Point: the muscle metaboreflex does restore blood flow to contracting muscles.
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Adaptation, Physiological↗
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Relation between muscle contraction speed and hydraulic performance in skeletal muscle ventricles.
BACKGROUND: The fatigue resistance and power-to-weight ratio of skeletal muscle that has been conditioned by electrical stimulation makes cardiac assistance from a graft of such muscle a realistic prospect. A skeletal muscle must be surgically reconfigured to act on the circulating blood, but little is known about the power losses that accompany such interventions. We investigated in acute experiments the hydraulic performance of approximately cylindrical pumps made from sheep latissimus dorsi (LD) muscles, having first characterized the performance of each muscle in situ. METHODS AND RESULTS: Force-length and force-velocity relations were measured in situ for LD that had received either 8 weeks of stimulation at 2 Hz or no chronic stimulation. Two sizes of skeletal muscle ventricle (SMV) were formed from the same muscles, and their hydraulic performance was measured. The hydraulic performance was also calculated from the linear data, models of the force-length and force-velocity curves, and a description of the stress distribution within the SMV wall. The model predicted well the isovolumetric function of the ventricles and the optimum afterload but overestimated the flow and therefore the power. In conditioned ventricles the performance was particularly poor because of the slow contractile properties of the muscles. CONCLUSIONS: If SMVs are to pump effectively against the arterial impedance, the pressure drop caused by flow (or the internal resistance) should be lower than that of the ventricles we constructed. Progress can be made through refinement of surgical technique and stimulation protocols that generate faster fatigue-resistant muscles.
Animals↗
Counterpoint: the muscle metaboreflex does restore blood flow to contracting muscles.
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Adaptation, Physiological↗
Role of myosin light chain kinase in muscle contraction.
In resting striated muscles of the rabbit muscle in vivo, the phosphorylatable light chain is partially phosphorylated. Tetanic stimulation increased the level of phosphorylation more rapidly in fast twitch than in slow twitch muscle. In both types of muscle the rate of dephosphorylation was relatively slow. In rabbit fast twitch muscles, phosphorylation levels persisted significantly above the resting value for some time after posttetanic potentiation had disappeared. The role of myosin light chain kinase in modulating contractile response in striated muscle is uncertain. In vertebrate smooth muscle the role of myosin phosphorylation appears to be different from that in striated muscle despite the general similarity of the actomyosin system in both tissues. Although phosphorylation in vitro increases the Mg2+ -ATPase of actomyosin, a number of features imply that a somewhat complex relationship exists between the level of phosphorylation and the actin activation of the Mg2+ -ATPase in vertebrate smooth muscle. Contrary to many earlier reports, preparations of smooth muscle actomyosin can be obtained with Mg2+ -ATPase activities comparable to those of actomyosin from skeletal muscle. Preliminary evidence is presented that suggests that phosphorylation changes the Ca2+ sensitivity of the Mg2+ -ATPase of smooth muscle actomyosin.
Actomyosin↗
[Changes in the sensitivity of the muscle spindles of fast and slow-contracting muscle fibers following chronic deafferentation].
The activity of muscle spindles was investigated in fast (m. EDL) and slow (m. sol) muscles of the cat 2-5 weeks after chronic deefferentation. The spontaneous activity of spindles in both muscles remains unchanged. The background activity and activity in dynamic and static phases of stretching both in primary and in secondary endings was much in chronic denervated muscle than in control. This increase in spindle activity was more pronounced in the slow muscle.
Muscle Contraction↗
Role of Rho-kinase in guinea-pig gallbladder smooth muscle contraction.
Guinea-pig gallbladder smooth muscle contractions can be elicited pharmacologically by a range of mechanisms. The involvement of Rho-kinase in contractions mediated by receptor-dependent and receptor-independent mechanisms was investigated using the Rho-kinase inhibitor (+)-(R)-trans-4-(1-aminoethyl)-N-(4-pyridyl) cyclohexane carboxamide (Y-27632). In a separate series of experiments, the role of Rho-kinase in the contractile response to Ca2+ entry through store-operated Ca2+ channels and to electrical field stimulation was also examined. Y-27632 (10 microM), which caused a significant decrease (P<0.0005) in basal resting tone, significantly inhibited gallbladder contractions evoked by cumulative additions of the G-protein-coupled agonists, carbachol (1 nM-100 microM; P<0.05) and cholecystokinin (10 nM-1 microM; P<0.005). Y-27632 also inhibited the contractions evoked by a single addition of the sarcoplasmic reticulum ATPase inhibitor, thapsigargin (1 microM; P<0.0005) and cumulative additions of KCl (10-85 mM; P<0.0005). The contractile response to Ca2+ entry through store-operated Ca2+ channels was significantly inhibited by Y-27632 (P<0.05) as were the contractile responses evoked by electrical field stimulation (2-25 Hz; P<0.0005). In contrast, Y-27632 had no significant effect on contractions evoked by phorbol 12,13-dibutyrate (0.1 nM-1 microM; a protein kinase C activator) or by the phosphatase inhibitor, cantharidin (100 microM). In conclusion, Rho-kinase contributes to the contractile response in guinea-pig gallbladder smooth muscle evoked by both G-protein-coupled and non-G-protein-coupled mechanisms in addition to contributing to the maintenance of basal tone. It also contributes to the contractile responses resulting from electrical field stimulation and store-operated Ca2+ channel entry.
