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Is the human masticatory system devoid of recurrent inhibition?

The aim of the present study was to investigate the existence or otherwise of a functional recurrent inhibitory system (Renshaw cell system) in the motoneurons that innervate human masticatory muscles. In a previous study, L: -acetylcarnitine (L: -Ac), a substance known to potentiate recurrent inhibition in humans was found to alter, in a specific way, the discharge variability, and the synchronous activity of motor units depending on the presence or absence of recurrent inhibition in the corresponding motoneuron pool. Using a similar paradigm, we have recorded the tonic discharge activity of motor unit pairs from the masseter muscle during voluntary isometric contraction while subjects were undergoing continuous intravenous saline (SAL, NaCl 0.9%) perfusion. Following a brief baseline-recording period, the subjects were given a test injection of either L: -Ac or isotonic saline (SAL) in a double blind manner. The variability, synchronization, and coherence between the motor unit discharges were analysed during three successive periods: pre-injection, during injection, and post-injection, each lasting 2-3 min. Neither L: -Ac nor SAL injection induced a significant change in the inter-spike interval (ISI) or the coefficient of variation of the ISIs in the motor units tested. There were also no significant changes in the pattern of synchronous activity or in the coherence, which reflects the common frequency content of the unit discharges. Reminiscent of what had been observed previously with motoneurons without recurrent inhibition in the Abductor Digitorum Minimi muscle, the lack of effects of L: -Ac injection on the firing behaviour of masseter motoneurons may suggest that classical Renshaw cell inhibition is lacking in this motoneuron pool.

Acetylcarnitine↗

Motor performance changes induced by muscle vibration.

The possibility that mechanical stimulation of selected muscles can act directly on the nervous system inducing persistent changes of motor performances was explored. On the basis of literature, stimulating parameters were chosen to stimulate the central nervous system and to avoid muscle fibre injuries. A sinusoidal mechanical vibration was applied, for three consecutive days, on the quadriceps muscle in seven subjects that performed a muscular contraction (VC). The same stimulation paradigm was applied on seven subjects in relaxed muscle condition (VR) and seven subjects were not treated at all (NV). Two sessions (PRE and POST) of isometric and isotonic tests were performed separated for 21 days, in all studied groups 7 days before and 15 days after stimulation, whilst an isokinetic test was performed on VC only. In the isometric test, the time of force development showed a significant decrease only in VC (POST vs PRE mean 27.8%, P < 0.05). In the isotonic test, the subjects' had to perform a fatiguing leg extension against a load. In this condition, the fatigue resistance increased greatly in VC (mean 40.3%, P < 0.001), increased slightly in VR and there was no difference in NV. In Isokinetic test, at several angular velocities, significantly less time was required to reach the force peak (mean 20.2% P < 0.05). The findings could be ascribed to plastic changes in proprioceptive processing, leading to an improvement in knee joint control. Such action delineates a new tool in sports training and in motor rehabilitation.

Adaptation, Physiological↗

Effect of indomethacin on electrical field stimulation-induced contractions of isolated transverse and longitudinal rat gastric fundus strips.

AIM: To study the effects of indomethacin on the isolated transverse and longitudinal rat gastric fundus strips. METHODS: The strips were suspended in an organ bath containing oxygenated Krebs solution, and contractile responses to electrical field stimulation were recorded on a physiograph in an isotonic manner after administration of cumulative concentrations of indomethacin. The effects of indomethacin on the strips pretreated with K(ATP) channel modulators, diazoxide and glybenclamide were studied. RESULTS: Treatment of the transverse strips with indomethacin resulted in a concentration-dependent inhibitory response. In longitudinal strips, biphasic responses were seen, which included a stimulatory response at low concentrations of indomethacin, followed by an inhibitory response at higher concentrations. Diazoxide pre-treatment inhibited the stimulatory response of longitudinal strips. Glybenclamide pre-treatment not only blocked inhibitory effect of the low concentrations of indomethacin on transverse strips, but also increased the amplitude of contractions. Moreover, the drug decreased the amplitude of contractions in longitudinal strips. CONCLUSION: Responses of the isolated longitudinal and transverse rat gastric fundus strips to indomethacin are not similar, and are influenced by K(ATP) channel modulators.

Animals↗

Effects of proctolin on contractions, membrane resistance, and non-voltage-dependent sarcolemmal ion channels in crustacean muscle fibers.

