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Results for “Muscle Contraction”

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At least 181 records · Page 10Linked to original sources

PubMed1995

Peptidergic innervation of leg muscles of the cockroach, Periplaneta americana (L.), and a possible role in modulation of muscle contraction.

FMRFamide-related peptides of insects are particularly important because of their possible function as neurohormones and neuromodulators on a wide variety of tissues. Part of this study was an investigation of the immunofluorescent staining of motor nerves which arise in the metathoracic ganglion, examined in wholemount using an antiserum that recognizes extended -RFamide peptides (generally recognized to be of the FMRFamide family). This antiserum revealed immunochemical staining of numerous cell bodies in the metathoracic ganglion and of axons in peripheral nerve 5, a large nerve which contains both motor and sensory fibres. Axons staining positive for FMRFamide-related peptides were traced in nerve 5 as far as the femur-tibia joint, and into the first (sensory-motor) and third (motor only) ramus of nerve 5. Reverse-phase HPLC with radioimmunoassay revealed a peak of FMRFamide-related peptide activity in nerve 5 that was coincident with a peak found when thoracic ganglia were processed in the same fashion. A physiological assay was devised to test the ability of various non-native peptides to alter the characteristics of contraction of skeletal muscles of the legs. Using neurally evoked contractions of coxal depressor muscles of the metathoracic leg it was determined that several non-native peptides could potentiate muscle contractions. The results of this study suggest that muscles of the legs receive innervation by identifiable, FMRFamide-related peptide-containing neurons and that the release of peptide(s) at the muscle may be yet another method of modulating the mechanics of muscle contraction.

Animals↗

PubMed1995

Effects of voluntary leg muscle contractions on cardiac output while standing.

To clarify the contribution of voluntary muscle contractions on the cardiovascular variables of humans, we measured stroke volume (SV), heart rate (HR), and cardiac output (CO) by impedance plethysmography in young males maintaining an upright standing position with 1) no voluntary muscle contractions owing to as little movement as possible (control condition), 2) voluntary muscle contractions in the calves along with a forward sway of the body, and 3) muscle contractions throughout the legs along with a backward sway. Muscle contraction in the calves did not provoke any significant increase in either SV or CO. Voluntary contractions throughout the legs, on the other hand, caused a reduction in SV and CO. From these observations we may conclude that contractions along with forward or backward swaying dose not enhance venous return unless the abdominal muscle is also contracting and unless the contractions are synchronous to one-minute wave in body fluid volume change.

Adolescent↗

PubMed2005

D-Glutamic acid-induced muscle contraction in the silkworm, Bombyx mori.

Agonists for muscle contraction in silkworms were screened by injecting test solutions into the hemolymph of decapitated silkworm larvae. Kainic acid, a glutamate receptor agonist, and D-glutamic acid induced muscle contractions, and D-aspartic acid was partially effective, whereas NMDA and AMPA, representative mammalian glutamate receptor agonists, did not induce contraction. L-Glutamic acid inhibited the kainic acid or D-glutamic acid-induced contraction. Amino acid analysis revealed that 3% of the total glutamic acid in the silkworm hemolymph is D-glutamic acid. These results suggest that d-glutamic acid acts physiologically as an agonist for muscle contraction in silkworms, and that L-glutamic acid functions as an inhibitor.

Animals↗

PubMed1984

Pardaxin produces postjunctional muscle contraction in guinea-pig intestinal smooth muscle.

The action of pardaxin (PX), a toxin isolated from the secretion of the Red Sea flatfish, Pardachirus marmoratus, was studied on longitudinal muscle of guinea-pig ileum. Pardaxin contracted the ileum and subsequently abolished muscle contraction to 5-hydroxytryptamine (5-HT), but did not affect the responses to acetylcholine (ACh) and substance P(SP). Pardaxin-induced contraction was only partially suppressed by atropine and not affected by tetrodotoxin or morphine. Preparations desensitized to 5-HT or SP responded normally to pardaxin. Pardaxin-induced contractions were normal in K+-depolarizing Krebs Ringer solution and not affected by black widow spider venom. It is concluded that the pardaxin-induced muscle contractions are not mediated through the release of neurotransmitters and do not involve 5-HT, SP or ACh receptors, but are due to a direct action on the muscle contractile mechanism.

