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 505 records · Page 28Linked to original sources
PubMed1979

Inhibition of intestinal smooth muscle contraction by surface-active alkyltrimethylammonium salts.

The effects of surface-active alkyltrimethylammonium salts (C10--C20) on the contractile activity of isolated rat jejunum and on the gastrointestinal motility in anaesthetized rats were studied. The surfactants caused a dose-dependent depression of spontaneous contractions and of acetyl-beta-methylcholine and BaCl2 induced contractions of isolated rat jejunum. The depressant activity of the surface-active alkyltrimethylammonium salts on smooth muscle contraction increased with an increase in the length of the alkyl chain to maximum activity at C16. It is suggested that the depressant activity of the surface-active alkyltrimethylammonium salts on smooth muscle contraction is due to a non-specific interaction of the surfactants with the cellmembrane of the muscle cells. No effect on gastric and intestinal motility in vivo was observed following intragastric or intraintestinal administrations of surface-active alkyltrimethylammonium salts. This lack of effect upon intraintestinal or intragastric administration probably depends on an inability of the surfactants to reach the site of action when administered from the mucosal side.

Acetylcholine↗
PubMed1976

Myotonia congenita with painful muscle contractions.

We present a family with dominantly inherited myotonia congenita and painful, electrically silent muscle contractions after exertion. In two family members, painful muscle contractions occurred coincident with hypothyroidism, and improved after thyroid replacement therapy. It is probable that this family represents a disease that is similar to but distinct from the dominant form of myotonia congenita.

Adult↗
PubMed2004

AMPK activation is not critical in the regulation of muscle FA uptake and oxidation during low-intensity muscle contraction.

To determine the role of AMP-activated protein kinase (AMPK) activation on the regulation of fatty acid (FA) uptake and oxidation, we perfused rat hindquarters with 6 mM glucose, 10 microU/ml insulin, 550 microM palmitate, and [14C]palmitate during rest (R) or electrical stimulation (ES), inducing low-intensity (0.1 Hz) muscle contraction either with or without 2 mM 5-aminoimidazole-4-carboxamide-1-beta-D-ribofuranoside (AICAR). AICAR treatment significantly increased glucose and FA uptake during R (P < 0.05) but had no effect on either variable during ES (P > 0.05). AICAR treatment significantly increased total FA oxidation (P < 0.05) during both R (0.38 +/- 0.11 vs. 0.89 +/- 0.1 nmol x min(-1) x g(-1)) and ES (0.73 +/- 0.11 vs. 2.01 +/- 0.1 nmol x min(-1) x g(-1)), which was paralleled in both conditions by a significant increase and significant decrease in AMPK and acetyl-CoA carboxylase (ACC) activity, respectively (P < 0.05). Low-intensity muscle contraction increased glucose uptake, FA uptake, and total FA oxidation (P < 0.05) despite no change in AMPK (950.5 +/- 35.9 vs. 1,067.7 +/- 58.8 nmol x min(-1) x g(-1)) or ACC (51.2 +/- 6.7 vs. 55.7 +/- 2.0 nmol x min(-1) x g(-1)) activity from R to ES (P > 0.05). When contraction and AICAR treatment were combined, the AICAR-induced increase in AMPK activity (34%) did not account for the synergistic increase in FA oxidation (175%) observed under similar conditions. These results suggest that while AMPK-dependent mechanisms may regulate FA uptake and FA oxidation at rest, AMPK-independent mechanisms predominate during low-intensity muscle contraction.

AMP-Activated Protein Kinases↗
PubMed2006

Sarcopenia in the Caenorhabditis elegans pharynx correlates with muscle contraction rate over lifespan.

In muscles, sarcopenia, the loss of muscle mass, is the major cause of aging-related functional decline and frailty. Several factors are correlated with sarcopenia during aging, including contraction-related cellular injury, oxidative stress, endocrine changes and reduced regenerative potential. However the involvement of these factors has not been experimentally investigated. Here, we report that contraction-related injury may significantly promote the progression of sarcopenia in the pharynx of the nematode, Caenorhabditis elegans, a model of aging in non-regenerative tissues. Both functional and structural declines in the pharynx during aging were significantly delayed in mutants with reduced muscle contraction rates. We also examined the role of bacteria in pharynx muscle decline during aging, as previous studies reported that antimicrobial treatments could extend C. elegans lifespan. Although microbial infection may have enhanced functional decline in the pharynx during aging, it was not the sole cause of decreased pumping rates in old animals. This study identifies contraction-related injury as a factor affecting the initiation and progression of sarcopenia during aging. Further, characterization of the specific types of damage induced by muscle contraction will be helpful for understanding the underlying causes of sarcopenia.