The neuropeptide proctolin in nanomolar concentrations enhances the contraction of crustacean muscle fibers manyfold. The cellular mechanisms underlying this potentiation were investigated in single, isolated, fast-contracting abdominal extensor muscle fibers of a small crustacean, the marine isopod Idotea baltica. Force measurements and current-clamp experiments revealed two actions of proctolin on the muscle fibers. In half of the preparations, proctolin (10(-9)-10(-6) M) increased the fiber's input resistance by up to 25%. In about one-fourth of the preparations, proctolin induced all-or-none action potentials in response to depolarizing current pulses in muscle fibers that showed graded electric responses under control conditions. In both cases, proctolin potentiated the peak force of muscle contractions (between 1.5- and 18-fold for 5 x 10(-9) M proctolin). Proctolin affected neither the membrane resting potential nor the threshold for excitation-contraction coupling. Using cell-attached patches on the sarcolemmal membrane, we identified non-voltage-dependent ion channels which contribute to the passive membrane properties of the muscle fibers. A 53 +/- 6 pS channel had its reversal potential near rest and carried outward current at depolarized potentials with physiological saline in the recording pipette. With isotonic K+ saline in the patch pipette, the reversal potential was +85 +/- 12 mV depolarized from the resting potential and single-channel conductances ranged from 36 to 166 pS. Proctolin modulated the activity of all these putative K+ channels by reducing the number of functionally active channels. The effects of proctolin on force of contraction, input resistance, and single-channel activity were mimicked by a membrane-permeating analog of cAMP. Conversely, a monothio analog of cAMP (Rp-cAMPS), a blocker of protein kinase A activity, substantially decreased the membrane input resistance of the muscle fibers. The results suggest that activation of the cAMP signal pathway and phosphorylation of non-voltage-dependent K+ channels by protein kinase A are involved in the potentiation of contractions by proctolin in the muscle fibers of this crustacean.

1-Methyl-3-isobutylxanthine↗

Mechanisms of mechanotransduction by specialized low-threshold mechanoreceptors in the guinea pig rectum.

The guinea pig rectum, but not the colon, is innervated by a specialized class of distension-sensitive mechanoreceptors that have transduction sites corresponding to rectal intraganglionic laminar endings (rIGLEs). Rectal mechanoreceptors recorded in vitro had low threshold to circumferential stretch, adapted slowly, and could respond within 2 ms to mechanical stimulation by a piezo-electric probe. Antagonists to ionotropic N-methyl-D-aspartate (NMDA; CGS 19755, memantine) and non-NMDA (6,7-dinitroquinoxaline-2,3-dione) glutamate receptors did not affect mechanotransduction. In normal Krebs solution, the P2X purinoreceptor agonist alpha,beta-methylene ATP reduced mechanoreceptor firing evoked by distension but simultaneously relaxed circular smooth muscle and inhibited stretch-induced contractions. Neither ATP nor alpha,beta-methylene ATP affected mechanotransduction when transduction sites were directly compressed with von Frey hairs. The P2 purinoreceptor antagonist pyridoxal phosphate-6-azophenyl-2',4'-disulfonic acid did not affect stretch-induced firing but reduced the inhibitory effect of alpha,beta-methylene ATP on stretch-induced firing. Under isometric conditions, blocking synaptic transmission in Ca2+-free solution reduced stretch-evoked firing but not when basal tension was restored to control levels. Under isotonic condition, Ca2+-free solution did not significantly affect load-evoked firing. The blockers of mechanogated and/or transient receptor potential channels, benzamil, Gd3+, SKF 96365, and ruthenium red inhibited stretch-induced firing but, in parallel, significantly reduced stretch-induced contractions. Benzamil and SKF 96365 were able to inhibit mechanotransduction when transduction sites were compressed with von Frey hairs. The results show that mechanotransduction is rapid but does not depend on fast exocytotic release of mediators. It is likely that stretch-activated ion channels on rIGLEs are involved in direct, physical mechanotransduction by rectal low-threshold mechanoreceptors.

Adenosine Triphosphate↗

Compartmentation of high-energy phosphates in resting and working rat skeletal muscle.

