extension curve similar to that during stretch, which disappeared over approximately 2 s. This component was removed by a small, quick release, leaving a longer-lasting component. The critical amplitude of release required to produce this result was found by clamping the fiber to a load at which there was zero velocity of shortening. This amplitude increased with time up to the angle in the force record during stretch, was constant for the remainder of the stretch, and decreased with time after the end of stretch; it was consistently less than the critical amplitude of stretch required to reach the breakpoint of force enhancement during stretch but was also independent of sarcomere length. The force drop accompanying the critical release showed a small increase up to an optimum magnitude at 2.4--2.7 microns sarcomere length, with a decrease at longer lengths.


1979 ◽  
Vol 59 (4) ◽  
pp. 639-647 ◽  
Author(s):  
R. W. CURRIE ◽  
F. H. WOLFE

Beef muscles were sampled at various times post-mortem both on and off carcass, and the pH, sarcomere length, and isotonic contraction profiles under various loads recorded. The results demonstrate that muscle under light load will begin to contract at pH 6.3 but more heavily loaded muscle will not contract until pH 5.8. Rapid pH fall produced an earlier initiation of contraction than slow pH fall, but the pH required for initiation of contraction under equal loads was the same. The results of isometric tension development followed by unrestrained contraction during the course of rigor development are presented. The authors suggest that both carcass cooling rate and rate of pH fall are implicated in prerigor contraction of postmortem beef muscle.


1960 ◽  
Vol 198 (6) ◽  
pp. 1333-1342 ◽  
Author(s):  
John T. Fales ◽  
S. Richard Heisey ◽  
Kenneth L. Zierler

The amount of extra oxygen consumed by skeletal muscle following work (isotonic contractions) or isometric contractions was measured in the normally circulated gastrocnemius-plantaris muscle group of the dog. Work was varied by: a) having the muscle perform the same work a repeated number of times; b) varying the load against which the muscle-contracted, c) varying the amount of shortening of the muscle by limiting the duration of stimulation. The effect of frequency of stimulation was assessed by using two frequencies of stimulation in conditions a) and c). Finally, the extra oxygen consumed following isotonic work was compared with the extra oxygen consumed following isometric tension development. It was found that extra oxygen consumption of skeletal muscle following activity was not a direct consequence of the work done nor was it related linearly to the amount of shortening. The extra oxygen consumption appeared to be a response to the number of nervous stimuli delivered to the muscle. At a sufficiently low frequency each stimulus evoked the consumption of a constant quantum of oxygen. At higher frequencies, after a relatively small number of stimuli, oxygen consumption per stimulus decreased with successive stimuli.


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