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At least 163 records · Page 9Linked to original sources
PubMed1997

A thermodynamic approach to the compromise between power and efficiency in muscle contraction.

An analysis of muscle contraction based on irreversible thermodynamics is presented in this work. From reported experimental results, it is shown that a muscle, as an energy converter, does not obey linear phenomenological relations. Some more suitable nonlinear phenomenological relations are found and discussed from an evolutionary point of view. In those relations a parameter alpha appears which is related to the nonlinearity of the equations. It is suggested that this parameter determines the compromise between the power output and the efficiency reached by the muscle. By analysing the energetics of some suitable performance regimes, we suggest that the fact that alpha values greater than 0.4 are not found in muscles of higher species, can be interpreted as an evolutionary necessity.

Animals↗
PubMed1991

Optimization of the timing of skeletal to cardiac muscle contraction during dynamic cardiomyoplasty: analysis using a mathematical model.

Cardiomyoplasty, or the use of skeletal muscle to assist the failing heart, has been studied for many years but has enjoyed only minimal success. It has been suggested that a delay in the start of skeletal muscle contraction relative to the QRS complex would enhance aortic flow. To study the effects of simulated changes in the relative timing of skeletal muscle contraction, heart rate and skeletal muscle contraction duration, a mathematical model was used to predict the vascular pressures and flows during cardiomyoplasty. The vascular pressures and cardiac output generated by the model for both the normal and heart failure state were similar to previously published canine data. Skeletal muscle contraction synchronous with cardiac mechanical systole (i.e., delayed approximately 50-75 ms from the QRS) was able to provide improvements in cardiac output, arterial blood pressure and aortic flow velocity up to 40% over the baseline heart failure state. A delay in the start of skeletal muscle contraction, prolonged skeletal muscle contraction duration or an increase in the heart rate from 90 to 120/min reduced this benefit. Thus, mechanical synchrony of skeletal and cardiac muscle contraction optimizes hemodynamics during cardiomyoplasty.

Heart Failure↗
PubMed1999

Role of M2 muscarinic receptors in airway smooth muscle contraction.

Airway smooth muscle expresses both M2 and M3 muscarinic receptors with the majority of the receptors of the M2 subtype. Activation of M3 receptors, which couple to Gq, initiates contraction of airway smooth muscle while activation of M2 receptors, which couple to Gi, inhibits beta-adrenergic mediated relaxation. Increased sensitivity to intracellular Ca2+ is an important mechanism for agonist-induced contraction of airway smooth muscle but the signal transduction pathways involved are uncertain. We studied Ca2+ sensitization by acetylcholine (ACh) and endothelin-1 (ET-1) in porcine tracheal smooth muscle by measuring contractions at constant [Ca2+] in strips permeabilized with Staphylococcal alpha-toxin. Both ACh and ET-1 contracted airway smooth muscle at constant [Ca2+]. Pretreatment with pertussis toxin for 18-20 hours reduced ACh contractions, but had no effect on those of ET-1 or GTPgammaS. We conclude that the M2 muscarinic receptor contributes to airway smooth muscle contraction at constant [Ca2+] via the heterotrimeric G-protein Gi.

Acetylcholine↗
PubMed1979

Early cellular changes and circular muscle contraction associated with the induction of decidualization by intrauterine oil in mice.

Intrauterine instillations of oil or saline distended the uterus in ovariectomized mice treated with progesterone + oestrogen to sensitize the uterus to a decidualizing stimulus. Saline does not induce decidualization, and therefore uterine distension per se is not the trigger to decidual induction. Oil induces decidualization, but does not involve gross damage to the epithelium, penetration of oil into the stroma or release of epithelial lipid into the stroma. Instillation (oil, saline or sham) induced a contraction of the circular muscles along the length of the uterus which closed the uterine lumen, expelled most of the oil and located the remainder primarily in the antimesometrial cleft of the lumen. Progesterone inhibited longitudinal muscle contraction and facilitated circular muscle contraction. These effects are discussed in relation to the spacing and implantation of blastocysts.

Animals↗
PubMedDate not supplied

Cyclosporine does not affect in vitro bronchial smooth muscle contractions in treated Lewis rats.

The purpose of this study was to investigate whether cyclosporine treatment could modify airway responses, thus playing a role in bronchial hyperresponsiveness observed in patients after lung transplantation. We have studied the effect of cyclosporine treatment in rats on subsequent bronchial responses to electrical field stimulation, to exogeneous 5-hydroxytryptamine, and acetylcholine in organ baths. The isometric force of contraction of bronchial smooth muscle was measured. Voltage and frequency responses produced by electrical field stimulation were similar in control and in rat bronchi treated with cyclosporine. Concentration-response curves to exogeneous acetylcholine were superimposed for both groups of animals, as were those to 5-hydroxytryptamine. Our results show that cyclosporine treatment does not affect bronchial smooth muscle contraction and rule out possible contribution of cyclosporine to the bronchial hyperresponsiveness described after lung transplantation.

