scholarly journals Variation of muscle stiffness with force at increasing speeds of shortening.

1975 ◽  
Vol 66 (3) ◽  
pp. 287-302 ◽  
Author(s):  
F J Julian ◽  
M R Sollins

Single frog skeletal muscle fibers were attached to a servo motor and force transducer by knotting the tendons to pieces of wire at the fiver insertions. Small amplitude, high frequency sinusoidal length changes were then applied during tetani while fibers contracted both isometrically and isotonically at various constant velocities. The amlitude of the resulting force oscillation provides a relative measure of muscle stiffness. It is shown from an analysis of the transient force responses observed after sudden changes in muscle length applied both at full and reduced overlap and during the rising phase of short tetani that these responses can be explained on the basis of varying numbers of cross bridges attached at the time of the length step. Therefore, the stiffness measured by the high frequency legth oscillation method is taken to be directly proportional to the number of cross bridges attached to thin filament sittes. It is found that muscle stiffness measured in this way falls with increasing shortening velocity, but not as rapidly as the force. The results suggest that at the maximum velocity of shortening, when the external force is zero, muscle stiffness is still substantial. The findings are interpreted in terms of a specific model for muscle contraction in which the maximum velocity of shortening under zero external load arises when a force balance is attained between attached cross bridges somr interpretations of these results are also discussed.

1987 ◽  
Vol 65 (8) ◽  
pp. 1798-1801 ◽  
Author(s):  
J. M. Renaud ◽  
R. B. Stein ◽  
T. Gordon

Changes in force and stiffness during contractions of mouse extensor digitorum longus and soleus muscles were measured over a range of extracellular pH from 6.4 to 7.4. Muscle stiffness was measured using small amplitude (<0.1% of muscle length), high frequency (1.5 kHz) oscillations in length. Twitch force was not significantly affected by changes in pH, but the peak force during repetitive stimulation (2, 3, and 20 pulses) was decreased significantly as the pH was reduced. Changes in muscle stiffness with pH were in the same direction, but smaller in extent. If the number of attached cross-bridges in the muscle can be determined from the measurement of small amplitude, high frequency muscle stiffness, then these findings suggest that (a) the number of cross-bridges between thick and thin filaments declines in low pH and (b) the average force per cross-bridge also declines in low pH. The decline in force per cross-bridge could arise from a reduction in the ability of cross-bridges to generate force during their state of active force production and (or) in an increased percentage of bonds in a low force, "rigor" state.


1990 ◽  
Vol 68 (1) ◽  
pp. 209-219 ◽  
Author(s):  
M. Okazawa ◽  
P. Pare ◽  
J. Road

We applied the technique of sonomicrometry to directly measure length changes of the trachealis muscle in vivo. Pairs of small 1-mm piezoelectric transducers were placed in parallel with the muscle fibers in the posterior tracheal wall in seven anesthetized dogs. Length changes were recorded during mechanical ventilation and during complete pressure-volume curves of the lung. The trachealis muscle showed spontaneous fluctuations in base-line length that disappeared after vagotomy. Before vagotomy passive pressure-length curves showed marked hysteresis and length changed by 18.5 +/- 13.2% (SD) resting length at functional residual capacity (LFRC) from FRC to total lung capacity (TLC) and by 28.2 +/- 16.2% LFRC from FRC to residual volume (RV). After vagotomy hysteresis decreased considerably and length now changed by 10.4 +/- 3.7% LFRC from FRC to TLC and by 32.5 +/- 14.6% LFRC from FRC to RV. Bilateral supramaximal vagal stimulation produced a mean maximal active shortening of 28.8 +/- 14.2% resting length at any lung volume (LR) and shortening decreased at lengths above FRC. The mean maximal velocity of shortening was 4.2 +/- 3.9% LR.S-1. We conclude that sonomicrometry may be used to record smooth muscle length in vivo. Vagal tone strongly influences passive length change. In vivo active shortening and velocity of shortening are less than in vitro, implying that there are significant loads impeding shortening in vivo.


