Course Of Isometric Contraction Research Articles

Asynchronous Muscle: A Primer

The asynchronous muscles of insects are characterized by asynchrony between muscle electrical and mechanical activity, a fibrillar organization with poorly developed sarcoplasmic reticulum, a slow time course of isometric contraction, low isometric force, high passive stiffness and delayed stretch activation and shortening deactivation. These properties are illustrated by comparing an asynchronous muscle, the basalar flight muscle of the beetle Cotinus mutabilis, with synchronous wing muscles from the locust, Schistocerca americana. Because of delayed stretch activation and shortening deactivation, a tetanically stimulated beetle muscle can do work when subjected to repetitive lengthening and shortening. The synchronous locust muscle, subjected to similar stimulation and length change, absorbs rather than produces work.

Effects of hypoxia, simulated ischemia and reoxygenation on the contractile function of human atrial trabeculae.

Hypoxia, ischemia and reoxygenation cause contractile dysfunction which will be characterized by the time course of isometric contraction of human atrial trabeculae. Post-rest potentiation (PRP) and postextrastimulatory potentiation (PEP) were elicited to obtain indirect information about the the role of the sarcoplasmic reticulum (SR) in excitation-contraction coupling. As lipid peroxidation could cause SR dysfunction, thiobarbituric acid reactive substances (TBARS) were measured. After 30 min of hypoxia (H) or simulated ischemia (H combined with acidosis-SI), contractile force decreased to 15% and 6%, respectively, of control (p < or = 0.05), whereas the normalized rate of both contraction and relaxation increased. In group H, rapid reoxygenation produced a recovery of contractile force to about 60%. After post-hypoxic reoxygenation the TBARS concentration was increased. In group SI, rapid reoxygenation and a rather gradual correction of acidosis produced complete recovery of contractile force. PRP and PEP were maintained during H and SI. Particularly post-ischemic reoxygenation caused a marked depression of PRP and partly of PEP. Thus, alteration of SR Ca2+ handling occurs predominantly during reoxygenation rather than during H or SI, probably associated with the damaging effect of increased oxygen radicals. The depression of potentiation occurred along with delayed relaxation, temporary increased resting force, mechanical alternans, and spontaneous activity which are further characteristics for SR dysfunction. Thus, for a possibly beneficial effect of low pH during SI combined with its gradual correction during reoxygenation on the recovery of contractile function, developed force should not be the only index.

A modified force-velocity equation for smooth muscle contraction.

It has been suggested that in skeletal muscle the force-velocity relationship may not be a simple hyperbolic one, as defined by Hill's equation. To determine whether smooth muscle demonstrated the same properties, quick-release force-velocity curves were obtained from canine tracheal smooth muscle. The results showed that the observed data points for tracheal smooth muscle systematically deviated from a hyperbola. Such deviation occurred at values of force (P) approaching maximum isometric force (Po) for curves elicited by quick release at 2 and 10 s in the course of isometric contractions. Shortening velocities under a given afterload were overestimated at the high-force end (P > 75% Po) by Hill's equation; this implied that a relationship more complex than a simple hyperbola was involved at high loads. We next focused on finding an equation to also fit those directly measured data points that did not conform to a hyperbola. Our rationale in developing the equation was that a plot of the linearized transform of Hill's equation should yield a straight line over the entire range of loads at which velocities were measured. The plot demonstrated that, in the low-load high-velocity portion of the curve, a peak value was reached at 70-80% Po, which decreased as load increased in the high-load low-velocity portion.(ABSTRACT TRUNCATED AT 250 WORDS)

Contractile behaviour of skinned papillary muscle in mitral valve disease.

