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PubMed1984

Fade in voluntary muscle contractions of patients with sequelae after poliomyelitis.

The isometric contraction pattern was followed in three female and two male patients with lower motoneuron paralysis due to sequelae from poliomyelitis in 1942-48. In uninstructed contractions, force increased slowly to an almost horizontal level which could be kept up for as long as desired. During rapid maximal voluntary contractions, a "biphasic" mechanogram was seen in 49% of 204 contractions, with a first maximum after 0.3 s (0.1-0.9), separated by a notch from a second maximum after 1.1 s (0.3-2.3). In the rest of the contractions, force could not be generated rapidly, despite the intention of the subjects, and a single maximum in the mechanogram was seen after 0.9 s (0.2-2.4). In contractions where a biphasic contraction pattern was seen, the electromyographic activity was greatest during approximately the first one half second of the contraction. In the other contractions the electromyographic activity was about the same during the whole contraction. The results suggest that the mechanograms are composed of a high innervation threshold, fast phasically active component, and a low innervation threshold, slow tonically active component. Fade represents the waning of tension in the phasically active component present in some contractions, while this component appears to be eliminated by poliomyelitis in other muscle contractions.

Adult↗
PubMed1989

Capillary tortuosity in skeletal muscles of mammals depends on muscle contraction.

Capillary orientation (anisotropy) was compared in hindlimb muscles of mammals of different size and/or different aerobic capacity (dog, goat, pony, and calf). All muscles were fixed by vascular perfusion at sarcomere lengths ranging from 1.5 to 2.7 micron. The ratios of capillary counts per fiber cross-sectional area on two sets of sections (0 and 90 degrees) to the muscle fiber axis were used to estimate capillary anisotropy and the coefficient c(K,0) relating 1) capillary counts on transverse sections (a commonly used parameter to assess muscle capillarity) and 2) capillary length per volume of fiber (i.e., capillary length density). Capillary orientation parallel to the muscle fiber axis decreased substantially with muscle fiber shortening. In muscles fixed at sarcomere lengths of 2.69 microns (dog vastus intermedius) and 1.52 microns (dog gastrocnemius), capillary tortuosity and branching added 7 and 64%, respectively, to capillary length density. The data obtained in this study are highly consistent with the previously demonstrated relationship between capillary anisotropy and sarcomere length in extended vs. contracted rat muscles, by use of the same method. Capillary anisotropy in mammalian locomotory muscles is curvilinearly related to sarcomere length. No systematic difference was found in capillary tortuosity with either body size, athletic ability, or aerobic capacity. Capillary tortuosity is a consequence of fiber shortening rather than an indicator of the O2 requirements of the tissue.

Animals↗
PubMed1992

Strength increases from the motor program: comparison of training with maximal voluntary and imagined muscle contractions.

1. This study addressed potential neural mechanisms of the strength increase that occur before muscle hypertrophy. In particular we examined whether such strength increases may result from training-induced changes in voluntary motor programs. We compared the maximal voluntary force production after a training program of repetitive maximal isometric muscle contractions with force output after a training program that did not involve repetitive activation of muscle; that is, after mental training. 2. Subjects trained their left hypothenar muscles for 4 wk, five sessions per week. One group produced repeated maximal isometric contractions of the abductor muscles of the fifth digit's metacarpophalangeal joint. A second group imagined producing these same, effortful isometric contractions. A third group did not train their fifth digit. Maximal abduction force, flexion/extension force and electrically evoked twitch force (abduction) of the fifth digit were measured along with maximal integrated electromyograms (EMG) of the hypothenar muscles from both hands before and after training. 3. Average abduction force of the left fifth digit increased 22% for the Imagining group and 30% for the Contraction group. The mean increase for the Control group was 3.7%. 4. The maximal abduction force of the right (untrained) fifth digit increased significantly in both the Imagining and Contraction groups after training (10 and 14%, respectively), but not in the Control group (2.3%). These results are consistent with previous studies of training effects on contralateral limbs. 5. The abduction twitch force evoked by supramaximal electrical stimulations of the ulnar nerve was unchanged in all three groups after training, consistent with an absence of muscle hypertrophy. The maximal force of the left great toe extensors for individual subjects remained unchanged after training, which argues against strength increases due to general increases in effort level. 6. Increases in abduction and flexion forces of the fifth digit were poorly correlated in subjects of both training groups. The fifth finger abduction force and the hypothenar integrated EMG increases were not well correlated in these subjects either. Together these results indicate that training-induced changes of synergist and antagonist muscle activation patterns may have contributed to force increases in some of the subjects. 7. Strength increases can be achieved without repeated muscle activation. These force gains appear to result from practice effects on central motor programming/planning. The results of these experiments add to existing evidence for the neural origin of strength increases that occur before muscle hypertrophy.