1990 ◽  
Vol 259 (4) ◽  
pp. H1118-H1125 ◽  
Author(s):  
J. S. Herland ◽  
F. J. Julian ◽  
D. G. Stephenson

The slack test method has been adapted for measurement of unloaded velocity of shortening in rat ventricular trabeculae that were skinned with saponin (50 micrograms/ml for 30 min). The method was sensitive enough to detect a 17% reversible change in the unloaded velocity of shortening produced by a 3 degrees C change in temperature. At pCa 5.30 (80-90% activation), halothane, enflurane, and isoflurane each slowed the shortening velocity by 25-30% at dose levels of 8 mM or greater but not at 4 mM or less. At pCa 5.48 (50-60% activation), halothane slowed the shortening velocity by 20-45% at dose levels of 4 mM or greater but not at 2 mM. The slowing effect of anesthetics on shortening velocity showed saturation at 8 mM for halothane, enflurane, and isoflurane when activation was at pCa 5.30. Saturation occurred at 4 mM for halothane when the pCa was 5.48. This result indicates that the dose-response relationship may be narrow, such that it can be demonstrated between 2 and 4 mM halothane for pCa 5.48 and between 4 and 8 mM halothane for pCa 5.30. The anesthetic dose dependence of isometric force and length axis intercept did not generally follow the same relationship as for the shortening velocity. Thus in several instances force did not significantly decrease when the velocity of shortening did. This may be interpreted as lack of simple inhibition by anesthetics on the number of interacting cross-bridges and as direct influence by anesthetics on the cross-bridge cycle.


1992 ◽  
Vol 165 (1) ◽  
pp. 121-136 ◽  
Author(s):  
G. J. Ettema ◽  
P. A. Huijing ◽  
A. de Haan

The aim of the present study was to investigate the effect of an active stretch during the onset of a muscle contraction on subsequent active behaviour of the contractile machinery within an intact mammalian muscle-tendon complex. Muscle length and shortening velocity were studied because they may be important variables affecting this so-called prestretch effect. Seven gastrocnemius medialis (GM) muscles of the rat were examined. Tetanic, isovelocity shortening contractions from 3 mm above muscle optimum length (l0) to l0 - 2 mm, at velocities of 10–50 mm s-1 (dynamic experiments), were preceded by either an isometric contraction (PI) or an active stretch (PS). By imposing quick length decreases between the prephase and the concentric phase, all excess force generated in the prephase was instantaneously eliminated. This procedure only allowed small force changes during subsequent shortening (caused by the intrinsic properties of the contractile machinery). In this way, the influence of series elastic structures on subsequent muscle performance was minimized. Experiments were also performed at lengths ranging from l0 + 2.5 mm to l0 - 1.5 mm, keeping the length constant after the initial quick length changes (isometric experiments). For the dynamic experiments, enhancement of the performance of the contractile machinery (potentiation) was calculated as the ratio of the average force level over each millimetre of shortening during PS to that during PI conditions (PS/PI). For the isometric experiments, the PS/PI force ratio after 300 ms of stimulation was used. The main result of the present study confirmed results reported in the literature and experiments on isolated muscle fibres. For all conditions, a potentiation effect was found, ranging from about 2 to 16%. Muscle length appeared to have a large positive effect on the degree of potentiation. At the greatest lengths potentiation was largest, but at lengths below optimum a small effect was also found. A negative influence of shortening velocity was mainly present at increased muscle lengths (l0 + 2.5 mm and l0 + 1.5 mm). For the dynamic experiments, no interaction was found between the effects of muscle length and shortening velocity on potentiation. However, there was a clear difference between the isometric and dynamic responses: the dependence of potentiation on muscle length was significantly greater for the isometric contractions than for the dynamic ones. These isometric-dynamic differences indicate that the processes underlying prestretch effects operate differently under isometric and dynamic conditions.(ABSTRACT TRUNCATED AT 400 WORDS)


2002 ◽  
Vol 282 (1) ◽  
pp. H165-H174 ◽  
Author(s):  
Michael J. Davis ◽  
Judy Davidson

