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At least 865 records · Page 48Linked to original sources
PubMed1986

[Inability to establish a single equilibrium value for the angle of a joint and its relation to the hysteretic properties of muscle contraction].

The processes of joint angle setting were studied on the simple experimental model of a joint. The model consisted of gastrocnemius muscles prepared on both hindlimbs of the anesthetized cat. The muscles were tied in antagonistic manner with a rotation-type registrator. Depending on the order of the muscle activation two different values of the joint angle were in the model system. It has been shown that indeterminacy of the equilibrium value of the joint angle was caused by hysteretical properties of the muscle contraction.

Animals↗
PubMed1998

Regulation of second messengers associated with airway smooth muscle contraction and relaxation.

Agonist-receptor interactions regulate airway smooth muscle tone through activation of guanine nucleotide binding proteins (G proteins), which are coupled to second messenger pathways that mediate changes in the tissue's contractile state. With respect to airway smooth muscle (ASM) contraction, receptor activation elicits phosphatidylinositol turnover that results in the formation of the second messengers, 1,2,-diacylglyserol, which activates protein kinase C (PKC), and inositol 1,4,5,-trisphosphate (Ins[1,4,5]P3), which binds to its intracellular receptor to mobilize intracellular calcium (Ca2+). Both the mobilization of Ca2+ and activation PKC play critical roles in initiating and acutely modulating the intensity and duration of the ASM contraction response. In contrast, bronchodilator agonist-mediated receptor activation is typically coupled to an enhanced accumulation of the second messenger, adenosine 3',5'-cyclic monophosphate (cAMP) which, through activation of cAMP-dependent protein kinase, induces the phosphorylation of specific proteins, leading to ASM relaxation. For activation of both of these functionally distinct signal transduction pathways, the agonist-receptor complexes interact with specific G proteins, which in turn modulate the enzymes regulating the production of their respective second messengers. Perturbations in Ins(1,4,5)P3 accumulation, its metabolism and intracellular binding may underlie changes in ASM contractility. Comparably, changes in ASM relaxation responsiveness, secondary to perturbations in cAMP accumulation, may be due to altered receptor/G protein modulation of adenylate cyclase activity, as well as to altered binding of Ins(1,4,5)P3 to its Ca2+-mobilizing intracellular receptor. This review begins with an overview of the structural and functional characteristics of G protein-linked receptors, followed by descriptions of the role of G proteins, their transmembrane signaling processes, and mechanisms regulating second messenger-coupled ASM contraction and relaxation, and concludes with new information underscoring the important roles of altered receptor/G protein-coupled expression and regulatory interactions between signaling pathways in modulating second-messenger accumulation and action in the "pro-asthmatic" sensitized airway smooth muscle.

Binding Sites↗
PubMed1987

Polarization changes in light diffracted from contracting muscle fibers.

Single fibers were isolated from the semitendinosus muscle of frog and illuminated with an He-Ne laser. The polarization of the laser beam was varied by a photoelastic modulator. The time course of the degree of polarization of light diffracted from the muscle fiber during an isometric contraction was measured directly with a time resolution of 1 ms. Tension, sarcomere length, and diffraction intensity were also measured. During the contraction cycle, the degree of polarization of the active fiber exhibited a biphasic variation relative to that of the resting fiber. Analysis identifies the movement of heavy meromyosin toward actin and the rise in myoplasmic calcium ion concentration as the main contributors to the polarization transient of active fibers. A quantitative theory describing the polarized diffraction from muscle fibers is formulated. There is good agreement between the theory and measurements.

Actins↗
PubMed1998

An algorithm for detecting the onset of muscle contraction by EMG signal processing.

The Generalized Likelihood Ratio (GLR) test is proposed for estimating the time instant of muscle contraction onset via electromyographic (EMG) signal processing. In contrast to commonly used threshold-based estimation methods, the proposed algorithm proves to be reasonably accurate even for low levels of EMG activity; the improved behaviour of the GLR test comes with just a modest increase in the computational complexity. A set of computer simulation experiments are presented, where the proposed algorithm and two different threshold-based estimators are studied; also, we discuss the results of analysing the EMG recordings of selected proximal muscles of the upper limb in a hemiparetic subject.

