Artykuły w czasopismach na temat „Slow component amplitude”
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Morton, R. Hugh. "&OV0312;O2 SLOW COMPONENT AMPLITUDE". Medicine and Science in Sports and Exercise 34, nr 2 (luty 2002): 381–82. http://dx.doi.org/10.1097/00005768-200202000-00028.
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Bearden, Shawn E., i Robert J. Moffatt. "&OV0312;O2 SLOW COMPONENT AMPLITUDE". Medicine and Science in Sports and Exercise 34, nr 2 (luty 2002): 382. http://dx.doi.org/10.1097/00005768-200202000-00029.
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Siniatchkin, M., E. Kirsch, P. Kropp, U. Stephani i W.-D. Gerber. "Slow Cortical Potentials in Migraine Families". Cephalalgia 20, nr 10 (grudzień 2000): 881–92. http://dx.doi.org/10.1046/j.1468-2982.2000.00132.x.
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Amplitude and habituation of event-related potentials are abnormal in migraine. We investigated 43 migraine and 41 healthy families to evaluate the influences of age, sex and familial contribution on the variance of amplitude and habituation of the contingent negative variation (CNV). Analysis of individual differences in relation to the CNV habituation was performed. The study demonstrated that habituation of the early CNV component characterizes migraine considerably better than the CNV amplitudes. Habituation, however, is strongly influenced by age. Migraine adults and children generally showed reduced habituation. Surprisingly, more than 30% of the healthy adults demonstrated a marked loss of habituation. The reduced CNV habituation represented a high sensitivity but low specificity to migraine, especially in children. CNV amplitude and habituation parameters revealed a considerable familial contribution associated with migraine. No familial influence on either morphology or habituation of the CNV in healthy families or between healthy members of migraine families was observed. The low specificity and familial transmission of CNV parameters in members of migraine families suggest that increased amplitudes and reduced habituation of CNV do not constitute a primary risk factor for migraine, but rather represent a predisposition. Genetic components probably affect variation of the CNV amplitude and habituation.
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Reznik, G. M. "Geostrophic adjustment with gyroscopic waves: barotropic fluid without the traditional approximation". Journal of Fluid Mechanics 743 (10.03.2014): 585–605. http://dx.doi.org/10.1017/jfm.2014.59.
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AbstractWe study geostrophic adjustment in rotating barotropic fluid when the angular speed of rotation $\boldsymbol{\Omega}$ does not coincide in direction with the acceleration due to gravity; the traditional and hydrostatic approximations are not used. Linear adjustment results in a tendency of any localized initial state towards a geostrophically balanced steady columnar motion with columns parallel to $\boldsymbol{\Omega}$. Nonlinear adjustment is examined for small Rossby numbers Ro and aspect ratio $H/L$ ($H$ and $L$ are the layer depth and the horizontal scale of motion), using multiple-time-scale perturbation theory. It is shown that an arbitrary perturbation is split in a unique way into slow and fast components evolving with characteristic time scales $(\mathit{Ro}f)^{-1}$ and $f^{-1}$, respectively, where $f $ is the Coriolis parameter. The slow component does not depend on depth and is close to geostrophic balance. On times $O(1/f\, \mathit{Ro})$ the slow component is not influenced by the fast one and is described by the two-dimensional fluid dynamics equation for the geostrophic streamfunction. The fast component consists of long gyroscopic waves and is a packet of inertial oscillations modulated by an amplitude depending on coordinates and slow time. On times $O(1/f\, \mathit{Ro})$ the fast component conserves its energy, but it is coupled to the slow component: its amplitude obeys an equation with coefficients depending on the geostrophic streamfunction. Under the traditional approximation, the inertial oscillations are trapped by the quasi-geostrophic component; ‘non-traditional’ terms in the amplitude equation provide a meridional dispersion of the packet on times $O(1/f\, \mathit{Ro})$, and, therefore, an effective radiation of energy from the initial perturbation domain. Another important effect of the non-traditional terms is that on longer times $O(1/f\, \mathit{Ro}^{2})$ a transfer of energy between the fast and the slow components becomes possible.
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Dityatev, A. E., i H. P. Clamann. "Reliability of spike propagation in arborizations of dorsal root fibers studied by analysis of postsynaptic potentials mediated by electrotonic coupling in the frog spinal cord". Journal of Neurophysiology 76, nr 5 (1.11.1996): 3451–59. http://dx.doi.org/10.1152/jn.1996.76.5.3451.
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1. Postsynaptic potentials were recorded in lumbar motoneurons of the frog in response to electrical activation of dorsal roots. After chemical synaptic transmission was blocked by replacing Ca2+ with Mg2+ in the superfusion medium, it was confirmed that the remaining electrical excitatory postsynaptic potentials (EEPSPs) recorded in motoneurons consisted of potential changes-produced by electrical coupling between the motoneurons and the stimulated axons. The EEPSPs could then be used as an assay to study the reliability of spike propagation into presynaptic terminals. 2. EEPSPs typically consisted of three components. The first was a small positive deflection (prespike or presynaptic volley) that could also be recorded extracellularly. The second component was a spikelike fast positive component and the third was a slow positive component that followed the second but had a distinct maximum and a slow decay. The amplitude of the fast component did not correlate with that of either the prespike or the slow component. 3. 4-Aminopyridine (0.1 mM), which widens action potentials by blocking K+ channels, increased the amplitude and width of EEPSPs. Heptanol (1-4 mM), which is known to be a blocker of electrical coupling, could block EEPSPs. 4. The amplitudes of EEPSPs evoked by dorsal root stimulation were compared at different temperatures (7.5-19.5 degrees C). A slight decrease of the amplitude of the fast component with increasing temperature (Q10 = 0.8) was within limits predicted by resistance-capacitance filtering of the presynaptic spike at the different temperatures, suggesting that the temperature does not affect propagation of the spike in this synapse. 5. The amplitude of the fast component of EEPSPs evoked by single-pulse and paired-pulse stimulation did not fluctuate more than the baseline noise in 37 experiments in which the SD of baseline noise was < 100 microV. We conclude that electrical synaptic transmission does not fluctuate intermittently in this system, and that branch points conduct or fail to conduct for periods of time longer than the longest period in the analyzed experiments.
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Kropp, P., i W.-D. Gerber. "Contingent Negative Variation During Migraine Attack and Interval: Evidence for Normalization of Slow Cortical Potentials During the Attack". Cephalalgia 15, nr 2 (kwiecień 1995): 123–28. http://dx.doi.org/10.1046/j.1468-2982.1995.015002123.x.
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The contingent negative variation (CNV) amplitudes of 16 subjects with migraine without aura were studied during pain-free intervals and during attacks and the results were compared with those of 22 healthy subjects. In 32 trials the CNV amplitudes were calculated for (a) “total interval”, (b) “early CNV component”, (c) “late CNV component”, and (d) habituation. There was a significantly higher total CNV amplitude in migraine subjects during pain-free intervals compared to that of the healthy subjects and migraine patients during an attack. Healthy subjects as well as subjects studied during the attack showed a significant habituation whereas migraine subjects studied during pain-free intervals did not. This suggests that the higher CNV amplitude in migraine patients studied between pain-free attacks may be due in part to impaired habituation.
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Carra, J., R. Candau, S. Keslacy, F. Giolbas, F. Borrani, G. P. Millet, A. Varray i M. Ramonatxo. "Addition of inspiratory resistance increases the amplitude of the slow component of O2 uptake kinetics". Journal of Applied Physiology 94, nr 6 (1.06.2003): 2448–55. http://dx.doi.org/10.1152/japplphysiol.00493.2002.
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The contribution of respiratory muscle work to the development of the O2consumption (V˙o 2) slow component is a point of controversy because it has been shown that the increased ventilation in hypoxia is not associated with a concomitant increase inV˙o 2 slow component. The first purpose of this study was thus to test the hypothesis of a direct relationship between respiratory muscle work andV˙o 2 slow component by manipulating inspiratory resistance. Because the conditions for aV˙o 2 slow component specific to respiratory muscle can be reached during intense exercise, the second purpose was to determine whether respiratory muscles behave like limb muscles during heavy exercise. Ten trained subjects performed two 8-min constant-load heavy cycling exercises with and without a threshold valve in random order. V˙o 2 was measured breath by breath by using a fast gas exchange analyzer, and the V˙o 2 response was modeled after removal of the cardiodynamic phase by using two monoexponential functions. As anticipated, when total work was slightly increased with loaded inspiratory resistance, slight increases in baseV˙o 2, the primary phase amplitude, and peak V˙o 2 were noted (14.2%, P < 0.01; 3.5%, P > 0.05; and 8.3%, P < 0.01, respectively). The bootstrap method revealed small coefficients of variation for the model parameter, including the slow-component amplitude and delay (15 and 19%, respectively), indicating an accurate determination for this critical parameter. The amplitude of the V˙o 2 slow component displayed a 27% increase from 8.1 ± 3.6 to 10.3 ± 3.4 ml · min−1 · kg−1( P < 0.01) with the addition of inspiratory resistance. Taken together, this increase and the lack of any differences in minute volume and ventilatory parameters between the two experimental conditions suggest the occurrence of aV˙o 2 slow component specific to the respiratory muscles in loaded condition.