Acetylcholine↗

PubMed1998

Skeletal muscle contractions stimulate cGMP formation and attenuate vascular smooth muscle myosin phosphorylation via nitric oxide.

Nitric oxide generated by neuronal nitric oxide synthase in contracting skeletal muscle fibers may regulate vascular relaxation via a cGMP-mediated pathway. Neuronal nitric oxide synthase content is greatly reduced in skeletal muscles from mdx mice. cGMP formation increased in contracting extensor digitorum longus muscles in vitro from C57 control, but not mdx mice. The increase in cGMP content was abolished with NG-nitro-L-arginine. Sodium nitroprusside treatment increased cGMP levels in muscles from both C57 and mdx mice. Skeletal muscle contractions also inhibited phenylephrine-induced phosphorylation of smooth muscle myosin regulatory light chain. Arteriolar dilation was attenuated in contracting muscles from mdx but not C57 mice. NO generated in contracting skeletal muscle may contribute to vasodilation in response to exercise.

Animals↗

PubMed1997

The swinging lever-arm hypothesis of muscle contraction.

The molecular mechanism of muscle contraction is a problem that has exercised biophysicists and biochemists for many years. The common view of the mechanism is embodied in the 'cross-bridge hypothesis', in which the relative sliding of thick (myosin) and thin (actin) filaments in cross-striated muscle is brought about by the 'cross-bridges', parts of the myosin molecules which protrude from the thick filaments and interact cyclically with the actin filaments, transporting them by a rowing action that is powered by the hydrolysis of ATP. This hypothesis is, however, rather vague on the molecular details of cross-bridge movement and, in the light of the recently determined crystal structures of myosin and actin, it has evolved into the more precise 'swinging lever-arm hypothesis'.

Actins↗

PubMed2004

A phenomenological model for estimating metabolic energy consumption in muscle contraction.

A phenomenological model for muscle energy consumption was developed and used in conjunction with a simple Hill-type model for muscle contraction. The model was used to address two questions. First, can an empirical model of muscle energetics accurately represent the total energetic behavior of frog muscle in isometric, isotonic, and isokinetic contractions? And second, how does such a model perform in a large-scale, multiple-muscle model of human walking? Four simulations were conducted with frog sartorius muscle under full excitation: an isometric contraction, a set of isotonic contractions with the muscle shortening a constant distance under various applied loads, a set of isotonic contractions with the muscle shortening over various distances under a constant load, and an isokinetic contraction in lengthening. The model calculations were evaluated against results of similar thermal in vitro experiments performed on frog sartorius muscle. The energetics model was then incorporated into a large-scale, multiple-muscle model of the human body for the purpose of predicting energy consumption during normal walking. The total energy estimated by the model accurately reflected the observed experimental behavior of frog muscle for an isometric contraction. The model also accurately reproduced the experimental behavior of frog muscle heat production under isotonic shortening and isokinetic lengthening conditions. The estimated rate of metabolic energy consumption for walking was 29% higher than the value typically obtained from gait measurements.

Animals↗

PubMed1997

Indices of skeletal muscle damage and connective tissue breakdown following eccentric muscle contractions.