Algorithms↗
PubMed1997

Methods to find aponeurosis and tendon stiffness and the onset of muscle contraction.

A method to measure small movements of living tissues either large or small is presented. The method is based on the detection of changes in reflected infrared light. An optocoupler (coupled photodiode and photodetector) and a small (< 1 cm2) mirror were used. The optocoupler (OC) has a low cost and it can be calibrated easily. It can be also used as the transducer of a strain-gage. Three different uses are shown: (a) as a strain-gage transducer; (b) detection of tendon and aponeurosis movements in large muscles (cat soleus); (c) detection of the onset of muscle contraction. Movements of less than 1 microm can be detected with the aid of automatic averaging of the signals. Concerning the second use (b), it permits the estimation of tendon stretch. Concerning the third use, the onset of muscle movement precedes by at least 2 ms that of the force recorded at the tendon.

Achilles Tendon↗
PubMed1987

Mast cells are not required for anaphylatoxin-induced ileal smooth muscle contraction.

The complement-derived anaphylatoxin peptides, C3a and C5a, have long been considered to manifest their spasmogenic activities primarily through stimulation of mast cells. Although mast cells represent the major non-circulating repository for histamine, these cells also elaborate a number of additional, highly potent spasmogenic mediators derived from arachidonic acid. The same lipid mediators can be released by many other cell types. As a result, evaluation of the role of mast cells in anaphylatoxin-dependent responses cannot be based exclusively upon an analysis of the mediators released. We evaluated the role of mast cells in anaphylatoxin-induced ileal smooth muscle contractions by testing isolated segments of ileal tissues derived from genetically mast cell-deficient mice and their congenic normal (+/+) littermates. Isolated tissues from either congenic normal (+/+) or mast cell-deficient Sl/Sld mice responded similarly to acetylcholine, histamine, serotonin, prostaglandin E2, and the thromboxane A2 analog, U-46619. At 1 microgram/ml, histamine induced contractions of greater magnitude in tissues from mast cell-deficient animals; however, this mediator also desensitized the tissues to repeat challenge with histamine at the same concentration. C5a at 1 nM resulted in contractions equivalent to approximately 50% of the maximal KCl response; normal and mast cell-deficient tissues responded in a similar manner. C5a also released histamine from the normal mouse ileum, in addition to causing contraction of the tissues. C3a at 200 nM also produced similar contractile responses in both +/+ and S1/S1d tissues. These studies show that the anaphylatoxin peptides C3a and C5a are capable of contracting smooth muscle-containing tissues by a mechanism completely independent of mast cells. In addition, we also demonstrated that mast cell degranulation does not necessarily provoke ileal contraction. Thus compound 48/80, a mast cell degranulating agent unrelated to the anaphylatoxins, did not induce contractions in ileal tissues, even when used at concentrations as high as 100 micrograms/ml. Compound 48/80 did release histamine from the +/+ ileum, however, indicating that the agent was able to cause degranulation of ileal mast cells. Taken together, these data indicate that spasmogenic responses to anaphylatoxins (and possibly other agents) that are associated with mast cell degranulation need not necessarily require mast cell mediator release for their expression.

Animals↗
PubMed1999

Long-latency contributions to reciprocal inhibition during various levels of muscle contraction.

Reciprocal inhibition is a functional term and refers to the proportional decrease in antagonist motoneuron activity that accompanies an agonist contraction. A condition-test (C-T) H-reflex paradigm (conditioned stimulus applied to the common peroneal nerve; test reflex elicited by posterior tibial nerve stimulation) was used during: (1) rest, (2) a tonic isometric tibialis anterior (TA) contraction at 10% of its maximal voluntary contraction (MVC) and, (3) a TA contraction at 25% MVC. The purpose of the study was to assess whether or not long-latency contributions to reciprocal inhibition of soleus H-reflexes changed with increasing levels of TA contraction. C-T intervals ranged from 5 to 150 ms. Subjects (n=14) had long-latency inhibition at rest (x = -35.0 +/- 18.7%). This inhibition was enhanced during 10% (x = -46.1 +/- 17.9%; p = 0.17) and 25% MVCs (x = -56.3 +/- 14.0%; p < 0.01). Findings indicate that long-latency contributions to reciprocal inhibition of the soleus motoneuron pool are enhanced with increasing force of TA muscle contraction up to 25% MVC. These results indicate that long-latency contributions to reciprocal inhibition of soleus H-reflexes are not static but rather are task-specific and change in relation to levels of TA muscle activity.

