The Experts below are selected from a list of 165 Experts worldwide ranked by ideXlab platform
Jean Marc Renaud - One of the best experts on this subject based on the ideXlab platform.
-
effect of tolbutamide on the rate of fatigue and recovery in frog sartorius muscle
Journal of Pharmacology and Experimental Therapeutics, 1995Co-Authors: Alain Comtois, P Light, Jean Marc RenaudAbstract:The goal of this study was to determine how blocking ATP-sensitive K+ channels with tolbutamide affects the excitability and contractility of intact frog sartorius muscle during fatigue development. Fatigue was elicited with one Tetanic Contraction every sec for 3 min. During fatigue the resting potential decreased by 10 mV although the action potential overshoot remained constant. The addition of 2 mmol.liter-1 tolbutamide 60 min before fatigue did not modify the effect of fatigue on the resting potential and action potential overshoot. During fatigue development the half-repolarization time of control muscles increased by 0.26 msec in control muscles, although it increased by 0.77 msec in the presence of 2 mmol.liter-1 tolbutamide; the difference was significant. The decrease in force during fatigue development was not affected by 2 mmol.liter-1 tolbutamide (added 60 min before fatigue), whereas the recovery of force after fatigue was slower in tolbutamide- exposed muscles than in control muscles. Addition of 2 mmol.liter-1 tolbutamide after 5 min of recovery reduced the recovery rate of the resting potential and half-repolarization time, but did not affect the recovery of Tetanic force during the first 40 min. Our results are consistent with the hypothesis that ATP-sensitive K+ channels are activated during fatigue development and that they contribute to the repolarization phase of action potentials, but they do not support the hypothesis that ATP-sensitive K+ channels contribute to the decrease in force.
-
na and k effect on contractility of frog sartorius muscle implication for the mechanism of fatigue
American Journal of Physiology-cell Physiology, 1995Co-Authors: R Bouclin, E Charbonneau, Jean Marc RenaudAbstract:Although a decrease in extracellular Na+ and an increase in K+ concentration are believed to contribute to the decrease in force during fatigue, the force of unfatigued muscle decreases only with quite large changes in Na+ and K+ concentration. The objective of this study was to determine whether concomitant and smaller changes in Na+ and K+ concentration have greater effects on muscle contractility than individual changes. At 3 mM K+, a large decrease in Na+ from 120 to 60 mM had no effect on the twitch force, while the Tetanic force decreased by 31.2%. At 120 mM Na+, an increase in K+ from 3 to 9 mM potentiated the twitch force by 41.1%, had no effect on the Tetanic force at 7 mM, and decreased the Tetanic force by 40.4% at 9 mM; both the twitch force and Tetanic force were completely abolished at 11 mM K+. The potentiation of the twitch force between 3 and 9 mM K+ was less at 60, 80, and 100 mM than at 120 mM Na+. A reduction in Na+ concentration also reduced the K+ concentration at which the twitch force and Tetanic force decreased and were completely abolished. It is shown that the combined effects of Na+ and K+ on the twitch and Tetanic Contractions were greater than the sum of their individual effects. Furthermore, it is proposed that neither Na+ nor K+ alone can be considered as an important factor in the decrease in force during fatigue, whereas together they are important for the Tetanic Contraction, but not for the twitch Contraction.
