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 559 records · Page 31Linked to original sources

PubMed2002

The effect of muscle contraction on kinaesthesia.

Kinaesthesia is our conscious awareness of body position and movement. Experiments are described examining kinaesthetic acuity in human subjects. The results showed a reduced ability to detect limb movement and match limb position during co-contraction of elbow extensors and flexors compared to when these muscles were relaxed. We also report results from animal experiments showing a reduction in muscle spindle stretch sensitivity during fusimotor and skeletomotor activation, a factor that might contribute to the decreased kinaesthetic acuity observed during muscle contraction.

Animals↗

PubMed1996

Smooth muscle fatty acid binding protein: a regulator of smooth muscle contraction?

A fatty acid binding protein has been isolated from chicken gizzard smooth muscle. The partial amino acid sequence (EMBL P80565) of this protein shows high sequence similarities with other members of the fatty acid binding protein family. This is the first fatty acid binding protein isolated from smooth muscle. It may be involved in the regulation of smooth muscle contraction by transporting polyunsaturated fatty acids (e.g. arachidonic acid).

Amino Acid Sequence↗

PubMed1990

[In electric nerve stimulation can the distance from the nerves be inferred from the intensity of muscle contraction? Possible parameters and sources of error].

Electrical nerve stimulation is a useful tool in regional anesthesia; it assists in locating the nerves. This investigation deals with electrical resistances at adhesive electrodes attached to the skin. The influence of external electrical resistance on the stimulating impulse is demonstrated. A new type of nerve stimulator is described; which integrates a measuring device that indicates the electrical impulse actually flowing in the patient. With this device, relationships between stimulating impulse, intensity of muscle contraction, and distance of the puncture cannula from the nerve can be assessed. MATERIALS AND METHODS. The electrical curve I = f (R) was determined using 3 different nerve stimulators (R = 1 - 15k omega). On each of five test persons, five adhesive electrodes were attached to the skin 10 cm apart. The resistance was assessed between these electrodes and a subcutaneously inserted puncture needle. The right and left brachial plexuses of the 5 subjects were punctured, using the axillary approach. A synchronized video camera simultaneously recorded the following values: (1) electrical impulse; (2) corresponding muscle contraction; and (3) the position of the puncture cannula. A scale ranging from 0-5 was applied to define the strength of the muscle contractions. RESULTS. The external resistance as measured under clinical conditions may limit the output impulse of nerve stimulators. In this case, the exerting impulse is lower than that indicated by the appliance. This error can only be identified using an impulse-measuring device. Nerve stimulators not equipped with a measuring device increase the risk of malpuncture, potentially resulting in nerve lesions. Skin resistance at adhesive electrodes varied from patient to patient within a range of 1.1 to 8.2 K omega. Preparing the skin appropriately (wiping with sandpaper) decreased the resistance by only 6% during the first 30 min. Within a distance of 50 cm to the puncture needle, the position of the adhesive electrode did not play a significant role. Axillary puncture of the brachial plexus resulted in the following values: (1) A stimulating impulse (cross-wave) of 1 mA and 1 ms exerted at a distance of 4 mm to the nerve induced a contraction of strength 3. (2) Reducing the impulse at this site by one-half (0.55 mA) resulted in just-visible contractions (strength 1). (3) Advancing the cannula at a stimulating impulse of 0.55 mA inside the neurovascular sheath again produced contractions of strength 3. (4) Performing the puncture with a blunt needle and tracing a distinct resistance, the impulse of 0.6 mA elicited contractions of strength 2. The needle tip was still outside the vascular nerve sheath. If this resistance was overcome and the needle tip lay inside the neurovascular sheath, the impulse could be reduced by one-half (0.32 mA) to produce contractions of strength 2.

Anesthesia, Conduction↗

PubMed1996

The role of the four Ca2+ binding sites of troponin C in the regulation of skeletal muscle contraction.