The subcellular distribution of high-energy phosphates in various types of skeletal muscle of the rat was analysed by subfractionation of tissues in non-aqueous solvents. Different glycolytic and oxidative capacities were calculated from the ratio of phosphoglycerate kinase and citrate synthase activities, ranging from 25 in m. soleus to 130 in m. tensor fasciae latae. In the resting state, the subcellular contents of ATP, creatine phosphate and creatine were similar in m. soleus, m. vastus intermedius, m. gastrocnemius and m. tensor fasciae latae but, significantly, a higher extramitochondrial ADP-content was found in m. soleus. A similar observation was made in isometrically and isotonically working m. gastrocnemius. The extramitochondrial, bound ADP accounted fully for actin-binding sites in resting fast-twitch muscles, but an excess of bound ADP was found in m. soleus and working m. gastrocnemius. The amount of non-actin-bound ADP reached maximal values of approx. 1.2 nmol/mg total protein. It could not be enhanced further by prolonged isotonic stimulation or by increased isometric force development. It is suggested that non-actin-bound ADP is accounted for by actomyosin-ADP complexes generated during the contraction cycle. Binding of extramitochondrial ADP to actomyosin complexes in working muscles thus acts as a buffer for cytosolic ADP in addition to the creatine system, maintaining a high cytosolic phosphorylation potential also at increasing rates of ATP hydrolysis during muscle contraction.

Adenosine Diphosphate↗

Mechanisms implicated in the histamine response of the sheep ureterovesical junction.

The isotonic response of the sheep ureterovesical junction to histamine receptor agonists and antagonists was studied in vitro. Histamine (10(-7)-10(-4) M) produced a concentration-dependent contraction which was dependent on the extracellular calcium concentrations. Nifedipine (10(-9)-10(-6) M) partially inhibited the contractile response to histamine. 2-Methylhistamine and 2-pyridylethylamine elicited contractile effect in a concentration-related manner. The order of potency was histamine greater than 2-methylhistamine greater than 2-pyridylethylamine. Dimaprit and 4-methylhistamine produced no response in this tissue. The histamine contraction was antagonized by mepyramine, the pA2 value being 8.41, but not by cimetidine (10(-4) M). Scopolamine (10(-5) M) and indomethacin (10(-6) M) had an inhibitory effect. Phentolamine (10(-5) M), propranolol (10(-7)) and hexamethonium (10(-6) M) did not alter the histamine-induced contractions. The present results indicate that the response to histamine in sheep ureterovesical junction is mediated mainly by a direct action on the smooth muscle through excitatory histamine H1-receptors and partly by an indirect action via the stimulation of intramural cholinergic nerves.

Animals↗

Electromyographic fatigue in neck/shoulder muscles and endurance in women with repetitive work.

EMG was recorded with surface electrodes from the trapezius and deltoid muscles during a static endurance test at approximately 20% of maximal voluntary contraction. Objective parameters for localized muscular fatigue were derived from the time course of the root mean square (RMS) and mean power frequency (MPF) of the EMG recordings. Isotonic regression is introduced as a tool for assessment of such parameters. The most pronounced sign of fatigue for trapezius was an increase in the RMS values, while for deltoid it was a decrease in the MPF values. This could be explained by the different functions of the two muscles. The endurance time for a group of 11 women in industrial work with repetitive short-cycled work tasks who were diagnosed with neck/shoulder disorders (tension neck) was significantly shorter (p less than 0.05) than for a group with the same work, but without neck/shoulder disorders (n = 11), and shorter than for a control group (n = 11). Regarding the EMG fatigue measures, there were no significant differences between the three groups. We did not find any relationships between endurance time and the EMG parameters. The results indicate that neck/shoulder disorders were not associated with divergent mechanisms for developing fatigue in the muscles, as recorded with surface EMG.

Adult↗

Impairment and restoration of rat urinary bladder responsiveness following distension.

Micturition and bladder responsiveness in vitro were impaired in rats fed isotonic sucrose, afflicted with diabetes mellitus or diabetes insipidus. Their urinary output which was seven times control, initiated micturition responses at volumes three times control. Nerve-induced contractions by bladders from these rats developed substantially less pressure than control. Contractions elicited at 1 Hz by control and impaired bladders were potentiated equally by tetraethylammonium chloride (TEA) (5 mM) or by carbachol (2 X 10(-7) M). Contractions elicited at 20 Hz by normal bladders were not potentiated, those by impaired bladders were. TEA, by increasing transmitter release, and carbachol, by a postjunctional action, substantially reversed bladder dysfunction. Because control and impaired bladders were equally enhanced by TEA, prejunctional and contractile element (CE) activity at 1 Hz were probably unaffected by distension. However, postjunctional sensitivity was probably reduced. Impaired bladders, more compliant than controls, became less compliant after carbachol without elevating resting pressure. Whereas the action of carbachol to enhance bladder responsiveness did not involve tension development, there may have been cholinoceptor facilitation and shortening of CE.

