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At least 811 records · Page 45Linked to original sources
PubMed1989

Increased muscle tension and reduced elasticity of affected muscles in recent-onset Graves' disease caused primarily by active muscle contraction.

In 3 patients with Graves' disease of recent onset, length-tension diagrams were made during surgery for squint under eyedrop anesthesia. The affected muscles were found to be very stiff when the other eye looked straight ahead. It was expected that these stiff muscles would be able to shorten to some extent but would be unable to lengthen, due to fibrosis of the muscle. We found that the affected muscles did not shorten very much when the other eye looked into the field of action of the muscle. Unexpectedly however, they lengthened considerably when the other eye looked out of the field of action of the muscle. This finding implies that the raised muscle tension and reduced elasticity of affected muscles in these cases of Graves' disease of recent onset were primarily caused by active muscle contraction, not by fibrosis.

Diplopia↗
PubMed2004

Diabetes decreases rabbit bladder smooth muscle contraction while increasing levels of myosin light chain phosphorylation.

The effect of diabetes mellitus on the regulation of urinary bladder smooth muscle contraction was studied. Diabetes was induced in the rabbit by alloxan injection followed by 16 wk of housing. The bladder was harvested and strips of wall devoid of both mucosa and serosa were examined. Intact strips of bladder smooth muscle from diabetic animals produced less stress in response to membrane depolarization than muscle from control animals; sensitivity to KCl was not changed. Carbachol responses were similar in muscle strips from the two animal groups. Basal myosin light chain (MLC) phosphorylation levels were significantly elevated in response to most stimuli in muscle strips from diabetic animals, although levels of stress were either unchanged or lower. alpha-Toxin-permeabilized strips that allow for control of the intracellular environment while maintaining excitation-contraction coupling showed increased levels of MLC phosphorylation but decreased sensitivity to activator Ca2+ in smooth muscle from diabetic animals. MLC phosphatase contents were similar in smooth muscle from the two animal groups; however, MLC phosphatase activity was greater in muscle from control compared with diabetic animals. These results suggest that diabetes mellitus uncouples basal MLC phosphorylation from force in the bladder smooth muscle cell.

Animals↗
PubMed2003

Muscle contraction: energy rate equations in relation to efficiency and step-size distance.

We derive the energy rate equation for muscle contraction. Our equation has only two parameters m, the maintenance heat rate and 1/S, the shortening heat coefficient. The impulsive model (previously described in earlier papers) provides a physical basis for parameter 1/S as well as for constants a and b in Hill's force-velocity equation. We develop new theory and relate the efficiency and the step-size distance to our energy rate equation. Correlation between the efficiency and the step-size distance is established. The various numbers are listed in Table 1: we use data from five different muscles in the literature. In summary, our analysis strongly supports the impulsive model as the correct model of contraction.

Animals↗
PubMedDate not supplied

[The mechanism of muscle contraction: along the path carved by Academician G.M Frank].

On the issue of the mechanism of muscle contraction, the views of the late G.M. Frank, to whom this symposium is dedicated, differed fundamentally from those of the then-current orthodoxy. Frank could not accept the idea of filament sliding brought about by swinging cross-bridges. He seemed particularly moved by two observations from his laboratory: the first, that the A-band shortened during active contraction; and the second, that sarcomere shortening occurred in stepwise fashion. From these findings principally, Frank came to the view that contraction involved a stepwise shortening of thick filaments. Although this view is broadly held to be incorrect, I will present evidence that it may constitute at least a partial answer. I will consider the evidence that both of Frank's principal findings-stepwise shortening and thick filament shortening-may be valid attributes of the contractile mechanism. I will then go on to show how these two attributes fit into an overall mechanism-not dissimilar to the one put forth by Frank.

Actins↗
PubMed1999

A thermodynamic optimization analysis of a possible relation between the parameters that determine the energetics of muscle contraction in steady state.

Given the phenomenological relations for muscle's steady-state contraction and proper definitions of power p and efficiency eta, the behavior of these quantities is analysed in terms of the parameters that determine the energetics of the muscle, here denoted by s(o)and alpha. s(o)is proportional to the so-called maintenance heat, while alpha is the parameter that determines the curvature of the Hill's force-velocity curve. The dependence of the muscle's power and efficiency, averaged over the whole range of force the muscle can exert, on the parameters s(o)and alpha is studied. The average power p(avg)is a function only of alpha, and is a growing function that approaches 1/6 asymptotically as alpha goes to infinity. The average efficiency eta(avg)is a function of both alpha and s(o). With the value of s(o)fixed, the graph of the function eta(avg)(s(o), alpha) is a convex curve with a single maximum. The value and the position of this maximum point both depend on s(o). In the limit alpha-->0, s(o)-->0, eta(avg)tends to 1. The points (s(o), alpha(m)(s(o))), with alpha(m)(s(o)) the value of alpha that maximizes eta(avg)for a given s(o), are fitted by the curve alpha=s(o 1/2). This relation was experimentally found by A.V. Hill in his early studies of muscle energetics. Other experimental data are found to qualitatively satisfy the same relation. Although some dynamical microscopic models for muscle contraction, based upon Huxley's cross-bridge model, show that the same kinetic parameters control both the maintenance heat (s(o)) and the muscle's power output (alpha), we suggest that the exact relation between them has been reached due to the evolutive stresses that made individuals with equally powerful and more efficient muscles more suitable to reproduce.