We compared the shortening velocity of smooth muscle in arterioles that had low or high levels of myogenic tone or norepinephrine (NE)-induced tone. We hypothesized that enhanced myogenic tone of arterioles reflects an enhanced maximum velocity of shortening of arteriolar smooth muscle in a way that is different from that produced by NE. These concepts are untested assumptions of arteriolar mechanics. Second-order arterioles from hamster cheek pouch (passive diameter at 40 mmHg = 42 μm) were isolated and cannulated for in vitro study. In the absence of flow, pressure was controlled by hydraulic pumps so that servo control of wall tension could be achieved from measurement of internal diameter and pressure. Isotonic quick-release protocols were used to measure the initial velocity of shortening following release from control wall tension (afterload) to a series of fractional afterloads. After release, the initial rates of shortening were fit to the Hill equation to obtain coefficients for a hyperbolic fit of the velocity-afterload relationship. The maximal unloaded shortening velocity for partially activated arterioles ( V′max) was determined from the y-intercept of each plot. Using this procedure, we compared V′max from two groups of arterioles equilibrated at low or high pressure, i.e., with low or high myogenic tone. Arterioles with higher myogenic tone had higher values of V′max than arterioles with lower myogenic tone. V′max for arterioles partially activated with NE at low pressure was comparable to V′max for arterioles with high myogenic tone, but NE produced high velocities at low force, whereas enhanced myogenic tone produced roughly parallel shifts in velocity and force. The results suggest that increased myogenic tone does indeed reflect enhanced activation of arteriolar smooth muscle, and this effect is mechanically different from that produced by NE.


1998 ◽  
Vol 275 (6) ◽  
pp. H1957-H1962 ◽  
Author(s):  
Yasutake Saeki ◽  
Satoshi Kurihara ◽  
Kimiaki Komukai ◽  
Tetsuya Ishikawa ◽  
Kiyohiro Takigiku

To study the effects of mechanical constraints on the Ca2+ affinity of cardiac troponin C, we analyzed the tension and aequorin light (AL) responses to sinusoidal length changes (5–10% of the initial muscle length) in aequorin-injected, tetanized cardiac muscles. The amplitude of the quasi-sinusoidal tension and AL responses decreased with increasing length-perturbation frequency from 0.5 to 1 Hz at 24°C and from 1 to 3 Hz at 30°C. The increase in AL corresponded well to the decrease in tension; likewise, the decrease in AL to the increase in tension and the tension response lagged behind the length change. A further increase in frequency (>1 Hz at 24°C and >3 Hz at 30°C) markedly increased the amplitude of the tension responses but decreased the amplitude of the AL responses. The increase in AL lagged behind the decrease in tension; likewise, the decrease in AL lagged behind the increase in tension, and the tension response led the length change. From previous mechanistic interpretations of the frequency dependence of the amplitude of tension response, we argue that the Ca2+affinity of cardiac troponin C changes in parallel with the active tension (i.e., the number of active cross bridges) but not with the passive tension produced by the length perturbation-induced cross-bridge strain.


1965 ◽  
Vol 163 (991) ◽  
pp. 215-223 ◽  

Shortening velocities of the frog rectus abdominis muscle during isotonic releases in potassium contracture have been determined under various conditions of initial length, initial tension and load. The velocity of shortening under constant load at any particular muscle length is dependent upon the length and tension of the muscle before release; there is no unique force-velocity relation at constant length. An empirical formulation of the relations between shortening velocity and length is given. These results cannot be explained in terms of a simple model of the muscle in which there is an undamped elastic element in series with a contractile component whose shortening velocity is instantaneously determined by tension. Some possible explanations of the phenomena are discussed, and it is tentatively suggested that the transient condition following an isotonic release is dependent upon the rates of formation and breakage of cross-linkages between the actin and myosin filaments in the muscle.


