PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “Muscle contraction”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 109 records · Page 6Linked to original sources

Animal electricity, Ca2+ and muscle contraction. A brief history of muscle research.

This brief review attempts to summarize some of the major phases of muscle research from Leeuwenhoek's description of sarcomeres in 1674, through Galvani's observation of "animal electricity" in 1791, to the discovery of Ca2+ as the key messenger in the coupling of nerve excitation to muscle contraction. The emerging molecular mechanism of the contraction process is one of the great achievements of biology, reflecting the intimate links between physics, chemistry and the life Sciences in the solution of biological problems.

Animals↗

Segmental and plurisegmental modulation of pressure pain thresholds during static muscle contractions in healthy individuals.

The purpose of this study was to assess possible segmental (uni- and/or bilateral) and plurisegmental changes in pressure pain thresholds (PPTs) during static muscle contractions. Twenty-four healthy subjects (12 female, 12 male) performed a standardised isometric contraction with the dominant m. quadriceps femoris (MQF) and m. infraspinatus (MI), respectively. PPTs were assessed using pressure algometry at the contracting muscle, at the contralateral (resting) muscle and at a distant resting muscle (MI during contraction of MQF and vice versa). The PPT assessments were performed before, during and 30min. following each contraction. The contractions were held until exhaustion or for a maximum of 10 PPT assessments/muscle. During contraction of MQF PPTs increased compared to baseline at the middle ( p<0.001) and the end (p<0.001) of the contraction period at all assessed sites alike. During contraction of MI PPTs increased compared to baseline at the middle (p<0.001) and the end (p<0.007) of the contraction period at all sites. The increase was more pronounced at the contracting muscle compared to the contralateral (p<0.002; p<0.01) and the distant (p<0.002; p<0.002) site. No statistically significant difference was seen in PPTs between the latter two. Following the contractions PPTs returned to baseline. Submaximal isometric contraction of MQF and MI gave rise to a statistically significant increase in PPTs at the contracting muscle, the resting homologous contralateral muscle and at the distant resting muscle indicating that generalised pain inhibitory mechanisms were activated. Contraction of MI, but not of MQF, gave rise to an additional activation of unilateral segmental antinociceptive effects.

Adult↗

Blood indices of muscle injury associated with eccentric muscle contractions.

Serum muscle enzyme activities of eight healthy men (22-32 years old) were measured before and 48 h after separate bouts of repetitive concentric, eccentric, and isometric contractions of the lower leg anterior compartments. Serum creatine kinase and glutamic oxaloacetic acid transaminase levels were both elevated 2 days after the eccentric exercise regimen, exclusively (36 and 17%, respectively). Lactic dehydrogenase levels were not affected by any of the protocols. Delayed muscle soreness was exclusively reported from the eccentrically exercised limb. We suggest that the high tensions developed during eccentric exercise cause mechanical damage, possibly including sarcolemmal degeneration. Subsequently, muscle enzymes are released to the blood. We conclude that postexercise serum levels of some muscle enzymes, at the time of maximal soreness, are qualitative markers of muscle damage.

Adult↗

The sarcoplasmic reticulum and the control of muscle contraction.

Activation of muscle contraction is a rapid event that is initiated by electrical activity in the surface membrane and transverse (T) tubules. This is followed by release of calcium from the inner membrane system, the sarcoplasmic reticulum (SR). Using electron microscopy (EM), K. R. Porter and his laboratory defined the SR, the unique junctions between SR and T tubules, and the continuity between T tubules and surface membrane. Current research in this area centers on the interaction between T tubules and SR. This is mediated by 2 well-identified calcium channels: the dihydropyridine receptors (DHPRs) that act as voltage sensors in the T tubules, and the ryanodine receptors (RyRs) or calcium release channels of the SR. The relative positions of these 2 molecules differ significantly in skeletal and cardiac muscle, and this correlates well with known functional differences in the control of contraction. Molecular biology experiments combined with EM indicate that DHPRs are linked to RyRs in skeletal but probably not in cardiac muscle.

Animals↗

Progression of partial experimental injury to peripheral nerve. Part 1: Periodic measurements of muscle contraction strength.