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Koga, Shunsaku, Tomoyuki Shiojiri, Manabu Shibasaki, Narihiko Kondo, Yoshiyuki Fukuba i Thomas J. Barstow. "Kinetics of oxygen uptake during supine and upright heavy exercise". Journal of Applied Physiology 87, nr 1 (1.07.1999): 253–60. http://dx.doi.org/10.1152/jappl.1999.87.1.253.
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It is presently unclear how the fast and slow components of pulmonary oxygen uptake (V˙o 2) kinetics would be altered by body posture during heavy exercise [i.e., above the lactate threshold (LT)]. Nine subjects performed transitions from unloaded cycling to work rates representing moderate (below the estimated LT) and heavy exercise (V˙o 2 equal to 50% of the difference between LT and peakV˙o 2) under conditions of upright and supine positions. During moderate exercise, the steady-state increase in V˙o 2was similar in the two positions, butV˙o 2 kinetics were slower in the supine position. During heavy exercise, the rate of adjustment ofV˙o 2 to the 6-min value was also slower in the supine position but was characterized by a significant reduction in the amplitude of the fast component ofV˙o 2, without a significant slowing of the phase 2 time constant. However, the amplitude of the slow component was significantly increased, such that the end-exerciseV˙o 2 was the same in the two positions. The changes inV˙o 2 kinetics for the supine vs. upright position were paralleled by a blunted response of heart rate at 2 min into exercise during supine compared with upright heavy exercise. Thus the supine position was associated with not only a greater amplitude of the slow component forV˙o 2 but also, concomitantly, with a reduced amplitude of the fast component; this latter effect may be due, at least in part, to an attenuated early rise in heart rate in the supine position.
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Kito, Yoshihiko, Retsu Mitsui, Sean M. Ward i Kenton M. Sanders. "Characterization of slow waves generated by myenteric interstitial cells of Cajal of the rabbit small intestine". American Journal of Physiology-Gastrointestinal and Liver Physiology 308, nr 5 (1.03.2015): G378—G388. http://dx.doi.org/10.1152/ajpgi.00308.2014.
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Slow waves (slow wavesICC) were recorded from myenteric interstitial cells of Cajal (ICC-MY) in situ in the rabbit small intestine, and their properties were compared with those of mouse small intestine. Rabbit slow wavesICC consisted of an upstroke depolarization followed by a distinct plateau component. Ni2+ and nominally Ca2+-free solutions reduced the rate-of-rise and amplitude of the upstroke depolarization. Replacement of Ca2+ with Sr2+ enhanced the upstroke component but decreased the plateau component of rabbit slow wavesICC. In contrast, replacing Ca2+ with Sr2+ decreased both components of mouse slow wavesICC. The plateau component of rabbit slow wavesICC was inhibited in low-extracellular-Cl−-concentration (low-[Cl−]o) solutions and by 4,4′-diisothiocyanostilbene-2,2′-disulfonic acid (DIDS), an inhibitor of Cl− channels, cyclopiazonic acid (CPA), an inhibitor of internal Ca2+ pumps, or bumetanide, an inhibitor of Na+-K+-2Cl− cotransporter (NKCC1). Bumetanide also inhibited the plateau component of mouse slow wavesICC. NKCC1-like immunoreactivity was observed mainly in ICC-MY in the rabbit small intestine. Membrane depolarization with a high-K+ solution reduced the upstroke component of rabbit slow wavesICC. In cells depolarized with elevated external K+, DIDS, CPA, and bumetanide blocked slow wavesICC. These results suggest that the upstroke component of rabbit slow wavesICC is partially mediated by voltage-dependent Ca2+ influx, whereas the plateau component is dependent on Ca2+-activated Cl− efflux. NKCC1 is likely to be responsible for Cl− accumulation in ICC-MY. The results also suggest that the mechanism of the upstroke component differs in rabbit and mouse slow wavesICC in the small intestine.
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Clemens, Stefan, i Paul S. Katz. "Identified Serotonergic Neurons in the TritoniaSwim CPG Activate Both Ionotropic and Metabotropic Receptors". Journal of Neurophysiology 85, nr 1 (1.01.2001): 476–79. http://dx.doi.org/10.1152/jn.2001.85.1.476.
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Although G-protein-coupled (metabotropic) receptors are known to modulate the production of motor patterns, evidence from the escape swim central pattern generator (CPG) of the nudibranch mollusk, Tritonia diomedea, suggests that they might also participate in the generation of the motor pattern itself. The dorsal swim interneurons (DSIs), identified serotonergic neurons intrinsic to the Tritonia swim CPG, evoke dual component synaptic potentials onto other CPG neurons and premotor interneurons. Both the fast and slow components were previously shown to be due to serotonin (5-HT) acting at distinct postsynaptic receptors. We find that blocking or facilitating metabotropic receptors in a postsynaptic premotor interneuron differentially affects the fast and slow synaptic responses to DSI stimulation. Blocking G-protein activation by iontophoretically injecting the GDP-analogue guanosine 5′- O-(2-thiodiphosphate) (GDP-β-S) did not significantly affect the DSI-evoked fast excitatory postsynaptic potential (EPSP) but decreased the amplitude of the slow component more than 50%. Injection of the GTP analogues guanosine 5′- O-(3-thiotriphosphate) (GTP-γ-S) and 5′-guanylyl-imidodiphosphate, to prolong G-protein activation, had mixed effects on the fast component but increased the amplitude and duration of the slow component of the DSI-evoked response and, with repeated DSI stimulation, led to a persistent depolarization. These results indicate that the fast component of the biphasic synaptic potential evoked by a serotonergic CPG neuron onto premotor interneurons is mediated by ionotropic receptors (5-HT-gated ion channels), whereas the slow component is mediated by G-protein-coupled receptors. A similar synaptic activation of metabotropic receptors might also be found within the CPG itself, where it could exert a direct influence onto motor pattern generation.
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Chu, Zhaobi, Rui Zhang, Bo Chen i Hua Li. "Estimation of symmetrical components and their orthogonal components under unknown frequencies and unknown biases". Modern Physics Letters B 31, nr 19-21 (27.07.2017): 1740085. http://dx.doi.org/10.1142/s0217984917400851.
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An algorithm to estimate symmetrical components, orthogonal components and amplitudes of each sinusoidal component in three-phase power system signal under unknown frequencies and unknown biases is presented. The algorithm consists of a signal transformation, a biased adaptive orthogonal decomposition (BAOD) and a symmetrical component estimation. The BAOD can be regarded as a combination of a low pass filter and a number of three-phase frequency estimators in parallel. The symmetrical component estimation employs addition and multiplication rather than operations of trigonometry, division and phase shift. The decomposition property and the convergence property were investigated by Lyapunov theorem, integral manifold of slow adaptation and average method. Two design parameters, bandwidth parameter and frequency adaptive gains, give different effects on the convergence property of frequency adaptation and amplitude estimation independently. Simulation results demonstrate the performance of the method.
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FREIDLIN, MARK. "ON STOCHASTIC PERTURBATIONS OF DYNAMICAL SYSTEMS WITH FAST AND SLOW COMPONENTS". Stochastics and Dynamics 01, nr 02 (czerwiec 2001): 261–81. http://dx.doi.org/10.1142/s0219493701000138.
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Dynamical systems with fast and slow components are considered. We show that small random perturbations of the fast component can lead to essential changes in the limiting slow motion. For example, new stable equilibria or deterministic oscillations with amplitude and frequency of order 1 can be introduced by the perturbations. These are stochastic resonance type effects, and they are considered from the point of view of large deviations theory.
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Barker, Alan R., Emily Trebilcock, Brynmor Breese, Andrew M. Jones i Neil Armstrong. "The effect of priming exercise on O2 uptake kinetics, muscle O2 delivery and utilization, muscle activity, and exercise tolerance in boys". Applied Physiology, Nutrition, and Metabolism 39, nr 3 (marzec 2014): 308–17. http://dx.doi.org/10.1139/apnm-2013-0174.
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This study used priming exercise in young boys to investigate (i) how muscle oxygen delivery and oxygen utilization, and muscle activity modulate oxygen uptake kinetics during exercise; and (ii) whether the accelerated oxygen uptake kinetics following priming exercise can improve exercise tolerance. Seven boys that were aged 11.3 ± 1.6 years completed either a single bout (bout 1) or repeated bouts with 6 min of recovery (bout 2) of very heavy-intensity cycling exercise. During the tests oxygen uptake, muscle oxygenation, muscle electrical activity and exercise tolerance were measured. Priming exercise most likely shortened the oxygen uptake mean response time (change, ±90% confidence limits; –8.0 s, ±3.0), possibly increased the phase II oxygen uptake amplitude (0.11 L·min−1, ±0.09) and very likely reduced the oxygen uptake slow component amplitude (–0.08 L·min−1, ±0.07). Priming resulted in a likely reduction in integrated electromyography (–24% baseline, ±21% and –25% baseline, ±19) and a very likely reduction in Δ deoxyhaemoglobin/Δoxygen uptake (–0.16, ±0.11 and –0.09, ±0.05) over the phase II and slow component portions of the oxygen uptake response, respectively. A correlation was present between the change in tissue oxygenation index during bout 2 and the change in the phase II (r = –0.72, likely negative) and slow component (r = 0.72, likely positive) oxygen uptake amplitudes following priming exercise, but not for muscle activity. Exercise tolerance was likely reduced (change –177 s, ±180) following priming exercise. The altered phase II and slow component oxygen uptake amplitudes in boys following priming exercise are linked to an improved localised matching of muscle oxygen delivery to oxygen uptake and not muscle electrical activity. Despite more rapid oxygen uptake kinetics following priming exercise, exercise tolerance was not enhanced.
