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At least 343 records · Page 19Linked to original sources

PubMed1986

Control of respiration by the hypothalamus and by feedback from contracting muscles in cats.

Central command and feedback from contracting muscles are two mechanisms which are thought to control the respiratory and cardiovascular systems during exercise. In this study, we compared the individual and combined responses to activation of central command and to muscular contraction in anesthetized cats. Continuous electrical stimulation of the subthalamic locomotor region (STLR) was used to simulate central command (Eldridge et al., 1985). Static (tetanic) contraction of hindlimb muscles was produced by stimulating the cut peripheral ends of the L7-S1 ventral roots. Despite similar increases in arterial pressure, STLR stimulation caused larger increases in cardiac frequency and respiration than that evoked by muscular contraction. When performed during muscular contraction, STLR still caused large increases in respiration, arterial pressure and cardiac frequency. In contrast, muscular contraction when induced during STLR stimulation caused only small increases in respiration and modest changes in arterial pressure and cardiac frequency. These results suggest that central command and feedback from contracting muscles exert different respiratory and cardiovascular effects when activated simultaneously than when activated individually. In addition, central command, as activated by STLR stimulation, predominates over the responses caused by muscular contraction.

Animals↗

PubMed2002

Esophageal striated muscle contractions in patients with Chagas' disease and idiopathic achalasia.

Chagas' disease causes degeneration and reduction of the number of intrinsic neurons of the esophageal myenteric plexus, with consequent absent or partial lower esophageal sphincter relaxation and loss of peristalsis in the esophageal body. The impairment of esophageal motility is seen mainly in the distal smooth muscle region. There is no study about esophageal striated muscle contractions in the disease. In 81 patients with heartburn (44 with esophagitis) taken as controls, 51 patients with Chagas' disease (21 with esophageal dilatation) and 18 patients with idiopathic achalasia (11 with esophageal dilatation) we studied the amplitude, duration and area under the curve of esophageal proximal contractions. Using the manometric method and a continuous perfusion system we measured the esophageal striated muscle contractions 2 to 3 cm below the upper esophageal sphincter after swallows of a 5-ml bolus of water. There was no significant difference in striated muscle contractions between patients with heartburn and esophagitis and patients with heartburn without esophagitis. There was also no significant difference between patients with heartburn younger or older than 50 years or between men and women or in esophageal striated muscle contractions between patients with heartburn and Chagas' disease. The esophageal proximal amplitude of contractions was lower in patients with idiopathic achalasia than in patients with heartburn. In patients with Chagas' disease there was no significant difference between patients with esophageal dilatation and patients with normal esophageal diameter. Esophageal striated muscle contractions in patients with Chagas' disease have the same amplitude and duration as seen in patients with heartburn. Patients with idiopathic achalasia have a lower amplitude of contraction than patients with heartburn.

Adolescent↗

PubMed1994

G-proteins in alpha 1-adrenoceptor mediated prostatic smooth muscle contraction.

The role of signal transducing guanine-nucleotide binding proteins (G-proteins) in alpha 1-receptor mediated smooth muscle contractions was investigated in human hyperplastic prostatic tissue. The selective alpha 1-receptor agonist phenylephrine (PE) evoked dose dependent contractions antagonized by the alpha 1-receptor blockers prazosin (EC50 10 nM) and YM617 (EC50 3 nM). Application of nifedipine (1-10,000 nM), a blocker of voltage-dependent L-type Ca(2+)-channels (VDCC), inhibited the PE evoked contraction up to 65.4%. Pretreating the tissue strips with pertussis toxin (PTX, exotoxin from Bordetella pertussis; 5-25 micrograms/ml), inactivating a subpopulation of G-proteins, inhibited the PE induced contractions up to 73.9%. PTX pretreatment had no effect on contractions elicited by 125 mM K+. Application of nifedipine to PTX pretreated tissue led to an additional inhibition of 13.7%. Our findings demonstrate the involvement of PTX-sensitive G-proteins in the signal transduction pathway of alpha 1-receptor induced contractions of prostatic smooth muscle. The remaining contractility of PTX pretreated tissue suggests additional participation of PTX insensitive mechanisms in alpha 1-receptor mediated prostatic smooth muscle contractions.