Indirect indices of exercise-induced human skeletal muscle damage and connective tissue breakdown were studied following a single bout of voluntary eccentric muscle contractions. Subjects (six female, two male), mean (SD) age 22 (2) years performed a bout of 50 maximum voluntary eccentric contractions of the knee extensors of a single leg. The eccentric exercise protocol induced muscle soreness (P < 0.05 Wilcoxon test), chronic force loss, and a decline in the 20:100 Hz percutaneous electrical myostimulation force ratio [P < 0.01, repeated measures analysis of variance (ANOVA)]. Serum creatine kinase (CK) and lactate dehydrogenase (LDH) activities were elevated (P < 0.01, repeated measures ANOVA) following the bout. The mean (SD) CK and LDH levels recorded 3 days post-exercise were 2815 (4144) IU.l-1 and 375 (198) IU.l-1, respectively. Serum alkaline phosphatase activity showed no changes throughout the study, and a non-significant increase (P = 0.058, repeated measures ANOVA) in pyridinoline was recorded following the bout. Urinary hydroxyproline (HP) and hydroxylysine (HL) excretion, expressed in terms of creatinine (Cr) concentration, increased after exercise (P < 0.05 and P < 0.01, respectively, repeated measures ANOVA). An increased HP:Cr was recorded 2 days post-exercise and HL:Cr was increased above baseline on days 2, 5, and 9 post-exercise. This indirect evidence of exercise-induced muscle damage suggests that myofibre disruption was caused by the eccentric muscle contractions. Elevated urine concentrations of indirect indices of collagen breakdown following eccentric muscle contractions suggests an increased breakdown of connective tissue, possibly due to a localised inflammatory response.

Adult↗

PubMed2003

The inhibitory effect of adrenomedullin in the rat ileum: cross-talk with beta3-adrenoceptor in the serotonin-induced muscle contraction.

In contrast to vascular muscles, the contribution of a hypotensive peptide adrenomedullin (AM) to the regulation of visceral smooth muscles is obscure. The content, synthesis, and effects of AM on the muscular tone in rat ileum were explored. It was found that there was immunoreactive AM (301 pg/mg of protein) and AM mRNA expression (162 fg/pg actin mRNA) in the ileum and that AM evoked relaxation in ileal strips (Ki = 0.85 nM) precontracted with serotonin. Antagonists of both AM (AM(22-52)) and calcitonin gene-related peptide (CGRP(8-37)) receptors did not affect this AM-induced relaxation, whereas it was suppressed by a selective blocker of beta3-adrenoreceptor (SR 59230A). The AM-induced relaxation was accompanied by a production of cAMP. Antagonists of protein kinases A (KT 5720 and H-7) and an inhibitor of the ATP-dependent K(+)-channels (glibenclamide) attenuated the effect of AM. We suggest that AM is a local regulator of the ileal tone, with an inhibitory action on muscle contraction. AM may activate the beta3-adrenoceptors, resulting in protein kinase A activation, which in turn opens the ATP-dependent K(+)-channels.

Adrenomedullin↗

PubMed1998

A molecular model for muscle contraction.

The molecular mechanism of muscle contraction has been elucidated by a combination of electron microscopy, biochemistry and X-ray diffraction from fibres and crystals. Protein crystallography provided the essential molecular anatomy for understanding this problem. Synchrotron radiation has played a crucial role.

Animals↗

PubMedDate not supplied

[Morphological data correlated with the mechanism of striated muscle contraction].

The classical theory of muscle contraction (Huxley, 1957) could not entirely explain a series of theoretical and experimental data. This theory sustains a longitudinal sliding of thin filaments on thick ones, by the tilting of myosin cross-bridges. Under different stimuli inducing contractions, the stereospecific conformations of cross-bridges appear to be different as it is shown using electron microscopy, fluorescence polarization, electron paramagnetic resonance (EPR) spectroscopy and equatorial X-ray diffraction. Our optic microscopy data also suggest the existence of such conformations, induced by different contractile stimuli.

Animals↗

PubMed1994

The biochemical basis of the regulation of smooth-muscle contraction.

The primary signal for smooth-muscle contraction is an increase in sarcoplasmic free Ca2+ concentration ([Ca2+]i). This triggers activation of calmodulin-dependent myosin light-chain kinase, which catalyses myosin phosphorylation, thereby activating crossbridge cycling and the development of force or contraction of the muscle cell. Restoration of resting [Ca2+]i deactivates the kinase; myosin is dephosphorylated by myosin light-chain phosphatase and the muscle relaxes. Recent evidence suggests that other signal-transduction pathways can modulate the contractile state of a smooth-muscle cell by affecting specific steps in the myosin phosphorylation-dephosphorylation mechanism.