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French, A. S. "Two components of rapid sensory adaptation in a cockroach mechanoreceptor neuron". Journal of Neurophysiology 62, nr 3 (1.09.1989): 768–77. http://dx.doi.org/10.1152/jn.1989.62.3.768.
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1. The femoral tactile spine of the cockroach is innervated by a single sensory neuron with its cell body in the spine. A step deflection of the spine produces a burst of action potentials which decays to zero in approximately 1 s. This rapid adaptation occurs during encoding of action potentials and can be studied by extracellular electrical stimulation of the sensory neuron. 2. The threshold current of the neuron is labile, increasing with depolarization and decreasing with mild hyperpolarization. During rapid adaptation, the threshold current increases to exceed any steady stimulating current. 3. The dynamic behavior of the threshold current in the tactile spine neuron was observed following step changes in membrane current. The threshold current followed a trajectory which could always be well fitted by a sum of two exponential decays with time constants of approximately 100 and 1,000 ms. 4. The amplitude of the slow component of threshold change was proportional to the size of the step change in membrane current but saturated at strong hyperpolarizations. Its time constant decreased monotonically with depolarization. In contrast, the fast component had more complex behavior, changing biphasically with step amplitude and reversing with initial hyperpolarizations. Its time constant was maximal at the resting membrane potential. 5. The amplitude of the fast component was strongly reduced by treatment with N-chlorosuccinimide (NCS), an agent which reduces sodium channel inactivation. It was not affected by some agents known to block potassium channels. 6. The slow component was not affected by NCS, tetraethyl-ammonium chloride, apamin, or charybdotoxin. 7. Approximate contributions of the two components to the steady-state threshold were reconstructed from step responses. These indicate that the slow component dominates when the receptor is hyperpolarized. However, during depolarizations from rest, as occur with normal stimulation, the two components contribute approximately equally to threshold changes.
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Knippenberg, J. M. J., E. L. J. M. van Luijtelaar i J. H. R. Maes. "Slow Late Component in Conditioned Stimulus-Evoked Potentials From the Amygdala After Fear Conditioning in the Rat". Neural Plasticity 9, nr 4 (2002): 261–72. http://dx.doi.org/10.1155/np.2002.261.
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Male Wistar rats were subjected to a differential Pavlovian fear conditioning procedure in which one of two tones (6 or 10 kHz) was followed by an electric shock (CS+) and the other was not (CS-). Before and after fear conditioning, we recorded the evoked potentials elicited byCS+andCS-from electrodes aimed at the lateral nucleus of the amygdala. Before conditioning, a slow, negative component with peak amplitude around 150 ms was present in the evoked potentials. This component was sensitive to habituation. After fear conditioning, bothCS+andCS-elicited the same late component, albeit with a larger amplitude. This enhancement was temporary: decreasing amplitude was observed in the course of CS test presentations under extinction. Prior research revealed a comparable slow component in the amygdala of the cat under similar experimental conditions. The collective results indicate that the large late component in the amygdala is enhanced by fear conditioning, suggesting that such enhancement reflects the anticipation of a biologically significant event.
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Pineda, J. C., E. Galarraga, J. Bargas, M. Cristancho i J. Aceves. "Charybdotoxin and apamin sensitivity of the calcium-dependent repolarization and the afterhyperpolarization in neostriatal neurons". Journal of Neurophysiology 68, nr 1 (1.07.1992): 287–94. http://dx.doi.org/10.1152/jn.1992.68.1.287.
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1. Intracellular recordings from neostriatal neurons in an in vitro slice preparation of the rat brain were used to analyze the pharmacological sensitivity of the action potential (AP) repolarization and the afterhyperpolarization (AHP) that follows a single action potential. The interspike voltage trajectory and the AHP could be divided into two main parts: a fast component lasting a few milliseconds and better observed during a train of spikes, and a slow component lasting approximately 250 ms and that comprises the main portion of the AHP. In some cells, a slow (up to 1 s) component of low amplitude was also detected. 2. Single APs were elicited at two imposed membrane potentials (around -60 and around -80 mV). The AP amplitude was larger, the repolarization rate was faster, and the duration was shorter when spikes were evoked at -80 mV. When measured from the -60 mV holding potential, the afterpotential was an AHP with peak amplitude of -5 mV. The afterpotential became a delayed depolarization (DD) at -80 mV. 3. Firing frequency adaptation was voltage sensitive. The firing of APs induced by long intracellular current pulses from a holding potential of -80 mV exhibited only a slow-frequency adaptation (time constant of seconds). However, at -60 mV, an initial and faster frequency adaptation was evident (time constant of tens of milliseconds). 4. The Ca2+ channel blocker Cd2+ retarded AP repolarization rate. This effect correlated with a significant block of the fast and slow components of the AHP. In contrast, Ni2+ had no significant effects on the same parameters.(ABSTRACT TRUNCATED AT 250 WORDS)
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Vogalis, F., i K. M. Sanders. "Excitatory and inhibitory neural regulation of canine pyloric smooth muscle". American Journal of Physiology-Gastrointestinal and Liver Physiology 259, nr 1 (1.07.1990): G125—G133. http://dx.doi.org/10.1152/ajpgi.1990.259.1.g125.
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Studies were performed to characterize the intrinsic innervation of the circular muscle layer of the canine pylorus. Cross-sectional strips of muscle were studied with intracellular recording techniques, and junction potentials were elicited with transmural nerve stimulation. Neurally mediated responses were recorded from cells at several points through the thickness of the circular layer. Excitatory junction potentials (EJPs) increased and inhibitory junction potentials (IJPs) decreased in amplitude with distance from the myenteric border of the circular muscle. Atropine blocked EJPs throughout the circular layer, demonstrating that excitatory inputs are primarily cholinergic. The gradient in IJP amplitude persisted after blockade of EJPs. Three components of IJPs were identified: 1) a fast, apamin-sensitive component that reached a peak and decayed within approximately 1 s; 2) a slower, apamin-insensitive component that reached a peak within 800 ms but decayed slowly over 5 s; and 3) a very slow component that reached a maximum in 7-10 s. Junctional potentials affected the pattern of myogenic electrical activity. Transmural stimulation could evoke premature slow waves in the myenteric portion of the circular layer but when excitatory inputs were blocked, IJPs greatly reduced the amplitude of slow waves. EJPs elicited action potentials in submucosal portion of circular muscles, and IJPs hyperpolarized these cells. The influence of intrinsic nerves on contractile patterns of pyloric muscles was also characterized. These data demonstrate that a neuromuscular apparatus exists within the gastroduodenal junction for 1) local regulation of slow waves and 2) independent control of the myenteric and submucosal regions of the circular layer.
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Goo, Yong Sook, Wonil Lim i Keith S. Elmslie. "Ca2+ Enhances U-Type Inactivation of N-Type (CaV2.2) Calcium Current in Rat Sympathetic Neurons". Journal of Neurophysiology 96, nr 3 (wrzesień 2006): 1075–83. http://dx.doi.org/10.1152/jn.01294.2005.
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Ca2+-dependent inactivation (CDI) has recently been shown in heterologously expressed N-type calcium channels (CaV2.2), but CDI has been inconsistently observed in native N-current. We examined the effect of Ca2+ on N-channel inactivation in rat sympathetic neurons to determine the role of CDI on mammalian N-channels. N-current inactivated with fast (τ ∼ 150 ms) and slow (τ ∼ 3 s) components in Ba2+. Ca2+ differentially affected these components by accelerating the slow component (slow inactivation) and enhancing the amplitude of the fast component (fast inactivation). Lowering intracellular BAPTA concentration from 20 to 0.1 mM accelerated slow inactivation, but only in Ca2+ as expected from CDI. However, low BAPTA accelerated fast inactivation in either Ca2+ or Ba2+, which was unexpected. Fast inactivation was abolished with monovalent cations as the charge carrier, but slow inactivation was similar to that in Ba2+. Increased Ca2+, but not Ba2+, concentration (5–30 mM) enhanced the amplitude of fast inactivation and accelerated slow inactivation. However, the enhancement of fast inactivation was independent of Ca2+ influx, which indicates the relevant site is exposed to the extracellular solution and is inconsistent with CDI. Fast inactivation showed U-shaped voltage dependence in both Ba2+ and Ca2+, which appears to result from preferential inactivation from intermediate closed states (U-type inactivation). Taken together, the data support a role for extracellular divalent cations in modulating U-type inactivation. CDI appears to play a role in N-channel inactivation, but on a slower (sec) time scale.
