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PubMed1989

Impedance of the chest wall during sustained respiratory muscle contraction.

We measured total chest wall impedance (Zw), "pathway impedances" of the rib cage (Zrcpath), and diaphragm-abdomen (Zd-apath), and impedance of the belly wall including abdominal contents (Zbw+) in five subjects during sustained expiratory (change in average pleural pressure [Ppl] from relaxation = 10 and 20 cmH2O) and inspiratory (change in Ppl = -10 and -20 cmH2O) muscle contraction, using forced oscillatory techniques (0.5-4 Hz) we have previously reported for relaxation (J. Appl. Physiol. 66: 350-359, 1989). Chest wall configuration and mean lung volume were kept constant. Zw, Zrcpath, Zd-apath, and Zbw+ all increased greatly at each frequency during expiratory muscle contraction; increases were proportional to effort. Zw, Zrcpath, and Zd-apath increased greatly during inspiratory muscle contraction, but Zbw+ did not. Resistances and elastances calculated from each of the impedances showed the same changes during muscle contraction as the corresponding impedances. Each of the resistances decreased as frequency increased, independent of effort; elastances generally increased with frequency. These frequency dependencies were similar to those measured in relaxed or tetanized isolated muscle during sinusoidal stretching (P.M. Rack, J. Physiol. Lond. 183: 1-14, 1966). We conclude that during respiratory muscle contraction 1) chest wall impedance increases, 2) changes in regional chest wall impedances can be somewhat independent, depending on which muscles contract, and 3) increases in chest wall impedance are due, at least in part, to changes in the passive properties of the muscles themselves.

Adult↗
PubMed1986

A dynamic model of smooth muscle contraction.

A dynamic model of smooth muscle contraction is presented and is compared with the mechanical properties of vascular smooth muscle in the rat portal vein. The model is based on the sliding filament theory and the assumption that force is produced by cross-bridges extending from the myosin to the actin filaments. Thus, the fundamental aspects of the model are also potentially applicable to skeletal muscle. The main concept of the model is that the transfer of energy via the cross-bridges can be described as a 'friction clutch' mechanism. It is shown that a mathematical formulation of this concept gives rise to a model that agrees well with experimental observations on smooth muscle mechanics under isotonic as well as isometric conditions. It is noted that the model, without any ad hoc assumptions, displays a nonhyperbolic force-velocity relationship in its high-force portion and that it is able to maintain isometric force in conditions of reduced maximum contraction velocity. Both these findings are consistent with new experimental observations on smooth muscle mechanics cannot be accounted for by the classical Hill model.

Animals↗
PubMed1999

Conformational changes of contractile proteins and their role in muscle contraction.

The review summarizes the results of studies on conformational changes in contractile proteins that occur during muscle contraction. Polarized fluorescence of tryptophan residues in actin and of fluorescent probes bound specifically to different sites on actin, myosin, or tropomyosin in muscle fibers was measured. The results show that the transition of actomyosin complex from the weak to the strong-binding state is accompanied by a change in the orientation of F-actin subunits with the C and N termini moving opposite to a large part of the subunit. Myosin light chains and some areas in the 20-kDa domain of myosin head move in the same direction as the C- and N-terminal regions of actin. It is established that troponin, caldesmon, calponin, and myosin systems of regulation of muscle contraction modify intramolecular actomyosin rearrangements in a Ca(2+)-dependent manner. The role of intramolecular movements of contractile proteins in muscle contraction is discussed.

Actins↗
PubMed1999

Regulation of Ca2+-independent smooth muscle contraction by alternative staurosporine-sensitive kinase.

It is well known that inhibition of myosin phosphatase induces smooth muscle contraction in the absence of Ca2+. We characterized the kinase(s) which plays a role in Ca2+-independent, microcystin-LR-induced contraction in permeabilized smooth muscle of the rabbit portal vein. Assessments of various protein kinase inhibitors revealed this kinase(s) (1) was sensitive to staurosporine (1 microM), but resistant to other agents including wortmannin (10 microM), Y-27632 ((R)-(+)-trans-N-(4-pyridyl)-4-(1-aminoethyl)-cyclohexanecarboxamide+ ++, 100 microM). HA1077 (1-(5-isoquinolinylsulfonyl)-homopiperazine, 100 microM), H-7 (1-(5-isoquinolinylsulfonyl)-2-methylpiperazine, 100 microM), and calphostin C (100 microM), and (2) induced phosphorylation of 20 kDa myosin light chain at serine-19. We concluded that other kinases exist which phosphorylate myosin light chain at serine-19 and induce Ca2+-independent smooth muscle contraction, distinct from Rho-associated kinase, myosin light chain kinase, and protein kinase C.