Amides↗
[Recruiting of motor units and changes of their firing rate as mechanisms of muscle contraction control].
Main mechanisms of muscle contraction control: recruiting of motor units and changes of their firing rate are discussed in the review. Relative contribution of these mechanisms at different types of muscular activity (tonic contraction, vibration reflex, locomotion) is considered.
Action Potentials↗
[Some new perspectives on V. I. Deshcherevskiy's kinetic theory of muscle contraction].
Deshcherevsky's kinetic theory of muscle contraction (Deshcherevsky, 1968, 1971) is considered in the light of the modern experimental data. The data are discussed, which support the validity of some propositions and conclusions of the theory, including the postulate on the negligibly small probability of pulling cross-bridge detachment. It is shown that if this postulate is accepted and the distance between the neighbouring actin sites for the given myosin cross-bridge attachment on the actin filament is taken as an actin filament half-turn (Sydorenko, 1982, 1984), then simple explanations, which don't contradict the cross-bridge hypothesis of force generation, could be given to a number of muscle behaviour features such as the high efficiency, stepwise shortening, repeated tension recovery after repeated forced step-wise shortening of activated muscle with the time-interval less than 10 ms, step-size up to 90nm powered by a single ATP molecule and so on.
Adenosine Triphosphate↗
Electric dipole theory and thermodynamics of actomyosin molecular motor in muscle contraction.
Movements in muscles are generated by the myosins which interact with the actin filaments. In this paper we present an electric theory to describe how the chemical energy is first stored in electrostatic form in the myosin system and how it is then released and transformed into work. Due to the longitudinal polarized molecular structure with the negative phosphate group tail, the ATP molecule possesses a large electric dipole moment (p(0)), which makes it an ideal energy source for the electric dipole motor of the actomyosin system. The myosin head contains a large number of strongly restrained water molecules, which makes the ATP-driven electric dipole motor possible. The strongly restrained water molecules can store the chemical energy released by ATP binding and hydrolysis processes in the electric form due to their myosin structure fixed electric dipole moments (p(i)). The decrease in the electric energy is transformed into mechanical work by the rotational movement of the myosin head, which follows from the interaction of the dipoles p(i) with the potential field V(0) of ATP and with the potential field Psi of the actin. The electrical meaning of the hydrolysis reaction is to reduce the dipole moment p(0)-the remaining dipole moment of the adenosine diphosphate (ADP) is appropriately smaller to return the low negative value of the electric energy nearly back to its initial value, enabling the removal of ADP from the myosin head so that the cycling process can be repeated. We derive for the electric energy of the myosin system a general equation, which contains the potential field V(0) with the dipole moment p(0), the dipole moments p(i) and the potential field psi. Using the previously published experimental data for the electric dipole of ATP (p(0) congruent with 230 debye) and for the amount of strongly restrained water molecules (N congruent with 720) in the myosin subfragment (S1), we show that the Gibbs free energy changes of the ATP binding and hydrolysis reaction steps can be converted into the form of electric energy. The mechanical action between myosin and actin is investigated by the principle of virtual work. An electric torque always appears, i.e. a moment of electric forces between dipoles p(0) and p(i)(/M/ > or = 16 pN nm) that causes the myosin head to function like a scissors-shaped electric dipole motor. The theory as a whole is illustrated by several numerical examples and the results are compared with experimental results.
Actomyosin↗
[Effect of thyroxine and noradrenaline on the energetics of muscle contraction].
The highly sensitive thermometric method (1.10(-5) degrees C/mm) revealed that the heat production of single contraction of the isolated rat diaphragmal muscle with artificial hyperthyrosis (HD) is nearly double of that of the normal muscle (ND). Noradrenaline added to the inculation solution entailed a greater increase of heat production of the muscle contraction in HD and had no significant effect on ND. However, calorific effect of thyroid hormone was about twice and a half as great as that of noradrenaline. These data suggest that thyroxin acts independently in the energy regulation during the cold acclimation of the organism, and the calorific effects of both hormones can be more effectively realized just at the moment of muscle contraction.