Adrenergic alpha-Antagonists↗

PubMed2002

In vivo electrophysiological responses of pedunculopontine neurons to static muscle contraction.

The pedunculopontine nucleus (PPN) has previously been implicated in central command regulation of the cardiorespiratory adjustments that accompany exercise. The current study was executed to begin to address the potential role of the PPN in the regulation of cardiorespiratory adjustments evoked by muscle contraction. Extracellular single-unit recording was employed to document the responses of PPN neurons during static muscle contraction. Sixty-four percent (20/31) of neurons sampled from the PPN responded to static muscle contraction with increases in firing rate. Furthermore, muscle contraction-responsive neurons in the PPN were unresponsive to brief periods of hypotension but were markedly activated during chemical disinhibition of the caudal hypothalamus. A separate sample of PPN neurons was found to be moderately activated during systemic hypoxia. Chemical disinhibition of the PPN was found to markedly increase respiratory drive. These findings suggest that the PPN may be involved in modulating respiratory adjustments that accompany muscle contraction and that PPN neurons may have the capacity to synthesize muscle reflex and central command influences.

Anesthesia↗

PubMed1994

Latency of skeletal muscle contraction after pulse train stimulation: an important factor in correct timing of skeletal muscle cardiac assist devices.

Various configurations of conditioned skeletal muscle are under investigation for cardiac assistance in patients with end-stage cardiac failure. Optimal timing of conditioned skeletal muscle contraction is essential for effective cardiac augmentation. However, unlike mechanical methods of assistance, skeletal muscle requires time to develop peak tension. We measured "time to 50% peak tension" and "time to 90% peak tension" using an electrical strain gauge in 12 canine latissimus dorsi muscles (6 untrained controls and 6 trained with 3 months of electrical stimulation at 25 Hz with a 15% duty cycle). The "time to 50% relaxation" and the "time to 90% relaxation" after discontinuation of the stimulus were also measured. Conditioned skeletal muscle required significantly more time to develop peak tension than unconditioned skeletal muscle. Relaxation was also significantly prolonged in conditioned muscle. Notably, conditioned lattisimus needed, on average, 0.35 sec to develop peak tension and 0.20 sec for 90% relaxation. Thus, 0.55 sec of each muscle contraction/relaxation cycle was devoted to development of peak tension and subsequent relaxation. At normal canine heart rates of approximately 120 beats per minute (0.50 sec per cardiac cycle), conditioned skeletal muscle may take up to 70% of each cardiac cycle (0.35 sec) to develop 90% of peak tension. The recognition of this phenomenon in conditioned skeletal muscle is important for effective contraction timing of both human and animal skeletal muscle assist devices. Development of proper conditioning regimens for such devices may benefit from identification of those training parameters which produce a minimal "time to peak tension."

Animals↗

PubMed1976

Cyclic nucleotide levels during carbachol-induced smooth muscle contractions.

Cyclic nucleotide levels and tension were measured at various times during carbachol-induced smooth muscle contractions. Cyclic GMP levels were markedly increased during contractions of rat vas deferens, guinea pig myometrium and guinea pig taenia coli, but were unchanged during contractions of rat uterus or guinea pig ileum. No significant changes in cyclic GMP levels could be detected in estrogen-primed rat uteri at any of the times or drug concentrations studied. Even in tissues in which large increases in cyclic GMP levels could be detected during carbachol-induced contractions (i.e. guinea pig myometrium and taenia coli) the contractions appeared to precede the cyclic GMP increases by several seconds. No significant changes in cyclic AMP levels were observed during carbachol-induced contractions in any of the smooth muscles studied. Thus, changes in tissue levels of the cyclic nucleotides do not appear to be responsible for the initiation of carbachol-induced smooth muscle contractions.

Animals↗

PubMed2004

Ca2+ and AMPK both mediate stimulation of glucose transport by muscle contractions.