Amides↗
PubMed1985

Nifedipine inhibits human bronchial smooth muscle contractions induced by leukotrienes C4 and D4, prostaglandin F2 alpha, and potassium.

The effects of nifedipine, a calcium channel blocker, on human bronchial smooth muscle contractions induced by leukotrienes C4 and D4 (LTC4, LTD4), prostaglandin F2 alpha (PGF2 alpha), and potassium were studied in vitro. The LTC4, LTD4, PGF2 alpha, and potassium caused bronchial smooth muscle contractions. After incubation with nifedipine at 2.9 X 10(-6)M, the contractions caused by LTC4, LTD4, PGF2 alpha, and potassium were significantly decreased. Nifedipine also significantly reversed human bronchial smooth muscle contractions previously initiated by these agonists. The effect of nifedipine on potassium contraction was significantly greater than that on LTC4, LTD4, and PGF2 alpha-induced contractions. The pharmacologic feature of nifedipine is that it inhibits the calcium influx associated with membrane depolarization. Therefore, these results suggest that there are two mechanisms of calcium movements in human bronchial smooth muscle contractions induced by LTC4, LTD4, and PGF2 alpha: membrane-depolarization-dependent and -independent mechanisms.

Aged↗
PubMed1985

Muscle contraction and free energy transduction in biological systems.

Muscle contraction occurs when the actin and myosin filaments in muscle are driven past each other by a cyclic interaction of adenosine triphosphate (ATP) and actin with cross-bridges that extend from myosin. Current biochemical studies suggest that, during each adenosine triphosphatase cycle, the myosin cross-bridge alternates between two main conformations, which differ markedly in their strength of binding to actin and in their overall structure. Binding of ATP to the cross-bridge induces the weak-binding conformation, whereas inorganic phosphate release returns the cross-bridge to the strong-binding conformation. This cross-bridge cycle is similar to the kinetic cycle that drives active transport and illustrates the general principles of free energy transduction by adenosine triphosphatase systems.

Actins↗
PubMed1988

Biochemical events associated with activation of smooth muscle contraction.

Biochemical events associated with activation of smooth muscle contraction were studied in neurally stimulated bovine tracheal smooth muscle. A latency period of 500 ms preceded increases in isometric force and myosin light chain phosphorylation. However, stimulation resulted in the rapid hydrolysis of inositol phospholipids as demonstrated by increases in inositol phosphates by 500 ms. Inositol trisphosphate increased 2-fold with no significant change in inositol tetrakisphosphate. The apparent activation state of myosin light chain kinase was assessed indirectly through measurements of the fractional activation of a second calmodulin-dependent enzyme, cyclic nucleotide phosphodiesterase. The fractional activation of cyclic nucleotide phosphodiesterase increased after neural stimulation to a maximal extent by 500 ms and remained at this level for at least 4 s. The monophosphorylation of myosin light chain increased after 500 ms and reached a maximum value by 2 s. Diphosphorylation also occurred but to a much lesser extent. Fractional activation of cyclic nucleotide phosphodiesterase and myosin light chain phosphorylation both decreased after 10 min continuous stimulation, although the force response remained at a maximal level. These observations demonstrate that inositol trisphosphate formation and activation of cyclic nucleotide phosphodiesterase (and hence most likely myosin light chain kinase) by calmodulin precede myosin light chain phosphorylation and that these events are sufficiently rapid to mediate the contractile response of neurally stimulated tracheal smooth muscle.

Animals↗
PubMed2004

The effect of high frequency electric pulses on muscle contractions and antitumor efficiency in vivo for a potential use in clinical electrochemotherapy.