Animals↗
Effects of ventrolateral medullary NMDA-receptor antagonism on biogenic amines and pressor response to muscle contraction.
Effects of D(-)2-amino-7-phosphonohepatanoic acid (AP-7), an N-methyl-D-aspartic acid (NMDA) receptor antagonist, administered into rostral ventrolateral medulla (RVLM) on changes in mean arterial pressure (MAP), heart rate (HR), extracellular levels of serotonin (5-HT), dopamine (DA), and norepinephrine (NE) during static muscle contraction were investigated in anesthetized rats. Tibial nerve stimulation-evoked muscle contraction increased MAP and HR by 25+/-3 mmHg and 29+/-4 bpm, respectively. Microdialysis of AP-7 (1 microM) into the RVLM for 30 min attenuated the contraction-evoked cardiovascular responses with similar developed muscle tensions, without baseline HR or blood pressure changes. Administration of AP-7 into the caudal ventrolateral medulla had no effect on MAP or HR responses during contraction. Muscle contraction increased extracellular 5-HT in the RVLM by 144+/-35%, DA by 104+/-15% and NE by 62+/-12%. Perfusion of AP-7 for 30 min into the RVLM attenuated contraction-evoked increases in monoamines, concomitant to attenuating cardiovascular responses. Results demonstrate that NMDA-receptor blockade within the RVLM, but not the CVLM, inhibits cardiovascular responses during muscle contraction. Furthermore, NMDA receptor antagonism within the RVLM results in a decrease of biogenic amine release during muscle contraction, suggesting that extracellular biogenic amine concentrations are modulated by NMDA receptors.
2-Amino-5-phosphonovalerate↗
Molecular mechanism of ATP-dependent actin-myosin interaction in muscle contraction.
Among a variety of energy transduction mechanisms in biological systems, the mechanism of chemo-mechanical energy conversion in muscle contraction has been studied most intensively. From the standpoint of muscle biochemistry, muscle contraction is essentially the actomyosin ATPase reaction in solution. From the standpoint of muscle physiology, on the other hand, muscle contraction is the relative sliding between the thick and thin filaments resulting from the attachment-detachment cycle between actin and myosin. Although the large gap between muscle physiology and muscle biochemistry is now being gradually eliminated by various new experimental techniques such as the flash photolysis of caged compounds and in vitro motility assay systems, there still remain a number of uncertainties concerning the molecular mechanism of actin-myosin interaction coupled with hydrolysis of ATP. As described in this article, attention of most investigators in this research field has been focused on the detection of myosin head rotation coupled with muscle force generation. Unfortunately, however, attempts to detect the myosin head rotation have not yet been successful, despite the efforts of many investigators with various techniques including X-ray diffraction, quick freezing, and use of various probes attached to the myosin head. It seems therefore possible that the mechanism of muscle contraction might be different from the mechanism which have been generally accepted. This possibility seems to be supported, for example, by the unexpected dissociation between the ATPase activity and the force development in muscle fibers treated with anti-S-2 antibody (Fig. 9C).
Actins↗
Effects of nitric oxide donors and nitric oxide synthase substrates on ciliary muscle contracted by carbachol and endothelin for possible use in myopia prevention.
Research has suggested that the development of myopia may possibly be prevented by the use of drugs which facilitate relaxation of the intraocular ciliary muscle. We examined the effects of five nitric oxide-producing agents--two nitric oxide donors, hydralazine and sodium nitrite, and three nitric oxide synthase substrates, L-arginine, L-canavanine, and N-benzoyl-L-arginine ethyl ester--on isolated bovine ciliary muscle maximally contracted with either carbachol or endothelin-1. Of these agents, hydralazine and L-canavanine produced a relaxing effect on endothelin-1-contracted muscle that was significantly greater than relaxing effect on carbachol-contracted muscle. These results indicate that hydralazine and L-canavanine could possibly be used for the prevention of myopia by relaxing the ciliary muscle with few anticholinergic and cycloplegic side effects.
Animals↗
Bladder instillation of Escherichia coli lipopolysaccharide alters the muscle contractions in rat urinary bladder via a protein kinase C-related pathway.