Adult↗
PubMed1995

Changes in fusimotor discharge rate provoked by isotonic fatiguing muscle contractions in decerebrate cats.

Changes in discharge rate of 26 fusimotor neurones to medial gastrocnemius muscle were studied during isotonic fatiguing contractions of lateral gastrocnemius and soleus muscles in decerebrate cats. Muscle contractions were elicited by either continuous or repetitive electrical stimulation of the muscle nerves. The muscles were considered to be fatigued when, against a load equal to one third of the tension developed at the onset of an isometric contraction, i.e. to the tension indicating isometrically-induced fatigue, they returned to the length at which the isometric contraction was elicited. At the onset of muscle contraction an increase in discharge rate, lasting for 5-220 s, occurred in all except one of the neurones. In 73% of the units a late increase developed in addition in parallel with muscle fatigue outlasting the contraction for 5-180 s. All but one of the remaining neurones exhibited a short lasting burst of spike discharges coincident with the end of contraction. Enhancement of the late increase by muscle ischaemia indicates contribution of chemosensitive small-diameter muscle afferents, while the short lasting burst is supposed to be elicited rather by the mechanosensitive units sensitized by metabolic products liberated during contraction and/or fatigue. Differences of the fusimotor reflex responses to isotonic vs. isometric contraction and/or fatigue and their possible functional role are discussed.

Animals↗
PubMed1998

Persistent attenuation and enhancement of the earthworm main muscle contraction generator response induced by repeated stimulation of a peripheral neuron.

Responses evoked in the earthworm, Amynthas hawayanus, main muscle contraction generator M-2 (postsynaptic mechanical-stimulus-sensitive) neuron by threshold mechanical stimuli in 2-s intertrial intervals (ITI) were used as the control or unconditioned responses (UR). Their attenuation induced by decreasing these intervals in non-associative conditioning and their enhancement induced by associating the unconditioned stimuli (US) to a train of short (0.1 s) hyperpolarizing electrical substitutive conditioning stimuli (SCS) in the Peri-Kästchen (PK) neuron were measured in four parameters, i.e., peak numbers (N) and amplitude (AMP) averaged from 120 responses, sum of these amplitudes (sigma AMP) and the highest peak amplitude (V) over a period of 4 min. Persistent attenuation similar to habituation was induced by decreasing the control ITI to 0.5 s and 2.0 s in non-associative conditioning within less than 4 min. Dishabituation was induced by randomly pairing one of these habituated US to an electrical stimulus in the PK neuron. All four parameters of the UR were enhanced by forward (SCS-US), but not backward (US-SCS), association of the US with 25, 100 and 250-Hz trains of SCS with 40-ms interstimulus intervals (ISI) for 4 min and persisted for another 4 min after turning off the SCS. The enhancement of these parameters was proportional to the SCS frequencies in the train. No UR was evoked by the SCS when the US was turned off after 4 min of classical conditioning.

Animals↗
PubMed1985

The inhibition of muscle contraction by adenosine 5' (beta, gamma-imido) triphosphate and by pyrophosphate.