Animals↗
PubMed2003

Chronic O2 exposure enhances vascular and airway smooth muscle contraction in the newborn but not adult rat.

Neonatal rats exposed to 60% O(2) for 14 days develop lung changes compatible with human bronchopulmonary dysplasia and pulmonary hypertension. Our aim was to evaluate and compare the newborn and adult rat pulmonary vascular and airway smooth muscle force generation and relaxation potential after exposure to 60% O(2) for 14 days. Vascular and airway intrapulmonary rings 100 microm in diameter were mounted on a myograph and bathed in Krebs-Henseleit solution bubbled with air- 6% CO(2) at 37 degrees C. Significant age-dependent changes in intrapulmonary arteries and their neighboring airway muscle properties were observed. Whereas hyperoxia enhanced force in neonatal vascular and airway muscle, the opposite was seen in adult samples. No changes in endothelium-dependent vascular relaxation were observed at either age, but the dose response to an endothelium-independent NO donor was altered. In the newborn experimental animals, the relaxation was reduced, whereas, in their adult counterparts, it was enhanced. After O(2) exposure, the bronchial muscle relaxation response to epithelium-dependent and -independent stimulation was not altered in either age group, whereas the epithelium-dependent response was decreased only in the adult. The antioxidant Trolox, or an endothelin-A and -B receptor antagonist, reversed the vascular and airway muscle's hyperoxia-induced changes. We conclude that chronic O(2) exposure in the newborn rat results in enhanced lung vascular and airway muscle contraction potential via a mechanism involving reactive oxygen species and the endothelin pathway. The present findings also suggest that the newborn is more susceptible to airway hyperresponsiveness after chronic O(2) exposure.

Aging↗
PubMed1999

Effects of age on the reciprocal peak torque ratios during knee muscle contractions in elite soccer players.

To investigate the effects of age on the reciprocal peak torque ratios during knee muscle contractions, 25 elite male soccer players, aged 22.3 +/- 3.8 yr (18-28), volunteered for the present study. The players were grouped as adult (> 21 years, n = 13) and young players (< or = 21 years, n = 12). Maximal concentric (CON) and eccentric (ECC) isokinetic thigh muscle strength was measured at angular velocities of 30 degrees, 180 degrees, 240 degrees and 300 degrees/s. ECC and CON peak torques of knee flexors (hamstring, HAM) and CON peak torques of knee extensors (quadriceps, QUA) in the dominant knee were greater (P < 0.05) in adult players than in young players at 180, 240 and 300 degrees/s. ECC HAM/CON QUA peak torque ratio at 300 degrees/s was greater (P < 0.05) for adult players compared to young players in the dominant knee but not in the nondominant knee. Furthermore, conventional HAM/QUA peak torque ratios of the dominant knee at all angular velocities for ECC contraction were higher (P < 0.05) in adult players than in young players. In conclusion, the findings of the present study indicate that the reciprocal torque ratio is influenced by age in the dominant knee of elite soccer players. Because there was no effect of age for the nondominant leg, the findings of the present study are more likely to be the result of the training background of the players than their age.

Adolescent↗
PubMed2006

Anticholinesterase drugs stimulate smooth muscle contraction of the rat trachea through the Rho-kinase pathway.

We performed this study to determine the effects of Rho-kinase inhibitors, Y-27632 and fasudil, on the anticholinesterase (anti-ChE)-induced contractile and phosphatidylinositol responses of the rat trachea. In vitro measurements of isometric tension and [3H] inositol monophosphate (IP1) that was formed were conducted by using rat tracheal rings or slices. Neostigmine- and pyridostigmine-induced contractions were almost completely inhibited by Y-27632 and fasudil at 30 microM each, whereas acetylcholine-induced contraction was inhibited incompletely, i.e., by 56% by Y-27632 and by 51% by fasudil, at 100 microM for each, respectively. The inhibitory effects of fasudil on neostigmine- and acetylcholine-induced contractions were completely reversed by calyculin-A, a myosin phosphatase inhibitor. Neostigmine-induced IP1 accumulation was attenuated by fasudil at 100 microM. The results suggest that anti-ChEs cause airway smooth muscle contraction, in part, through activation of the Rho-kinase pathway.