Aging↗
PubMed1997

Effects of ventrolateral medullary AMPA-receptor antagonism on pressor response during muscle contraction.

Effects of administering 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) at a concentration that preferentially blocks alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA) receptors into rostral ventrolateral medulla (rVLM) or caudal ventrolateral medulla (cVLM) on cardiovascular responses elicited during static muscle contraction were investigated using anesthetized rats. Two microdialysis probes were inserted bilaterally into either the rVLM or the cVLM using stereotaxic guides. A tibial nerve stimulation-evoked static muscle contraction for 30 s increased mean arterial pressure (MAP) and heart rate (HR) by 27 +/- 3 mmHg and 28 +/- 4 beats/min, respectively. Microdialysis of CNQX into the rVLM for 30 min attenuated the contraction-evoked increases in MAP and HR (10 +/- 2 mmHg and 12 +/- 2 beats/min). Developed tensions were similar during the contractions before and after microdialyzing CNQX. In contrast, administration of CNQX into the cVLM potentiated the muscle contraction-evoked cardiovascular responses (MAP, 25 +/- 4 vs. 39 +/- 6 mmHg; HR, 27 +/- 3 vs. 42 +/- 3 beats/min), with no change in developed tensions. Results demonstrate that AMPA receptors within the rVLM and the cVLM appear to play opposite modulatory roles in the central integration of cardiovascular responses elicited during static muscle contraction.

6-Cyano-7-nitroquinoxaline-2,3-dione↗
PubMed1999

Muscarinic cholinoceptor subtypes mediating tracheal smooth muscle contraction and inositol phosphate generation in guinea pig and rat.

The effects of the muscarinic cholinoceptor antagonists atropine (non-selective), pirenzepine (M1-selective), methoctramine (M2-selective) and 4-diphenylacetoxy-N-methylpiperidine methiodide (4-DAMP; M3-selective) were examined on the responsiveness of guinea pig and rat tracheal tissue to acetylcholine and carbachol. Results indicate that smooth muscle contraction in isolated tracheal tissue from both species was mediated primarily by muscarinic M3 cholinoceptors. The effects of atropine, pirenzepine and 4-DAMP were similar against the contractile actions of acetylcholine and carbachol in both species and in epithelium-intact and epithelium-denuded tissue. In contrast, differences in the effects of methoctramine in antagonising contractile responses to acetylcholine and carbachol were observed between the two species and following epithelium removal in the guinea pig. Thus, whilst this study has found that tracheal smooth muscle contraction in the guinea pig and rat is mediated primarily by muscarinic M3 cholinoceptors, anomalies in the functional inositol phosphate generation results obtained with the muscarinic cholinoceptor antagonists highlight species differences in the actions of acetylcholine and carbachol in eliciting smooth muscle contraction suggesting the possible existence of functional non-M3 muscarinic cholinoceptors.

Animals↗
PubMed2003

Short chain fatty acids stimulate feline colonic smooth muscle contraction.

The effect of short chain fatty acids (SCFA) on feline colonic smooth muscle contraction was evaluated in vitro. Colonic tissue was obtained from seven healthy male and female adult cats and seven healthy male and female kittens. Longitudinal and circular colonic smooth muscle strips from proximal and distal colon were incubated with SCFA (acetate, butyrate and propionate; 1-100mM). SCFA-induced contractions were compared to responses obtained using maximal concentrations (10(-4)M) of acetylcholine (ACh). The calcium dependence of the SCFA response was investigated by incubating with nifedipine (1 microM) or verapamil (1 microM). Acetate, butyrate and propionate elicited isometric stress responses (0.25-1.98 x 10(4)N/m(2)) in longitudinal, but not circular, smooth muscle from both the proximal and distal colon of adult cats. Maximal responses were attained at 50 and 100mM SCFA. Maximal butyrate and propionate responses were 29 and 19% of the maximal ACh response (10(-4)M), respectively. Acetate was least effective in stimulating contractile responses. Nifedipine and verapamil abolished all responses. Contractile responses in kittens were similar to those observed in adult cats, but were smaller in amplitude. Results of these studies have shown that SCFA stimulate longitudinal colonic smooth muscle contractions in kittens and adult cats in vitro. These SCFA-induced contractions involve activation of calcium influx. These in vitro findings may account for some of the effects of dietary fiber on feline colonic motility in vivo.