Isometric measurements of muscle contraction in response to single as well as tetanic volleys of supramaximal stimuli were recorded from the limbs of 32 monkeys with noninjured or partially lacerated tibial nerves. Nerve action potentials (NAP) and muscle action potentials (MAP) were also determined at intervals varying from 1 hour to 52 weeks after injury. Limbs with mobilized noninjured nerve sustained small but definite decreases in muscle contraction strength particularly if the interval between operations was brief. Partially lacerated nerves had immediate averaged decreases in single twitch and supramaximal contraction strengths of 32.8% and 30.4% despite maintenance of NAP velocity. One week following injury, muscle contraction had decreased by another 21.6% and 19.7% respectively while NAP velocity was decreased by 18.5%. Measurements were also reduced at 2, 4, and 8 weeks and to a lesser degree at 12 weeks; at 24 and 36 weeks, muscle contraction was less than pre-injury data but not when compared to recordings 15 minutes after injury. Values recorded at 52 weeks reflected partial reinnervation of Achilles musculature. Studies over a 24-hour period following partial laceration demonstrated significant further decreases in muscle power by 8 hours. The authors conclude that nerve activity following partial laceration fluctuates as function diminishes during the early hours to weeks following injury.

Action Potentials↗

Influence of muscle contraction on whiplash kinematics.

It is unclear whether reflexive muscle contraction in unaware occupants can alter spinal kinematics to mitigate injury in the unaware occupant subjected to whiplash loading. Whiplash injury likely occurs during the non-physiologic S-curvature phase of spinal kinematics, present during the first 100 msec after the initiation of T1 acceleration. Experimental investigations using human volunteers have reported 45 to 60 msec delays prior to electrical activity of the sternocleidomastoid. The effects of reflexive contraction of the neck muscles were investigated using a validated head-neck computational model consisting of head, cervical spine, and first thoracic vertebra. Intervertebral discs. spinal ligaments, and facet joints were modeled using discrete elements. Passive and active musculature were incorporated using the Hill-type muscle model. The computational model was subjected to 2.6 m/sec rear impact velocity, applied to T1. Reflexive muscle contraction in the unaware occupant model was incorporated using a 54-msec muscle delay, 13-msec electromechanical delay, and an 81-msec muscle rise time. Results of the unaware occupant model were compared to the model exercised without muscle contraction. Reflexive muscle contraction altered segmental angulations by less than 10% and facet joint capsular ligament distractions by less than 16% during the time of maximum S-curvature. At the C5-C6 and C6-C7 levels, muscle contraction increased capsular ligament distractions. Due to the nominal affect of reflexive muscle contraction on segmental angulations and facet joint capsular ligament distractions during S-curvature, it is unlikely that this contraction can alter the cervical kinematics responsible for whiplash injury.

Acceleration↗

The efficiency of muscle contraction.

When a muscle contracts and shortens against a load, it performs work. The performance of work is fuelled by the expenditure of metabolic energy, more properly quantified as enthalpy (i.e., heat plus work). The ratio of work performed to enthalpy produced provides one measure of efficiency. However, if the primary interest is in the efficiency of the actomyosin cross-bridges, then the metabolic overheads associated with basal metabolism and excitation-contraction coupling, together with those of subsequent metabolic recovery process, must be subtracted from the total heat and work observed. By comparing the cross-bridge work component of the remainder to the Gibbs free energy of hydrolysis of ATP, a measure of thermodynamic efficiency is achieved. We describe and quantify this partitioning process, providing estimates of the efficiencies of selected steps, while discussing the errors that can arise in the process of quantification. The dependence of efficiency on animal species, fibre-type, temperature, and contractile velocity is considered. The effect of contractile velocity on energetics is further examined using a two-state, Huxley-style, mathematical model of cross-bridge cycling that incorporates filament compliance. Simulations suggest only a modest effect of filament compliance on peak efficiency, but progressively larger gains (vis-à-vis the rigid filament case) as contractile velocity approaches Vmax. This effect is attributed primarily to a reduction in the component of energy loss arising from detachment of cross-bridge heads at non-zero strain.

Actomyosin↗

Stretch-shortening contraction in Parkinson patients: evidence of normal muscle contraction execution with low efficiency.

The aim of this study was to compare different muscle contraction types in Parkinson patients and controls. Ten patients with mild to moderate Parkinsonism (7 men, 3 women, mean age 62.3) and 11 controls (7 men, 4 women, mean age 66.0) were investigated. Measurements in eccentric, concentric contraction and stretch-shortening contraction were made using modified Cybex 11 equipment. The torque areas in ankle dorsiflexors at 30 degrees/second, 120 degrees/second and 180 degrees/second were measured. The power (Nm/second) was calculated in a defined range of motion. The power at different angular velocities and contraction types was significantly lower in the patient group than in the control group. In both groups the power in eccentric and stretch-shortening contraction was significantly larger than in concentric contraction. The relative improvement in power in stretch-shortening contraction in patients was equal to the improvement made by the controls. Patients generated significantly more EMG than controls in concentric and eccentric contractions. The EMG in the stretch-shortening cycle was the same in both groups at higher velocities. The patients performed voluntary isolated muscle contraction in the same way as controls, but with a lower efficiency in contraction. The eccentric torque and the supplement of torque generated from the combined eccentric and concentric (stretch-shortening) contraction might be important for achievement of adequate dynamic movements in patients with Parkinson's disease.