Muscle contractions present the main source of unpleasant sensations for patients undergoing electrochemotherapy. The contractions are a consequence of high voltage pulse delivery. Relatively low repetition frequency of these pulses (1 Hz) results in separate muscle contractions associated with each single pulse that is delivered. It would be possible to reduce the number of unpleasant sensations by increasing the frequency of electric pulses above the frequency of tetanic contraction, provided that the antitumor efficiency of electrochemotherapy remains the same. These assumptions were investigated in the present paper by measuring the muscle torque at different pulse repetition frequencies and at two different pulse amplitudes in rats and studying the antitumor efficiency of electrochemotherapy at different pulse repetition frequencies on tumors in mice. Measurements of muscle torque confirmed that pulse frequencies above the frequency of tetanic contraction (>100 Hz) reduce the number of individual contractions to a single muscle contraction. Regardless of the pulse amplitude, with increasing pulse frequency muscle torque increases up to the frequency of 100 or 200 Hz and then decreases to a value similar to that after application of a 1 Hz pulse train. Electrochemotherapy in vivo with higher repetition frequencies inhibits tumor growth and is efficient at all pulse frequencies examined (1 Hz-5 kHz). These results suggest that there is a considerable potential for clinical use of high frequency pulses in electrochemotherapy.

Animals↗
PubMed2000

Modulation of extracellular glutamate and pressor response to muscle contraction during NMDA-receptor blockade in the rostral ventrolateral medulla.

Recently our laboratory demonstrated increases in extracellular glutamate concentrations within the rostral ventrolateral medulla (RVLM) during static muscle contraction (Caringi, D.C., Maher, T., Chaiyakul, P., Asmundsson, G., Ishide, T., Ally, A. Pflügers Arch. Eur. J. Physiol., 435:465-471, 1998). In this study, we determined effects of microdialyzing D(-)2-amino-7-phosphonohepatanoic acid (AP-7), an NMDA-receptor antagonist, into the RVLM on changes in mean arterial pressure (MAP), heart rate (HR), and extracellular glutamate levels during muscle contraction in anesthetized rats. Bilateral placements of microdialysis probes into the RVLM were verified by perfusing L-glutamate and obtaining a pressor response. Muscle contraction for 2 min, increased MAP and HR by 22+/-4 mmHg and 28+/-5 bpm, respectively. Extracellular glutamate as determined by microdialysis increased from 0.8+/-0.2 to 6.3+/-1.2 ng/5 microl. Microdialysis of AP-7 (1.0 microM) for 30 min inhibited contraction-evoked MAP and HR responses (10+/-3 mmHg and 13+/-3 bpm) and attenuated increases in glutamate during muscle contraction. Developed tensions did not differ during contractions before and after AP-7. Results demonstrate that NMDA-receptor blockade in the RVLM inhibits cardiovascular responses during static muscle contraction via a reduction in extracellular glutamate levels.

2-Amino-5-phosphonovalerate↗
PubMed1989

[Effect of phosphorylation of light chain myosin and Ca2+ on the conformation of F-actin during skeletal muscle contraction].

The dependence of polarized fluorescence of rhodaminylphalloin specifically bound to F-actin and the tension developed by a fiber upon phosphorylation of myosin (18.5 kD) light chains as well as on the concentration of free Ca2+ was observed during the contraction of glycerinated rabbit skeletal muscle fibers. Still greater changes in the polarized fluorescence and higher values of tension were recorded for fibers with phosphorylated light chains at low (0.6 microM) Ca2+ concentrations as well as for those with dephosphorylated light chains at high (10 microM) Ca2+ concentrations. It is concluded that phosphorylation of myosin light chains modulates skeletal muscle contraction. The mechanisms of modulation involve conformational changes in F-actin.

Actins↗
PubMed1998

Protein kinase C activation during Ca2+-independent vascular smooth muscle contraction.