We have studied the inhibition of the contraction of glycerinated rabbit psoas muscle caused by ligands that bind to the ATPase site of myosin. Two ligands, adenosine 5' (beta, gamma-imido) triphosphate (AMPPNP) and pyrophosphate (PPi), decreased the force and stiffness developed in isometric contractions and the velocity of shortening of isotonic contractions. The force exerted by isometric fibers was measured as a function of MgATP in the presence and absence of a constant concentration of the ligands. As the MgATP concentration decreased, the inhibition of tension caused by the ligand increased, reaching approximately 50% at 25 microM MgATP and either 2 mM MgPPi or 2 mM MgAMPPNP. The maximum velocity of shortening was also measured as a function of MgATP concentration in the presence of 1 and 2 mM MgPPi and 2.5 and 5 mM MgAMPPNP. Both ligands acted as pure competitive inhibitors with Ki = 3.0 mM for PPi and 5.1 mM for MgAMPPNP. These data show that both ligands are weak inhibitors of the contraction of fibers. The results provided information on the energetics of actin-myosin-ligand states that occur in the portion of the cross-bridge cycle where MgATP binds to myosin. A simple analysis of the inhibition of velocity suggests that MgAMPPNP binds to the actomyosin complex at this step of the cycle with an effective affinity constant of approximately 2 X 10(2) M-1.

Adenosine Triphosphate↗
PubMed2005

Possible involvement of CPI-17 in augmented bronchial smooth muscle contraction in antigen-induced airway hyper-responsive rats.

Airway hyper-responsiveness (AHR) associated with heightened airway resistance and inflammation is a characteristic feature of asthma. It has been demonstrated that contractile responsiveness and Ca(2+) sensitization to acetylcholine (ACh) in repeated antigen challenge-induced airway hyper-responsive bronchial preparation were significantly increased. The CPI-17 (PKC-potentiated inhibitory protein for heterotrimeric myosin light chain phosphatase of 17 kDa) is activated by protein kinase C and acts on a myosin light-chain phosphatase-specific target. The aim of the present study was to explore the role of CPI-17 in hyper-responsiveness of bronchial smooth muscle in antigen-induced AHR rats. In immunoblotting, the levels of expression of CPI-17 mRNA and protein were significantly increased in bronchus from rats that were repeatedly challenged with antigen. ACh-induced CPI-17 phosphorylation and translocation to membrane fraction were also significantly increased in bronchus from antigen-challenged rats. In conclusion, we suggest that augmented expression and activation of CPI-17 observed in the hyper-responsive bronchial smooth muscle might be responsible for the enhanced ACh-induced Ca(2+) sensitization of bronchial smooth muscle contraction associated with AHR.

Acetylcholine↗
PubMed2003

Eccentric muscle contractions: their contribution to injury, prevention, rehabilitation, and sport.

Muscles operate eccentrically to either dissipate energy for decelerating the body or to store elastic recoil energy in preparation for a shortening (concentric) contraction. The muscle forces produced during this lengthening behavior can be extremely high, despite the requisite low energetic cost. Traditionally, these high-force eccentric contractions have been associated with a muscle damage response. This clinical commentary explores the ability of the muscle-tendon system to adapt to progressively increasing eccentric muscle forces and the resultant structural and functional outcomes. Damage to the muscle-tendon is not an obligatory response. Rather, the muscle can hypertrophy and a change in the spring characteristics of muscle can enhance power; the tendon also adapts so as to tolerate higher tensions. Both basic and clinical findings are discussed. Specifically, we explore the nature of the structural changes and how these adaptations may help prevent musculoskeletal injury, improve sport performance, and overcome musculoskeletal impairments.

Accidental Falls↗
PubMed1984

Vascular permeability changes and smooth muscle contraction in relation to capsaicin-sensitive substance P afferents in the guinea-pig.