Adult↗
PubMed1998

A role for MAP kinase in differentiated smooth muscle contraction evoked by alpha-adrenoceptor stimulation.

The purpose of this study was to investigate the potential role of mitogen-activated protein (MAP) kinase in smooth muscle contraction by monitoring MAP kinase activation, caldesmon phosphorylation, and contractile force during agonist stimulation. Isometric tension in response to KCl and phenylephrine (PE) was measured from strips of ferret aorta. MAP kinase activation was monitored by Western blot using a phosphospecific p44/p42 MAP kinase antibody. Caldesmon phosphorylation was assessed using specific phosphocaldesmon antibodies. We report here that treatment of smooth muscle strips with PD-098059, a specific inhibitor of MAP kinase kinase, did not detectably modify the KCl-evoked contraction but significantly inhibited the contraction to PE in the absence of extracellular Ca2+. In this experimental condition, where the contraction occurs in the absence of increases in 20-kDa myosin light chain phosphorylation, PD-098059 also inhibited significantly MAP kinase and caldesmon phosphorylation. Collectively, these results demonstrate a direct cause-and-effect relationship between MAP kinase activation and Ca2+-independent smooth muscle contraction and support the concept of caldesmon phosphorylation as the missing link between both events.

Adrenergic alpha-Agonists↗
PubMed1981

The influence of recruitment order and temperature on muscle contraction with special reference to motor unit fatigue.

Although recruitment in man often proceeds from the slowest to fastest motor units, a variety of stimuli can alter this order. To study the effect of recruitment order on isometric performance, the tetanic tension of individual fast and slow twitch motor units was measured during fatiguing isometric contractions of the medial gastrocnemius muscle of the cat with recruitment proceeding from either the slowest to fastest or fastest to slowest motor units throughout the contractions. The muscles were stimulated electrically through the ventral roots of the spinal cord. Fatiguing isometric tensions were examined at 10, 20, 40, 70, or 100% of the initial strength of the muscles at 28 and 38 degrees C. The results of these experiments showed that for contractions at low isometric tensions (20 and 40% of the muscles' strength), especially at the lower temperature, the endurance was longer when recruitment proceeded from the slowest to fastest units. The reason for this appeared to be linked to the more rapid rate of fall of tension over time in fast as opposed to slow twitch motor units.

Animals↗
PubMed1999

Inhalation of mainstream and sidestream cigarette smoke retards embryo transport and slows muscle contraction in oviducts of hamsters (Mesocricetus auratus).

Prior experiments have shown that the functioning of hamster oviducts is impaired by in vitro exposure to cigarette smoke. To determine if cigarette smoke affects oviductal functioning in vivo, an inhalation experiment was done in which hamsters were exposed to doses of smoke similar to those received by human smokers. The effects of mainstream smoke (the bolus of smoke inhaled by active smokers) and sidestream smoke (the main component in environmental tobacco smoke) were compared. Transport of preimplantation embryos through the hamster oviduct was retarded in females inhaling doses of mainstream or sidestream smoke that produced serum cotinine levels within the range reported for women who actively or passively smoke during pregnancy. In addition, hamster oviductal muscle contraction rate decreased significantly during a single exposure of animals to either mainstream or sidestream smoke, and contraction rate failed to return to initial control values during a 25-min recovery period. Both preimplantation embryo transport and muscle contraction were more sensitive to sidestream than mainstream smoke. These data demonstrate that inhalation of doses of mainstream and sidestream cigarette similar to those received by active and passive human smokers adversely affects functioning of the oviduct and may explain the increased incidence of ectopic pregnancies reported in women who smoke.

Animals↗
PubMed1995

A direct regulatory role for troponin T and a dual role for troponin C in the Ca2+ regulation of muscle contraction.

Troponin (Tn), containing three subunits: Ca2+ binding (TnC), inhibitory (TnI), and tropomyosin binding (TnT), plays a crucial role in the Ca2+ regulation of vertebrate striated muscle contraction. These three subunits function by interacting with each other and with the other thin filament proteins. Previous studies suggested that the primary role of TnT is to anchor the TnI.TnC complex to the thin filament, primarily through its interactions with TnI and tropomyosin. We propose here a new role for TnT. Our results indicate that, when TnT is combined with the TnI.TnC complex, there is an activation of actomyosin ATPase that is Ca(2+)-dependent. To determine whether the latter results from a direct effect of TnC on TnT or indirectly from an effect of TnC on TnI which is transmitted to TnT, we prepared a deletion mutant (deletion of residues 1-57) of TnI, TnId57 (Sheng et al. (1992) J. Biol. Chem. 267, 25407-25413), which interacts with TnC but not TnT. Both wild type (TnI.TnC.TnT) and mutant (TnId57.TnC.TnT) Tn complexes demonstrated equivalent activity in the Ca2+ regulation of actomyosin-S1 ATPase activity. Similarly, both TnI and TnId57 could equally reconstitute TnI-depleted skinned muscle fibers. Therefore, since TnId57 does not interact with TnT, these results suggest that TnT reconstitutes native Ca2+ sensitivity via direct interaction with TnC. Thus Ca2+ binding to TnC would have a dual role: 1) release of the ATPase inhibition by TnI and 2) activation of the ATPase through interaction with TnT.