Acetylcholine↗
PubMed1992

Direct inhibitory mechanisms of halothane on canine tracheal smooth muscle contraction.

Halothane directly relaxes airway smooth muscle. To determine the direct inhibitory mechanisms of halothane on canine tracheal smooth muscle contraction, the effects of this anesthetic on the levels of several intracellular second messengers were investigated by measuring intracellular Ca2+ concentration ([Ca2+]i), Ca2+/phospholipid-dependent protein kinase (PKC) translocation, and intracellular cyclic adenosine monophosphate concentration ([cAMP]i). When carbachol (1 microM) was used to increase [Ca2+]i to the same concentration as that induced by high-K+ (72.7 mM), the carbachol-induced contraction was more than twice as great, indicating that carbachol enhances the sensitivity of contractile elements to Ca2+ or activates a Ca(2+)-independent mechanism. Similarly, 12-deoxyphorbol 13-isobutylate, a potent PKC activator, markedly potentiated high-K(+)-induced muscle contraction without an increase of [Ca2+]i. The addition of halothane (0.33, 0.75, 1.15, and 1.47 mM) decreased [Ca2+]i and the muscle tension induced by carbachol. However, the decrease of muscle tension was more marked than that of [Ca2+]i at the higher concentrations. Although [Ca2+]i in the presence of verapamil and carbachol was not affected by halothane, the anesthetic markedly decreased muscle force by decreasing the "Ca2+ sensitization" or the Ca(2+)-independent enhancement of tension observed with carbachol. Halothane (0.75 and 1.47 mM) significantly released the membrane-associated PKC to cytosol, which decreased PKC activity. [cAMP]i of the smooth muscle stimulated by carbachol was moderately but significantly increased by halothane. However, when equivalent relaxation was induced with forskolin, which acts via adenylate cyclase activation, a much higher [cAMP]i was observed, which suggests that halothane acts via an additional pathway.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2002

Comparison of sarcomere alterations after muscle contraction and tension loading in the rat soleus muscle.

Muscle contraction induced by 30 min of continuous nerve stimulation at 50 Hz resulted in sarcomere changes of the soleus muscle in the rat in our previous study. To further investigate the cause of sarcomere alterations, the sciatic nerve was electrically stimulated intermittently for 30 min. Nerve stimulation was also conducted after cutting the tendons of the soleus, gastrocnemius and plantaris muscles in order to prevent imposing tension on these muscles as a result to their own contractions. In addition, the muscles were pulled by weights via their tendons to load high tension for 30 min without nerve stimulation. Sarcomere alterations immediately after treatments were quantified by electron microscopy. The percentages of aberrant sarcomere areas of the soleus muscle were 25.7 +/- 16.4% (mean +/- SD) in the group of intermittent nerve stimulation with intact tendons and 21.1 +/- 35.4% in the group of tenotomy and continuous nerve stimulation, which were roughly equal to or more severe than the group of continuous nerve stimulation with intact tendons (18.8 +/- 15.8%) in our previous study. Sarcomere alterations consisted mainly of hypercontraction in these groups. Almost all sarcomere changes in the tension-loaded (pulled) soleus muscles were scarce myofilaments (1.7 +/- 1.0% by 600 g; 4.5 +/- 2.9% by 1200 g), and hypercontraction was not observed. These findings indicate that neither high tension nor a decrease of muscle blood flow during continuous contraction seems to be the primary cause of sarcomere alterations in the present study. There are probably other causes that produce aberrant sarcomeres.

Actin Cytoskeleton↗
PubMedDate not supplied

[Effect of the graded muscle contraction on the H reflex and long latency reflexes of the thenar and hypothenar muscles to a fixed threshold stimulus].

