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At least 253 records · Page 14Linked to original sources

PubMed1982

Electromyographic feedback: effects on voluntary muscle contractions in normal subjects.

To evaluate the efficacy and function of EMG feedback (FB) in muscle reeducation, voluntary muscle contractions with and without EMG FB were compared under controlled experimental conditions in normal human subjects (n=10). Each subject was instructed to produce 12 sustained, 30-second contractions of the left abductor hallucis muscle, 6 contractions in each of 2 sessions. For all subjects, EMG FB was provided in half of the trials, alternating with nonfeedback (NFB) trials. A ranking task was included to measure ability to discriminate contractions in the target muscle. EMG activity was significantly greater during muscle contractions attempted with EMG FB; this was due to increased motor unit recruitment early in the course of the trials, a positive response in normal subjects similar to that in paretic subjects in our previous study. Performance on the ranking task also indicated that subjects had little perceptual awareness of their muscle contractions. Our findings suggest that the positive response to EMG FB was due to the precise information it provided concerning small, poorly discriminated muscle contractions.

Biofeedback, Psychology↗

PubMed2005

Attenuation of the effect of remote muscle contraction on the soleus H-reflex during plantar flexion.

OBJECTIVE: We investigated to what extent the facilitation of the soleus (Sol) Hoffmann (H-) reflex during a phasic voluntary wrist flexion (Jendrássik maneuver, JM) can be modulated by graded plantar flexion force and conditioning wrist flexion force. METHODS: The subjects were asked to perform phasic wrist flexion under a reaction time condition. Sol H-reflex was evoked by stimulating the right tibial nerve at various time intervals (50-400ms) after the 'Go' signal for initiating JM while the ankle was at rest and while plantarflexing. The level of tonic plantar flexion force (isometric contraction of 10, 20 and 30% of maximal EMG) and conditioning wrist flexion (isometric contraction of 30, 50 and 80% of maximum voluntary contraction) during JM was graded systematically. RESULTS: Although JM facilitation could be seen 80-120ms after the flexor carpi radialis (FCR) EMG onset even while plantarflexing, the magnitude of JM facilitation under plantar flexion was significantly decreased compared to that at rest. The degree of decrease in JM facilitation did not depend on the level of plantar flexion force. In contrast, the degree of JM facilitation was proportional to the level of wrist flexion force while the ankle was at rest and while plantarflexing, though the amount of JM facilitation significantly decreased while plantarflexing. CONCLUSIONS: JM facilitation of Sol H-reflex is decreased while performing tonic voluntary contraction of the homonymous muscle. The degree of decrease in JM facilitation is independent of the level of homonymous muscle contraction, but depends on the level of remote FCR contraction. In clinical application, when we intend to elicit a maximum stretch reflex by JM, full relaxation of homonymous muscle should be carefully confirmed. SIGNIFICANCE: Our results provide evidence for better understanding of the features of JM and insight into its clinical application.

Acoustic Stimulation↗

PubMed1993

Antagonism of vasoconstriction by muscle contraction differs with alpha-adrenergic subtype.

It has been suggested that muscle contraction causes prejunctional inhibition of transmitter release from sympathetic nerves. In accordance with this, we found that second-order (50 microns ID) arterioles of the cat sartorius muscle dilate 40-80% more with muscle contraction during 2-, 4-, or 8-Hz sympathetic nerve stimulation than during equivalent constriction produced by intravenous norepinephrine injection. However, when constriction was to the selective alpha 1-agonist phenylephrine, the magnitude of dilation induced by muscle contraction was similar to that seen with sympathetic nerve stimulation, suggesting that prejunctional inhibition is not involved. Alternatively, different receptor subtypes may be activated by sympathetic nerve stimulation and exogenous norepinephrine. In support of this explanation, we found that approximately 50% of the vasoconstrictor effect of sympathetic nerve stimulation (8 Hz) was blocked by prazosin, an alpha 1-adrenergic antagonist, but no further diminution of tone was seen with addiction of yohimbine, an alpha 2-adrenergic antagonist. In contrast, the vasoconstrictor response to exogenous norepinephrine was not affected by prazosin, while addition of yohimbine almost completely blocked the response. These findings suggest that muscle contraction selectively attenuates vasoconstriction mediated by junctional receptors in second-order arterioles.