Uropathogenic Escherichia coli is a common cause of urinary tract infection. We determined the effects of intravesical instillation of E. coli lipopolysaccharide (LPS, endotoxin) on muscle contractions, protein kinase C (PKC) translocation, and inducible nitric oxide synthase (iNOS) expression in rat urinary bladder. The contractions of the isolated rat detrusor muscle evoked by electrical field stimulations were measured short-term (1 h) or long-term (24 h) after intravesical instillation of LPS. One hour after LPS intravesical instillation, bladder PKC-alpha translocation from cytosolic fraction to membrane fraction and endothelial (e)NOS protein was elevated, and detrusor muscle contractions were significantly increased. PKC inhibitors chelerythrine and Ro32-0432 inhibited this LPS-enhanced contractile response. Application of PKC activator beta-phorbol-12,13-dibutyrate enhanced the muscle contractions. Three hours after intravesical instillation of LPS, iNOS mRNA was detected in the bladder. Immunoblotting study also demonstrated that the induction of iNOS proteins is detected in bladder in which LPS was instilled. 24 h after intravesical instillation of LPS, PKC-alpha translocation was impaired in the bladder; LPS did not affect PKC-delta translocation. Muscle contractions were also decreased 24 h after LPS intravesical instillation. Aminoguanidine, a selective iNOS inhibitor, blocked the decrease in PKC-alpha translocation and detrusor contractions induced by LPS. These results indicate that there are different mechanisms involved in the alteration of urinary bladder contractions after short-term and long-term treatment of LPS; an iNOS-regulated PKC signaling may participate in causing the inhibition of muscle contractions in urinary bladder induced by long-term LPS treatment.
Animals↗
Effects of nitric oxide and GABA interaction within ventrolateral medulla on cardiovascular responses during static muscle contraction.
We hypothesized that nitric oxide (NO) has opposing roles in regulating cardiovascular responses within the rostral (RVLM) and caudal (CVLM) ventrolateral medulla by modulating release of gamma-aminobutyric acid (GABA). We have measured GABA concentrations within the RVLM and CVLM during increases in mean arterial pressure (MAP) and heart rate (HR) following a 2-min tibial nerve stimulation-evoked static muscle contraction before and after microdialysis of the NO precursor, L-arginine (1.0 microM), for 30 min, and after the NO inhibitor, L-NMMA (1.0 microM), for 30 min. In eight anesthetized rats, muscle contraction significantly increased MAP, HR and GABA levels within the RVLM area (from 0.53+/-0.09 to 1.22+/-0.10 ng/10 microl). Following microdialysis of L-arginine, muscle contraction augmented GABA levels (from 0.45+/-0.07 to 2.18+/-0.09 ng/10 microl) and attenuated changes in MAP and HR. Subsequent application of L-NMMA significantly decreased GABA levels (from 0.47+/-0.08 to 0.22+/-0.07 ng/10 microl) but potentiated MAP and HR responses to a muscle contraction. In contrast, muscle contraction significantly increased MAP and HR but decreased GABA concentrations within the CVLM (from 1.20+/-0.20 to 0.78+/-0.17 ng/10 microl). Following microdialysis of L-arginine, muscle contraction significantly attenuated GABA levels (from 1.34+/-0.19 to 0.33+/-0.10 ng/10 microl) and augmented changes in MAP and HR in response to muscle contraction. A subsequent microdialysis of L-NMMA into the CVLM reversed the effects of L-arginine. These results demonstrate that NO within the RVLM and CVLM differentially modulates cardiovascular responses during static muscle contraction and that NO influences exercise-induced cardiovascular responses by modulating GABA release within the ventrolateral medulla.
Afferent Pathways↗
Effect of calcium antagonists (omega-conotoxin GVIA, verapamil, gallopamil, diltiazem) on bronchial smooth muscle contractions induced by soman.