The cellular signaling mechanisms that modulate the sustained vascular smooth muscle contractions that occur in vasospasm are not known. We and others have hypothesized that a kinase cascade involving protein kinase C (PKC) modulates sustained vascular smooth muscle contraction. The purpose of this investigation was to develop a model in which the traditional contractile pathways involving myosin light chain phosphorylation are not activated and determine if the PKC pathway is activated under these conditions. The phosphorylation of caldesmon, myosin light chain (MLC20), and the specific PKC substrate, MARCKS (myristoylated, alanine-rich C-kinase substrate) was measured in bovine carotid arterial smoothmuscle (BCASM) stimulated with phorbol 12,13-dibutyrate (PDBu) under Ca2+-containing and Ca2+-free conditions. PDBu stimulation led to increases in caldesmon and MARCKS phosphorylation to the same degree in the presence or absence of Ca2+. PDBu stimulation but did not lead to increases in MLC20 phosphorylation over basal levels in Ca2+-free conditions. Immunoblot analysis of BCASM using PKC isoform-specific antibodies demonstrated the presence of one "Ca2+- dependent" PKC isoform: alpha, and two of the "Ca2+-independent" isoforms: epsilon and zeta. These data suggest that Ca2+-independent isoforms of PKC may play a role in the sustained phase of BCASM contractions through a kinase cascade that involves caldesmon and MARCKS phosphorylation but not MLC20 phosphorylation.

Animals↗
PubMed1998

Effect of barodenervation on c-Fos expression in the medulla induced by static muscle contraction in cats.

A previous study has shown increased Fos-like immunoreactivity (FLI), a marker of neural activation, in the nucleus of the solitary tract (NTS) and the ventrolateral medulla (VLM) after static muscle contraction elicited by electrical stimulation of L7 and S1 ventral roots of the spinal cord in anesthetized, baroreceptor-intact cats. Because the electrically induced static muscle contraction reflexly increased arterial blood pressure, the concomitant activation of the arterial baroreceptor reflex during static muscle contraction may have resulted in some of the FLI labeling that was observed in the medulla. The purpose of this study was to determine regions in the medulla that are activated by muscle contraction in the absence of arterial baroreceptor input. Electrical stimulation of L7 and S1 ventral roots of the spinal cord was used to elicit static muscle contraction, and FLI in the medulla was determined in barointact and barodenervated cats. In barointact contraction cats, FLI was observed in the lateral reticular nucleus (LRN), NTS, lateral tegmental field (FTL), subretrofacial nucleus (SRF), and A1 region of the medulla. In barodenervated contraction cats, FLI increased in the same regions; however, the number of FLI-labeled cells in the NTS, FTL, and A1 region was significantly less than in barointact contraction animals. No significant difference in the number of FLI-labeled cells was found in the LRN and SRF between the two groups. These results clearly demonstrate that cardiovascular regions in the medulla are activated by input from afferent activity originating in skeletal muscle independently of concomitant arterial baroreceptor reflex activation.

Afferent Pathways↗
PubMed2006

Alterations in the blood velocity profile influence the blood flow response during muscle contractions and relaxations.

The present study examined the influences of the muscle contraction (MCP) and relaxation (MRP) phases, as well as systole and diastole, on the blood velocity profile and flow in the conduit artery at different dynamic muscle contraction forces. Eight healthy volunteers performed one-legged dynamic knee-extensor exercise at work rates of 5, 10, 20, 30, and 40 W at 60 contractions per minute. The time- and space-averaged, amplitude-weighted, mean (V(mean)) and maximum (V(max)) blood flow velocities were continuously measured in the common femoral artery during the cardiosystolic (CSP) and cardiodiastolic (CDP) phases during MCP and MRP, respectively. The V(max)/V(mean) ratio was used as a flow profile index where a ratio of approximately (~) 1 indicates a "flat" velocity profile, and a ratio significantly greater than (>>) 1 indicates a "parabolic" velocity profile. At rest, a "steeper" parabolic velocity profile was found during the CDP (ratio: 1.75 +/- 0.06) than during the CSP (ratio: 1.31 +/- 0.02). During the MRP of exercise, the V(max)/V(mean) ratio shifted to be less steep (p < 0.05) than at rest during the CDP (ratio: 1.41-1.54) at 5, 10, 20, 30, and 40 W; whereas it was slightly higher (p < 0.05) at 30 and 40 W than at rest during the CSP (ratio: 1.43-1.46). During the MCP, the parabolic blood velocity profile was enhanced (p < 0.05) at higher contraction forces, 20 W during the CDP (ratio: 2.15-2.52) and 30 W during the CSP (ratio: 1.49-1.77), potentially because of a greater retrograde flow component. A higher blood flow furthermore appeared during the MRP compared to during the MCP, coinciding with a greater uniformity of the red blood cells moving at higher blood velocities during the MRP. Thus part of the difference in the magnitude of blood flow during the MRP vs. MCP may be due to the alterations of the blood velocity flow profile.