Aged↗

c-Fos expression in the midbrain periaqueductal gray during static muscle contraction.

The periaqueductal gray (PAG) of the midbrain is involved in the autonomic regulation of the cardiovascular system. The purpose of this study was to determine if static contraction of the skeletal muscle, which increases arterial blood pressure and heart rate, activates neuronal cells in the PAG by examining Fos-like immunoreactivity (FLI). Muscle contraction was induced by electrical stimulation of the L7 and S1 ventral roots of the spinal cord in anesthetized cats. An intravenous infusion of phenylephrine (PE) was used to selectively activate arterial baroreceptors. Extensive FLI was observed within the ventromedial region (VM) of the rostral PAG, the dorsolateral (DL), lateral (L), and ventrolateral (VL) regions of the middle and caudal PAG in barointact animals with muscle contractions, and in barointact animals with PE infusion. However, muscle contraction caused a lesser number of FLI in the VM region of the rostral PAG, the DL, L, and VL regions of the middle PAG and the L and VL regions of the caudal PAG after barodenervation compared with barointact animals. Additionally, the number of FLI in the DL and L regions of the middle PAG was greater in barodenervated animals with muscle contraction than in barodenervated control animals. Thus these results indicated that both muscle receptor and baroreceptor afferent inputs activate neuronal cells in regions of the PAG during muscle contraction. Furthermore, afferents from skeletal muscle activate neurons in specific regions of the PAG independent of arterial baroreceptor input. Therefore, neuronal cells in the PAG may play a role in determining the cardiovascular responses during the exercise pressor reflex.

Animals↗

The role of RhoA-mediated Ca2+ sensitization of bronchial smooth muscle contraction in airway hyperresponsiveness.

Smooth muscle contraction is mediated by Ca2+-dependent and Ca2+-independent pathways. The latter Ca2+-independent pathway, termed Ca2+ sensitization, is mainly regulated by a monomeric GTP binding protein RhoA and its downstream target Rho-kinase. Recent studies suggest a possible involvement of augmented RhoA/Rho-kinase signaling in the elevated smooth muscle contraction in several human diseases. An increased bronchial smooth muscle contractility, which might be a major cause of the airway hyperresponsiveness that is a characteristic feature of asthmatics, has also been reported in bronchial asthma. Here, we will discuss the role of RhoA/Rho-kinase-mediated Ca2+ sensitization of bronchial smooth muscle contraction in the pathogenesis of airway hyperresponsiveness. Agonist-induced Ca2+ sensitization is also inherent in bronchial smooth muscle. Since the Ca2+ sensitization is sensitive to a RhoA inactivator, C3 exoenzyme, and a Rho-kinase inhibitor, Y-27632, the RhoA/Rho-kinase pathway is involved in the signaling. It is of interest that the RhoA/Rho-kinase-mediated Ca2+ sensitization of bronchial smooth muscle contraction is markedly augmented in experimental asthma. Moreover, Y-27632 relaxes the bronchospasm induced by contractile agonists and antigens in vivo. Y-27632 also has an ability to inhibit airway hyperresponsiveness induced by antigen challenge. Thus, the RhoA/Rho-kinase pathway might be a potential target for the development of new treatments for asthma, especially in airway hyperresponsiveness.

Animals↗

Smooth muscle contraction as a model to study the mediator role of endogenous lipoxygenase products of arachidonic acid.

In the lung, the contraction of smooth muscle, or bronchospasm, is generally caused by an immunologic insult resulting in mast cell degranulation and the release of histamine, slow reacting substances, and other mediators of inflammation (1). Although the immediate response is bronchospasm, continued activation of this sequence of events results in a chronic inflammatory disease. In the uterus, numerous conditions can result in smooth muscle contraction. One major pathophysiological syndrome associated with increased uterine tone and severe rhythmic contraction is primary dysmenorrhea (2). In this disease state, prostaglandins have been shown to play a major role in these contractions (3,4), and inhibitors of cyclooxygenase have proven beneficial in clinical practice (5). Both dysmenorrhea and cervical ripening have been likened to inflammatory reactions due to varying degrees of vasodilation, invasion by inflammatory cells, proliferation of fibroblasts and smooth muscle contraction (6,7). Metabolism of arachidonic acid (AA) via cyclooxygenase to prostaglandins and thromboxanes and via lipoxygenase to hydroxyeicosatetraenoic acids (HETEs) and leukotrienes is an integral part of both the acute and chronic inflammatory reaction in the lung or uterus. The material reviewed here examines the effect of endogenous leukotrienes on both the lung and uterus and suggests that other smooth muscles and pathophysiological states may be more involved with the lipoxygenase pathway of AA metabolism than previously believed.

