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Twitch Force (twitch + force)
Selected AbstractsMouse diaphragm assay for detection of antibodies against botulinum toxin type BMOVEMENT DISORDERS, Issue 12 2005Dirk Dressler MD Abstract With the advent of a commercial preparation of botulinum toxin type B (BT-B) for treatment of cervical dystonia detection of antibodies against BT-B (BT-B-AB) becomes necessary. For this purpose, we carried out a mouse diaphragm assay (MDA) by continuous measurement of the twitch force of a mouse hemidiaphragm preparation elicited by electric stimulation of its phrenic nerve. After exposing the preparation to BT-B 3 ng/ml the time to half-maximal twitch force reduction (paralysis time [PT]) was 69 ± 4 min (n = 25). Addition of sera from patients with antibodies against BT-A produced a PT of 68 ± 5 min (n = 24), whereas addition of sera from controls with antibodies against tetanus toxoid produced a PT of 67 ± 6 min (n = 30). When defined amounts of BT-B-AB were added to the MDA, PT was prolonged. This prolongation was correlated closely to the amount of BT-B-AB added, thus producing a calibration curve. The threshold for BT-B-AB detection was 0.4 mU/ml. When sera from 7 patients (4 women, 3 men; age 50.6 ± 14.2 years) with cervical dystonia (Toronto Western Spasmodic Torticollis Rating Scale score, 18.9 ± 2.9) and complete secondary failure of BT-B therapy (NeuroBloc; Elan Pharmaceuticals, Shannon, Ireland; 12,229 ± 2,601 MU/injection series, 1.86 ± 0.69 injection series before complete secondary therapy failure; 100.4 ± 15.8 days between injection series with normal therapeutic effect) were tested, BT-B-AB titers of more than 10 mU/ml were found in all of them. The MDA can be used to measure neutralizing BT-B-AB titers quantitatively and with adequate sensitivity and specificity. Further studies are necessary to understand the role of intermediate BT-B-AB titers in partial BT-B therapy failure. © 2005 Movement Disorder Society [source] Mechanisms of force failure during repetitive maximal efforts in a human upper airway muscleMUSCLE AND NERVE, Issue 1 2002Christiana DelloRusso BS Abstract The upper airway respiratory muscles play an important role in the regulation of airway resistance, but surprisingly little is known about their contractile properties and endurance performance. We developed a technique that allows measurement of force and the electromyogram (EMG) of human nasal dilator muscles (NDMs). Endurance performance was quantified by measuring NDM "flaring" force and EMG activity as healthy human subjects performed 10 s maximal voluntary contractions (MVCs), separated by 10 s rest, until the area under the force curve fell to 50% MVC (the time limit of the fatigue task, Tlim), which was reached in 34.2 ± 3.1 contractions (685.0 ± 62.3 s). EMG activity was unchanged except at Tlim, where it averaged 78.7 ± 3.6% of pretest activity (P < 0.01). M-wave amplitude did not change, suggesting that neuromuscular propagation was not impaired. MVC force increased to 80% of the pretest level within 10 min of recovery but twitch force failed to recover, suggesting low-frequency fatigue. The data suggest that a failure of the nervous system to excite muscle could explain at most only a small fraction of the NDM force loss during an intermittent fatigue task, and then only at Tlim. Thus, the majority of the force failure during this task is due to impairment of mechanisms that reside within the muscle fibers. © 2002 Wiley Periodicals, Inc. Muscle Nerve 26: 94,100, 2002 [source] Fluctuations in isometric muscle force can be described by one linear projection of low-frequency components of motor unit discharge ratesTHE JOURNAL OF PHYSIOLOGY, Issue 24 2009Francesco Negro The aim of the study was to investigate the relation between linear transformations of motor unit discharge rates and muscle force. Intramuscular (wire electrodes) and high-density surface EMG (13 × 5 electrode grid) were recorded from the abductor digiti minimi muscle of eight healthy men during 60 s contractions at 5%, 7.5% and 10% of the maximal force. Spike trains of a total of 222 motor units were identified from the EMG recordings with decomposition algorithms. Principal component analysis of the smoothed motor unit discharge rates indicated that one component (first common component, FCC) described 44.2 ± 7.5% of the total variability of the smoothed discharge rates when computed over the entire contraction interval and 64.3 ± 10.2% of the variability when computed over 5 s intervals. When the FCC was computed from four or more motor units per contraction, it correlated with the force produced by the muscle (62.7 ± 10.1%) by a greater degree (P < 0.001) than the smoothed discharge rates of individual motor units (41.4 ± 7.8%). The correlation between FCC and the force signal increased up to 71.8 ± 13.1% when the duration and the shape of the smoothing window for discharge rates were similar to the average motor unit twitch force. Moreover, the coefficients of variation (CoV) for the force and for the FCC signal were correlated in all subjects (R2 range = 0.14,0.56; P < 0.05) whereas the CoV for force was correlated to the interspike interval variability in only one subject (R2= 0.12; P < 0.05). Similar results were further obtained from measures on the tibialis anterior muscle of an additional eight subjects during contractions at forces up to 20% of the maximal force (e.g. FCC explained 59.8 ± 11.0% of variability of the smoothed discharge rates). In conclusion, one signal captures most of the underlying variability of the low-frequency components of motor unit discharge rates and explains large part of the fluctuations in the motor output during isometric contractions. [source] Atrial Tachyarrhythmias Induced By Acetylcholine In Tilapia (Oreochromis SP.) Isolated AtriaCLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 5-6 2000Tsai-Chu Lin SUMMARY 1. Effects of the parasympathetic neuromediator acetylcholine (ACh) on atrial tissues vary greatly depending on the species, the type of atrial cells and experimental conditions. The aim of the present study was to investigate, with microelectrode techniques, the arrhythmogenic effects of ACh in tilapia (Oreochromis sp.) isolated atria at room (22,25°C) and high temperature (37°C). 2. Acetylcholine (1,10 ,mol/L) shortened action potential duration (APD), depressed action potential plateau and decreased twitch force in tilapia atria, as it did in human atrial fibres. In addition, ACh induced premature responses and re-entrant tachyarrhythmias (TA; frequency range from 7 to 25 Hz) in five of 19 and 14 of 22 tilapia atria tested at room and high temperature, respectively. The higher incidence of ACh-induced TA at 37°C compared with room temperature was statistically significant. 3. The ACh-induced TA consisted of high-frequency and uniform action potentials accompanied by tension oscillation and elevation of diastolic force (flutter). Acetylcholine-induced TA could be readily abolished by atropine (1 ,mol/L) and prevented by treatment with agents with local anaesthetic properties, such as 0.1 ,mol/L tetrodotoxin or 3 ,mol/L quinidine. The antagonistic action of quinidine occurred without significant prolongation of APD. 4. The present findings suggest that pharmacological concentrations of the cholinergic muscarinic agonist ACh readily induce TA (mainly atrial flutter) in tilapia atria, presumably via sodium channel-dependent re-entrant excitation. The poikilothermic tilapia appears to be an appropriate animal model for the study of atrial TA. [source] | ||||||||||