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Barker, Alan R., Andrew M. Jones i Neil Armstrong. "The influence of priming exercise on oxygen uptake, cardiac output, and muscle oxygenation kinetics during very heavy-intensity exercise in 9- to 13-yr-old boys". Journal of Applied Physiology 109, nr 2 (sierpień 2010): 491–500. http://dx.doi.org/10.1152/japplphysiol.00139.2010.
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The present study examined the effect of priming exercise on O2 uptake (V̇o2) kinetics during subsequent very heavy exercise in eight 9- to 13-yr-old boys. We hypothesised that priming exercise would 1) elevate muscle O2 delivery prior to the subsequent bout of very heavy exercise, 2) have no effect on the phase II V̇o2 τ, 3) elevate the phase II V̇o2 total amplitude, and 4) reduce the magnitude of the V̇o2 slow component. Each participant completed repeat 6-min bouts of very heavy-intensity cycling exercise separated by 6 min of light pedaling. During the tests V̇o2, muscle oxygenation (near infrared spectroscopy), and cardiac output (Q̇) (thoracic impedance) were determined. Priming exercise increased baseline muscle oxygenation and elevated Q̇ at baseline and throughout the second exercise bout. The phase II V̇o2 τ was not altered by priming exercise ( bout 1: 22 ± 7 s vs. bout 2: 20 ± 4 s; P = 0.30). However, the time constant describing the entire V̇o2 response from start to end of exercise was accelerated ( bout 1: 43 ± 8 s vs. bout 2: 36 ± 5 s; P = 0.002) due to an increased total phase II V̇o2 amplitude ( bout 1: 1.73 ± 0.33 l/min vs. bout 2: 1.80 ± 0.59 l/min; P = 0.002) and a reduced V̇o2 slow component amplitude ( bout 1: 0.18 ± 0.08 l/min vs. bout 2: 0.12 ± 0.09 l/min; P = 0.048). These results suggest that phase II V̇o2 kinetics in young boys is principally limited by intrinsic muscle metabolic factors, whereas the V̇o2 total phase II and slow component amplitudes may be O2 delivery sensitive.
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Kitano, M., K. Niiyama, T. Kasamatsu, E. E. Sutter i A. M. Norcia. "Retinotopic and nonretinotopic field potentials in cat visual cortex". Visual Neuroscience 11, nr 5 (wrzesień 1994): 953–77. http://dx.doi.org/10.1017/s0952523800003904.
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AbstractTwo types of field potentials were identified in cat visual cortex using contrast reversal of oriented bar gratings: a short-latency fast-local component with a retinotopic organization similar to that seen with single-unit discharges at the same cortical site, and a slow, nonretinotopic component with a longer peak latency. The slow-distributed component had an extensive receptive field mapped by measuring the amplitude of binary kernels and showed strong inhibitory interactions within the receptive field. The peak latency of the slow-local component increased with distance from the retinotopic center, suggesting a possible conduction delay. Both components showed some orientation bias depending on the laminar location, but the bias could be independent of the orientation preferred by single units in the immediate vicinity. The present findings indicate that locally generated field potentials reflect cortical mechanisms for nonlinear integration over wide areas of the visual field.
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Hegmann, F. A., i J. S. Preston. "Photoresponse of high Tc superconductor thin films". Canadian Journal of Physics 70, nr 10-11 (1.10.1992): 1133–37. http://dx.doi.org/10.1139/p92-183.
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A fast photoresponse is observed in a current-biased epitaxial YBa2Cu3O7 thin-film bridge structure exposed to 100 ps laser pulses. A bolometric response, with a pulse width of the order of 10 ns, dominates at temperatures close to Tc and at high laser fluences. At lower temperatures and fluences, the observed transient response contains distinct fast and slow components. Preliminary results indicate a pulse width for the fast component less than 500 ps. Application of a small magnetic field perpendicular to the sample increases the amplitude of the slow component while leaving the fast component relatively unaffected. Comparison of these results with resistance versus temperature measurements in the same magnetic field suggests that the fast component is nonthermal in origin.
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Ward, S. M., F. Vogalis, D. P. Blondfield, H. Ozaki, N. Fusetani, D. Uemura, N. G. Publicover i K. M. Sanders. "Inhibition of electrical slow waves and Ca2+ currents of gastric and colonic smooth muscle by phosphatase inhibitors". American Journal of Physiology-Cell Physiology 261, nr 1 (1.07.1991): C64—C70. http://dx.doi.org/10.1152/ajpcell.1991.261.1.c64.
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The effects of calyculin A, a phosphatase inhibitor isolated from the marine sponge Discodermia calyx, on the electrical activity of colonic and gastric muscles were studied. Calyculin A reduced the amplitude and duration of slow waves, primarily by inhibiting the plateau component. Okadaic acid, another phosphatase inhibitor, also reduced the amplitude and duration of gastric slow waves. The mechanism of action of calyculin A was investigated by studying its effects on inward currents of isolated gastric and colonic myocytes. Calyculin A reduced the amplitude of the peak and the sustained components of the inward current. Okadaic acid had similar effects. These data suggest that phosphorylation of Ca2+ channels of gastrointestinal smooth muscles may inhibit Ca2+ currents. This mechanism may provide an important means of regulating the currents responsible for excitation-contraction coupling in these muscles.
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Lakhina, G. S., S. V. Singh, A. P. Kakad, F. Verheest i R. Bharuthram. "Study of nonlinear ion- and electron-acoustic waves in multi-component space plasmas". Nonlinear Processes in Geophysics 15, nr 6 (27.11.2008): 903–13. http://dx.doi.org/10.5194/npg-15-903-2008.
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Abstract. Large amplitude ion-acoustic and electron-acoustic waves in an unmagnetized multi-component plasma system consisting of cold background electrons and ions, a hot electron beam and a hot ion beam are studied using Sagdeev pseudo-potential technique. Three types of solitary waves, namely, slow ion-acoustic, ion-acoustic and electron-acoustic solitons are found provided the Mach numbers exceed the critical values. The slow ion-acoustic solitons have the smallest critical Mach numbers, whereas the electron-acoustic solitons have the largest critical Mach numbers. For the plasma parameters considered here, both type of ion-acoustic solitons have positive potential whereas the electron-acoustic solitons can have either positive or negative potential depending on the fractional number density of the cold electrons relative to that of the ions (or total electrons) number density. For a fixed Mach number, increases in the beam speeds of either hot electrons or hot ions can lead to reduction in the amplitudes of the ion-and electron-acoustic solitons. However, the presence of hot electron and hot ion beams have no effect on the amplitudes of slow ion-acoustic modes. Possible application of this model to the electrostatic solitary waves (ESWs) observed in the plasma sheet boundary layer is discussed.
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Kida, M., i A. Imai. "Cognitive performance and event-related brain potentials under simulated high altitudes". Journal of Applied Physiology 74, nr 4 (1.04.1993): 1735–41. http://dx.doi.org/10.1152/jappl.1993.74.4.1735.
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The effects of hypobaric hypoxia on cognitive processing in humans were studied by recording event-related potentials (ERPs) from the scalp in a go/no-go reaction time (RT) paradigm under various simulated high altitudes. Most subjects indicated abrupt impairment of RT at high altitudes. RTs lengthened in association with changes in latency and amplitude of the N2-P3 components, reflecting sensory discrimination and evaluation processes. Some subjects did not suffer any changes in RT up to an extremely high altitude of 6,000 m. In the latter case, although the N2-P3 components did not undergo any changes, the P3 component was followed by a sequence of negative on-going (frontal maximum) and positive on-going (parietal maximum) slow waves. The amplitudes of these slow waves increased as altitude increased. Although these same waves appeared in the ERPs of subjects who demonstrated the increase in RTs at high altitudes, when the subjects failed in the RT task, both of the slow waves either disappeared or diminished. Such slow waves may be associated with attempts to maintain RTs against the deteriorative effects of hypobaric hypoxia.
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Porciatti, V., R. Alesci i P. Bagnoli. "Evoked responses to sinusoidal gratings in the pigeon optic tectum". Visual Neuroscience 2, nr 2 (luty 1989): 137–45. http://dx.doi.org/10.1017/s0952523800011998.
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AbstractTectal evoked potentials (TEPs) in response to sinusoidal gratings of different contrast, spatial and temporal frequency have been recorded from the tectal surface of the pigeon. Responses have been digitally filtered in order to isolate transient oscillatory (fast) potentials (50–150 Hz), transient slow potentials (1–50 Hz), and the steady-state second-harmonic component (16.6 Hz). Transient slow potentials, as well as the steady-state second-harmonic component, are band-pass spatially tuned with a maximum at 0.5 cycles/deg and attenuation at higher and lower spatial frequencies. The high spatial frequency cutoff is 4–5 cycles/deg. Both transient slow potentials and the steady-state second-harmonic component increase in amplitude as a function of log contrast and saturate at about 20% contrast. The contrast sensitivity, as determined by extrapolating TEP amplitude to 0 V is 0.1–0.2%. These characteristics of spatial-frequency selectivity and contrast sensitivity are similar to those reported for single tectal cells. Unlike slow potentials, oscillatory potentials are not band-pass spatially tuned. In addition, their contrast response function does not saturate at moderate contrast. These differences suggest that tectal evoked slow and fast potentials reflect the activity of different neuronal mechanisms.