Adult↗
PubMed1996

Perfused skeletal muscle contraction and metabolism improved by angiotensin II-mediated vasoconstriction.

In the present study, the effects of angiotensin II (ANG II) on tension development and associated metabolism during twitch and tetanic stimulation via the sciatic nerve of the gastrocnemius-plantaris-soleus muscle group of the perfused rat hindlimb were investigated. Rat hindlimbs were perfused at constant flow with an erythrocyte-containing medium equilibrated with 95% air-5% CO2 at 37 degrees C, and determinations of oxygen and glucose uptake, lactate and glycerol release, and 2-deoxy-D-[1-3H]glucose uptake (Rg') into individual muscles were carried out. ANG II (1 nM) infusion alone caused vasoconstriction with increased oxygen (55%) and glucose (98%) uptake and lactate (37%) and glycerol (64%) release. ANG II infusion during muscle contraction gave less vasoconstriction but increased the tension development during tetanic stimulation by 80% and increased the contraction-induced oxygen uptake and Rg' by plantaris and gastrocnemius red and white muscles. These effects of ANG II may have been due to increased nutritive flow to contracting muscles or to redirection of flow from noncontracting and type I fiber muscles to the type II fiber contracting muscles in the hindlimb. The results indicate that the regulation of flow by the vasculature is an important regulator of muscle contraction and metabolism.

Angiotensin II↗
PubMed2000

Circulatory responses to voluntary and electrically induced muscle contractions in humans.

BACKGROUND AND PURPOSE: Transcutaneous electrical nerve stimulation (TENS) increases regional blood flow when applied at intensities sufficient to cause skeletal muscle contraction. It is not known whether increases in blood flow elicited by TENS differ from those caused by voluntary muscle contraction. The purpose of this study, therefore, was to compare the hemodynamic effects of these 2 types of muscle contraction. SUBJECTS AND METHODS: Fourteen people with no known pathology, aged 18 to 49 years (mean=28, SD=8), served as subjects. Calf blood flow (venous occlusion plethysmography), heart rate (electrocardiogram), blood pressure (automated sphygmomanometry), and force (footplate transducer) were measured during electrically induced and voluntary contractions. RESULTS: Both modes of exercise caused rapid, but short-lived vasodilation (calf vascular resistance [mean(SEM]: (53%(3% for voluntary contractions versus (57%(4% for electrically induced contractions). The vasodilation caused by electrically induced contractions persisted for at least 15 seconds in the postexercise period, whereas the vasodilation elicited by voluntary contractions had resolved by this time point. CONCLUSION AND DISCUSSION: The hemodynamic changes elicited by voluntary and electrically induced muscle contractions are similar in magnitude but different in duration.

Adult↗
PubMed2001

Larval muscle contraction fails to produce torsion in a trochoidean gastropod.

The causes and effects of ontogenetic torsion in gastropods have been debated intensely for more than a century (1-19). Occurring rapidly and very early in development, torsion figures prominently in shaping both the larval and adult body plans. We show that mechanical explanations of the ontogenetic event that invoke contraction of larval retractor muscles are inadequate to explain the observed consequences in some gastropods. The classic mechanical explanation of Crofts (4, 5) and subsequent refinements of her explanation have been based on species with rigid larval shell properties (18, 19) that cannot be extrapolated to all gastropods. We present visual evidence of the lack of rigidity of the uncalcified larval shell in a basal trochid gastropod, Margarites pupillus (Gould), and provide photographic confirmation of our prediction that larval retractor muscle contraction is insufficient to produce more than local deformation or dimpling at the site of muscle insertion. These findings do not refute muscular contraction as a primary cause of ontogenetic torsion in gastropods that calcify their larval shells prior to the onset of torsion, nor do they refute the monophyly of torsion. They do, however, suggest that torsion may be a loosely constrained developmental process with multiple pathways to the more constrained end result (20, 21).

Animals↗