It is now generally accepted that activation of AMP-activated protein kinase (AMPK) is involved in the stimulation of glucose transport by muscle contractions. However, earlier studies provided evidence that increases in cytosolic Ca(2+) mediate the effect of muscle contractions on glucose transport. The purpose of this study was to test the hypothesis that both the increase in cytosolic Ca(2+) and the activation of AMPK are involved in the stimulation of glucose transport by muscle contractions. Caffeine causes release of Ca(2+) from the sarcoplasmic reticulum. Incubation of rat epitrochlearis muscles with a concentration of caffeine that raises cytosolic Ca(2+) to levels too low to cause contraction resulted in an approximate threefold increase in glucose transport. Caffeine treatment also resulted in increased phosphorylation of calmodulin-dependent protein kinase (CAMK)-II in epitrochlearis muscle. The stimulation of glucose transport by caffeine was blocked by the Ca(2+)-CAMK inhibitors KN62 and KN93. Activation of AMPK with 5-aminoimidazole-4-carboxamide ribonucleoside (AICAR) also resulted in an approximate threefold increase in glucose transport in the epitrochlearis. The increases in glucose transport induced by AICAR and caffeine were additive, and their combined effect was not significantly different from that induced by maximally effective contractile activity. KN62 and KN93 caused an approximately 50% inhibition of the stimulation of glucose transport by contractile activity. Our results provide evidence that both Ca(2+) and AMPK are involved in the stimulation of glucose transport by muscle contractions. They also suggest that the stimulation of glucose transport by Ca(2+) involves activation of CAMK.

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

PubMed1998

Evidence for the essential role of myosin subfragment-2 in the ATP-dependent actin-myosin sliding in muscle contraction.

The role of myosin subfragment-2 (myosin S-2) in muscle contraction was studied by using an in vitro motility assay system in which the ATP-dependent sliding between myosin-coated polystyrene beads and actin filament arrays (actin cables) of giant algal cells were recorded under constant external loads provided with a centrifuge microscope. With antibody to myosin S-2 below 0.3 mg/ml, the maximum "isometric" force generated by myosin molecules on the bead decreased markedly, but the unloaded bead-sliding velocity along actin cables did not change appreciably, indicating a decrease in the number of myosin molecules interacting with actin cables. The antibody at 0.3-1.5 mg/ml decreased not only the maximum isometric force, but also the unloaded bead-sliding velocity in a dose-dependent manner. With the antibody at 1.5-3 mg/ml, the beads eventually stopped moving to remain attached to actin cables. These beads could be readily detached from actin cables with very small centrifugal forces, indicating very weak actin-myosin linkages. The antibody had no effect on rigor actin-myosin linkages formed before the antibody application. These results are consistent with the view that myosin S-2 plays an essential role in muscle contraction.

Actins↗

PubMed2006

Effects of pelvic floor muscle contraction on anal canal pressure.

The role of pelvic floor muscle contraction in the genesis of anal canal pressure is not clear. Recent studies have suggested that vaginal distension increases pelvic floor muscle contraction. We studied the effects of vaginal distension on anal canal pressure in 15 nullipara asymptomatic women. Anal pressure, rest, and squeeze were measured using station pull-through manometry techniques with no vaginal probe, a 10-mm vaginal probe, and a 25-mm vaginal probe in place. Rest and squeeze vaginal pressures were significantly higher when measured with the 25-mm probe compared with the 10-mm probe, suggesting that vaginal distension enhances pelvic floor contraction. In the presence of the 25-mm vaginal probe, rest and squeeze anal pressures in the proximal part of the anal canal were significantly higher compared with no vaginal probe or the 10-mm vaginal probe. On the other hand, distal anal pressures were not affected by any of the vaginal probes. Ultrasound imaging of the pelvic floor revealed that vaginal distension increased the anterior-posterior length of the puborectalis muscle. Atropine at 15 micro g/kg had no influence on the rest and squeeze anal pressures with or without vaginal distension. Our data suggest that pelvic floor contractions increase pressures in the proximal part of the anal canal, which is anatomically surrounded by the puborectalis muscle. We propose that pelvic floor contraction plays an important role in the fecal continence mechanism by increasing anal canal pressure.

Adult↗

PubMed1990

Cardiovascular response to sustained maximal voluntary static muscle contraction.