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Olschewski, Andrea, Michael E. Bräu, Gunter Hempelmann, Werner Vogel i Boris V. Safronov. "Differential Block of Fast and Slow Inactivating Tetrodotoxin-sensitive Sodium Channels by Droperidol in Spinal Dorsal Horn Neurons". Anesthesiology 92, nr 6 (1.06.2000): 1667–76. http://dx.doi.org/10.1097/00000542-200006000-00026.
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Background Dorsal horn neurons of the spinal cord participate in neuronal pain transmission. During spinal and epidural anesthesia, dorsal horn neurons are exposed to local anesthetics and opioids. Droperidol is usually given with opioids to avoid nausea and vomiting. A recently developed method of "entire soma isolation" has made it possible to study directly the action of droperidol on different components of Na+ current in dorsal horn neurons. Methods Using a combination of the whole-cell patch-clamp recording from spinal cord slices and the entire soma isolation method, we studied the direct action of droperidol on two types of Na+ currents in dorsal horn neurons of young rats. Results The tetrodotoxin-sensitive Na+ current in isolated somata consisted of a fast inactivating (tauF, 0.5-2 ms; 80-90% of the total amplitude) and a slow inactivating (tauS, 6-20 ms; 10-20% of the total amplitude) component. Droperidol, at concentrations relevant for spinal and epidural anesthesia, selectively and reversibly suppressed the fast component with a half-maximum inhibiting concentration (IC50) of 8.3 microm. The slow inactivating component was much less sensitive to droperidol; the estimated IC50 value was 809 microm. Conclusions Droperidol selectively blocks fast Na+ channels, the fast and slow components of the Na+ current in dorsal horn neurons are carried through pharmacologically distinct types of Na+ channels, and the effects of droperidol differ from those of local anesthetics and tetrodotoxin, which equipotently suppress both components. Droperidol may be suggested as a pharmacologic tool for separation of different types of inactivating tetrodotoxin-sensitive Na+ channel.
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Dimoska, Aneta, Stuart J. Johnstone, Dale Chiswick, Robert J. Barry i Adam R. Clarke. "A Developmental Investigation of Stop-Signal Inhibition". Journal of Psychophysiology 21, nr 2 (styczeń 2007): 109–26. http://dx.doi.org/10.1027/0269-8803.21.2.109.
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Abstract. The present study examined the development of response inhibition in the stop-signal task across child (8-13 years), young-adult (18-22 years), and middle-aged adult (29-47 years) groups through a dissociation of low- and higher-frequency ERP activity. Fifty-one subjects (n = 17 in each group) performed the stop-signal task, which consisted of a visual choice reaction time (RT) task and auditory stop-signals, while EEG was recorded. The original EEG data (0.01-30 Hz) was subsequently filtered to separate slow-wave (0.01-2 Hz) and residual (2-30 Hz) activity. Performance findings revealed that stop-signal reaction time (SSRT) decreased from the child to young-adult group and then showed a small increase in the middle-aged adult group. Original ERPs revealed decreasing N1 and N2 amplitudes and increasing P2 and P3 amplitudes across the scalp with increasing age for successful-stop trials. These developmental effects did not occur in the residual waveforms after removal of slow-wave activity. For failed-stop trials, a response-locked negative component, identified as the error-negativity (Ne), showed an age-related decrease in amplitude across the scalp in the residual, but not the original, waveform. The error-positivity (Pe) increased in amplitude with age in the original data, but this was accounted for by a positive slow-wave (PSW). Together, the findings suggest that underlying slow-wave activity accounts for a large number of developmental effects in the traditionally quantified ERP components, but may also obscure effects occurring in residual activity. These findings highlight the importance of dissociating low- and higher-frequency ERP activity in developmental research.
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Chorley, Alan, Richard P. Bott, Simon Marwood i Kevin L. Lamb. "Bi-exponential modelling of $$W^{^{\prime}}$$ reconstitution kinetics in trained cyclists". European Journal of Applied Physiology 122, nr 3 (18.12.2021): 677–89. http://dx.doi.org/10.1007/s00421-021-04874-3.
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Abstract Purpose The aim of this study was to investigate the individual $$W^{^{\prime}}$$ W ′ reconstitution kinetics of trained cyclists following repeated bouts of incremental ramp exercise, and to determine an optimal mathematical model to describe $$W^{^{\prime}}$$ W ′ reconstitution. Methods Ten trained cyclists (age 41 ± 10 years; mass 73.4 ± 9.9 kg; $$\dot{V}{\text{O}}_{2\max }$$ V ˙ O 2 max 58.6 ± 7.1 mL kg min−1) completed three incremental ramps (20 W min−1) to the limit of tolerance with varying recovery durations (15–360 s) on 5–9 occasions. $$W^{^{\prime}}$$ W ′ reconstitution was measured following the first and second recovery periods against which mono-exponential and bi-exponential models were compared with adjusted R2 and bias-corrected Akaike information criterion (AICc). Results A bi-exponential model outperformed the mono-exponential model of $$W^{^{\prime}}$$ W ′ reconstitution (AICc 30.2 versus 72.2), fitting group mean data well (adjR2 = 0.999) for the first recovery when optimised with parameters of fast component (FC) amplitude = 50.67%; slow component (SC) amplitude = 49.33%; time constant (τ)FC = 21.5 s; τSC = 388 s. Following the second recovery, W′ reconstitution reduced by 9.1 ± 7.3%, at 180 s and 8.2 ± 9.8% at 240 s resulting in an increase in the modelled τSC to 716 s with τFC unchanged. Individual bi-exponential models also fit well (adjR2 = 0.978 ± 0.017) with large individual parameter variations (FC amplitude 47.7 ± 17.8%; first recovery: (τ)FC = 22.0 ± 11.8 s; (τ)SC = 377 ± 100 s; second recovery: (τ)FC = 16.3.0 ± 6.6 s; (τ)SC = 549 ± 226 s). Conclusions W′ reconstitution kinetics were best described by a bi-exponential model consisting of distinct fast and slow phases. The amplitudes of the FC and SC remained unchanged with repeated bouts, with a slowing of W′ reconstitution confined to an increase in the time constant of the slow component.
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Yoshimura, M., C. Polosa i S. Nishi. "Afterhyperpolarization mechanisms in cat sympathetic preganglionic neuron in vitro". Journal of Neurophysiology 55, nr 6 (1.06.1986): 1234–46. http://dx.doi.org/10.1152/jn.1986.55.6.1234.
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A long-lasting afterhyperpolarization (AHP) follows the antidromic or current-induced action potential of sympathetic preganglionic neurons (SPNs) studied in slices of cat spinal cord maintained in vitro. Duration and amplitude of the AHP that follows a single spike were 2.8 +/- 0.3 s and 16.0 +/- 0.7 mV (mean +/- SE), respectively. In most cases two components could be distinguished, an initial faster and usually larger component [fast (F) AHP] followed by a slowly decaying component [slow (S) AHP]. An increase in membrane conductance was associated with the AHP. The amplitude of both components increased with membrane depolarization and decreased with hyperpolarization. Both fast and slow component were nullified at a voltage of -90 mV in 3.6 mM K+. Peak AHP amplitude decreased as K+ was increased from 1.5 to 7.0 mM. The null point for both fast (F) AHP and slow (S) AHP shifted in the depolarizing or hyperpolarizing direction when K+ was increased or decreased, respectively. These data suggest that an increase in K+-conductance is the mechanism underlying the AHP. The two components of the AHP could be separated by their differential sensitivity to superfusion with the Ca2+-channel blocker cobalt (2 mM) or with low Ca2+ (0.25 mM). These procedures resulted in an AHP of much shorter duration (330 ms, range 150-600), presumably the FAHP. These observations indicate that a Ca2+-activated K+-conductance is likely to be involved in the generation of the SAHP. The FAHP was depressed during superfusion with tetraethylammonium (TEA) (20 mM) and intracellular cesium injection. The SAHP was enhanced by TEA and enhanced or depressed by cesium. In 3.6 mM K+ the FAHP reversed in polarity at membrane voltages more negative than -90 mV. This component had an approximately linear relation of amplitude to membrane potential. The SAHP did not reverse in most cells. In the few cases in which it reversed, the change in amplitude for a given change in membrane voltage was much smaller on the negative than on the positive side of the null potential. Thus the SAHP shows voltage-dependent, nonlinear characteristics. This difference in behavior of the two components was also observed when the null point was displaced in high or low K+. In the presence of tetrodotoxin (TTX) the AHP persisted in temporal association with a high-threshold, TTX-resistant, cobalt-sensitive spike. During the time course of the AHP the efficacy of synaptic input decreased, suggesting that the AHP has an important role in regulating the firing rate of the SPN.
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Skinner, Julianne, Antimo Buonocore i Ziad M. Hafed. "Transfer function of the rhesus macaque oculomotor system for small-amplitude slow motion trajectories". Journal of Neurophysiology 121, nr 2 (1.02.2019): 513–29. http://dx.doi.org/10.1152/jn.00437.2018.