-
effects of k on the twitch and Tetanic Contraction in the sartorius muscle of the frog rana pipiens implication for fatigue in vivo
Canadian Journal of Physiology and Pharmacology, 1992Co-Authors: Jean Marc Renaud, Peter E LightAbstract:The effects of increasing the extracellular K+ concentration on the capacity to generate action potentials and to contract were tested on unfatigued muscle fibers isolated from frog sartorius muscle. The goal of this study was to investigate further the role of K+ in muscle fatigue by testing whether an increased extracellular K+ concentration in unfatigued muscle fibers causes a decrease in force similar to the decrease observed during fatigue. Resting and action potentials were measured with conventional microelectrodes. Twitch and Tetanic force was elicited by field stimulation. At pHo (extracellular pH) 7.8 and 3 mmol K+.L-1 (control), the mean resting potential was -86.6 +/- 1.7 mV (mean +/- SEM) and the mean overshoot of the action potential was 5.6 +/- 2.5 mV. An increased K+ concentration from 3 to 8.0 mmol.L-1 depolarized the sarcolemma to -72.2 +/- 1.4 mV, abolished the overshoot as the peak potential during an action potential was -12.0 +/- 3.9 mV, potentiated the twitch force by 48.0 +/- 5.7%, but did not affect the Tetanic force (maximum force) and the ability to maintain a constant force during the plateau phase of a tetanus. An increase to 10 mmol K+.L-1 depolarized the sarcolemma to -70.1 +/- 1.7 mV and caused large decreases in twitch (31.6 +/- 26.1%) and Tetanic (74.6 +/- 12.1%) force. Between 3 and 9 mmol K+.L-1, the effects of K+ at pHo 7.2 (a pHo mimicking the change in interstitial pH during fatigue) and 6.4 (a pHo known to inhibit force recovery following fatigue) on resting and action potentials as well as on the twitch and Tetanic force were similar to those at pHo 7.8. Above 9 mmol K+.L-1 significant differences were found in the effect of K+ between pHo 7.8 and 7.2 or 6.4. In general, the decrease in peak action potential and twitch and Tetanic force occurred at higher K+ concentrations as the pHo was more acidic. The results obtained in this study do not support the hypothesis that an accumulation of K+ at the surface of the sarcolemma is sufficiently large to suppress force development during fatigue. The possibility that the K+ concentration in the T tubules reaches the critical K+ concentration necessary to cause a failure of the excitation-Contraction coupling mechanism is discussed.
J L Taylor - One of the best experts on this subject based on the ideXlab platform.
-
Twitch interpolation: Superimposed twitches decline progressively during a Tetanic Contraction of human adductor pollicis
Journal of Physiology, 2013Co-Authors: Simon C Gandevia, T. J. Carroll, Chris J. Mcneil, J L TaylorAbstract:The assessment of voluntary activation of human muscles usually depends on measurement of the size of the twitch produced by an interpolated nerve or cortical stimulus. In many forms of fatiguing exercise the superimposed twitch increases and thus voluntary activation appears to decline. This is termed 'central' fatigue. Recent studies on isolated mouse muscle suggest that a peripheral mechanism related to intracellular calcium sensitivity increases interpolated twitches. To test whether this problem developed with human voluntary Contractions we delivered maximal Tetanic stimulation to the ulnar nerve (≥60 s at physiological motoneuronal frequencies, 30 and 15 Hz). During the tetani (at 30 Hz) in which the force declined by 42%, the absolute size of the twitches evoked by interpolated stimuli (delivered regularly or only in the last second of the tetanus) diminished progressively to less than 1%. With stimulation at 30 Hz, there was also a marked reduction in size and area of the interpolated compound muscle action potential (M wave). With a 15 Hz tetanus, a progressive decline in the interpolated twitch force also occurred (to ∼10%) but did so before the area of the interpolated M wave diminished. These results indicate that the increase in interpolated twitch size predicted from the mouse studies does not occur. Diminution in superimposed twitches occurred whether or not the M wave indicated marked impairment at sarcolemmal/t-tubular levels. Consequently, the increase in superimposed twitch, which is used to denote central fatigue in human fatiguing exercise, is likely to reflect low volitional drive to high-threshold motor units, which stop firing or are discharging at low frequencies.
Jon Scott - One of the best experts on this subject based on the ideXlab platform.
-
the dynamic response of golgi tendon organs to Tetanic Contraction of in series motor units
Brain Research, 1995Co-Authors: P Davies, J Petit, Jon ScottAbstract:Abstract Golgi tendon organs (TOs) display a dynamic response related to the rate of tension development by the motor units (MUs) which activate each TO. When several MUs are activated together the response increases non-linearly with respect to tension. The dynamic response has been re-examined by recording the responses of TOs, in the adult cat, to Tetanic, isometric Contractions of one or more MUs and has been found to comprise two components: for each MU-TO pair the instantaneous frequency between the first two impulses of the response was linearly related to the rate of rise of the tension, the slope of the relationship being greatest for the slow units. Similarly, when activating MUs were stimulated together, the relationships between the frequency and the initial rate of tension rise were linear. When the relationships were expressed in terms of relative tension rate the organs were found to be most strongly activated by the IIb muscle fibres, the responsiveness at the level of the whole muscle being reduced by unloading effects. The later component of the response showed an exponential relationship between discharge frequency and rate of tension development, the slope of the relationship between frequency and the logarithm of tension rate being independent of MU size. Although absolute tension increases during a Contraction, this did not appear to impinge on the response which was dominated by the dynamic parameters of the Contraction.