Animals↗

NaHCO3-induced alkalosis reduces the phosphocreatine slow component during heavy-intensity forearm exercise.

During heavy-intensity exercise, the mechanisms responsible for the continued slow decline in phosphocreatine concentration ([PCr]) (PCr slow component) have not been established. In this study, we tested the hypothesis that a reduced intracellular acidosis would result in a greater oxidative flux and, consequently, a reduced magnitude of the PCr slow component. Subjects (n = 10) performed isotonic wrist flexion in a control trial and in an induced alkalosis (Alk) trial (0.3g/kg oral dose of NaHCO3, 90 min before testing). Wrist flexion, at a contraction rate of 0.5 Hz, was performed for 9 min at moderate- (75% of onset of acidosis; intracellular pH threshold) and heavy-intensity (125% intracellular pH threshold) exercise. 31P-magnetic resonance spectroscopy was used to measure intracellular [H+], [PCr], [Pi], and [ATP]. The initial recovery data were used to estimate the rate of ATP synthesis and oxidative flux at the end of heavy-intensity exercise. In repeated trials, venous blood sampling was used to measure plasma [H+], [HCO3-], and [Lac-]. Throughout rest and exercise, plasma [H+] was lower (P < 0.05) and [HCO3-] was elevated (P < 0.05) in Alk compared with control. During the final 3 min of heavy-intensity exercise, Alk caused a lower (P < 0.05) intracellular [H+] [246 (SD 117) vs. 291 nmol/l (SD 129)], a greater (P < 0.05) [PCr] [12.7 (SD 7.0) vs. 9.9 mmol/l (SD 6.0)], and a reduced accumulation of [ADP] [0.065 (SD 0.031) vs. 0.098 mmol/l (SD 0.059)]. Oxidative flux was similar (P > 0.05) in the conditions at the end of heavy-intensity exercise. In conclusion, our results are consistent with a reduced intracellular acidosis, causing a decrease in the magnitude of the PCr slow component. The decreased PCr slow component in Alk did not appear to be due to an elevated oxidative flux.

Acid-Base Equilibrium↗

The offset cortical potential: an electrical correlate of movement inhibition in man.

Nine normal subjects were asked to make either a brisk isometric pinch of a force transducer held between the forefinger and thumb, or to hold a pinch for approximately 15 s and then release the force suddenly without any overt antagonist contraction. EEG activity was averaged about the onset or offset of EMG activity, and movements were made in the subjects' own time. All subjects found the task simple. The EEG activity preceding offset of contraction (offset cortical potential) was significantly smaller in lateral leads than that seen before onset of contraction. Midline activation was similar in both tasks. We suggest that in the onset task, motor cortex activity related to the act to be performed contributes substantially to the EEG potentials in lateral leads. This activity is absent in the offset task which requires only withdrawal of tonic input to motor cortex. Midline activity, common to both onset and offset tasks, could reflect timing, attentional, or other processes. The results are discussed in relation to previous data from an isotonic relaxation task.

Adult↗

Active trunk extensor contributions to dynamic posteroanterior lumbar spinal stiffness.

BACKGROUND: Assessments of posteroanterior (PA) spinal stiffness using mobilization apparatuses have demonstrated an increase in PA spine stiffness during voluntary contraction of the lumbar extensor muscles; yet, little work has been done to this degree in symptomatic subjects. OBJECTIVE: To use a previously validated dynamic mechanical impedance procedure to quantify changes in PA dynamic spinal stiffness at rest and during lumbar isotonic extension tasks in patients with low back pain (LBP). METHODS: Thirteen patients with LBP underwent a dynamic spinal stiffness assessment in the prone-resting position and again during lumbar extensor efforts. Stiffness assessments were obtained using a handheld impulsive mechanical device equipped with an impedance head (load cell and accelerometer). PA manipulative thrusts (approximately 150 N, <5 milliseconds) were delivered to skin overlying the L3 left and right transverse processes (TPs) and to the L3 spinous process (SP) in a predefined order (left TP, SP, right TP) while patients were at rest and again during prone-lying lumbar isotonic extension tasks. Dynamic spinal stiffness characteristics were determined from force and acceleration measurements using the apparent mass (peak force/peak acceleration, kg). Apparent mass measurements for the resting and active lumbar isotonic task trials of each patient were compared using a 2-tailed, paired t test. RESULTS: A significant increase in the PA dynamic spinal stiffness was noted for thrusts over the SP (apparent mass [17.0%], P=.0004) during isotonic trunk extension tasks compared with prone resting, but no statistically significant changes in apparent mass were noted for the same measures over the TPs. CONCLUSIONS: These findings add support to the significance of the trunk musculature and spinal posture in providing increased spinal stability.