Animals↗

PubMed1995

Indirect coupling of phosphate release to de novo tension generation during muscle contraction.

A key question in muscle contraction is how tension generation is coupled to the chemistry of the actomyosin ATPase. Biochemical and mechanochemical experiments link tension generation to a change in structure associated with phosphate release. Length-jump and temperature-jump experiments, on the other hand, implicate phase 2slow, a significantly faster, markedly strain-sensitive kinetic process in tension generation. We use a laser temperature jump to probe the kinetics and mechanism of tension generation in skinned rabbit psoas fibers--an appropriate method since both phosphate release and phase 2slow are readily perturbed by temperature. Kinetics characteristic of the structural change associated with phosphate release are observed only when phosphate is added to fibers. When present, it causes a reduction in fiber tension; otherwise, no force is generated when it is perturbed. We therefore exclude this step from tension generation. The kinetics of de novo tension generation by the temperature-jump equivalent of phase 2slow appear unaffected by phosphate binding. We therefore propose that phosphate release is indirectly coupled to de novo tension generation via a steady-state flux through an irreversible step. We conclude that tension generation occurs in the absence of chemical change as the result of an entropy-driven transition between strongly bound crossbridges in the actomyosin-ADP state. The mechanism resembles the operation of a clock, with phosphate release providing the energy to tension the spring, and the irreversible step functions as the escapement mechanism, which is followed in turn by tension generation as the movement of the hands.

Actomyosin↗

PubMed2002

Mice lacking M2 and M3 muscarinic acetylcholine receptors are devoid of cholinergic smooth muscle contractions but still viable.

Cholinergic agents elicit prominent smooth muscle contractions via stimulation of muscarinic receptors that comprise five distinct subtypes (M1-M5). Although such contractions are important for autonomic organs, the role of each subtype has not been characterized precisely because of the poor selectivity of the currently available muscarinic ligands. Here, we generated a mutant mouse line (M2-/-M3-/- mice) lacking M2 and M3 receptors that are implicated in such cholinergic contractions. The relative contributions of M2 and M3 receptors in vitro was approximately 5 and 95% for the detrusor muscle contraction and approximately 25 and 75% for the ileal longitudinal muscle contraction, respectively. Thus, M1, M4, or M5 receptors do not seem to play a role in such contractions. Despite the complete lack of cholinergic contractions in vitro, M2-/-M3-/- mice were viable, fertile, and free of apparent intestinal complications. The urinary bladder was distended only in males, which excludes a major contribution by cholinergic mechanisms to the urination in females. Thus, cholinergic mechanisms are dispensable in gastrointestinal motility and female urination. After 10 Hz electrical field stimulation, noncholinergic inputs were found to be increased in the ileum of M2-/-M3-/- females, which may account for the lack of apparent functional deficits. Interestingly, the M2-/-M3-/- mice had smaller ocular pupils than M3-deficient mice. The results suggest a novel role of M2 in the pupillary dilation, contrary to the well known cholinergic constriction. These results collectively suggest that an additional mechanism operates in the control of pupillary constriction-dilatation.

Animals↗

PubMed1988

Muscle PO2 in the initial phase of increased local oxygen demand (rhythmical muscle contraction) in rats with portacaval shunt (PCA).

The influence of a hyperdynamic syndrome caused by PCA on PO2 distribution in skeletal muscle of rats during the initial phase of muscle activity was examined. Rhythmical muscle contraction of the m. biceps femoris was induced by direct electrical stimulation. Tissue PO2 of the contracting muscle was recorded continuously from the start of the 210 s-long activity period up to 140 s after the last contraction using a multiwire surface electrode. In comparison with controls no different behaviour of mean muscle PO2 in the initial phase of contraction was found. After muscle activity mean PO2 decreased to a lower level in rats with PCA than in controls. This might be a further indication of the disturbing influence of a hyperdynamic syndrome on the regulating mechanisms of the microcirculation.