INTRODUCTION: To determine the percentage of appearance of the H reflex and long latency reflexes (LLRs) in the thenar and hypothenar muscles of normal subjects to a fixed threshold mixed nerve electrical stimulus and variable degrees of muscle contraction. METHODS: Fifteen subjects aged 21 to 32 years of age without any prior history of central or peripheral neurological diseases volunteered for the study. The stimulation was a constant currrent given at the wrist with the cathode positioned proximally; started at 1 mA and it was gradually increased mA by mA until the M response appeared with the subject relaxed. The intensity of the stimulation was thereafter kept constant. The contraction was an abducting movement of the thumb in the case of the thenar muscle and abduction of the digiti minimi in the case of the hypothenar muscle and was sustained throughout the study. The reflexes were elicited with a repetition rate of 3 Hz, the stimulus was a square pulse of 0.5 ms. We used a low frequency pass filter of 10 Hz and a high frequency pass filter of 10 kHz. The sweep speed was set a 10 ms per division. The responses were averaged 200 times and then smoothed. RESULTS: The mean intensity of the stimulus that evoked the H response, for all subjects, was 7.5 2.8 mA. The mean latency of the H reflex elicited with stimulation of the median nerve was 26 ms 2.03 ms (std. error 0.28, maximum 28.2, minimum 22.0). The mean latency of the H reflex elicited with stimulation of the ulnar nerve was 25.1 ms 1.64 ms (std. error 0.230, maximum 28, minimum 22.3). The difference between the percentage of responses attained under a relaxed condition and with any kind of muscle contraction was highly significant statistically using the Chi square method (p < 0.001). When we compared the percentage of the H responses obtained with slight, moderate, strong contraction, and contraction against resistance, between them, we did no find a significant difference. The LLRs appeared only in the trials with strong contraction. CONCLUSIONS: The H reflexes and the LLRs of the thenar and hypothenar muscle were not obtained with threshold stimulation when these muscles were relaxed. With any degree of muscle contraction the H reflex in these muscles could be obtained in 94 percent of the trials. Maximal contraction and contraction against resistance were the best conditions to elicit long latency responses.

Adult↗
PubMed1997

Extracellular serotonin changes in VLM during muscle contraction: effects of 5-HT1A-receptor activation.

This study determined whether muscle contraction causes an increase in extracellular levels of serotonin (5-HT) in the rostral (rVLM) or caudal ventrolateral medulla (cVLM) in anesthetized rats. Muscle contraction, evoked by tibial nerve stimulation, increased mean arterial blood pressure (MAP) by 27 +/- 4 mmHg (n = 8). In addition, 5-HT levels in the rVLM were elevated by 65 +/- 9% during the contraction (n = 8). Results were similar over two repeated contractions. In contrast, muscle contraction increased MAP, but not 5-HT, levels in the cVLM (n = 6). Tibial nerve stimulation after muscle paralysis had no effect on either MAP or 5-HT levels in both rVLM and cVLM. Microdialysis of a 5-HT1A agonist, 8-OH-DPAT (10 mM), into the rVLM for 30 min (n = 6) blunted the MAP change and reduced 5-HT release during contraction. Administration of NAN-190, a 5-HT1A antagonist, into the rVLM had no effect on 5-HT release and cardiovascular responses during muscle contraction and blocked the changes in 5-HT, MAP, and heart rate to static contraction after subsequent microdialysis of 8-OH-DPAT. Results demonstrate that 5-HT levels in the rVLM increase during muscle contraction and that 5-HT1A-receptor activation in the rVLM blunts MAP response to muscle contraction via a decrease in the extracellular concentration of 5-HT.

8-Hydroxy-2-(di-n-propylamino)tetralin↗
PubMed1991

[The manifestation of the hysteresis effects of muscle contraction in the cortically evoked coactivation of muscle antagonists].

Hysteretic after-effects of muscle contraction were studied on unanaesthetized cats during intracortical microstimulation of two sites in the motor cortex. Equilibrium in the joint-external load system was shown to be dependent on the order of stimulation of the sites in the motor cortex. Coactivation of antagonistic muscles led to an increase in both the joint stiffness and uncertainty of the equilibrium value of the joint angle.

Animals↗
PubMed2004

Considerations on the history dependence of muscle contraction.

When a skeletal muscle that is actively producing force is shortened or stretched, the resulting steady-state isometric force after the dynamic phase is smaller or greater, respectively, than the purely isometric force obtained at the corresponding final length. The cross-bridge model of muscle contraction does not readily explain this history dependence of force production. The most accepted proposal to explain both, force depression after shortening and force enhancement after stretch, is a nonuniform behavior of sarcomeres that develops during and after length changes. This hypothesis is based on the idea of instability of sarcomere lengths on the descending limb of the force-length relationship. However, recent evidence suggests that skeletal muscles may be stable over the entire range of active force production, including the descending limb of the force-length relationship. The purpose of this review was to critically evaluate hypotheses aimed at explaining the history dependence of force production and to provide some novel insight into the possible mechanisms underlying these phenomena. It is concluded that the sarcomere nonuniformity hypothesis cannot always explain the total force enhancement observed after stretch and likely does not cause all of the force depression after shortening. There is evidence that force depression after shortening is associated with a reduction in the proportion of attached cross bridges, which, in turn, might be related to a stress-induced inhibition of cross-bridge attachment in the myofilament overlap zone. Furthermore, we suggest that force enhancement is not associated with instability of sarcomeres on the descending limb of the force-length relationship and that force enhancement has an active and a passive component. Force depression after shortening and force enhancement after stretch are likely to have different origins.

Animals↗
PubMed1991

Changes in the baroreceptor reflex at the start of muscle contraction in the decerebrate cat.