Animals↗

PubMed2003

ATP concentrations and muscle tension increase linearly with muscle contraction.

Previous studies have suggested that activation of ATP-sensitive P2X receptors in skeletal muscle play a role in mediating the exercise pressor reflex (Li J and Sinoway LI. Am J Physiol Heart Circ Physiol 283: H2636-H2643, 2002). To determine the role ATP plays in this reflex, it is necessary to examine whether muscle interstitial ATP (ATPi) concentrations rise with muscle contraction. Accordingly, in this study, muscle contraction was evoked by electrical stimulation of the L7 and S1 ventral roots of the spinal cord in 12 decerebrate cats. Muscle ATPi was collected from microdialysis probes inserted in the muscle. ATP concentrations were determined by the HPLC method. Electrical stimulation of the ventral roots at 3 and 5 Hz increased mean arterial pressure by 13 +/- 2 and 16 +/- 3 mmHg (P < 0.05), respectively, and it increased ATP concentration in contracting muscle by 150% (P < 0.05) and 200% (P < 0.05), respectively. ATP measured in the opposite control limb did not rise with ventral root stimulation. Section of the L7 and S1 dorsal roots did not affect the ATPi seen with 5-Hz ventral root stimulation. Finally, ventral roots stimulation sufficient to drive motor nerve fibers did not increase ATP in previously paralyzed cats. Thus ATPi is not largely released from sympathetic or motor nerves and does not require an intact afferent reflex pathway. We conclude that ATPi is due to the release of ATP from contracting skeletal muscle cells.

Adenosine Triphosphate↗

PubMed2003

[Effects of TWP on capacity of muscle contraction].

OBJECTIVE: To investigate the direct effects of Tripterygium Wilfordii Polyglycosidium (TWP) on capability of muscle contraction. METHODS: Using electronic stimulator to stimulate the phrenic nerve of the isolated phrenic nerve diaphragm preparation of 30 rats or directly stimulate the isolated gastrocnemius muscle preparation of 45 toads in vitro, we studied the effects of TWP on capability of muscle intrinsic contraction. RESULTS: TWP in 20 mg/L increased the amplitude of muscle contraction in initial 60 min but did not make further increase of the amplitude of muscle contraction from 60 min to 90 min in the isolated phrenic nerve diaphragm preparation of rat under one-third optimal stimulus. TWP in 40 mg/L and in 60 mg/L did not cause decrease of amplitude of muscle contraction in initial 60 min in isolated phrenic nerve diaphragm preparation of rat under one-third optimal stimulus. TWP in 60 mg/L did not cause decrease of tension of signal-contraction in initial 30 min in isolated gastrocnemius muscle preparation of toad under one-third optimal direct stimulus. Solvent DMSO could obviously reduce the tension of muscle contraction both in isolated phrenic nerve diaphragm preparation of rat and in isolated gastrocnemius muscle preparation of toad under one-third optimal stimulus. CONCLUSION: TWP can limitedly enhance the capability of muscle contraction; Solvent DMSO can restrain muscle contraction.

Animals↗

PubMed2002

EMG discharge patterns during human grip movement are task-dependent and not modulated by muscle contraction modes: a transcranial magnetic stimulation (TMS) study.

Our previous study revealed that, during tonic muscle contraction, remarkable functional differences among intrinsic and extrinsic muscles were observed during two different grip movements, i.e., precision and power grips. To verify whether this evidence is true even under the phasic muscle contraction, magnetic stimulation was delivered over the left scalp while a normal human subject performed phasic precision or power grip responses of the right-hand fingers in a simple reaction time (SRT) paradigm. Magnetic stimulation delivered during the latent period revealed different cortico-motoneuronal excitations between the two grip responses. In particular, the contributions of extensor carpi radialis (ECR) muscle were definitely different between the two grip responses, although motor-evoked potentials (MEPs) of first dorsal interosseous (FDI) prior to, and after EMG onset of movement initiation, were not different. These results were similar to previous results obtained during tonic muscle contraction. Thus, we have concluded that the task-dependent EMG discharge pattern in finger manipulation could not be modulated by muscle contraction modes.

Action Potentials↗

PubMed2003

Changes in segmental and motor cortical output with contralateral muscle contractions and altered sensory inputs in humans.