Acetylcholine↗
PubMedDate not supplied

Quadriceps muscle contraction protects the anterior cruciate ligament during anterior tibial translation.

The proposed skiing injury mechanism that suggests a quadriceps muscle contraction can contribute to anterior cruciate ligament rupture was biomechanically investigated. The effect of quadriceps muscle force on a knee specimen loaded to anterior cruciate ligament failure during anterior tibial translation was studied in a human cadaveric model. In both knees from six donors, average age 41 years (range, 31 to 65), the joint capsule and ligaments, except the anterior cruciate ligament, were cut. The quadriceps tendon, patella, patellar tendon, and menisci were left intact. One knee from each pair was randomly selected to undergo destructive testing of the anterior cruciate ligament by anterior tibial translation at a displacement rate of 30 mm/sec with a simultaneously applied 889 N quadriceps muscle force. The knee flexion during testing was 30 degrees. As a control, the contralateral knee was loaded correspondingly, but only 5 N of quadriceps muscle force was applied. The ultimate load for the knee to anterior cruciate ligament failure when tested with 889 N quadriceps muscle force was 22% +/- 18% higher than that of knees tested with 5 N of force. The linear stiffness increased by 43% +/- 30%. These results did not support the speculation that a quadriceps muscle contraction contributes to anterior cruciate ligament failure. In this model, the quadriceps muscle force protected the anterior cruciate ligament from injury during anterior tibial translation.

Adult↗
PubMed1983

Effect of tubocurarine and decamethonium on voluntary muscle contractions in man.

Six healthy, young male subjects performed repeated brisk maximal voluntary muscle contractions (MVC) with the knee and hip extensors. Three MVCs were performed every minute. On separate days decamethonium 0.03 mg X kg-1 and tubocurarine 0.01 mg X kg-1 were administered intravenously during repeated MVCs. While ordinary MVCs showed a slow rate of rise of tension over approximately 1 s, brisk MVCs showed a steep rate of rise of tension and a biphasic configuration appeared, as a notch was seen 370-480 ms after the initiation of the contraction curve. An arbitrary straight line was drawn connecting the starting point of the contraction curve and the notch. The tension time integral to the left and above this line (alpha component), respectively to the right and below the line (beta component) was measured during the first 600 ms of the contraction. Tubocurarine affected the beta component until 70% reduced. With further curarization, the remainder of the beta component was reduced together with the alpha component. Decamethonium, in contrast, affected the alpha component together with 30% of the beta component. Thereafter, the rest of the beta component was increasingly affected. The results suggest that the isometric mechanogram is composed of a phasically active component with a high innervation threshold primarily sensitive to decamethonium, and a tonically active component with a lower innervation threshold, and primarily sensitive to tubocurarine.

Decamethonium Compounds↗
PubMed1982

Cholinergic-independent effects of amphetamine on mammalian skeletal muscle contractions.

Studies were designed to investigated the cholinergic-independent mechanism(s) by which (+)-amphetamine produces a biphasic modification of directly stimulated contractions of skeletal muscle in the rat phrenic nerve-diaphragm preparation. In tissues pretreated with alpha-bungarotoxin, low concentrations of (+)-amphetamine (2.7-1.08 x 10(-4) M) enhanced muscle blockade. In other studies (Gerald, Meldrum and Skau, Res. Commun, chem. Path. Pharmac., 1982), high K+ concentrations or low Na+ concentrations antagonized amphetamine-enhancement of the twitch, while potentiating the blockade; in contrast K+-free media augmented amphetamine-induced enhancement of contractions. Low concentrations of amantadine, tetracaine, and tetrodotoxin increased the facilitatory response to (+)-amphetamine while the inhibitory effects of (+)-amphetamine were potentiated by higher concentrations of these antagonists; similar biphasic effects were observed with (-)-amphetamine and tetracaine. (+)-Amphetamine reserved the marked enhancement of the twitch produced by veratridine while, conversely, this neurotoxin failed to alter muscle contractions after (+)-amphetamine pretreatment. These findings suggest that amphetamine-induced enhancement and blockade of directly-stimulated skeletal muscle resulted from alterations in Na+ fluxes, possibly through interactions with membrane ionic channels.

Amantadine↗
PubMed2003

Phosphatidylinositol 3-kinase modulates vascular smooth muscle contraction by calcium and myosin light chain phosphorylation-independent and -dependent pathways.