Steve S Segal - One of the best experts on this subject based on the ideXlab platform.
-
regional activation of rapid onset vasodilatation in mouse skeletal muscle regulation through α adrenoreceptors
The Journal of Physiology, 2010Co-Authors: Ale W Moore, Shaw E Earde, Steve S SegalAbstract:Exercise onset entails motor unit recruitment and the initiation of vasodilatation. Dilatation can ascend the arteriolar network to encompass proximal feed arteries but is opposed by sympathetic nerve activity, which promotes vasoconstriction and inhibits ascending vasodilatation through activating α-adrenoreceptors. Whereas contractile activity can antagonize sympathetic vasoconstriction, more subtle aspects of this interaction remain to be defined. We tested the hypothesis that constitutive activation of α-adrenoreceptors governs blood flow distribution within individual muscles. The mouse gluteus maximus muscle (GM) consists of Inferior and Superior regions. Each muscle region is supplied by its own motor nerve and feed artery with an anastomotic arteriole (resting diameter ∼25 μm) that spans both muscle regions. In anaesthetized male C57BL/6J mice (3–5 months old), the GM was exposed and superfused with physiological saline solution (35°C; pH 7.4). Stimulating the inferior gluteal motor nerve (0.1 ms pulse, 100 Hz for 500 ms) evoked a brief Tetanic Contraction and produced rapid (<1 s) onset vasodilatation (ROV; diameter change, 10 ± 1 μm) of the anastomotic arteriole along the active (Inferior) muscle region but not along the inactive (Superior) region (n= 8). In contrast, microiontophoresis of acetylcholine (1 μm micropipette tip, 1 μA, 500 ms) initiated dilatation that travelled along the anastomotic arteriole from the Inferior into the Superior muscle region (diameter change, 5 ± 2 μm). Topical phentolamine (1 μm) had no effect on resting diameter but this inhibition of α-adrenoreceptors enabled ROV to spread along the anastomotic arteriole into the inactive muscle region (dilatation, 7 ± 1 μm; P < 0.05), where remote dilatation to acetylcholine then doubled (P < 0.05). These findings indicate that constitutive activation of α-adrenoreceptors in skeletal muscle can restrict the spread of dilatation within microvascular resistance networks and thereby increase blood flow to active muscle regions.
Walter Herzog - One of the best experts on this subject based on the ideXlab platform.
-
increased non uniformity in in vivo sarcomere length during a Tetanic Contraction
Biophysical Journal, 2017Co-Authors: Eng Kuan Moo, T R Leonard, Walter HerzogAbstract:IntroductionThe maximal, steady-state, isometric force produced by a muscle depends on its sarcomere length (SL). In previous studies in single myofibrils, it was found that sarcomere length non-uniformities increased during activation and force production. However, single myofibrils lack much of the structural proteins that provide stability to entire muscles, thus the observed SL non-uniformities in myofibrils might not occur in whole muscles. This study was aimed at investigating the change in SL distribution during Tetanic Contractions in an intact muscles of live mice.MethodsMice were anaesthetized using isoflurane. The proximal femur and foot of the left lower limb were clamped. The skin over the left tibialis anterior (TA) muscle was opened and stretched to form a bath for a saline solution that allowed for imaging using a water-immersion objective. The TA was supra-maximally stimulated using a nerve cuff electrode on the sciatic nerve using 0.1ms square wave pulses at 60Hz for 1s. SL were measured using second harmonic generation microscopy for the fully stretched TA. Measurements were made for the passive and activated TA over an area of 160x3 µm2 in the mid-belly of the muscle.ResultsSLs for the passive muscle were 2.53±0.06µm (mean±sd). During Contraction, sarcomeres shortened by ∼12% to 2.24±0.12µm. The coefficient of variation of the SLs doubled from 2.4% at rest to 5.2% during Tetanic Contractions. The range of SLs increased from the passive (2.36-2.71µm) to the active state (1.85-2.62µm).ConclusionSL non-uniformity doubled during muscle activation and differed by more than 0.7 µm. The functional implications of these massive SL non-uniformities need to be explored, and the common practice of representing muscles with a single SL value needs to be reconsidered.