Motor or sensory activity in one arm can affect the other arm. We tested the hypothesis that a voluntary contraction can affect the motor pathway to the contralateral homologous muscle and investigated whether alterations in sensory input might mediate such effects. Responses to transcranial magnetic stimulation [motor-evoked potentials (MEPs)], stimulation of the descending tracts [cervicomedullary MEPs (CMEPs)], and peripheral nerve stimulation (H-reflex) were recorded from the relaxed right flexor carpi radialis (FCR), while the left arm underwent unilateral interventions (5 s duration) that included voluntary contraction, muscle contraction evoked through percutaneous stimulation, tendon vibration, and cutaneous and mixed nerve stimulation. During moderate to strong voluntary wrist flexion on the left, MEPs in the right FCR increased, CMEPs were unaffected, and the H-reflex was depressed. These results are consistent with an increase in excitability of the motor cortex, no effect on the motoneuron pool, and presynaptic inhibition of Ia afferents. In contrast, percutaneous muscle stimulation facilitated both MEPs and the H-reflex. However, muscle contraction produced by a combination of voluntary effort and electrical stimulation also reduced the contralateral H-reflex. After voluntary contractions, the H-reflex remained depressed for 35 s, but after stimulation-evoked contractions, it rapidly returned to baseline. Under both conditions, MEPs recovered rapidly. After voluntary contractions, CMEPs were also depressed for approximately 10 s despite their lack of change during contractions. Wrist tendon vibration (100 Hz) did not affect, and 20-Hz median nerve stimulation or forearm medial cutaneous nerve stimulation mildly facilitated, the H-reflex without affecting MEPs. Voluntary wrist extension, similarly to wrist flexion, increased MEPs and depressed H-reflexes. However, ankle dorsiflexion facilitated the H-reflex akin to the Jendrassik maneuver. These data suggest that a unilateral voluntary muscle contraction has contralateral effects at both cortical and segmental levels and that the segmental effects are not replicated by stimulated muscle contraction or by input from muscle spindles or non-nociceptive cutaneous afferents.

Adult↗

PubMed1991

Electromyographic basis of inaccurate movement; its dependence upon the mode of muscle contraction.

The electromyographic basis of inaccurate performance was investigated in two rapid precision-grip skills controlled by concentric and eccentric muscle contractions respectively. Surface electromyograms, recorded from the first dorsal interosseous (DI), adductor pollicis (AP) and abductor pollicis brevis, were utilised to identify changes in the timing and intensity of muscle activation which may be responsible for inaccurate performance. The results showed that when fast precision-grip skills were controlled by concentric DI and AP muscle contraction, variations in the intensity of muscle contraction were responsible for inaccurate performance. However, when these skills were controlled by eccentric DI and AP muscle contractions, inaccurate performance resulted from variations in the timing of muscle activation. It was concluded that the nature of the deficiency in the patterns of muscle activation resulting in inaccurate performance was dependent upon the type of muscle contraction used in the skill.

Adult↗

PubMed1992

[Effects of pH on vascular smooth muscle contraction].

Effects of pH on vascular smooth muscle contractility were reviewed. Basic effect of acidosis seems to be the inhibition of K channels and L-type Ca channels. Inhibition of K channels results in a membrane depolarization, opening of L-type Ca channels, increase in Ca influx and muscle contraction. Inhibition of Ca channels results in an opposit effect. Thus, the effect of acidosis is determined by the relative potency of these two contradictory effects. This may be the reason why acidosis induces contraction in polarized muscle whereas it slightly inhibits contraction in depolarized muscle. In addition, measurements of cytosolic Ca level simultaneously with muscle tension suggest that acidosis increases Ca sensitivity of contractile elements, and this effect also helps acidosis to induce contraction in vascular smooth muscle.

Animals↗

PubMed1984

Sites in the rabbit flocculus specifically related to eye blinking and neck muscle contraction.

In alert rabbits, the cerebellar flocculus was mapped for effects of local stimuli delivered through glass microelectrodes. Triple-barreled glass microelectrodes were used, each barrel of which was filled with solution containing one of three different dyes (Fast Green FCF, Pontamine Sky Blue and Nigrosine) for differentially labeling the sites exhibiting different stimulus effects. In addition to eye movements reported earlier, eye blinking and contraction of dorsal neck muscles were elicited from limited areas of the flocculus. Eye blinking sites were concentrated rostroventrally and neck muscle contraction sites caudoventrally within the flocculus. The present results suggest that the rabbit flocculus contains specific sites devoted to the control of eye blinking and neck posture.