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Two main types of small eye movements occur during gaze fixation: microsaccades and slow ocular drifts. While microsaccade generation has been relatively well studied, ocular drift control mechanisms are unknown. Here we explored the degree to which monkey smooth eye movements, on the velocity scale of slow ocular drifts, can be generated systematically. Two male rhesus macaque monkeys tracked a spot moving sinusoidally, but slowly, along the horizontal or vertical direction. Maximum target displacement in the motion trajectory was 30 min arc (0.5°), and we varied the temporal frequency of target motion from 0.2 to 5 Hz. We obtained an oculomotor “transfer function” by measuring smooth eye velocity gain (relative to target velocity) as a function of frequency, similar to past work with large-amplitude pursuit. Monkey eye velocities as slow as those observed during slow ocular drifts were clearly target motion driven. Moreover, as with large-amplitude smooth pursuit, eye velocity gain varied with temporal frequency. However, unlike with large-amplitude pursuit, exhibiting low-pass behavior, small-amplitude motion tracking was band pass, with the best ocular movement gain occurring at ~0.8–1 Hz. When oblique directions were tested, we found that the horizontal component of pursuit gain was larger than the vertical component. Our results provide a catalog of the control abilities of the monkey oculomotor system for slow target motions, and they also support the notion that smooth fixational ocular drifts are controllable. This has implications for neural investigations of drift control and the image-motion consequences of drifts on visual coding in early visual areas. NEW & NOTEWORTHY We studied the efficacy of monkey smooth pursuit eye movements for very slow target velocities. Pursuit was impaired for sinusoidal motions of frequency less than ~0.8–1 Hz. Nonetheless, eye trajectory was still sinusoidally modulated, even at velocities lower than those observed during gaze fixation with slow ocular drifts. Our results characterize the slow control capabilities of the monkey oculomotor system and provide a basis for future understanding of the neural mechanisms for slow ocular drifts.
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Liu, Louis W. C., i Jan D. Huizinga. "Canine colonic circular muscle generates action potentials without the pacemaker component". Canadian Journal of Physiology and Pharmacology 72, nr 1 (1.01.1994): 70–81. http://dx.doi.org/10.1139/y94-012.
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Two dominant types of action potentials in canine colon are slow wave type action potentials (slow waves) and spike-like action potentials (SLAPs). The slow waves, originating at the submuscular surface where a network of interstitial cells of Cajal (ICCs) is found, possess a pacemaker component. Activation of the pacemaker component is insensitive to voltage changes and L-type calcium channel blockers, and is postulated to involve a metabolic clock sensitive to cyclic AMP. SLAPs are more prominent in the longitudinal muscle. To understand the contribution circular muscle cells make to the generation of these action potentials, a circular muscle preparation (devoid of the submuscular ICC – smooth muscle network, longitudinal muscle, and myenteric plexus) was developed. Circular muscle preparations were spontaneously quiescent, with a resting membrane potential of −62.9 ± 0.6 mV. Ba2+ (0.5 mM) depolarized the cells to −51.8 ± 0.6 mV and induced electrical oscillations with a frequency, duration, amplitude, and rate of rise equal to 6.6 ± 0.4 cpm, 2.2 ± 0.2 s, 19.4 ± 0.9 mV, and 21.8 ± 1.7 mV/s, respectively. In most cases, Ba2+-induced oscillations were preceded by a prepotential of 4.4 ± 0.3 mV, with a rate of rise of 1.1 ± 0.1 mV/s. Ba2+-induced oscillations were abolished by 1 μM D600 as well as by repolarization of 6–12 mV. Addition of 0.1 μM Bay K8644 in the presence of Ba2+ further depolarized circular muscle cells to −42.4 ± 0.8 mV and increased the oscillation frequency to 16.8 ± 1.8 cpm. The electrical oscillations induced in circular muscle preparations by Ba2+ and Bay K8644 were similar to the SLAPs exhibited by the isolated longitudinal muscle layer, indicating that generation of SLAPs is an intrinsic property of smooth muscle cells. Forskolin (1 μM), previously shown to dramatically decrease the frequency but not the amplitude of slow waves in preparations including the submuscular ICC network, decreased the amplitude of the Ba2+-induced oscillations in circular muscle preparations without changing the frequency. These results provide strong evidence for the hypothesis that the submuscular ICC – smooth muscle network is essential for the initiation of the pacemaker component of the colonic slow waves. The mechanism for regulating the frequency of slow waves is different from that responsible for the Ba2+-induced oscillations in circular muscle preparations. Circular muscle cells are shown to be excitable and capable of generating oscillatory activity dominated by L-type calcium channel activity, which is regulated by K+ conductance.Key words: interstitial cells of Cajal, smooth muscle, dog colon, barium chloride, potassium conductance, Bay K8644, pacemaking activity.
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Carter, Helen, Andrew M. Jones, Thomas J. Barstow, Mark Burnley, Craig Williams i Jonathan H. Doust. "Effect of endurance training on oxygen uptake kinetics during treadmill running". Journal of Applied Physiology 89, nr 5 (1.11.2000): 1744–52. http://dx.doi.org/10.1152/jappl.2000.89.5.1744.
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The purpose of this study was to examine the effect of endurance training on oxygen uptake (V˙o 2) kinetics during moderate [below the lactate threshold (LT)] and heavy (above LT) treadmill running. Twenty-three healthy physical education students undertook 6 wk of endurance training that involved continuous and interval running training 3–5 days per week for 20–30 min per session. Before and after the training program, the subjects performed an incremental treadmill test to exhaustion for determination of the LT and the V˙o 2 max and a series of 6-min square-wave transitions from rest to running speeds calculated to require 80% of the LT and 50% of the difference between LT and maximal V˙o 2. The training program caused small (3–4%) but significant increases in LT and maximalV˙o 2 ( P < 0.05). TheV˙o 2 kinetics for moderate exercise were not significantly affected by training. For heavy exercise, the time constant and amplitude of the fast component were not significantly affected by training, but the amplitude of theV˙o 2 slow component was significantly reduced from 321 ± 32 to 217 ± 23 ml/min ( P< 0.05). The reduction in the slow component was not significantly correlated to the reduction in blood lactate concentration ( r = 0.39). Although the reduction in the slow component was significantly related to the reduction in minute ventilation ( r = 0.46; P < 0.05), it was calculated that only 9–14% of the slow component could be attributed to the change in minute ventilation. We conclude that theV˙o 2 slow component during treadmill running can be attenuated with a short-term program of endurance running training.
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Ufret-Vincenty, Carmen A., Deborah J. Baro i L. F. Santana. "Differential contribution of sialic acid to the function of repolarizing K+ currents in ventricular myocytes". American Journal of Physiology-Cell Physiology 281, nr 2 (1.08.2001): C464—C474. http://dx.doi.org/10.1152/ajpcell.2001.281.2.c464.
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We investigated the contribution of sialic acid residues to the K+ currents involved in the repolarization of mouse ventricular myocytes. Ventricular K+ currents had a rapidly inactivating component followed by slowly decaying and sustained components. This current was produced by the summation of three distinct currents: I to, which contributed to the transient component; I ss, which contributed to the sustained component; and I K,slow, which contributed to both components. Incubation of ventricular myocytes with the sialidase neuraminidase reduced the amplitude of I to without altering I K,slow and I ss. We found that the reduction in I to amplitude resulted from a depolarizing shift in the voltage of activation and a reduction in the conductance of I to. Expression of Kv4.3 channels, a major contributor to I to in the ventricle, in a sialylation-deficient Chinese hamster ovary cell line (lec2) mimicked the effects of neuraminidase on the ventricular I to. Furthermore, we showed that sialylated glycolipids have little effect on the voltage dependence of I to. Finally, consistent with its actions on I to, neuraminidase produced an increase in the duration of the action potential of ventricular myocytes and the frequency of early afterdepolarizations. We conclude that sialylation of the proteins forming Kv4 channels is important in determining the voltage dependence and conductance of I to and that incomplete glycosylation of these channels could lead to arrhythmias.
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Baeyens, Jean-Pierre, Ben Serrien, Maggie Goossens, Katia Veekmans, Regs Baeyens, Walter Daems, Erik Cattrysse i Ron Clijsen. "Effects of Rehearsal Time and Repertoire Speed on Extensor Carpi Radialis EMG in Conservatory Piano Students". Medical Problems of Performing Artists 35, nr 2 (1.06.2020): 81–88. http://dx.doi.org/10.21091/mppa.2020.2013.