The occurrence of neurogenic inflammation as indicated by Evans blue extravasation was studied in various organs of the guinea-pig. Electrical stimulation of the trigeminal nerve caused Evans blue extravasation due to increased vascular permeability in the nasal mucosa and gingiva. Vagal stimulation induced extravasation in the epiglottis, larynx, trachea, bronchial tree and esophagus. Splanchnic stimulation induced Evans blue extravasation in the gall bladder, bile ducts and superior mesenteric artery. Stimulation of the inferior mesenteric ganglion caused a marked extravasation in the upper and middle part of both ureters, while pelvic activation induced a reaction in the lower ureter, urinary bladder, urethra and vagina. I.v. substance P (SP) (3 nmol X kg11) or capsaicin (1 mumol X kg-1) both induced extravasation in many tissues including those in which nerve stimulation produced a response. The extravasation responses to SP, capsaicin or nerve stimulation all had similar border-line zones, such as esophagus to stomach, bile ducts to duodenum, rectum to anal mucosa, pulmonary artery to heart and vagina to uterus. Quantitative determinations showed especially large permeability effects in the trachea, umbilical ligament and ureter. The permeability effect of capsaicin and nerve stimulation was abolished in capsaicin-pretreated animals, while the response to SP was still present. Capsaicin pretreatment caused an almost total loss of SP in several visceral organs including the respiratory and urinary tracts. The SP content in these tissues was correlated (r = 0.97) to the Evans blue extravasation following nerve stimulation or i.v. capsaicin. SP and capsaicin caused contractions in vitro of the esophagus, ureter, urinary bladder, trachea and gall bladder. The capsaicin-induced contraction of the trachea was resistant to tetrodotoxin pretreatment. The non-cholinergic, non-adrenergic contraction of the urinary bladder upon field stimulation was still present in capsaicin-pretreated animals. In conclusion, neurogenic inflammation occurs in several organs with a highly region-specific distribution, which is accompanied by the presence of capsaicin-sensitive SP neurons. Both parasympathetic and sympathetic pathways contain capsaicin-sensitive afferent fibres which mediate an increase in vascular permeability most likely by releasing SP. In addition, both capsaicin and SP cause smooth muscle contraction in several visceral organs.

Animals↗
PubMed1999

Effects of newly synthesized analogs of MIF-1 containing unnatural amino acids on electrically evoked smooth muscle contractions.

New MIF-1 (Pro-Leu-Gly-NH2) analogs containing unnatural amino acids such as L-canavanine (Cav) and L-cysteic acid S-(2-aminoethyl)amide (sLys) have been synthesized and in vitro experiments were performed to study their action on neurotransmission in target tissues with adrenergic and cholinergic neurotransmission. The experiments were carried out on electrically stimulated proximal guinea pig ileum (GPI) and the prostatic part of rat and rabbit vasa deferentia (VDR, VDRabb). The present results show that the newly synthesized Cav2-MIF and sLys2-MIF might affect electrically evoked smooth muscle contractions.

Adrenergic Agents↗
PubMed1990

Comparison of microscopic and laser diffraction methods for measuring sarcomere lengths of contracted muscle fibers of chicken pectoralis major muscle.

The objective of the present study was to compare the effectiveness of a microscopy method with a laser diffraction method for measuring sarcomere lengths of chicken pectoralis major (p. major) muscle fibers exhibiting various contraction states. Chicken p. major muscles were excised from the animals at death. Samples of each muscle were treated with pH-buffered (5.0 and 7.5) isoionic CaCl2, KCl, or ethylene glycol bis-(b-aminoethyl ether) N,N,N',N'-tetraacetic acid (EGTA) solutions in order to produce variability in the degree of fiber contraction. Sarcomere lengths (SL) of the fibers were observed using light microscopy and a laser diffraction method. The methods gave comparable results for sarcomere lengths greater than 1.6 microns. However, for SL less than 1.6 microns, sarcomere contraction was not accurately assessed by the laser diffraction method.

Animals↗
PubMed1994

Magnetically induced muscle contraction is caused by motor nerve stimulation and not by direct muscle activation.

When magnetically stimulating peripheral nerves, a local cocontraction of muscle under the coil is observed. We assessed whether this contraction results from: (1) magnetic stimulation of motor nerves, or (2) direct depolarization of the muscle membrane. Wrist extensor muscles of normal subjects were magnetically stimulated with the coil placed directly above the muscle. Neuromuscular transmission was then blocked by atracurium using a technique of local curarization. As a reference, the radial nerve was stimulated electrically. Magnetic and electrical stimuli were applied alternatingly every 10 s. Twitch force of wrist extension was measured isometrically over a period of about 70 min including the phase of complete neuromuscular block. Twitch amplitudes elicited by magnetic and electrical stimuli were equivalent during the whole experiment. These results suggest that muscle cocontraction following magnetic stimulation results from depolarization of terminal motor nerve branches.

Action Potentials↗