Animals↗

PubMed1992

Studies on the mechanism of 5-HT1 receptor-induced smooth muscle contraction in dog saphenous vein.

1. We have investigated the mechanism of smooth muscle contraction evoked by activation of 5-HT1-like receptors in dog isolated saphenous vein. 2. In the presence of the 5-HT2 receptor antagonist, ritanserin (0.1 microM), concentration-effect curves (10 nM-300 microM) for 5-hydroxytryptamine (5-HT)-induced smooth muscle contraction were biphasic. This could be attributed to a direct action on 5-HT1-like receptors at low concentrations of 5-HT (10 nM-10 microM) and an indirect (through the release of noradrenaline from sympathetic neurones) activation of postjunctional alpha-adrenoceptors at higher 5-HT concentrations. In contrast, concentration-effect curves (100 nM-100 microM) for sumatriptan-induced contractions were not biphasic, and were due solely to activation of 5-HT1-like receptors. 3. Smooth muscle contractions evoked either by low concentrations of 5-HT or by sumatriptan were abolished by removal of extracellular calcium and were markedly inhibited, but not abolished, by the calcium channel blocker, verapamil (1-30 microM). In contrast, contractions evoked by high concentrations of 5-HT were markedly less sensitive to removal of extracellular calcium or to verapamil. 4. 5-HT and sumatriptan also inhibited (to a maximum of about 50%) prostaglandin E2 (PGE2, 5 microM)-stimulated adenosine 3':5'-cyclic monophosphate (cyclic AMP) formation. This effect was mimicked by the alpha 2-adrenoceptor agonist, azepexole (B-HT933) but not by the alpha 1-adrenoceptor agonist, methoxamine.5. In contrast to mediation of smooth muscle contraction, the 5-HT1-like receptor-mediated inhibition of PGE2-stimulated cyclic AMP formation evoked by 5-HT or sumatriptan was not attenuated by removal of extracellular calcium or by verapamil (1 microM).6. A directly-acting inhibitor of adenylyl cyclase, 2',3'-dideoxyadenosine (1 mM) inhibited PGE2-stimulated cyclic AMP formation but did not produce smooth muscle contraction.7. These results suggest that contractile responses of dog isolated saphenous vein arising through activation of 5-HT1-like receptors are associated with both an influx of extracellular calcium ions (to a large extent via voltage-dependent channels) and an inhibition of adenylyl cyclase. However, although these two responses are coupled to the same receptor, they appear to be independent.

Adenylyl Cyclase Inhibitors↗

PubMed2000

Low-temperature modification of the inhibitory effects of volatile anesthetics on airway smooth muscle contraction in dogs.

BACKGROUND: Because exposure to low temperature can modify the effect of volatile anesthetics on airway smooth muscle contraction, this study was conducted to investigate low-temperature modifications of the inhibitory effects of isoflurane and sevoflurane on canine tracheal smooth muscle tone by simultaneously measuring the muscle tension and intracellular concentration of Ca2+ ([Ca2+]i) and by measuring voltage-dependent Ca2+ channel activity. METHODS: [Ca2+]i was monitored by the 500-nm light emission ratio of preloaded fura-2, a Ca2+ indicator. Isometric tension was measured simultaneously. Whole cell patch clamp recording techniques were used to observe voltage-dependent Ca2+ channel activity in dispersed muscle cells. Isoflurane (0-3.0%) or sevoflurane (0-3%) was introduced to a bath solution at various temperatures (37, 34, or 31 degrees C). RESULTS: Low temperature (34 or 31 degrees C) reduced high-K+-induced (72.7 mm) muscle contraction and increased [Ca2+]i, but it enhanced carbachol-induced (1 microm) muscle contraction with a decrease in [Ca2+]i. The volatile anesthetics tested showed significant inhibition of both high-K+-induced and carbachol-induced airway smooth muscle contraction, with a concomitant decrease in [Ca2+]i. The inhibition of the carbachol-induced muscle contraction by volatile anesthetics was abolished partially by exposure to low temperature. Volatile anesthetics and low-temperature exposure significantly inhibited voltage-dependent Ca2+ channel activity of the smooth muscle. CONCLUSIONS: Exposure of airway smooth muscle to low temperature leads to an increase in agonist-induced muscle contractility, with a decrease in [Ca2+]i. The inhibition of voltage-dependent Ca2+ channel activity by exposure to low temperature and by volatile anesthetics cam be attributed, at least in part, to the decrease in [Ca2+]i.