Animals↗
PubMed1994

Fusimotor responses to fatiguing muscle contractions in non-denervated hindlimb of decerebrate cats.

Changes in discharge rate of 21 fusimotor neurons to medial gastrocnemius muscle during long-lasting fatiguing contractions of lateral gastrocnemius and soleus muscles were recorded in decerebrate cats with innervation of the same hindlimb preserved. Both the spontaneous activity and reflex responses of fusimotor neurons differed from those found previously in preparations with denervated hindlimb. Higher proportion of units fired at rest at rates above 20 impulses/s, the initial increase in discharge rate at the onset of muscle contraction was markedly prolonged, lasting in the majority of units throughout the muscle contraction, while the late increase in discharge rate developing with muscle fatigue was either absent or short-lasting. It is suggested that the increase in spontaneous firing rate occurs in dynamic fusimotor neurons being supported by afferent inflow from secondary muscle spindle endings from non-contracting muscles, the enhancement of the early responses to be primarily due to recurrent disinhibition and the differences in changes of early and late responses to reflect their partly different origin. The possibility is raised that the late reflex responses are lacking more often in static than in dynamic fusimotor neurons. From the functional point of view the differences in fusimotor reflex responses in innervated versus denervated hindlimb may indicate their susceptibility to modifications by changes in afferent inflow according, supposedly, to the current demands of motor control of the active and/or fatigued muscle.

Animals↗
PubMed2001

Rapid cardiac adaptation to exercise demand signal and execution of maximal leg muscle contraction.

We investigated the neural regulation of the cardiac interval to an exercise demand signal and to a repeated exercise in 20 healthy human subjects. Electrocardiogram (ECG), muscle torque, and electromyogram (EMG) were simultaneously measured and their time relationships compared before and during the exercise. The R-R interval of ECG was directly increased by the exercise demand signal itself before the onset of EMG but not reflexly by muscle contraction. The cardiac interval decreased at the onset of exercise. Under the condition of repeated maximum eccentric training, the resting cardiac interval decreased prior to the exercise, whereas the brief increase in cardiac interval to the exercise demand signal remained unchanged. These results suggested that when autonomic nerve activity to the pacemaker is activated by the exercise demand signal, an initial effect of vagal nerve activity appears, and an effect of vagal nerve withdrawal and/or sympathetic nerve activity then appears. The responses of the heart and leg skeletal muscle at the onset of exercise are not synchronized, and the cardiac interval is controlled by vagal and sympathetic nerve activities to effect a transition to a high heart rate as quickly and smoothly as possible.

Adaptation, Physiological↗
PubMedDate not supplied

Prevention of persistent cerebral smooth muscle contraction in response to whole blood.

Using an in vitro system designed to measure arterial constriction, we have demonstrated the importance of platelet function in maintaining cerebral smooth muscle contraction after whole blood injection. We tested two agents, acetyl salicylic acid (ASA) and phthalazinol, both known to interfere with platelet function. In control tests normal rabbit and monkey blood produced a reliable and persistent arterial constriction. In experimental tests blood drawn from animals premedicated with ASA and phthalazinol failed to produce a persistent contraction. These results support the hypothesis that chemicals released during platelet aggregation may be important in persistent vasospasm.

Animals↗
PubMed1995

Attenuation of the reflex responses to muscle contraction by the coadministration of antagonists to substance P and somatostatin into the dorsal horn.