Animals↗

Expression of c-fos-like immunoreactivity in the feline brainstem in response to isometric muscle contraction and baroreceptor reflex changes in arterial pressure.

This study compared whether activation of muscle ergoreceptor afferents caused by isometric muscle contraction, activation of baroreceptor afferents induced by i.v. infusion of phenylephrine, or baroreceptor afferent inactivation, caused by carotid artery occlusion, elicit similar patterns of c-Fos induction in brainstem areas. Adult cats were anesthetized with alpha-chloralose, and in each case, the experimental intervention caused an increase in the arterial blood pressure. There were two sets of control experiments: in both, animals underwent the same surgical procedures but then either remained at rest for the entire study, or the tibial nerve was stimulated, as in the contraction group, following muscle paralysis with tubocurarine. Following the procedures, animals rested for 90 min to allow neuronal expression of c-Fos. Control cats showed very little c-Fos immunoreactivity (c-Fos-ir) in the brainstem. Muscle contraction induced c-Fos-ir expression mainly in the nucleus tractus solitarius, lateral reticular nucleus, lateral tegmental field, vestibular nucleus, subretrofacial nucleus, spinal trigeminal tract and in a lateral region of the periaqueductal grey (P 0.5-1.0). The majority of the c-Fos-ir was found in brainstem areas contralateral to the contracted muscle. In addition, muscle contraction induced c-Fos-ir in the dorsal horns of spinal segments L6-S1 on the ipsilateral side of the spinal cord. Phenylephrine infusion caused c-Fos-ir expression in the nucleus tractus solitarius, spinal trigeminal tract, solitary tract, and dorsal motor nucleus of the vagus. No c-Fos-ir was apparent in the periaqueductal grey. Carotid occlusions induced c-Fos-ir expression in the area postrema, nucleus tractus solitarius, solitary tract, and spinal trigeminal tract. Expression was bilateral. Areas that exhibited c-Fos-ir correspond to sites previously reported to release various neuropeptides in response to muscle contraction or carotid occlusions. These results indicate that the exercise pressor reflex and baroreflex activate similar, but not completely identical, sites in the brainstem.

Afferent Pathways↗

A four-state cross bridge model for muscle contraction. Mathematical study and validation.

A mathematical model of contracting skeletal muscle is studied. The model is composed by an elastic element (SE) in series with a contractile element (CE) that describes the cross bridge kinetics with a formulation derived by that proposed by Eisenberg and Hill (1978). An analytical study of the system of nonlinear partial differential equations of the model allows the existence and the uniqueness of the solution to be proved. A suitable approach to the numerical solution is defined and a series of numerical tests are performed. These tests lead to select an appropriate set of parameters and allow to compare model predictions and experimental observations on frog skeletal muscle.

Actins↗

Molecular aspects of muscle contraction and regulation.

Current views regarding some aspects of the contraction of muscle and its regulation are reviewed. Recent work bearing on the segmental flexibility of myosin is related to cross-bridge movements and ATP metabolism in living muscle. Interaction of troponin with calcium, the process that initiates activation of actin-myosin interaction, is discussed in terms of Ca-induced conformational changes and protein-protein interactions.

Actins↗

Antinociceptive and smooth muscle contracting activities of the methanolic extract of Cassia tora leaf.

The leaves of Cassia tora Linn. (Family: Caesalpiniaceae) were soxhlet extracted with methanol. The spasmogenic effects of the extract were evaluated on guinea pig ileum, rabbit jejunum and mice intestinal transit. Antinociceptive activity of the extract was also evaluated in the mice. The LD(50) values of the extract in mice were >2000 mg/kg i.p. and p.o. The extract contracted smooth muscles of guinea pig ileum and rabbit jejunum in a concentration-dependent manner. Atropine reversibly blocked this activity. Mepyramine also reduced the contractile amplitude due to the extract in a concentration-dependent manner. The extract increased intestinal transit in mice dose dependently. C. tora extract significantly (P<0.05) reduced the number of acetic acid induced abdominal constrictions in mice and the effect was comparable to that of aspirin (150 mg/kg i.p.). The extract also significantly (P<0.05) reduced the nociceptive response of mice to increased force (g). The effects were dose-dependent. The studies suggest that the use of C. tora, traditionally, as a purgative and in the treatment of other ailments is justifiable.

Analgesics↗