Anesthetics, Inhalation↗

PubMed1990

Sonographic imaging of muscle contraction and fasciculations: a correlation with electromyography.

Precise quantitation of fasciculations with EMG is difficult because of their random location and discharge frequency in muscle. We studied the clinical value of real-time ultrasound in the study of normal voluntary muscle contraction and in the identification of fasciculations in 22 patients. Sonography effectively imaged fasciculations, demonstrating them in both resting and actively contracting extremity muscles and in less accessible muscles such as the tongue. In two instances ultrasound identified fasciculations not apparent on EMG. Analysis of the video images generated quantitative data on fasciculation duration (averaging 500 msec), size, and location and provided unique insight into the process of normal muscle contraction and motor unit physiology.

Electromyography↗

PubMed2004

Effects of muscle contraction on somatosensory event-related EEG power and coherence changes.

Effects of isometric muscle contraction on amplitude and coherence changes of EEG rhythms during repetitive cutaneous electrical stimulation were analyzed in 10 right-handed subjects. Subjects received electrical stimuli at intensity above pain threshold to their right middle finger while either squeezing a rubber tube with the right index finger and thumb, or keeping their ipsilateral hand muscles relaxed. EEG was recorded using 111 closely spaced electrodes. Somatosensory stimuli were followed by reduction of the relative 8-12 and 16-24 Hz band power (at 0.2-0.4 s) in bilateral primary sensorimotor cortices (S1/M1) and medial frontal cortex, and by a subsequent increase in 16-24 Hz band power (at 0.9 s). Isometric muscle contraction strongly suppressed these band power changes. The 8-12 and 16-24 Hz mean coherence in a wide region surrounding the contralateral S1/M1 and in the medial frontal cortex showed an initial decrease, partially paralleling band power changes, and later an increase. Ipsilateral S1/M1 showed a decrease in 8-12 Hz coupling only with the central and frontal electrodes of the same hemisphere. Muscle contraction reduced all coherence changes, but enhanced the 8-12 Hz coherence between ipsilateral S1/M1 and posterior parietal cortex. Early post-stimulus decrease of oscillatory coupling between S1/M1 and premotor cortex and between S1/M1 and medial frontal cortex suggests that these cortical regions act rather independently during processing of somatosensory information, and synchronize only later when the band power in contralateral S1/M1 increases. Motor cortex activation associated with ipsilateral hand muscle contraction interferes with cortical processing of somatosensory stimuli in S1/M1 cortices.

Adult↗

PubMedDate not supplied

Theoretical study of the effects of vascular smooth muscle contraction on strain and stress distributions in arteries.

To study the effects of smooth muscle contraction and relaxation on the strain and stress distribution in the vascular wall, a mathematical model was proposed. The artery was assumed to be a thick-walled orthotropic tube made of nonlinear, incompressible elastic material. Considering that the contraction of smooth muscle generates an active circumferential stress in the wall, a numerical study was performed using data available in the literature. The results obtained showed that smooth muscle contraction affects the residual strains which exist in a ring segment cut out from the artery and exposed to no external load. When the ring specimen is cut radially, it springs open with an opening angle. The predicted monotonic increase of the opening angle with increasing muscular tone was in agreement with recent experimental results reported in the literature. It was shown that basal muscular tone, which exists under physiological conditions, reduces the strain gradient in the arterial wall and yields a near uniform stress distribution. During temporary changes in blood pressure, the increase in muscular tone induced by elevated pressure tends to restore the distribution of circumferential strain in the arterial wall, and to maintain the flow-induced wall shear stress to normal level.

Animals↗

PubMed1998

Extracellular glutamate increases in rostral ventrolateral medulla during static muscle contraction.