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BACKGROUND: Repetitive actions while playing piano may overload forearm muscles and tendons, leading to playing-related musculoskeletal disorders (PRMDs), including lateral epicondylitis. METHODS: In this pilot study, surface electromyography (sEMG) activity of the extensor carpi radialis (ECR) was captured in 10 conservatory piano students while playing a fast and a slow music score selected from the individual’s repertoire, each 3 minutes long. Measurements were made at baseline and again after 2 hrs and 4 hrs of rehearsal time of the piano études. The amplitude of the sEMG signal was processed by a smoothing algorithm, and the frequency component with a non-orthogonal wavelets procedure. Amplitude of the sEMG was expressed in percent of maximal voluntary contraction (%MVC) at baseline. Statistical analysis encompassed 2-way repeated measures ANOVAs for the amplitude and frequency components of the sEMG signal (a set at 5%). The students also rated the intensity of rehearsals using a VAS. RESULTS: The ECR presented with a mean amplitude of 23%MVC for the slow scores, which increased significantly to 36%MVC for the fast scores. The sEMG signal presented a significant though small decrease of 1.9%MVC in amplitude between baseline and 4 hrs of rehearsal time and no shift in frequency, which may indicate that the rehearsals were held at a physiological steady-state and suggesting optimization or complementary muscle loading. CONCLUSIONS: These data accentuated that the loading of the ECR (as reflected in the amplitude component) was higher than that seen for computer keyboard workers. The augmented loading of the ECR and reduced blood flow to forearm muscles may be a factor in the development of PRMDs in pianists.
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Berger, Nicolas J. A., i Andrew M. Jones. "Pulmonary O2 uptake on-kinetics in sprint- and endurance-trained athletes". Applied Physiology, Nutrition, and Metabolism 32, nr 3 (marzec 2007): 383–93. http://dx.doi.org/10.1139/h06-109.
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Pulmonary O2 uptake kinetics during “step” exercise have not been characterized in young, sprint-trained (SPT), athletes. Therefore, the objective of this study was to test the hypotheses that SPT athletes would have (i) slower phase II kinetics and (ii) a greater oxygen uptake “slow component” when compared with endurance-trained (ENT) athletes. Eight sub-elite SPT athletes (mean ( ± SD) age = 25 (±7) y; mass = 80.3 (±7.3) kg) and 8 sub-elite ENT athletes (age= 28 (±4) y; mass = 73.2 (±5.1) kg) completed a ramp incremental cycle ergometer test, a Wingate 30 s anaerobic sprint test, and repeat “step” transitions in work rate from 20 W to moderate- and severe-intensity cycle exercise, during which pulmonary oxygen uptake was measured breath by breath. The phase II oxygen uptake kinetics were significantly slower in the SPT athletes both for moderate (time constant, τ; SPT 32 (±4) s vs. ENT 17 (±3) s; p < 0.01) and severe (SPT 32 (±12) s vs. ENT 20 (±6) s; p < 0.05) exercise. The amplitude of the slow component (derived by exponential modelling) was not significantly different between the groups (SPT 0.55 (±0.12) L·min–1 vs. ENT 0.50 (±0.22) L·min–1), but the increase in oxygen uptake between 3 and 6 min of severe exercise was greater in the SPT athletes (SPT 0.37 (±0.08) L·min–1 vs. ENT 0.20 (±0.09) L·min–1; p < 0.01). The phase II τ was significantly correlated with indices of aerobic exercise performance (e.g., peak oxygen uptake (moderate-intensity r = –0.88, p < 0.01; severe intensity r = –0.62; p < 0.05), whereas the relative amplitude of the oxygen uptake slow component was significantly correlated with indices of anaerobic exercise performance (e.g., Wingate peak power output; r = 0.77; p < 0.01). Thus, it could be concluded that sub-elite SPT athletes have slower phase II oxygen uptake kinetics and a larger oxygen uptake slow component compared with sub-elite ENT athletes. It appears that indices of aerobic and anaerobic exercise performance differentially influence the fundamental and slow components of the oxygen uptake kinetics.
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Fernández de Sevilla, David, Marco Fuenzalida, Ana B. Porto Pazos i Washington Buño. "Selective Shunting of the NMDA EPSP Component by the Slow Afterhyperpolarization in Rat CA1 Pyramidal Neurons". Journal of Neurophysiology 97, nr 5 (maj 2007): 3242–55. http://dx.doi.org/10.1152/jn.00422.2006.
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Pyramidal neuron dendrites express voltage-gated conductances that control synaptic integration and plasticity, but the contribution of the Ca2+-activated K+-mediated currents to dendritic function is not well understood. Using dendritic and somatic recordings in rat hippocampal CA1 pyramidal neurons in vitro, we analyzed the changes induced by the slow Ca2+-activated K+-mediated afterhyperpolarization (sAHP) generated by bursts of action potentials on excitatory postsynaptic potentials (EPSPs) evoked at the apical dendrites by perforant path-Schaffer collateral stimulation. Both the amplitude and decay time constants of EPSPs (τEPSP) were reduced by the sAHP in somatic recordings. In contrast, the dendritic EPSP amplitude remained unchanged, whereas τEPSP was reduced. Temporal summation was reduced and spatial summation linearized by the sAHP. The amplitude of the isolated N-methyl-d-aspartate component of EPSPs (EPSPNMDA) was reduced, whereas τNMDA was unaffected by the sAHP. In contrast, the sAHP did not modify the amplitude of the isolated EPSPAMPA but reduced τAMPA both in dendritic and somatic recordings. These changes are attributable to a conductance increase that acted mainly via a selective “shunt” of EPSPNMDA because they were absent under voltage clamp, not present with imposed hyperpolarization simulating the sAHP, missing when the sAHP was inhibited with isoproterenol, and reduced under block of EPSPNMDA. EPSPs generated at the basal dendrites were similarly modified by the sAHP, suggesting both a somatic and apical dendritic location of the sAHP channels. Therefore the sAHP may play a decisive role in the dendrites by regulating synaptic efficacy and temporal and spatial summation.
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Olcese, Riccardo, Daniel Sigg, Ramon Latorre, Francisco Bezanilla i Enrico Stefani. "A Conducting State with Properties of a Slow Inactivated State in a Shaker K+ Channel Mutant". Journal of General Physiology 117, nr 2 (29.01.2001): 149–64. http://dx.doi.org/10.1085/jgp.117.2.149.
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In Shaker K+ channel, the amino terminus deletion Δ6-46 removes fast inactivation (N-type) unmasking a slow inactivation process. In Shaker Δ6-46 (Sh-IR) background, two additional mutations (T449V-I470C) remove slow inactivation, producing a noninactivating channel. However, despite the fact that Sh-IR-T449V-I470C mutant channels remain conductive, prolonged depolarizations (1 min, 0 mV) produce a shift of the QV curve by about −30 mV, suggesting that the channels still undergo the conformational changes typical of slow inactivation. For depolarizations longer than 50 ms, the tail currents measured during repolarization to −90 mV display a slow component that increases in amplitude as the duration of the depolarizing pulse increases. We found that the slow development of the QV shift had a counterpart in the amplitude of the slow component of the ionic tail current that is not present in Sh-IR. During long depolarizations, the time course of both the increase in the slow component of the tail current and the change in voltage dependence of the charge movement could be well fitted by exponential functions with identical time constant of 459 ms. Single channel recordings revealed that after prolonged depolarizations, the channels remain conductive for long periods after membrane repolarization. Nonstationary autocovariance analysis performed on macroscopic current in the T449V-I470C mutant confirmed that a novel open state appears with increasing prepulse depolarization time. These observations suggest that in the mutant studied, a new open state becomes progressively populated during long depolarizations (>50 ms). An appealing interpretation of these results is that the new open state of the mutant channel corresponds to a slow inactivated state of Sh-IR that became conductive.
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Bachoo, M., R. Yip i C. Polosa. "Effect of naloxone and prolonged preganglionic stimulation on noncholinergic transmission in the superior cervical ganglion of the cat". Canadian Journal of Physiology and Pharmacology 68, nr 8 (1.08.1990): 1093–99. http://dx.doi.org/10.1139/y90-164.
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In cats anesthetized with sodium pentobarbital, a supramaximal 40-Hz, 30-s train to the cervical sympathetic trunk, during block of ganglionic cholinergic transmission with hexamethonium and scopolamine, produced a delayed, slow, small amplitude contraction of the nictitating membrane that persisted for several minutes after the end of the stimulus train. The post-stimulus component of the response was due to afterdischarge of the ganglion cells, since section of the post-ganglionic axons at the end of the train resulted in elimination of this component. The amplitude of the slow nictitating membrane response was enhanced in a dose-dependent manner by i.v. injection of naloxone. The enhancement was detectable at a dose as low as 1 μg/kg and was maximal at 10 μg/kg. During continuous preganglionic stimulation at 40 Hz, the amplitude of the slow nictitating membrane response reached a peak in 2–4 min and then faded with time until it became undetectable. Time for 90% decay was 82 ± 5 min (n = 18). The nictitating membrane response to postganglionic nerve stimulation was not modified by prolonged preganglionic stimulation. In three cats, the cervical sympathetic trunk was split into two bundles and one bundle was stimulated continuously at 40 Hz until the slow response disappeared. At this time stimulation of the unconditioned bundle evoked a slow response of normal appearance. This suggests that the process underlying the fade involves only the conditioned axons. Recovery from the fade was slow, the response approaching control by 24 h post-stimulus. In contrast, the nictitating membrane response mediated by ganglionic nicotinic transmission was of amplitude similar to control within the 1st min after the end of a 2-h period of continuous 40 Hz stimulation. The fade and recovery of the slow response may be the consequence of presynaptic events and reflect the exhaustion followed by slow replenishment of the releasable stores of the noncholinergic transmitter. The enhancement of the slow response by naloxone suggests that an inhibitory noncholinergic transmitter, presumably an opioid, is also released by the preganglionic axon terminals.Key words: peptides, opioids, ganglionic transmission, cotransmitters, synapse.