OBJECTIVE: The aim was to determine if the coadministration of antagonists to substance P and somatostatin into the L7 dorsal horn blunts the reflex cardiovascular responses to static contraction to a greater extent than each antagonist alone. The possibility that this attenuation is mediated by blunting the contraction evoked increases in sympathetic outflow was also tested. METHODS: Using alpha chloralose anaesthetised cats (n = 8), static contraction and stretch of the triceps surae muscle were performed before and after microinjecting (1 microliter) 250 ng of the substance P antagonist, D-Pro2-D-Phe7-D-Trp9-substance P, and the somatostatin antagonist, cyclo(7-amino-heptanoyl-phenylalanyl-D-tryptophyl-lysyl-threonyl-[ benzyl]). The muscle was contracted by electrically stimulating the peripheral end of the cut L7 ventral root. RESULTS: Before injecting the antagonists, static muscle contraction increased mean arterial blood pressure by 40(SEM 6) mm Hg, heart rate by 13(2) beats.min-1, and renal sympathetic nerve activity (RSNA) by 41(7)%. These changes were blunted by the antagonists since the increases in blood pressure, heart rate, and RSNA were reduced to 21(3) mm Hg, 8(1) beats.min-1, and 23(5)%, respectively. In contrast, antagonist administration did not affect the pressor [33(5) v 31(5) mm Hg], heart rate [9(2) v 10(2) beats.min-1], or RSNA [23(4)% v 25(5)%] responses to muscle stretch. Microinjection of 2% lignocaine into the dorsal horn virtually abolished the reflex changes elicited by muscle stretch. CONCLUSIONS: The release of substance P and somatostatin in the spinal cord plays a role in mediating the cardiovascular changes caused by static contraction, but the release of other neurotransmitters/neuromodulators is also involved. The attenuation produced by these antagonists is mediated, at least in part, by reducing sympathetic outflow.

Animals↗
PubMed2004

Decavanadate as a biochemical tool in the elucidation of muscle contraction regulation.

Recently reported decameric vanadate (V(10)) high affinity binding site in myosin S1, suggests that it can be used as a tool in the muscle contraction regulation. In the present article, it is shown that V(10) species induces myosin S1 cleavage, upon irradiation, at the 23 and 74 kDa sites, the latter being prevented by actin and the former blocked by the presence of ATP. Identical cleavage patterns were found for meta- and decavanadate solutions, indicating that V(10) and tetrameric vanadate (V(4)) have the same binding sites in myosin S1. Concentrations as low as 50 muM decavanadate (5 muM V(10) species) induces 30% of protein cleavage, whereas 500 muM metavanadate is needed to attain the same extent of cleavage. After irradiation, V(10) species is rapidly decomposed, upon protein addition, forming vanadyl (V(4+)) species during the process. It was also observed by NMR line broadening experiments that, V(10) competes with V(4) for the myosin S1 binding sites, having a higher affinity. In addition, V(4) interaction with myosin S1 is highly affected by the products release during ATP hydrolysis in the presence or absence of actin, whereas V(10) appears to be affected at a much lower extent. From these results it is proposed that the binding of vanadate oligomers to myosin S1 at the phosphate loop (23 kDa site) is probably the cause of the actin stimulated myosin ATPase inhibition by the prevention of ATP/ADP exchange, and that this interaction is favoured for higher vanadate anions, such as V(10).

Animals↗
PubMed1989

Role of phosphoinositide metabolism in functional antagonism of airway smooth muscle contraction by beta-adrenoceptor agonists.

Histamine and the muscarinic agonists, methacholine, oxotremorine, and McN-A-343, were used to contract guinea-pig tracheal smooth muscle preparations. Cumulative dose-relaxation curves with isoprenaline were performed subsequently. In addition, the concentration-dependent induction of phosphoinositide metabolism by the contractile agonists was measured in bovine tracheal smooth muscle. All agonists were found to induce a decrease of the apparent affinity of isoprenaline and a loss of relaxation, depending on the concentration and type of contractile agonist used. The differential effects of the contractile agonists, especially at higher and supramaximal concentrations, on these beta-adrenergic parameters could be explained by differences in phosphoinositide metabolism.

(4-(m-Chlorophenylcarbamoyloxy)-2-butynyl)trimethy↗
PubMed2004

Chloride channels and alpha1-adrenoceptor-mediated pulmonary artery smooth muscle contraction: effect of pulmonary hypertension.

Noradrenaline induced concentration-dependent contractions of pulmonary artery segments from control and monocrotaline-treated rats. There was a significant decrease in the maximum response but not sensitivity in artery segments from monocrotaline-treated rats. At a concentration (10(-6) M) that abolished KCl-induced contraction, nifedipine attenuated but did not abolish, noradrenaline-induced contraction in both groups. However, noradrenaline-induced contraction in artery segments from pulmonary hypertensive rats was more susceptible to inhibition by nifedipine. Bumetanide (10(-4) M), a chloride transport inhibitor and niflumic acid, a chloride channel inhibitor, reduced noradrenaline-induced contraction of the pulmonary artery in control and pulmonary hypertensive groups. These compounds were more effective in ring segments from pulmonary hypertensive rats. It was concluded that activation of chloride channels was involved in noradrenaline-induced contraction and that the contribution of chloride channels was enhanced in pulmonary hypertensive rats.

Animals↗