Adult↗

Preloading and range of motion effect on plantarflexor muscle performance.

OBJECTIVE: To determine the effects of maximal preloading and range of motion (ROM) on the mechanical parameters of the plantarflexor muscles obtained while using the isotonic mode of testing of a Biodex dynamometer. DESIGN: A convenience sample of healthy subjects in the context of a descriptive comparative study. SETTING: Research laboratory in Canada. SUBJECTS: Fifteen volunteered subjects without history of injury or disorder to the right lower extremity. MEASUREMENTS: Four maximal isotonic tests were performed against a selected load of 27Nm. For the first two tests, the movement at the ankle ranged from -12 degrees (dorsiflexion) to +32 degrees (plantarflexion); one of these tests was preceded by a 2-second maximal preloading contraction, while the other was performed without preloading. For the other two tests, the ROM at the ankle was increased by 15 degrees of plantarflexion and thus ranged from -12 degrees to +47 degrees; again one of these tests was executed with preloading and the other without preloading. RESULTS: The four tests showed differences in the mechanical parameters (MANOVA p < .05). At angles of -10 degrees and +5 degrees, subjects produced higher torque and power but lower velocity values for the two tests preceded by a maximal preloading. The effect of ROM was demonstrated at +20 degrees where tests performed in a small amplitude reached a lower velocity than the corresponding tests performed in a larger amplitude. Based on the velocity profiles, the results also revealed that maximal preloading changed the selected isotonic movement of the Biodex dynamometer to an isoaccelerative movement characterized by high torque and power production. CONCLUSIONS: Isotonic assessment using the Biodex dynamometer provides different values of torque, velocity, and power depending on the testing conditions used. In clinical settings, it would be important to control these testing conditions.

Analysis of Variance↗

Mathematical modeling of relations between the kinetics of free intracellular calcium and mechanical function of myocardium.

The paper describes a mathematical model of cardiac muscle contraction based on the assumption of two types of co-operativity which control the formation of calcium-troponin complexes and on a simplified scheme of free intracellular calcium kinetics. Calcium transients are shown to be different in isotonic and isometric conditions, being dependent on initial muscle length as well. Numerical experiments and analysis of the model suggest that calcium uptake by the sarcoplasmic reticulum slows down with an increase in the intracellular concentration of free calcium. This suggestion enables the model to explain the disappearance of load-dependent relaxation observed experimentally at cardiac hypertrophy.

Calcium↗

Mechanisms of increased responses of the aorta to alpha-adrenoceptor agonists in streptozotocin-induced diabetic rats.

To investigate the influence of diabetes on the responsiveness of the cardiovascular system, we have examined the effects of various agents on the reactivity of the vascular smooth muscle of aortic strips obtained from age-matched control and diabetic rats. Norepinephrine (NE) contracted the aortic strips obtained from age-matched control and diabetic rats in a concentration-dependent manner, but maximal contraction of aortic strips in response to NE was enhanced in diabetic rats. The EC50 value for NE in the diabetic aortic strips was similar to that in the aorta from age-matched controls. Ca-induced contracture of the aortic strips which were depolarized with isotonic K+ (60 mM) was potentiated in aortic strips from diabetic rats, when compared with those from age-matched controls. Ca-induced contracture of aortic strips, preincubated with 10(-6) M NE and 10(-6) M nicardipine in Ca2+-free Krebs-Henseleit solution (KHS), was not significantly different in age-matched control and diabetic rats. Bay K 8644, an activator of calcium channels, produced an increase in the force of contraction of the slightly depolarized aorta from diabetic rats. Phasic contraction induced by phenylephrine (PE) in the presence of 10(-6) M nicardipine in Ca2+-free KHS was significantly enhanced in aortic strips obtained from diabetic rats. These results demonstrate that NE-induced contraction of the aortic strips obtained from diabetic rats was significantly enhanced, and that this increased contractile response of the aorta to NE may be due to an increased influx of extracellular calcium through the voltage-dependent Ca2+ channels, but not through the receptor-operated Ca2+ channels.(ABSTRACT TRUNCATED AT 250 WORDS)

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