The contractile behaviour of Triton-X 100 skinned left ventricular papillary muscle from 19 patients undergoing cardiac surgery for mitral valve stenosis: n = 6, mitral valve incompetence: n = 7, or combined mitral valve disease: n = 6 was analyzed. At supramaximal activation the "vibration induced force clamping technique" was used for isometric analysis of time course and extent of isometric postvibration force recovery. Afterloaded contractions were applied for extrapolation of the maximum shortening velocity at zero load (Vmax). The Calcium sensitivity was analysed by variation of the free EGTA-buffered Calcium concentration at a passive resting force of 2 mN at 26 degrees C. In different types of mitral valve disease the characteristics of isometric force development were unaltered in terms of maximum force development, force per square mm, Calcium sensitivity and the time course of isometric contraction after force clamping. However the capability to shorten as expressed by Vmax was reduced in mitral valve incompetence (3.87 +/- 0.37 ML/s) as compared with mitral valve stenosis (5.29 +/- 0.35 ML/s) or combined mitral valve disease (4.83 +/- 0.51 ML/s). The ratio between the inverse value of Vmax and the time constant of isometric force development after force clamping was significantly different in mitral valve incompetence as compared with other types of mitral valve disease (p < 0.0001). These data argue for the presence of different resistances against shortening in various types of mitral valve disease, due to altered cross-bridge cycling characteristics or to morphological factors.

Sodium fluoride produces a K + efflux by increasing intracellular Ca 2+ through Na +Ca 2+ exchange

Acute fluoride intoxication increases intracellular calcium (Ca i), manifested by increased twitch tension in cardiac muscle, and by potassium efflux (mediated by Ca 2+-dependent K + channels) in fluoridated erythrocytes. Fluoride, like isoproterenol, stimulates adenylate cyclase, and could increase Ca i via the effects of cAMP on Ca 2+ channels. However, while the inotropic effects of fluoride mimicked isoproterenol in rat atria, their effects on the time course of isometric contraction were quite different. In addition, acetylcholine negated isoproterenoPs effect on twitch tension but did not modulate the effects of fluoride. Further, the Ca 2+ channel antagonist verapamil had no effect on fluoride-stimulated K + efflux from erythrocytes. Fluoride also inhibits Na + -K + ATPase, and increases intracellular Na +, so could increase Ca i via Na + Ca 2+ exchange. Lanthanum, which blocks Na + -Ca 2+ exchange, blocks fluoride-induced K + efflux in erythrocytes. We conclude that the effects of fluoride on adenylate cyclase are not important in intact tissue, and that inhibition of Na + -K + ATPase and subsequent Na 2+ -Ca 2+ exchange may be the mechanism of increased Ca i in acute fluoride toxicity.

Differential effects of reoxygenation on intracellular calcium and isometric tension.

We used the bioluminescent Ca2+ indicator, aequorin to record intracellular calcium transients during reoxygenation of hypoxic ferret ventricular muscle in order to determine whether alterations in the amplitude and time course of isometric contraction are mediated by changes in [Ca2+]i. Papillary muscles less than or equal to 1 mm in diameter were removed from the hearts of male ferrets and perfused with a bicarbonate-buffered physiologic salt solution at 30 degrees C. Muscles were stimulated to contract isometrically at 0.33 Hz and were loaded with aequorin by a chemical procedure. Hypoxia was induced by changing the gas mixture bubbling the perfusate to 95% N2, 5% CO2; reoxygenation was accomplished by switching the gas mixture to 95% O2, 5% CO2. Hypoxia produced a decrease in peak Ca2+ and tension that was reversed by reoxygenation. However, the effects on tension of changes in oxygenation were greater than expected from the degree of change in [Ca2+]i. The time courses of the Ca2+ transient and isometric twitch moved in opposite directions and were respectively prolonged/abbreviated by hypoxia and abbreviated/prolonged by reoxygenation. These results indicate that changes in the amplitude and time course of the isometric twitch induced by hypoxia and reoxygenation cannot be attributed alone to changes in intracellular Ca2+ availability and are caused in part by a significant decrease in the calcium sensitivity of the contractile apparatus.

High force development and crossbridge attachment in smooth muscle from swine carotid arteries.