The cardiovascular response to maximal, voluntary, sustained 2-min static contraction by three different muscle groups (right hand finger flexors [RHF], right leg extensors [RLE], and both leg extensors [BLE]) was studied in young adult males (N = 13) and females (N = 14). Systolic blood pressure (SBP), diastolic blood pressure (DBP), and heart rate (HR) were recorded at 30 s intervals prior to, during, and after exercise. Mean arterial blood pressure (MABP) and pulse pressure (PP) were computed from SBP and DBP. The force of muscle contraction was monitored continuously throughout the 2-min task. Data were analyzed by MANOVA. The results showed that impulse (force x time) declined significantly throughout exercise, and there were significant differences in impulse among muscle groups. SBP, DBP, PP, and MABP increased significantly throughout the 2-min contraction period, while heart rate increased initially and then leveled off. The magnitudes of the blood pressure and HR responses were related to the muscles involved: BLE greater than RLE greater than RHF. Blood pressures during rest and exercise were significantly lower for females than for males, but there was no sex effect for heart rate. These findings suggest that blood pressure increases throughout sustained static muscular contractions despite significant reductions in force production. Heart rate, on the other hand, does not increase throughout exercise under these conditions. It appears that heart rate and blood pressure responses to sustained static contraction are mediated by different mechanisms, but these mechanisms are similar for males and females.

Adolescent↗

PubMed1999

Effects of thermal acclimation on nervous conduction and muscle contraction in the frog Rana temporaria.

The effects of season and acclimation temperature on the latency of the leg withdrawal reflex and three of its components have been studied: conduction velocity in the sciatic nerve, spinal conduction time, and contraction time of gastrocnemius muscle. The latency of the leg withdrawal reflex was markedly shortened by cold acclimation: the reaction times were at 6 degrees C 1.54 s in 4 degrees C acclimated and 3.97 s in 24 degrees C acclimated winter frogs. Also, the temperature dependence of the reflex latency was reduced by cold acclimation. Thus, frogs acclimated to cold responded to external stimuli in cold more rapidly than warm-acclimated ones. This cold adaptation of the reflex could not be explained by changes in its studied components. These made up only one-tenth of the reflex response time, and either did not show significant cold acclimation (muscle contraction and spinal conduction times in summer) or showed inverse acclimation, especially when measured at high temperatures (i.e. conduction velocities were reduced by acclimation to cold). Thus, the cold acclimation of the reflex response probably resides in the sensory component of the response. The inverse temperature adaptation response of conduction velocities may reflect a reduced ion permeability across cellular membranes in cold which decreases metabolic energy expenditure during inactive periods.

Adaptation, Physiological↗

PubMed1988

Differences in regulatory mechanisms of atrial and ventricular muscle contraction in bovine heart.

The purpose of this study was to characterize the regulatory mechanisms of atrial muscle contraction. Natural actomyosin (NAM) and tropomyosin-troponin (TM-TN) complex were prepared from atrial and ventricular muscle of the same bovine heart. The results were as follows: (1) Atrial NAM was more sensitive to Ca2+ than was ventricular NAM: the pCa required for 50% ATPase activation was 5.96 +/- 0.10 vs. 5.63 +/- 0.07, (mean +/- SE; n = 6; p less than 0.01); (2) reconstitution of desensitized actomyosin of rabbit skeletal muscle plus atrial or ventricular TM-TN complex produced higher Ca2+ sensitivity in atrial muscle than in ventricular muscle: the pCa required for 50% ATPase activation was 6.48 +/- 0.10 vs. 6.23 +/- 0.15 (n = 3; p less than 0.05); (3) the amount of inorganic phosphate covalently bound to atrial NAM was equivalent to that bound to ventricular NAM; (4) SDS-polyacrylamide gel electrophoresis of the two NAMs revealed several protein bands of different mobility from 16,000 to 30,000 daltons; and (5) the superprecipitation response of atrial NAM was characterized by a stepwise change in turbidity after the addition of MgATP, in contrast to the biphasic pattern of ventricular NAM. These data suggest that the free Ca ion concentration required for atrial muscle contraction is lower than that required for ventricular muscle contraction and that the difference is attributable to differences in atrial and ventricular regulatory proteins.