1988 ◽  
Vol 65 (3) ◽  
pp. 1410-1415
Author(s):  
G. S. Supinski ◽  
J. S. Arnold ◽  
S. G. Kelsen

The present study examined the effect of theophylline on the shortening velocity of submaximally activated diaphragmatic muscle (i.e., muscles were activated by the use of a level of stimulation, 50 Hz, within the range of phrenic neural firing frequencies achieved during breathing, whereas maximum activation is achieved at 300 Hz). Experiments were performed in vitro on strips of diaphragmatic muscle obtained from 21 Syrian hamsters. Muscle shortening velocity was assessed during isotonic contractions against a range of afterloads, and Hill's characteristic equation was used to calculate velocity at zero load. In addition, unloaded shortening velocity was also measured by the slack test, i.e., from the time required for muscles to take up slack after a sudden reduction in muscle length. Theophylline (160 mg/l) increased the velocity of muscle shortening against a wide range of external loads (0-14 N/cm2) and increased the extrapolated unloaded velocity of shortening from 6.4 +/- 0.9 to 7.9 +/- 1.1 (SE) lengths/s (P less than 0.01). Theophylline reduced the time required to take up slack for any given step change in muscle length, increasing the unloaded velocity of shortening assessed by the slack test from 7.6 +/- 0.9 to 9.3 +/- 1.1 lengths/s (P less than 0.002). The effect of theophylline on diaphragmatic shortening velocity was evident at concentrations as low as 40 mg/l and increased progressively as theophylline concentrations were increased to 320 mg/l. Theophylline increased the shortening velocity of fatigued as well as fresh muscles.(ABSTRACT TRUNCATED AT 250 WORDS)


1990 ◽  
Vol 258 (3) ◽  
pp. H861-H869 ◽  
Author(s):  
W. J. Leijendekker ◽  
W. D. Gao ◽  
H. E. ter Keurs

The stiffness of rat cardiac trabeculae was measured in vitro to distinguish between an increase in unstimulated force (Fu) caused by rapid cycling of cross bridges or caused by rigor bridges during hypoxia. The force was measured with a strain gauge, the sarcomere length was determined by laser diffraction techniques, and muscle length was controlled by means of a motor. Stiffness was analyzed by using small (less than 1% of muscle length) sinusoidal length perturbations of 1 and 100 Hz. The stiffness at 100 Hz increased linearly with force during tetani at a varied [Sr2+] (0.25-10 mM) in the Krebs-Henseleit (K-H) buffer, but remained virtually unchanged at 1 Hz. In contrast, the stiffness of both the passive muscle and the muscle exposed to either CN- or to PO2 less than 1.5 mmHg up to development of maximal Fu (Fumax) was similar at 1- and 100-Hz perturbations. Less profound hypoxia (PO2 6-10 mmHg) resulted in spontaneous sarcomere activity during the rise in Fu, and an increase in the ratio of stiffness at 100 Hz to stiffness at 1 Hz was detected. When oxidative phosphorylation was inhibited by CN- (2 mM) while the muscle was stimulated in the absence of both Ca2+ and Na+ (choline+substituted), the addition of Na+ at the time at which Fu had reached 30-40% of Fumax did not affect the rate of rise of Fu. These results show that the development of Fu during more complete anoxia in rat trabeculae is completely due to the formation of rigor links and that Ca2(+)-dependent cross-bridge activation can contribute to the rise in Fu during less severe hypoxia.


1999 ◽  
Vol 202 (2) ◽  
pp. 135-142 ◽  
Author(s):  
F. Lou ◽  
N.A. Curtin ◽  
R.C. Woledge

The production of work by the contractile component (CC) and the storage and release of work in the elastic structures that act in series (the series elastic component, SEC) with the contractile component were measured using white muscle fibres from the dogfish Scyliorhinus canicula. Heat production was also measured because the sum of work and heat is equivalent to the energy cost of the contraction (ATP used). These energy fluxes were evaluated in contractions with constant-velocity shortening either during stimulation or during relaxation. The muscle preparation was tetanized for 0.6 s and shortened by 1 mm (approximately 15 % of L0) at 3.5 or 7.0 mm s-1 (approximately 15 or 30 % of V0), where L0 is the muscle length at which isometric force is greatest and V0 is the maximum velocity of shortening. In separate experiments, the stiffness of the SEC was characterized from measurements of force responses to step changes in the length of contracting muscle. Using the values of SEC stiffness, we evaluated separately the work and heat associated with the CC and with the SEC. The major findings were (1) that work stored in the SEC could be completely recovered as external work when shortening occurred during relaxation (none of the stored work being degraded into heat) and (2) that, when shortening occurred progressively later during the contraction, the total energy cost of the contraction declined towards that of an isometric contraction.


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