In experiments designed to achieve maximal activation, the active force/cell cross-sectional area in tissues prepared from the swine carotid media was 6.7 +/- 0.3 (sd) X 10(5) N/m5. This value exceeds that reported for other vertebrate muscle cells and is striking because of the low smooth muscle myosin content. The hypothesis that high force generation may, in part, reflect an increase in the crossbridge duty cycle, i.e., the fraction of the cycle during which force is generated, was tested by determining the rate of force redevelopment after a step shortening and the ration of the load-bearing capacity of the contractile system to the developed stress during the course of isometric contractions. Maximal crossbridge cycling rates estimated by the rate of force redevelopment occurred 30 seconds after the onset of a high K+-induced contraction, and decreased thereafter, although the load-bearing capacity or maximum active stress was maintained. These results from isometric experiments support the hypothesis and provide further evidence that attached, non-cycling crossbridges contribute to force maintenance in tonically contracting arterial smooth muscle.

Myocardial sarcomere dynamics during isometric contraction.

1. Sarcomere lengths were measured during rest and throughout the time course of isometric contractions in thin, isolated rat papillary muscles using light diffraction techniques. 2. Shortening of the sarcomere length occurred upon contraction at all muscle lengths, averaging 7% at optimal length and more at shorter lengths. Relative to the narrow range of sarcomere lengths spanning the length--tension curve, this degree of shortening was considerable. 3. Local changes of sarcomere length were quantitatively paralleled by local changes of tissue segment length, the latter demarcated by microspheres lodged within the muscle tissue. At all but the shortest muscle lengths, sarcomere shortening was fully accounted for by equivalent lengthening of the non-striated regions near the clamped ends of the preparation. 4. It seems likely that these regions near the clamped ends of the preparation. 4. It seems constitute the source of the large series elasticity characteristic of isolated papillary muscle preparations such as this.

Beta-receptor blockade and myocardial effects of cardiac glycosides.

Because of suggestions that norepinephrine release from cardiac sympathetic nerves contributes to the myocardial action of digitalis, the effect of betareceptor blockade on these actions was determined. 10 -6 M propranolol did not alter the basal contractility of isolated kitten papillary muscles or of atrial strips from kittens, guinea pigs, rabbits, dogs, and chickens but decreased by 85% their inotropic response to norepinephrine released by tyramine or highintensity electrical stimulation. The same concentration of propranolol had no effect on cumulative inotropic concentration-effect curves for ouabain, acetylstrophanthidin, and digoxin in these preparations. Presence of propranolol did not modify the actions of cardiac glycosides on the time course of isometric contraction. Beta-receptor blockade was without effect on decreases in active tension and increases in resting tension induced by toxic concentrations of cardioactive steroids. The frequency of digitalis-induced automaticity in guinea pig atrial strips and kitten papillary muscles was significantly decreased by propranolol, presumably because of its direct electrophysiologic actions. Exposure of cat hearts to digoxin in vivo and to ouabain in vitro had no effect on myocardial norepinephrine concentrations. It is concluded that release of myocardial norepinephrine plays no role in the actions of cardiac glycosides on the heart.

On the contraction of glycerol-extracted muscle fibre bundles under highly isometric conditions.

Summary.A new technique for strictly isometric recording of glycerol‐extracted muscle fibre bundles is described. The apparatus works on the principle of a torsion balance.By comparing contractions of fibre bundles of different thickness from rabbit psoas conclusions can be drawn about the diffusion depth for ATP into the bundle. ATP in a concentration of 2.3 × 10‐4 M penetrates about 40 μ into a fibre bundle, probably via the endomysium, the diffusion into a single fibre amounting to only about 1 μ.The final isometric tension is proportional to the circumference of the fibre bundle, not to the cross section area.The magnitude of the final isometric tension and the rate of the isometric contraction have been studied as functions of the ATP concentration.The latency between the moment of immersion of the fibre bundle into the ATP solution and the start of the contraction is compatible with the assumption of an unstirred fluid layer of 30–45 μ around the fibre bundle.Possible factors influencing the course of isometric contraction of glycerol‐extracted muscle fibre bundles are discussed.