1. The action of muscle contraction on the sensitivity of the cardiac vagal component of the baroreceptor reflex was examined in decerebrate cats. 2. The sensitivity of the baroreceptor reflex was expressed as the difference between the maximum prolongation of the R-R interval in response to carotid sinus baroreceptor stimulation and the mean of ten R-R intervals immediately before carotid sinus pressure elevation. 3. Muscle contraction elicited by electrical stimulation of L7 ventral roots (50 Hz) significantly reduced the sensitivity of the baroreceptor reflex by reducing the prolongation of the R-R interval from 269 +/- 31 to 159 +/- 22 ms. 4. Inhibition of the cardiac vagal component of the baroreceptor reflex was seen just 1 s after the onset of contraction and with stimulation frequencies as low as 10 Hz. 5. These results show for the first time that changes in the sensitivity of the baroreceptor reflex during exercise result in part from afferent information originating in the contracting muscles.

Animals↗
PubMed1988

A self-induced translation model of myosin head motion along thin filament in muscle contraction.

Evidence has been accumulating that muscle contraction may not be associated with the power stroke of the cross-bridges tightly coupled with ATP hydrolysis cycle. We have constructed a new contraction model which includes a number of basic properties of contraction processes not taken into consideration in the models hitherto reported. The basic assumption is that, when one head of a myosin molecule attaches to an actin monomer on thin filament, conformational changes take place in the neighbouring actin monomers to result in their non-symmetrical charge distribution to exert electrostatic force on the unattached head of the same myosin molecule in one direction. Thus, the unattached head moves along thin filament to attach to another actin monomer, while the already attached head detaches from thin filament. These steps are repeated to cause muscle contraction. The above contraction model can explain the results of our X-ray diffraction experiments as well as the results reported by other authors.

Actin Cytoskeleton↗
PubMed2001

Mechanisms underlying stabilization of temporally summated muscle contractions in the lobster (Panulirus) pyloric system.

Muscles are the final effectors of behavior. The neural basis of behavior therefore cannot be completely understood without a description of the transfer function between neural output and muscle contraction. To this end, we have been studying muscle contraction in the well-investigated lobster pyloric system. We report here the mechanisms underlying stabilization of temporally summating contractions of the very slow dorsal dilator muscle in response to motor nerve stimulation with trains of rhythmic shock bursts at a physiological intraburst spike frequency (60 Hz), physiological cycle periods (0.5-2 s), and duty cycles from 0.1 to 0.8. For temporal summation to stabilize, the rise and relaxation amplitudes of the phasic contractions each burst induces must equalize as the rhythmic train continues. Stabilization could occur by changes in rise duration, rise slope, plateau duration, and/or relaxation slope. We demonstrate a generally applicable method for quantifying the relative contribution changes in these characteristics make to contraction stabilization. Our data show that all characteristics change as contractions stabilize, but their relative contribution differs depending on stimulation cycle period and duty cycle. The contribution of changes in rise duration did not depend on period or duty cycle for the 1-, 1.5-, and 2-s period regimes, contributing approximately 30% in all cases; but for the 0.5-s period regime, changes in rise duration increased from contributing 25% to contributing 50% as duty cycle increased from 0.1 to 0.8. At all cycle periods decreases in rise slope contributed little to stabilization at small duty cycles but increased to contributing approximately 80% at high duty cycles. The contribution of changes in plateau duration decreased in all cases as duty cycle increased; but this decrease was greater in long cycle period regimes. The contribution of changes in relaxation slope also decreased in all cases as duty cycle increased; but for this characteristic, the decrease was greatest in fast cycle period regimes, and in these regimes at high duty cycles these changes opposed contraction stabilization. Exponential fits to contraction relaxations showed that relaxation time constant increased with total contraction amplitude; this increase presumably underlies the decreased relaxation slope magnitude seen in high duty cycle, fast cycle period regimes. These data show that changes in no single contraction characteristic can account for contraction stabilization in this muscle and suggest that predicting muscle response in other systems in which slow muscles are driven by rapidly varying neuronal inputs may be similarly complex.

Animals↗
PubMed1991

Excited hydrogen bonds in the molecular mechanism of muscle contraction.

The mechanism of muscle contraction is considered. The hydrolysis of an ATP molecule is assumed to produce the excitation of hydrogen bonds A--H...B between electronegative atoms A and B, which are contained in the myosin head and actin filament. This excitation energy epsilon f depends on the interatomic distance AB = R and generates the tractive force f = -delta epsilon f/delta R, that makes atoms AB approach each other. The swing of the myosin head results in macroscopic mutual displacement of actin and myosin polymers. The motion of the actin filament under the action of this force is studied. The conditions under which a considerable portion of the excitation energy converts into the potential tension energy of the actin filament are analysed, and the probability of higher muscle efficiency existence is discussed.

Actins↗