Animals↗
PubMed2004

An expanded latch-bridge model of protein kinase C-mediated smooth muscle contraction.

A thin-filament-regulated latch-bridge model of smooth muscle contraction is proposed to integrate thin-filament-based inhibition of actomyosin ATPase activity with myosin phosphorylation in the regulation of smooth muscle mechanics. The model included two latch-bridge cycles, one of which was identical to the four-state model as proposed by Hai and Murphy (Am J Physiol Cell Physiol 255: C86-C94, 1988), whereas the ultraslow cross-bridge cycle has lower cross-bridge cycling rates. The model-fitted phorbol ester induced slow contractions at constant myosin phosphorylation and predicted steeper dependence of force on myosin phosphorylation in phorbol ester-stimulated smooth muscle. By shifting cross bridges between the two latch-bridge cycles, the model predicts that a smooth muscle cell can either maintain force at extremely low-energy cost or change its contractile state rapidly, if necessary. Depending on the fraction of cross bridges engaged in the ultraslow latch-bridge cycle, the model predicted biphasic kinetics of smooth muscle mechanics and variable steady-state dependencies of force and shortening velocity on myosin phosphorylation. These results suggest that thin-filament-based regulatory proteins may function as tuners of actomyosin ATPase activity, thus allowing a smooth muscle cell to have two discrete cross-bridge cycles with different cross-bridge cycling rates.

Animals↗
PubMed1991

Calcium reversal, relaxation by calcium ion of various smooth muscles contracted by carbachol, norepinephrine or a phorbol ester in calcium-ion free medium.

1. Ca reversal was reported on the longitudinal smooth muscle of rat uterus and the fundic part of the circular smooth muscle of guinea pig stomach; that is, addition of Ca ion to the Ca-free bathing solution in which the muscle is contracting to oxytocin or carbachol, respectively, relaxes the muscle. 2. We tested whether this inhibitory action of Ca ion is seen in other smooth muscles including vascular, air way, gastric and genital smooth muscles. 3. We found that Ca reversal was observed in the smooth muscle of rat thoracic aorta contracted by norepinephrine or by a phorbol ester, TPA, guinea pig tracheal smooth muscle contracted to carbachol, fundic smooth muscle of rat stomach to carbachol, corporal and antral smooth muscle of guinea pig stomach to carbachol and rat vas deferens to norepinephrine. 4. Ca reversal was observed not only when the muscle contracted by an agonist of the surface receptor such as oxytocin, norepinephrine or carbachol but also by a phorbol ester that is believed to cause contraction in the cell by activating phosphorylation. 5. Thus, we conclude that Ca reversal is a universal phenomenon in smooth muscles.

Animals↗
PubMed1993

Ovine tracheal muscle contraction in vitro: inhibition by calcium channel blockers gallopamil and verapamil.

We compared the inhibitory effects of calcium channel blockers, gallopamil and verapamil on acetylcholine (Ach)-induced contractions of ovine tracheal muscle in vitro. Adult sheep were sacrificed and tracheal strips were obtained by cutting the single tracheal rings from the mid-trachea. Tracheal strips were suspended in Krebs-Henseleit solution and isometric tension measured upon stimulation with cumulative doses of Ach (10(-7) to 10(-4) M) without and after pretreatment with gallopamil (10(-7) to 10(-6) M) or verapamil (10(-6) to 10(-5) M). In untreated tissues, the mean concentration of Ach required to produce 50% of maximal response (EC50) was 4.3 x 10(-6) M Ach. Both gallopamil and verapamil inhibited the Ach-induced contractions of ovine tracheal smooth muscle, by shifting the dose-response curves to Ach to the right. EC50 Ach for gallopamil (10(-6) M) and verapamil (10(-6) M) was 2.6 x 10(-5) and 5.2 x 10(-6) M, respectively. Dose ratio defined as postantagonist EC50 Ach/control EC50 Ach, was 7.7 for gallopamil and 2.0 for verapamil. Thus, the inhibitory effect of gallopamil was approximately 4-fold more potent than that of verapamil. Gallopamil was 17-fold more potent than verapamil in relaxing precontracted tracheal strips. The dose of calcium antagonists required to produce 25% relaxation (EC25) of tracheal strips precontracted with 10(-4) Ach was 3.7 x 10(-5) M for verapamil and 2.2 x 10(-6) M for gallopamil. These results indicate that gallopamil is effective against Ach-induced contractions of ovine trachealis muscles, and is more potent than verapamil.