Actomyosin↗

PubMed2005

Barakol suppresses norepinephrine-induced inhibition of spontaneous longitudinal smooth muscle contractions in isolated rat small intestine.

The present study aimed to investigate the purgative effects of barakol, the purified extract of Cassia siamea Lam., on the longitudinal smooth muscle contractions of the rat ileum. The extract increased the force of spontaneous muscle contractions in a concentration-dependent manner (EC50=0.3 mM). Saxitoxin (0.3 microM) abolished the stimulatory effects of barakol, a result indicating a neural mechanism of action. In addition, atropine (10 microM) but not propanolol (10 microM) or phentolamine (10 microM), partially inhibited barakol-induced smooth muscle contractions suggesting that cholinergic nerves were involved. The motor effects of barakol were further examined in muscle strips treated with catecholamines to suppress spontaneous contractile activity and decrease muscle tone. Norepinephrine or dopamine (10 microM) decreased the amplitude of spontaneous contractions by 72% and 18%, respectively. Pretreatment of the tissues with barakol (1 mM) significantly decreased the inhibitory effect of norepinephrine by 60%, but not that of dopamine. Its ability to potentiate atropine- and saxitoxin-sensitive contractions and inhibit the antimotility actions of norepinephrine suggests that barakol may increase longitudinal smooth muscle contractions by decreasing the inhibitory effect of norepinephrine on excitatory cholinergic motor neurons. Barakol may produce a purgative action in small intestine which may be clinically important in patients with intestinal hypomotility disorders.

Animals↗

PubMed1987

The mechanism of muscle contraction. Biochemical, mechanical, and structural approaches to elucidate cross-bridge action in muscle.

Muscle contraction occurs when the thin actin and thick myosin filaments slide past each other. It is generally assumed that this process is driven by cross-bridges which extend from the myosin filaments and cyclically interact with the actin filaments as ATP is hydrolysed. Current biochemical studies suggest that the myosin cross-bridge exists in two main conformations. In one conformation, which occurs in the absence of MgATP, the cross-bridge binds very tightly to actin and detaches very slowly. When all the cross-bridges are bound in this way, the muscle is in rigor and extremely resistant to stretch. The second conformation is induced by the binding of MgATP. In this conformation the cross-bridge binds weakly to actin and attaches and detaches so rapidly that it can slip from actin site to actin site, offering very little resistance to stretch. During ATP hydrolysis by isolated actin and myosin in solution, the cross-bridge cycles back and forth between the weak-binding and strong-binding conformations. Assuming a close correlation between the behaviour of isolated proteins in solution and the cross-bridge action in muscle, Eisenberg and Greene have developed a model for cross-bridge action where, in the fixed filament lattice in muscle, the transition from the weak-binding to the strong-binding conformation causes the elastic cross-bridge to become deformed and exert a positive force, while the transition back to the weak-binding conformation upon binding of MgATP, causes deformation which, during fibre shortening, leads to rapid detachment of the cross-bridge and its re-attachment to a new actin site. From the results of in vitro experiments, it was furthermore suggested that relaxation occurs when the transition from the weak-binding to the strong-binding conformation is blocked. Results of recent mechanical and X-ray diffraction experiments on skinned fibre preparations are consistent with the assumed close correlation between the behaviour of isolated proteins in solution and the behaviour of cross-bridges in muscle. Furthermore, X-ray diffraction experiments allowed to provide experimental evidence for the postulated structural difference between attached weak-binding and attached strong-binding cross-bridges. Finally, recent studies have confirmed the prediction of Eisenberg and Greene that the rate limiting step in vitro determines the rate of force generation in muscle.

Actins↗

PubMed1987

Effects of cholinergic drugs on muscle contraction in Moniliformis moniliformis (Acanthocephala).