The ventrolateral medulla is an important site involved in increases in arterial pressure and heart rate during static muscle contraction. Glutamate, an excitatory amino acid neurotransmitter, appears to play a role in mediating these responses. We measured glutamate concentration in the extracellular fluid of the rostral ventrolateral medulla during static muscle contraction in anesthetized rats. A 2-min tibial nerve stimulation-evoked muscle contraction increased blood pressure by 30 +/- 4 mmHg and heart rate by 32 +/- 4 bpm. Extracellular glutamate in the rostral ventrolateral medulla also increased from 9 +/- 1 pmol/4 microl to 14 +/- 1 pmol/4 microl. Results were repeatable over two subsequent contractions. Tibial nerve stimulation following neuromuscular blockade did not elicit changes in blood pressure, heart rate or extracellular fluid glutamate. Data demonstrate that muscle contraction increases extracellular fluid concentration of glutamate in the rostral ventrolateral medulla, suggesting that rostral ventrolateral medullary glutamate release is a neurochemical change associated with cardiovascular responses during static muscle contraction.

Animals↗

PubMed1994

Caldesmon and calponin phosphorylation in regulation of smooth muscle contraction.

Recent studies of the smooth muscle contractile system indicate that Ca(2+)-dependent phosphorylation of the 20-kDa myosin light chains, modulation of phosphoprotein phosphatases, and phosphorylation of thin-filament proteins are all potential features of contractile system regulation. The thin-filament proteins caldesmon and calponin are known to inhibit actomyosin ATPase in vitro and actin sliding velocity in the in vitro motility assay. Inhibition of actomyosin ATPase is relieved by phosphorylation of caldesmon or calponin. The notion that caldesmon and calponin phosphorylation-dephosphorylation is important in the living smooth muscle cell was tested using canine tracheal smooth muscle strips labeled with 32P. We found that both caldesmon and calponin phosphorylation increased in response to stimulation with carbachol. Carbachol induced a biphasic increase in [Ca2+]i in canine tracheal smooth muscle, an early transient increase in myosin phosphorylation, which decayed to 0.4 mol Pi/mol light chain, and a rapid transient increase in tissue shortening velocity. Relative changes in caldesmon phosphorylation correlate best with force development and the [Ca2+]i transient, both of which follow a similar time course. Calponin phosphorylation appears to be a rapid transient event more similar to the transient increase in unloaded shortening velocity. Our results are consistent with a potential role for both caldesmon and calponin phosphorylation in regulating smooth muscle contraction.

Animals↗

PubMed1986

Desensitization of aortic smooth muscle contraction in rats harboring pheochromocytoma.

Desensitization of smooth muscle contraction was studied in aortic ring segments obtained from New England Deaconness Hospital rats harboring pheochromocytomas, a norepinephrine-secreting tumor. Rats were studied 5 to 6 weeks after implantation of the pheochromocytoma, by which time severe hypertension had developed. Aortic ring segments from the pheochromocytoma rats were significantly less sensitive to the alpha-1 adrenergic agonist phenylephrine [log10 (ED50) = -7.21 +/- 0.09 vs. -7.63 +/- 0.11 in controls). In addition, the maximal force of contraction induced by phenylephrine was decreased in the aortas from pheochromocytoma rats (1.31 +/- 0.15 g) compared to controls (2.17 +/- 0.23 g). The potency of the thromboxane A2 receptor agonist U-46,619 was decreased in the aortic ring segments from pheochromocytoma rats compared to controls, although it elicited a similar maximal force of contraction. Desensitization of alpha receptor-mediated contraction was prevented by treating the pheochromocytoma-bearing rats with the reversible alpha adrenergic antagonist phentolamine (200 micrograms/kg/hr) via osmotic minipumps for 2 weeks. However, phentolamine did not decrease the hypertension in these rats. Also, large doses of the irreversible alpha adrenergic antagonist phenoxybenzamine (4 mg/kg/day i.p.) did not decrease blood pressure in rats harboring pheochromocytoma or did the drug completely block aortic alpha receptors in these rats as it did in controls. The results indicate that pheochromocytoma induces heterologous desensitization of smooth muscle contraction in rat aorta. The desensitization is due to direct effects of catecholamines unrelated to hypertension. The New England Deaconess Hospital rat harboring pheochromocytoma is an interesting model to study the effects of high concentrations of plasma catecholamines on smooth muscle contraction.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