The effect of the calcium antagonists omega-conotoxin GVIA, verapamil, gallopamil and diltiazem was investigated on in vitro bronchial smooth muscle contraction in the rat induced by the nerve agent soman. Soman inhibits the acetylcholinesterase activity irreversibly. The effect of the calcium channel antagonists on contractions induced by electrical field stimulation and carbachol was also investigated, in order to elucidate the mechanism by which calcium antagonists inhibit the soman induced contraction. omega-Conotoxin GVIA reduced the bronchial smooth muscle contraction induced by electrical field stimulation with an almost complete inhibition at approximately 1.0 x 10(-6) M. The soman induced contraction was only inhibited by 15% at a concentration of 3.0 x 10(-6) M omega-conotoxin GVIA. The organic calcium antagonists verapamil, gallopamil and diltiazem reduced both electrically and soman induced smooth muscle contraction. Complete inhibition of the contractions induced by soman was achieved at 1.4 x 10(-4) M for verapamil and gallopamil, while diltiazem inhibited the contraction to 7% of control at 1.4 x 10(-4) M. Verapamil, gallopamil and diltiazem increased the EC50 for carbachol significantly, while omega-conotoxin GVIA had no effect. None of the calcium antagonists had any effect on the maximal contraction induced by carbachol. Verapamil, gallopamil and diltiazem blocked, however, sub-maximal contractions induced by carbachol (10(-7)-10(-5) M) resulting in a right-shift of the dose response curve. The results show that omega-conotoxin GVIA inhibits the calcium-dependent release of acetylcholine which causes contraction of airway smooth muscle, while it has no effect on smooth muscle contraction induced by soman.(ABSTRACT TRUNCATED AT 250 WORDS)
Acetylcholinesterase↗
Use of ion channel blockers in studying the regulation of skeletal muscle contractions.
Effects of K(+)- and Cl(-)-channel blockers on the muscle contraction of mouse diaphragm in response to direct electrical muscle stimulation were studied. K(+)-channel blockers (0.1-1 mmol/l 4-aminopyridine, 0.4-1.2 mmol/l uranyl nitrate and 2-30 mmol/l tetraethylammonium chloride) and a Cl(-)-channel blocker (0.01-0.03 mmol/l 9-anthracene carboxylic acid) increased the contractile amplitudes in a limited extent not to exceed over 50% of control. However, the sequential applications of two different channel blockers at a rather low concentration markedly increased the contractile responses mostly over 300% of control except the combination of 4-aminopyridine and uranyl nitrate. It appears that two K(+)-channel blockers synergistically exerted their effects rather than additionally in the regulation of muscle contractions. Investigation on the possible mechanism of the synergistic action of K(+)-channel blockers suggested that prolongation of action potential durations was in a linear correlation with the increased contractions. On the other hand, the contractile potentiation induced by combination of K(+)- and Cl(-)-channel blockers was attributed to the production of repetitive action potential firings (150 +/- 12 Hz) upon a single electrical stimulation. Similar to Cl(-)-channel blocker, low Cl- as well as low Ca2+ enhanced K(+)-channel blockers in producing contractile potentiation accompanied with stimulus-bound repetitive discharges. Tetrodotoxin at a concentration of 0.03 mumol/l which did not affect the twitches evoked by electrical stimulations completely inhibited the contractile potentiation induced by the combined application of K(+)- and Cl(-)-channel blockers.(ABSTRACT TRUNCATED AT 250 WORDS)
Action Potentials↗
Glutamate neurotransmission and nitric oxide interaction within the ventrolateral medulla during cardiovascular responses to muscle contraction.
We previously reported that nitric oxide, within the RVLM and CVLM, plays an opposing role in modulating cardiovascular responses during static muscle contraction [B.J. Freda, R.S. Gaitonde, R. Lillaney, A. Ally, Cardiovascular responses to muscle contraction following microdialysis of nitric oxide precursor into ventrolateral medulla, Brain Res. 828 (1999) 60-67]. In this study, we determined whether the effects of administering L-arginine, a precursor for the synthesis of nitric oxide, and N(G)-monomethyl-L-arginine (L-NMMA), a nitric oxide synthase inhibitor, into the rostral (RVLM) and caudal (CVLM) ventrolateral medulla on cardiovascular responses elicited during static muscle contraction were mediated via an alteration of localized glutamate concentrations using microdialysis techniques. In experiments within the RVLM (n=8), muscle contraction increased MAP and HR by 21+/-2 mmHg and 22+/-3 bpm, respectively. Glutamate increased from 1.1+/-0.4 to 4.4+/- 0.6 ng/5 microl measured from bilateral RVLM areas. Microdialysis of L-arginine (1.0 microM) for 30 min attenuated the contraction-evoked increases in MAP, HR, and glutamate levels. After subsequent microdialysis of L-NMMA (1.0 microM) into the RVLM, contraction augmented the pressor and tachycardic responses and glutamate release. In experiments within CVLM (n=8), muscle contraction increased MAP and HR by 22+/-3 mmHg and 20+/-2 bpm, respectively. Glutamate increased from 0.8+/-0. 4 to 3.6+/-0.6 ng/5 microl measured from the CVLM. L-Arginine augmented the cardiovascular responses and glutamate release and L-NMMA attenuated all the effects. Results suggest that nitric oxide within the RVLM and CVLM plays opposing roles in modulating cardiovascular responses during static exercise via decreasing and increasing, respectively, extracellular glutamate levels.
Animals↗