Animals↗

PubMed1999

Phase-dependent heartbeat modulation by muscle contractions during dynamic handgrip in humans.

The influence of cardiac phase on the response of the cardiac pacemaker to dynamic hand contraction in eight healthy young men was studied to determine whether heart rate response to muscle contraction varied as a function of timing within the cardiac cycle. Changes in R-R interval (RRI) in response to muscle contraction were measured at various cardiac phases during heartbeat-synchronized handgrip at a rate of one contraction per two heartbeats. To extract the direct effect of the muscle contraction on the RRI, spontaneous slow variations and respiratory sinus arrhythmia were removed from the total RRI fluctuations in the frequency domain. Cross-correlograms between the extracted RRI fluctuations and muscle contraction showed that the coupling was strong when the muscle contraction occurred at the middle phase of the cardiac cycle. Muscle contraction at the systolic phase of the cardiac cycle had a tendency to produce a phase advance (shortening of RRI), whereas muscle contraction at the middle phase or later had a tendency to produce a phase delay (prolongation of RRI). The results showed the presence of a neuronal circuit that modulates the cardiac pacemaker activity depending on the timing of muscle contraction in the cardiac cycle.

Adult↗

PubMed1975

Electrical and mechanical activities of longitudinal muscle contraction elicited by transmural electric stimulation.

Intracellular electrical and mechanical activities were simultaneously recorded from the longitudinal muscle of isolated guinea-pig jejunum when the preparation was stimulated transmurally by square pulses of 1 msec, 10 Hz, 10-40 V. Transmural stimulation of more than 30 V induced co-ordinated peristaltic waves under intraluminal pressure at levels subthreshold for the peristaltic reflex. Transmural stimulation of less than 30 V induced various types of mechanical responses. After termination of stimulation, rebound excitation was observed. Electrical activities of the longitudinal muscle were compared with various mechanical responses. Slow depolarization without spike potential was recorded when the longitudinal muscle contracted without circular muscle contraction. However, spike potential was recorded from the longitudinal muscle when circular muscle contraction was present as a response. Hyperpolarization was observed soon after the beginning of stimulation. This hyperpolarization was persistent to atropine at 10(-6) g/ml. These electrical and mechanical responses to transmural stimulation disappeared when the preparation was treated with tetrodotoxin at 2 X 10(-7) g/ml.

Animals↗

PubMedDate not supplied

Leishmania parasites (Kinetoplastida: Trypanosomatidae) reversibly inhibit visceral muscle contractions in hemimetabolous and holometabolous insects.

Female sand flies can acquire protozoan parasites in the genus Leishmania when feeding on an infected vertebrate host. The parasites complete a complex growth cycle in the sand fly gut until they are transmitted by bite to another host. Recently, a myoinhibitory peptide was isolated from Leishmania major promastigotes. This peptide caused significant gut distension and reversible, dose-dependent inhibition of spontaneous hindgut contractions in the enzootic sand fly vector, Phlebotomus papatasi. The current study further characterizes myoinhibitory activity in L. major and other kinetoplastid parasites, using the P. papatasi hindgut and other insect organ preparations. Myoinhibitory activity was greatest in cultured promastigotes and in culture medium in late log-phase and early stationary-phase, coinciding with development of infective Leishmania morphotypes in the sand fly midgut. L. major promastigote lysates inhibited spontaneous contractions of visceral muscle preparations from hemimetabolous (Blattaria and Hemiptera) and holometabolous (Diptera) insects. Inhibition of visceral muscle contractions in three insect orders indicates a conserved mode of action. Myoinhibitory activity was detected also in Leishmania braziliensis braziliensis, a Sudanese strain of Leishmania donovani, and the kinetoplastid parasite Leptomonas seymouri. Protozoan-induced myoinhibition mimics the effect of insect myotropins. Inhibiting host gut contractions protects Leishmania parasites from being excreted after blood meal and peritrophic matrix digestion, allowing development and transmission of infective forms.

Animals↗