Regulation of smooth muscle contraction involves a number of signaling mechanisms that include both kinase and phosphatase reactions. The goal of the present study was to determine the role of one such kinase, phosphatidylinositol (PI)3-kinase, in vascular smooth muscle excitation-contraction coupling. Using intact medial strips of the swine carotid artery, we found that inhibition of PI3-kinase by LY-294002 resulted in a concentration-dependent decrease in the contractile response to both agonist stimulation and membrane depolarization-dependent contractions and a decrease in Ca(2+)-dependent myosin light chain (MLC) phosphorylation, the primary step in the initiation of smooth muscle contraction. Inhibition of PI3-kinase also depressed phorbol dibutyrate-induced contractions, which are not dependent on either Ca(2+) or MLC phosphorylation but are dependent on protein kinase C. To determine the Ca(2+)-dependent site of action of PI3-kinase, we determined the effect of several inhibitors of calcium metabolism on LY-294002-dependent inhibition of contraction. These inhibitors included nifedipine, SK&F-96365, and caffeine. Only SK&F-96365 blocked the LY-294002-dependent inhibition of contraction. Interestingly, all compounds blocked the LY-294002-dependent inhibition of MLC phosphorylation. Our results suggest that activation of PI3-kinase is involved in a Ca(2+)- and MLC phosphorylation-independent pathway for contraction likely to involve protein kinase C. In addition, our results also suggest that activation of PI3-kinase is involved in Ca(2+)-dependent signaling at the level of receptor-operated calcium channels.

Animals↗
PubMed2004

Control of respiration and bioenergetics during muscle contraction.

(1)H-NMR experiments have determined intracellular O(2) consumption (Vo(2)) with oxymyoglobin (MbO(2)) desaturation kinetics in human calf muscle during plantar flexion exercise at 0.75, 0.92, and 1.17 Hz with a constant load. At the onset of muscle contraction, myoglobin (Mb) desaturates rapidly. The desaturation rate constant of approximately 30 s reflects the intracellular Vo(2). Although Mb desaturates quickly with a similar time constant at all workload levels, its final steady-state level differs. As work increases, the final steady-state cellular Po(2) decreases progressively. After Mb desaturation has reached a steady state, however, Vo(2) continues to rise. On the basis of current respiratory control models, the analysis in the present report reveals two distinct Vo(2) phases: an ADP-independent phase at the onset of contraction and an ADP-dependent phase after Mb has reached a steady state. In contrast to the accepted view, the initial intracellular Vo(2) shows that oxidative phosphorylation can support up to 36% of the energy cost, a significantly higher fraction than expected. Partitioning of the energy flux shows that a 31% nonoxidative component exists and responds to the dynamic energy utilization-restoration cycle (which lasts for only milliseconds) as postulated in the glycogen shunt theory. The present study offers perspectives on the regulation of respiration, bioenergetics, and Mb function during muscle contraction.

Adenosine Diphosphate↗
PubMedDate not supplied

[Noradrenaline regulation of the energy of heat production and ATP utilization during normal single muscle contraction and in hyperoxia].

The effect of noradrenalin (NA, 0.008 microgram/ml) on the rate of heat release (V) during a single isometric contraction of an isolated diaphragm was investigated in rats kept in air and 99% oxygen for 3 hours. The effect was measured by the electrothermometric method in the presence and in the absence of ATP (0.01 mg/ml) in the incubation solution. Hyperoxia doubled V of muscle contraction. The calorigenic effect of NA was not detected in the norm and was very distinct during hyperoxia so that VNA = 0.14X XVinit + 10.88. ATP addition increased V both in the normal and hyperoxic state. However, the increase of the initial V level was 5.3-fold in the hyporexoc state and 1.5-fold in the norm. It is concluded that hyperoxia disturbs energy metabolism of muscle contraction through NA-dependent acceleration of ATP-lytic processes and increase of energy expenditures of heat formation in the course of muscle contraction.

Adenosine Triphosphate↗
PubMed1997

Local neurogenic regulation of rat hindlimb circulation: role of calcitonin gene-related peptide in vasodilatation after skeletal muscle contraction.