In order to study the role of the Ca2+-specific sites (I and II) and the high affinity Ca2+-Mg2+ sites (III and IV) of TnC in the regulation of muscle contraction, we have constructed four mutants and the wild type (WTnC) of chicken skeletal TnC, with inactivated Ca2+ binding sites I and II (TnC1,2-), site III (TnC3-), site IV (TnC4-), and sites III and IV (TnC3,4C-). All Ca2+ binding site mutations were generated by replacing the Asp at the X-coordinating position of the Ca2+ binding loop with Ala. The binding of these mutated proteins to TnC-depleted skinned skeletal muscle fibers was investigated as well as the rate of their dissociation from these fibers. The proteins were also tested for their ability to restore steady state force to TnC-depleted fibers. We found that although the NH2-terminal mutant of TnC (TnC1,2-) bound to the TnC-depleted fibers (with a lower affinity than wild type TnC (WTnC)), it was unable to reactivate Ca2+-dependent force. This supports earlier findings that the low affinity Ca2+ binding sites (I and II) in TnC are responsible for the Ca2+-dependent activation of skeletal muscle contraction. All three COOH-terminal mutants of TnC bound to the TnC-depleted fibers, had different rates of dissociation, and could restore steady state force to the level of unextracted fibers. Although both high affinity Ca2+ binding sites (III and IV) are important for binding to the fibers, site III appears to be the primary determinant for maintaining the structural stability of TnC in the thin filament. Moreover, our results suggest an interaction between the NH2- and COOH-terminal domains of TnC, since alteration of sites I and II lowers the binding affinity of TnC to the fibers, and mutations in sites III and IV affect the Ca2+ sensitivity of force development.

Animals↗

PubMed1985

Activation of tracheal smooth muscle contraction: synergism between Ca2+ and activators of protein kinase C.

The effects of divalent ionophores (A23187 and ionomycin), Ca2+ channel agonist (BAY K 8644), and protein kinase C (C-kinase) activators [phorbol 12-myristate 13-acetate (PMA), mezerein] on bovine tracheal smooth muscle contraction were investigated. A23187 (5 microM) and ionomycin (0.5 microM) produced a prompt but transient contraction. C-kinase activators either produced no effect--e.g., PMA at 200 nM--or produced a rise in tension that was slow in onset but then gradually increased--e.g., mezerein at 400 nM. In contrast, ionophores and C-kinase activators, in combination, acted synergistically to produce a prompt and sustained contractile response that is reminiscent of that observed in response to carbachol, a cholinergic agonist. In addition, BAY K 8644 (20 nM), which has a minimal effect on tension by itself, could significantly enhance contraction induced by C-kinase activators. The contraction induced by all of these agents was quickly reversed either by removal of extracellular Ca2+ or upon addition of forskolin, an activator of adenylate cyclase. A similar reversal of carbachol-induced contraction by forskolin was observed with carbachol-induced contraction. These findings strongly suggest that C-kinase plays an important role in mediating tracheal smooth muscle contraction.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗

PubMed1988

Biomechanical model calculation of muscle contraction forces: a double linear programming method.

This paper presents a novel scheme for the use of linear programming to calculate muscle contraction forces in models describing musculoskeletal system biomechanics. Models of this kind are frequently found in the biomechanics literature. In most cases they involve muscle contraction force calculations that are statically indeterminate, and hence use optimization techniques to make those calculations. We present a linear programming optimization technique that solves a two-objective problem with two sequential linear programs. We use the technique here to minimize muscle intensity and joint compression force, since those are commonly used objectives. The two linear program model has the advantages of low computation cost, ready implementation on a micro-computer, and stable solutions. We show how to solve the model analytically in simple cases. We also discuss the use of the dual problem of linear programming to gain understanding of the solution it provides.

Biomechanical Phenomena↗

PubMed1998

Muscle contraction as a Markov process. I: Energetics of the process.