In whole Moniliformis moniliformis spontaneous muscle contractions were rhythmic; longitudinal contractions were measured with a force transducer. The cholinergic agonists levamisole and nicotine significantly increased muscle tension in whole worms; these contractions were tonic and were antagonised by the ganglionic blocker pentolinium and by piperazine. In addition, levamisole-induced contractions were inhibited by gallamine, hexamethonium, and norepinephrine. In worm segments, where drugs in solution were injected through the worms, acetylcholine (ACh) and nicotinic agonists were effective in causing contractions, whereas muscarinic agonists in concentrations up to 1 mM had no effect. Although muscle contraction in M. moniliformis was induced by nicotinic agonists, these contractions were effectively antagonised by a range of chemicals that block ganglionic, skeletal, and muscarinic sites in vertebrates. The presence of ACh in M. moniliformis and the effects of nicotinic agonists on muscle contraction suggest that ACh is a putative excitatory neurotransmitter.

Acanthocephala↗

PubMed2002

Delay in initiation and termination of muscle contraction, motor impairment, and physical disability in upper limb hemiparesis.

The purpose of this study was to describe the relationship between the delay in initiation and termination of muscle contraction and clinical measures of motor impairment and physical disability in the affected upper limb of patients with hemiparesis. Electromyographic (EMG) activity of 26 long-term survivors of stroke was recorded during isometric wrist flexion and extension. Upper limb motor impairment and disability were assessed with the Fugl-Meyer motor assessment (FMA) and arm motor ability test (AMAT), respectively. Delay in initiation and termination of muscle contraction was significantly prolonged in the paretic arm. However, the delay was not significantly affected by stroke type, stroke level, side of hemiparesis, or presence of aphasia. Delay in initiation and termination of muscle contraction correlated significantly with FMA and AMAT. Abnormally delayed initiation and termination of muscle contraction may contribute to hemiparetic upper limb motor impairment and physical disability in hemiparetic patients.

Adult↗

PubMed1992

In vivo and in vitro correlation of trachealis muscle contraction in dogs.

Maximal trachealis muscle shortening in vivo was compared with that in vitro in seven anesthetized dogs. In addition, the effect of graded elastic loads on the muscle was evaluated in vitro. In vivo trachealis muscle shortening, as measured using sonomicrometry, revealed maximal active shortening to be 28.8 +/- 11.7% (SD) of initial length. Trachealis muscle preparations from the same animals were studied in vitro to evaluate isometric force generation, isotonic shortening, and the effect of applying linear elastic loads to the trachealis muscle during contraction from optimal length. Maximal isotonic shortening was 66.8 +/- 8.4% of optimal length in vitro. Increasing elastic loads decreased active shortening and velocity of shortening in vitro in a hyperbolic manner. The elastic load required to decrease in vitro shortening to the extent of the shortening observed in vivo was similar to the estimated load provided by the tracheal cartilage. We conclude that decreased active shortening in vivo is primarily due to the elastic afterload provided by cartilage.

Animals↗

PubMed1992

The Caenorhabditis elegans unc-93 gene encodes a putative transmembrane protein that regulates muscle contraction.

unc-93 is one of a set of five interacting genes involved in the regulation or coordination of muscle contraction in Caenorhabditis elegans. Rare altered-function alleles of unc-93 result in sluggish movement and a characteristic "rubber band" uncoordinated phenotype. By contrast, null alleles cause no visibly abnormal phenotype, presumably as a consequence of the functional redundancy of unc-93. To understand better the role of unc-93 in regulating muscle contraction, we have cloned and molecularly characterized this gene. We isolated transposon-insertion alleles and used them to identify the region of DNA encoding the unc-93 protein. Two unc-93 proteins differing at their NH2 termini are potentially encoded by transcripts that differ at their 5' ends. The putative unc-93 proteins are 700 and 705 amino acids in length and have two distinct regions: the NH2 terminal portion of 240 or 245 amino acids is extremely hydrophilic, whereas the rest of the protein has multiple potential membrane-spanning domains. The unc-93 transcripts are low in abundance and the unc-93 gene displays weak codon usage bias, suggesting that the unc-93 protein is relatively rare. The unc-93 protein has no sequence similarity to proteins listed in current data-bases. Thus, unc-93 is likely to encode a novel membrane-associated muscle protein. We discuss possible roles for the unc-93 protein either as a component of an ion transport system involved in excitation-contraction coupling in muscle or in coordinating muscle contraction between muscle cells by affecting the functioning of gap junctions.

Alleles↗