Acetylcholine↗
PubMedDate not supplied

100 Hz remains upper limit of synchronous muscle contraction--an anomaly resolved.

Wootton and Newman introduced a problem when they showed, by high-speed cinematography, that a minute hemipteran insect, the whitefly Trialeurodes vaporariorum, achieves a wing-beat frequency of up to 181 Hz. 100 Hz had been regarded as the upper limit of contraction by myoneural synchrony, and whitefly flight muscle had been placed in the 'synchronous' category on structural grounds. The problem is resolved by evidence presented here, which reclassifies the power-producing flight muscles of whiteflies as 'asynchronous'.

Animals↗
PubMed2005

Inhibition of stretch-activated channels during eccentric muscle contraction attenuates p70S6K activation.

Eccentric contractions (EC) are known to result in muscle hypertrophy, potentially through activation of the Akt-mammalian target of rapamycin-p70 S6 kinase (p70S6K) signaling pathway. Previous work has also demonstrated that EC result in the opening of stretch-activated channels (SAC), and inhibition of these channels resulted in an attenuation of EC-induced muscle hypertrophy. The purpose of this study was to test the hypothesis that a known intracellular pathway directly associated with muscle hypertrophy is coupled to the opening of SAC. Specifically, we measured the activation of the Akt, GSK-3beta, p70S6K, and ribosomal protein S6 following a single bout of EC in the rat tibialis anterior (TA) muscle. The TA muscles performed four sets of six repetitions of EC. In vivo blockade of SAC was performed by a continuous oral treatment with streptomycin in the drinking water (4 g/l) or by intravenous infusion of 80 micromol/kg gadolinium (Gd3+). EC increased the degree of Akt and p70S6K phosphorylation in the TA muscle, whereas in animals in which SAC had been inhibited, there was a reduced capacity for EC to induce Akt or p70S6K phosphorylation. Accompanying this reduced activation of Akt and p70S6K was a failure to phosphorylate GSK-3beta or S6 when SAC were inhibited. The results from these data indicate the necessity of functional SAC for the complete activation of Akt and p70S6K pathway in response to EC.

Adaptation, Physiological↗
PubMed1989

Muscle contraction headache: dexamethasone suppression test and response to amitriptyline.

Chronic muscle contraction headache (CMCH) and depression have many features in common. Patients with CMCH respond to antidepressants. We attempted to further elucidate this relationship through the use of the dexamethasone suppression test (DST) pattern of patients suffering from CMCH as well as their response to amitriptyline. Twenty drug-free patients suffering from CMCH of at least 6 months' duration were studied with DST and subsequently treated with amitriptyline 75 mg at bedtime. Nineteen patients completed the treatment trial and reported variable headache relief. All cortisol levels were within the expected range. We conclude CMCH patients do not display the DST pattern of endogenous depression.

Adult↗
PubMedDate not supplied

[Cytosolic calcium dynamics and smooth muscle contraction(II): Reticular calcium fluxes].

The contractile status of smooth muscle depends upon cytosolic Ca2+, the Ca(2+)-sensitivity of actin-myosin interaction and various calcium-independent mechanisms. This second part of our overview is devoted to the complex involvement of endoplasmic reticulum in the cytosolic Ca2+ signals related to smooth muscle contractile activity, with a focus on the functional structure of reticular membrane proteins that ensure the respective Ca2+ fluxes. Ca2+ release is activated by cytosolic Ca2+, involving reticular channels called inositol triphosphate receptors and ryanodine receptors. Beside calcium and inositol triphosphate, cyclic ADP-ribose and nicotinic acid adenine dinucleotide phosphate have recently emerged as intracellular signals that activate Ca2+ release. The reticular Ca2+ pump is essential both for the control of cytosolic Ca2+ and for the preservation of reticular stores.

Calcium↗
PubMed1998

Role of adenosine in regulation of carbohydrate metabolism in contracting muscle.

Adenosine production from AMP in the sarcoplasm and interstitial space of muscle is markedly enhanced during contractions. The produced adenosine may act as a 'local hormone' by binding to various types of adenosine receptors present in the membrane of adjacent cells, including skeletal muscle, vascular smooth muscle and neurons. Thus, interstitial adenosine may significantly contribute to regulation of muscle carbohydrate metabolism, both by adjusting metabolism and local blood flow to the energy needs imposed by a given degree of contratile activity on the muscle cell. The studies presented here demonstrate that endogenous adenosine via A1-adenosine receptors is able to directly stimulate insulin-mediated glucose transport in oxidative muscle cells during contractions. In addition, adenosine may further contribute to stimulation of muscle glucose uptake during contractions by increasing blood flow and thereby targetting glucose and insulin delivery to active muscle fibres. Furthermore, our findings demonstrate that adenosine via A1- and A2-receptors may inhibit glycogen breakdown in oxidative muscle tissue which during contractions is simultaneously exposed to insulin and beta-adrenergic stimulation. It is concluded that adenosine importantly contributes to regulation of carbohydrate metabolism in oxidative muscle fibers during contractions.

Adenosine↗