Force generation during muscle contraction can be understood in terms of cyclical length changes in segments of actin thin filaments moving through the three-dimensional lattice of myosin thick filaments. Recent anomalies discovered in connection with analysis of myosin step sizes in in vitro motility assays and with skinned fibres can be rationalized by assuming that ATP hydrolysis on actin accompanies these length changes. The paradoxically rapid regeneration of tension in quick release experiments, as well as classical energetic relationships, such as Hill's force-velocity curve, the Fenn effect, and the unexplained enthalpy of shortening, can be given mutually self-consistent explanations with this model. When muscle is viewed as a Markov process, the vectorial process of chemomechanical transduction can be understood in terms of lattice dependent transitions, wherein the phosphate release steps of the myosin and actin ATPases depend only on occurrence of allosteric changes in neighbouring molecules. Tropomyosin has a central role in coordinating the steady progression of these cooperative transitions along actin filaments and in gearing up the system in response to higher imposed loads.

Actins↗

PubMed1993

Microvascular responses to oxygen and muscle contraction in hypertensive Dahl rats.

We evaluated the possibility that increased arteriolar tone in salt-sensitive hypertension could be partially due to an altered vascular responsiveness to oxygen and/or tissue metabolites. The microvasculature of the superfused spinotrapezius muscle was studied with fluorescence microscopy in Dahl salt-sensitive rats fed low (0.45%) or high (7%) salt diets for 4 weeks. High salt intake produced hypertension (mean arterial pressure = 162 +/- 5 mm Hg vs 130 +/- 4 mm Hg for low salt rats, p < 0.05), and increased vascular tone at the level of the arcade arterioles but not in the smaller transverse or distal arterioles. Arcade arteriole constriction induced by increasing superfusate oxygen content (from 0% to 10% O2) was 60% greater in hypertensive rats than in normotensive rats, whereas oxygen-dependent constriction of transverse and distal arterioles was similar in the two groups. The oxygen-induced reduction in capillary perfusion (the fraction of time during which flow was observed in each vessel) was also greater in hypertensive than in normotensive rats. Arcade arteriole dilation during 2 Hz muscle contraction was significantly greater in hypertensive than in normotensive rats, but there were no differences between groups in the dilation of any other vessel type or in the capillary flow increases accompanying 2 or 8 Hz contraction. These results suggest that a hyperresponsiveness to the actions of blood-borne or tissue oxygen could contribute to increased arcade arteriolar tone in the spinotrapezius muscle of Dahl rats with salt-induced hypertension. The enhanced dilation of arcade arterioles during muscle contraction also suggests a localized hyperresponsiveness to tissue metabolites in this form of hypertension.

Animals↗

PubMed2001

Zipper-interacting protein kinase induces Ca(2+)-free smooth muscle contraction via myosin light chain phosphorylation.

The inhibition of myosin phosphatase evokes smooth muscle contraction in the absence of Ca(2+), yet the underlying mechanisms are not understood. To this end, we have cloned smooth muscle zipper-interacting protein (ZIP) kinase cDNA. ZIP kinase is present in various smooth muscle tissues including arteries. Triton X-100 skinning did not diminish ZIP kinase content, suggesting that ZIP kinase associates with the filamentous component in smooth muscle. Smooth muscle ZIP kinase phosphorylated smooth muscle myosin as well as the isolated 20-kDa myosin light chain in a Ca(2+)/calmodulin-independent manner. ZIP kinase phosphorylated myosin light chain at both Ser(19) and Thr(18) residues with the same rate constant. The actin-activated ATPase activity of myosin increased significantly following ZIP kinase-induced phosphorylation. Introduction of ZIP kinase into Triton X-100-permeabilized rabbit mesenteric artery provoked a Ca(2+)-free contraction. A protein phosphatase inhibitor, microcystin LR, also induced contraction in the absence of Ca(2+), which was accompanied by an increase in both mono- and diphosphorylation of myosin light chain. The observed sensitivity of the microcystin-induced contraction to various protein kinase inhibitors was identical to the sensitivity of isolated ZIP kinase to these inhibitors. These results suggest that ZIP kinase is responsible for Ca(2+) independent myosin phosphorylation and contraction in smooth muscle.