1. The mechanism of neurogenic regulation of skeletal muscle circulation was studied in the hindlimb of anaesthetized rats in vivo. Regional blood flow (RBF) of the hindlimb was recorded with a pulsed Doppler flow probe positioned in the iliac artery. 2. A short period (1 min) of sciatic nerve stimulation at 10 Hz caused a sustained increase in RBF (from 2.0 +/- 0.2 to 3.7 +/- 0.2 kHz at the peak), but no appreciable change in either MBP or HR, suggesting that the nerve stimulation produced local vasodilatation of the peripheral vasculature. The hyperaemic response reached a peak within 15 s and characteristically remained above the basal level for more than 5 min after the cessation of nerve stimulation. The response was regarded as a secondary response brought about by the contraction of skeletal muscles since (+)-tubocurarine (0.73 micromol kg(-1), i.a.) almost abolished it. 3. Lignocaine (43 micromol kg(-1), i.a.) and capsaicin (0.33 micromol kg(-1), i.a.) significantly suppressed the hyperaemic response to skeletal muscle contraction, suggesting that capsaicin-sensitive sensory nerves contribute to the hyperaemia. In contrast, an inhibitor of NO synthase, N(omega)-nitro-L-arginine methyl ester (1 micromol kg(-1) min(-1), i.v.), did not affect the hyperaemic response. 4. Serum levels of calcitonin gene-related peptide (CGRP) in iliac venous effluent significantly increased from 51 +/- 4 to 77 +/- 5 fmol ml(-1) during the hyperaemic response to skeletal muscle contraction. A bolus injection of CGRP (300 pmol kg(-1), i.a.) induced a long-lasting increase in RBF of the hindlimb. Moreover, CGRP(8-37) (100 nmol kg(-1) min(-1), i.v.), a specific CGRP1 receptor antagonist, significantly suppressed the hyperaemic response, especially the sustained phase of the response which was almost abolished by this antagonist. 5. These results suggest that CGRP, which is released from peripheral endings of capsaicin-sensitive sensory nerves, partly mediates the hyperaemia evoked by skeletal muscle contraction of the rat hindlimb.

Animals↗
PubMed1997

Optical isometric force transducer for measurement of rat skeletal muscle contraction in the NMR spectrometer.

In order to measure force of contraction of the rat gastrocnemius muscle in the NMR spectrometer with a simultaneous observation of 31P NMR spectra, an optical force transducer was constructed using gratings and optical fibers. Muscle contraction was accurately recorded in the spectrometer without interfering with NMR measurements. The half height width of the phosphocreatine (PCr) peak in the presence or absence of the transducer was 5 Hz. Decrease in PCr and increase in inorganic phosphate (Pi) in the muscle were successfully followed during monitoring of the force developed during exercise. The change in the PCr:(PCr + Pi) ratio correlated well with the time-force integral from the optical force transducer. In general, there was no interference with the 31P NMR spectrum when the transducer was attached to rat leg, so this optical force transducer should prove valuable for studying muscle physiology in the NMR spectrometer.

Animals↗
PubMed1999

Cardiovascular responses to an orthostatic challenge and electrical-stimulation-induced leg muscle contractions in individuals with paraplegia.

The purpose of this study was to investigate the cardiovascular and haemodynamic responses that occur during moderate orthostatic challenge in people with paraplegia, and the effect of electrical stimulation (ES)-induced leg muscle contractions on their responses to orthostatic challenge. Eight males with complete spinal lesions between the 5th and 12th thoracic vertebrae (PARA) and eight able-bodied individuals (AB) volunteered for this study. Changes in heart rate (fc), stroke volume (SV), cardiac output (Qc), mean arterial pressure (MAP), total peripheral resistance (TPR), limb volumes and indices of neural modulation of fc, [parasympathetic (PNS) and sympathetic (SNS) nervous system indicators] were assessed during: (1) supine rest (REST), (2) REST with lower-body negative pressure at -30 torr (LBNP -30, where 1 torr = 133.32 N/m2), and (3) for PARA only, LBNP -30 with ES-induced leg muscle contractions (LBNP + ES). LBNP -30 elicited a decrease in SV (by 23% and 22%), Qc (by 15% and 18%) and the PNS indicator, but an increase in fc (by 10% and 9%), TPR (by 23% and 17%) and calf volume (by 1.51% and 4.04%) in both PARA and AB subjects, respectively. The SNS indicator was increased in the AB group only. Compared to LBNP -30, LBNP + ES increased SV (by 20%) and Qc (by 16%), and decreased TPR (by 12%) in the PARA group. MAP was unchanged from REST during all trials, for both groups. The orthostatic challenge induced by LBNP -30 elicited similar cardiovascular adaptations in PARA and AB subjects. ES-induced muscle contractions during LBNP -30 augmented the cardiovascular responses exhibited by the PARA group, probably via reactivation of the skeletal muscle pump and improved venous return.

Adult↗