Amino Acid Sequence↗

PubMed1998

Signal transduction pathways mediating CCK-induced gallbladder muscle contraction.

The signal transduction that mediates CCK-induced contraction of gallbladder muscle was investigated in the cat. Contraction was measured by scanning micrometry in single muscle cells isolated enzymatically with collagenase. Production of D-myo-inositol 1,4, 5-trisphosphate (IP3) and sn-1,2-diacylglycerol (DAG) was quantitated using HPLC and TLC, respectively. Protein kinase C (PKC) activity was determined by measuring the phosphorylation of a specific substrate peptide from myelin basic protein, Ac-MBP-(4-14). CCK-induced contraction was blocked by incubation in strontium medium, pertussis toxin (PTx), and antibodies against Gialpha3 or betagamma-subunits but was not blocked by Ca2+-free medium or by antibodies against Gq/11alpha, Gialpha1-2, or Goalpha. The contraction induced by CCK was inhibited by the phospholipase C (PLC) inhibitor U-73122, anti-PLC-beta3 antibody, and the IP3 receptor antagonist heparin but was not inhibited by the the phospholipase D inhibitor propranolol or antibodies against PLC-beta1 or PLC-beta2. Western blot analysis of gallbladder muscle revealed the presence of PLC-beta2 and PLC-beta3 but not PLC-beta1. CCK caused a 94% increase in IP3 generation and an 86% increase in DAG generation. A low dose of CCK caused PKC translocation, and CCK-induced contraction was blocked by the PKC inhibitor H-7. A high dose of CCK, however, caused no PKC translocation, and its contraction was blocked by the calmodulin antagonist CGS9343B. In conclusion, CCK contracts cat gallbladder muscle by stimulating PTx-sensitive Gi 3 protein coupled with PLC-beta3, producing IP3 and DAG. Low doses activate PKC, whereas high doses activate calmodulin.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗

PubMedDate not supplied

Reflex muscle contraction in anterior shoulder instability.

Reduced proprioception may contribute to recurrent anterior shoulder instability. Twelve patients with unilateral shoulder instability were investigated for evidence of deficient proprioception with an activated pneumatic cylinder and surface electromyography electrodes; the contralateral normal shoulder was used as a control. The latency between onset of movement and the detection of muscle contraction was used as an index of proprioception. No significant difference in muscle contraction latency was detected between the stable and unstable shoulders, suggesting that there was no significant defect in muscular reflex activity. This study does not support the use proprioception-enhancing physiotherapy in the treatment of posttraumatic anterior shoulder instability.

Adult↗

PubMedDate not supplied

A technique to decrease breast shape deformity during muscle contraction in submuscular augmentation mammaplasty.

The main objective of this study was to decrease breast shape distortion during pectoralis muscle contraction following submuscular augmentation mammaplasty. We followed 348 patients who had retromuscular augmentation mammoplasty: 251 (72.1%) had polyurethane-covered gel-filled, 97 (27.9%) had textured-silicone gel-filled implants. Among the 348, 46 had surgery following the Regnault technique and 302 had surgery by the below-mentioned technique. Periareolar incision, bipartision of breast parenchyma down to the fascia, undermining of breast base from the fascia downward to the inframammary sulcus or a little below it, detaching of muscle off the thoracic cage, disinsertion of abdomino-costal pectoralis attachments. Full thickness incision of pectoralis muscle on a vertical line on the nipple projection for 2-5 inches. Placing of prosthesis. Drainage. Closure. No objective evaluation was used, only clinical judgments by three observers--the surgeon, a nurse and the patient herself. The results showed a definite decrease of the dynamic deformity among patients in whom the author's technical variation was carried out. This technique allows also, for decreasing the upward pushing of the implant during pectoralis muscle contraction and facilitates stretch of the breast tissue in patients with tighter breast envelopes. Despite lack of precise measurements, conclusions drawn from clinical judgments, taken as objectively as possible, suggest that the use of this technique may offer the solution of an otherwise disturbing collateral effect, frequently seen after this operation.

Breast Implantation↗

PubMed1986

Physiology and pathophysiology of skeletal muscle contractions. Part I. Dynamic activity.

An overview is presented of the physiology and pathophysiology of dynamic skeletal muscle contractions in the intact living organism. Dynamic muscle activities are divided into concentric contractions with shortening of muscle fibres and the production of positive work, and eccentric contractions with lengthening of muscle fibres and the production of negative work. In positive work, muscle tension overcomes external forces. In negative work, external forces overcome muscle tension. The latter phenomenon, with relatively few active motor units, explains the injuries induced by eccentric contractions. Both the contractile and non-contractile elements are involved in the muscle injuries and, clinically, they are referred to as myofibrositis.

Animals↗

PubMed2002

Muscle function during repetitive moderate-intensity muscle contractions in myoadenylate deaminase-deficient Dutch subjects.

We investigated whether the capacity for repetitive submaximal muscle contraction was reduced in a group of subjects (n=8) with a primary deficiency of myoadenylate deaminase (MAD). Quadriceps femoris muscle fatigue was evaluated using voluntary and electrically stimulated contractions during 20 min of repetitive voluntary isometric contractions at 40% of maximal force-generating capacity (MFGC). After 5 min of exercise, MFGC had declined significantly to 70.6+/-4.1% (mean+/-S.E.M.) and 87.2+/-1.6% of baseline values in MAD-deficient and sedentary control subjects (n=8) respectively (P=0.002 between groups). After 5 min of exercise, the half-relaxation time had increased significantly to 113.4+/-6.1% of baseline in MAD-deficient muscle, but had decreased significantly to 94.1+/-1.3% in control subjects (P=0.003 between groups). All control subjects completed the 20-min exercise test. Five of the MAD-deficient subjects had to stop exercising due to early muscle fatigue; however, three of the MAD-deficient subjects were able to complete the 20-min exercise test. In conclusion, although the capacity for repetitive submaximal isometric muscle contractions for the group of MAD-deficient subjects was significantly decreased, it remains uncertain whether MAD deficiency is the sole cause of pronounced muscle fatigue.

AMP Deaminase↗

PubMed1999

Characterization of 5-hydroxytryptamine receptors mediating circular smooth muscle contraction in the human umbilical artery.

The study was performed to characterize pharmacologically the contractile 5-hydroxytryptamine (5-HT) receptors in the circular smooth muscle of the isolated human umbilical artery. Effects of agonists and antagonists for different 5-HT receptor subtypes were studied in intact endothelium vessel segments. All agonists induced concentration-dependent circular smooth muscle contractions. The potency was in declining order 5-HT > alpha-methyl-5-HT > sumatriptan >/= 2-methyl-5-HT. The effects of 5-HT and alpha-methyl-5-HT were antagonized by ketanserin, as well as methiothepin. The contractile effect of sumatriptan was antagonized by methiothepin but not by ketanserin. The 5-HT3 receptor antagonist, MDL 72222, did not affect the contraction by any of the agonists, including 2-methyl-5-HT. It is concluded that the 5-HT-induced contraction in the circular smooth muscle of the human umbilical artery seems to be mediated by a mixed population of 5-HT1-like receptors and 5-HT2 receptors.

Adolescent↗

PubMed1985

Relationships between strength of low back muscle contraction and reported intensity of chronic low back pain.

The electromyographic patterns produced by recording the left and right paraspinal muscles of subjects while in motion (bending and rising) and still (standing upright, sitting supported and unsupported, and prone) were contrasted for people with: 1) no history of back pain; 2) past episodes of low back pain but currently pain free; and 3) chronic low back pain with various diagnosed etiologies. Each of the 83 individuals recorded during episodes of low back pain produced a unique pattern of muscle contraction which was relatively stable between weekly recording sessions. In every case, at least one of the six positions showed elevated contraction levels significantly above that of the 15 subjects with no history of back pain and the 28 with no current back pain. For nine of the eleven subjects who reported changes in pain intensity between recording sessions, a clearly positive correlation occurred between the reported intensity of pain and the level of contraction in the one position most different from the reference group. No diagnostic subgroup of low back pain subjects produced a single unique pattern. Furthermore, no single aspect of the EMG signal, such as bilateral asymmetry, had predictive value for any individual subject. Our recordings did not differ with respect to diagnostic category so further research will have to be done to determine whether the diagnostic categories currently in use do not fit the physiological bases for the problems and/or whether prolonged abnormal levels of muscle contraction eventually produce problems such as disc displacement.

Adolescent↗

PubMed1991

5-hydroxytryptamine-stimulated accumulation of 1,2-diacylglycerol in the rabbit basilar artery: a role for protein kinase C in smooth muscle contraction.

1. 5-Hydroxytryptamine (5-HT) produced a concentration-dependent increase in the membrane concentration of 1,2-diacylglycerol (DG) in the rabbit isolated basilar artery, but did not stimulate the hydrolysis of membrane phosphoinositide. 2. The 5-HT-induced accumulation of DG could be blocked with the putative phospholipase C inhibitor 2-nitro-4-carboxyphenyl-N,N-diphenylcarbamate (NCDC; 70 microM), but not with the protein kinase C inhibitor, 1-(5-isoquinolinesulphonyl)-2-methyl piperazine (H7; 50 microM). 3. Direct stimulation of protein kinase C with phorbol 12,13-dibutyrate (PDBu) produced sustained smooth muscle contraction which was fairly rapid in onset and could be reversed by H7 but not by NCDC. The inactive phorbol, 4 alpha phorbol 12,13-dideceonate, did not produce contraction in the basilar artery. 4. 5-HT-induced contractions (1 nM-100 microM) were blocked or greatly reduced in the presence of the protein kinase inhibitor H7 or polymyxin B, and with the phospholipase C inhibitor, NCDC. The concentrations of these inhibitors which abolished contraction to 5-HT, did not alter smooth muscle contraction produced in response to 30 mM K(+)-physiological salt solution (PSS). 5. These data suggest that DG production and the subsequent activation of PKC forms an important component of the cerebrovascular contractile response to 5-HT. As the DG does not appear to arise from membrane phosphatidylinositol, it appears that 5-HT can stimulate the production of this second messenger in cerebral arteries by a mechanism which is different from peripheral arteries.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗

PubMed1990

Electromyographic biofeedback with mental imagery and home practice in the treatment of children with muscle-contraction headache.

A multiple-baseline across subjects design was used to evaluate the effects of electromyographic (EMG) biofeedback on muscle-contraction headaches reported by two adolescent females. Subsequent to baseline, each child participated in seven treatment sessions conducted over an 8-week interval. Treatment sessions consisted of 10 min of adaptation (baseline), 15 min of EMG biofeedback, and 5 min of self-control during which the child continued to decrease muscle tension without feedback. Children were instructed to practice self-control of relaxation at home. Self-reports of headache frequency, duration and intensity were recorded throughout the study. Results indicate that headache activity was reduced as a function of EMG biofeedback, mental imagery, and home practice and remained below baseline levels during 6-month and 1-year follow-up assessments. Findings are discussed in terms of the paucity of published studies investigating the efficacy of EMG biofeedback as a treatment for pediatric muscle-contraction headache.

Adolescent↗