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Fawkner, Samantha G., i Neil Armstrong. "Longitudinal changes in the kinetic response to heavy-intensity exercise in children". Journal of Applied Physiology 97, nr 2 (sierpień 2004): 460–66. http://dx.doi.org/10.1152/japplphysiol.00784.2003.
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The purpose of this study was to investigate longitudinal changes with age in the kinetic response to cycling at heavy-intensity exercise in boys and girls. Twenty-two prepubertal children (13 male, 9 female) carried out a series of exercise tests on two test occasions with a 2-yr interval. On each test occasion, the subject completed multiple transitions from baseline to 40% of the difference between their previously determined V-slope and peak O2 uptake (V̇o2) for 9 min on an electronically braked cycle ergometer. Each subject's breath-by-breath responses were interpolated to 1-s intervals, time aligned, and averaged. The data after phase 1 were fit with 1) a double exponential model and 2) a single exponential model within a fitting window that was previously identified to exclude the slow component. There were no significant differences in the parameters of the primary component between each model. Subsequent analysis was carried out using model 2. The V̇o2 slow component was computed as the difference between the amplitude of the primary component and the end-exercise V̇o2 and was expressed as the percent contribution to the total change in V̇o2. Over the 2-yr period, the primary time constant (boys 16.8 ± 5.3 and 21.7 ± 5.3 s, girls 21.1 ± 8.1 and 26.4 ± 8.4 s, first and second occasion, respectively) and the relative amplitude of the slow component (boys 9.4 ± 4.6 and 13.8 ± 5.3%, girls 10.3 ± 2.4 and 15.5 ± 2.8%, first and second occasion, respectively) significantly increased with no sex differences. The data demonstrate that children do display a slow-component response to exercise and are consistent with an age-dependent change in the muscles' potential for O2 utilization.
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Hurst, R. S., R. Latorre, L. Toro i E. Stefani. "External barium block of Shaker potassium channels: evidence for two binding sites." Journal of General Physiology 106, nr 6 (1.12.1995): 1069–87. http://dx.doi.org/10.1085/jgp.106.6.1069.
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External barium ions inhibit K+ currents of Xenopus oocytes expressing ShH4 delta 6-46, the non-inactivating deletion of the Shaker K+ channel. At the macroscopic level, Ba2+ block comprises both a fast and a slow component. The fast component is less sensitive to Ba2+ (apparent dissociation constant at 0 mV, K(0), approximately 19.1 mM) than the slow component and is also less voltage dependent (apparent electrical distance, delta, approximately 0.14). The slow component (K(0), approximately 9.4 mM, delta approximately 0.25) is relieved by outward K+ current, which suggests that the corresponding binding site resides within the channel conduction pathway. At the single channel level, the fast component of block is evidenced as an apparent reduction in amplitude, suggesting an extremely rapid blocking and unblocking reaction. In contrast, the slow component appears to be associated with long blocked times that are present from the beginning of a depolarizing command. Installation of the slow component is much slower than a diffusion limited process; for example, the blocking time constant (tau) produced by 2 mM Ba2+ is approximately 159 s (holding potential, HP = -90 mV). However, the blocking rate of this slow component is not a linear function of external Ba2+ and tends to saturate at higher concentrations. This is inconsistent with a simple bi-molecular blocking reaction. These features of external Ba2+ block can be accounted for by a simple model of two sequential Ba2+ binding sites, where the deeper of the two sites produces the slow component of block.
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Reznik, G. M. "Geostrophic adjustment with gyroscopic waves: stably neutrally stratified fluid without the traditional approximation". Journal of Fluid Mechanics 747 (23.04.2014): 605–34. http://dx.doi.org/10.1017/jfm.2014.166.
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AbstractWe examine nonlinear geostrophic adjustment in a rapidly rotating (small Rossby number Ro) stably neutrally stratified (SNS) fluid consisting of a stratified upper layer with $N>f$ ($N$ is the buoyancy frequency, $f$ the Coriolis parameter) and a homogeneous lower layer, the density and other fields being continuous at the interface between the layers. The angular speed of rotation is non-parallel to gravity; the traditional and hydrostatic approximations are not used. The wave spectrum in the model consists of internal and gyroscopic waves. During the adjustment an arbitrary long-wave perturbation is split in a unique way into slow quasi-geostrophic (QG) and fast ageostrophic components with typical time scales $(Ro\, f)^{-1}$ and $f^{-1}$, respectively. The QG flow is governed by two coupled nonlinear equations of conservation of QG potential vorticity (PV) in the layers. The fast component is a sum of internal waves and inertial oscillations (long gyroscopic waves) confined to the homogeneous layer and modulated by an amplitude depending on coordinates and slow time. On times $t\sim (\, f\, Ro)^{-1}$ the slow component is not influenced by the fast one but the inertial oscillations amplitude is coupled to the QG flow and obeys an equation practically coinciding with that in the barotropic case (Reznik, J. Fluid Mech., vol. 743, 2014, pp. 585–605). A non-stationary boundary layer with large vertical gradients of horizontal velocity develops in the stratified layer near the interface to prevent penetration of the inertial oscillations into the stratified fluid; an analogous weaker boundary layer arises near the upper rigid lid. At large times the internal waves gradually decay because of dispersion and the resulting motion consists of the slow QG component and inertial oscillations confined to the barotropic lower layer.
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Rasouli, Omid, Egil A. Fors, Ottar Vasseljen i Ann-Katrin Stensdotter. "A Concurrent Cognitive Task Does Not Perturb Quiet Standing in Fibromyalgia and Chronic Fatigue Syndrome". Pain Research and Management 2018 (7.08.2018): 1–8. http://dx.doi.org/10.1155/2018/9014232.
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Background and Objectives. Cognitive complaints are common in fibromyalgia (FM) and chronic fatigue syndrome (CFS). Fatigue as well as pain may require greater effort to perform cognitive tasks, thereby increasing the load on processing in the central nervous system and interfering with motor control.Methods. The effect of a concurrent arithmetic cognitive task on postural control during quiet standing was investigated in 75 women (aged 19–49 years) and compared between FM, CFS, and matched controls (n=25/group). Quiet standing on a force plate was performed for 60 s/condition, with and without a concurrent cognitive task. The center of pressure data was decomposed into a slow component and a fast component representing postural sway and adjusting ankle torque.Results. Compared to controls, CFS and FM displayed lower frequency in the slow component (p<0.001), and CFS displayed greater amplitude in the slow (p=0.038andp=0.018) and fast (p=0.045) components. There were no interactions indicating different responses to the added cognitive task between any of the three groups.Conclusion. Patients displayed insufficient postural control across both conditions, while the concurrent cognitive task did not perturb quiet standing. Fatigue but not pain correlated with postural control variables.
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Garland, S. W., D. J. Newham i D. L. Turner. "The amplitude of the slow component of oxygen uptake is related to muscle contractile properties". European Journal of Applied Physiology 91, nr 2-3 (1.03.2004): 192–98. http://dx.doi.org/10.1007/s00421-003-0963-7.
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Salvadego, Desy, Stefano Lazzer, Carlo Busti, Raffaela Galli, Fiorenza Agosti, Claudio Lafortuna, Alessandro Sartorio i Bruno Grassi. "Gas exchange kinetics in obese adolescents. Inferences on exercise tolerance and prescription". American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 299, nr 5 (listopad 2010): R1298—R1305. http://dx.doi.org/10.1152/ajpregu.00038.2010.
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A functional evaluation of skeletal muscle oxidative metabolism was performed in a group of obese adolescents (OB). The various components of pulmonary O2 uptake (V̇o2) kinetics were evaluated during 10-min constant-load exercises (CLE) on a cycloergometer at different percentages of V̇o2max. The relationships of these components with the gas exchange threshold (GET) were determined. Fourteen male OB [age 16.5 ± 1.0 (SD) yr, body mass index 34.5 ± 3.1 kg·m−2] and 13 normal-weight, age-matched nonathletic male volunteers (control group) were studied. The time-constant (τf) of the fundamental component and the presence, pattern, and relative amplitude of the slow component of V̇o2 kinetics were determined at 40, 60, and 80% of V̇o2max, previously estimated during an incremental test. V̇o2max (l/min) was similar in the two groups. GET was lower in OB (55.7 ± 6.7% of V̇o2max) than in control (65.1 ± 5.2%) groups. The τf was higher in OB subjects, indicating a slower fundamental component. At CLE 60% (above GET in OB subjects, below GET in control subjects) a slow component was observed in nine out of fourteen OB subjects, but none in the control group. All subjects developed a slow component at CLE 80% (above GET in both OB and control). Twelve OB subjects did not complete the 10-min CLE 80% due to voluntary exhaustion. In nine OB subjects, the slow component was characterized by a linear increase in V̇o2 as a function of time. The slope of this increase was inversely related to the time to exhaustion. The above findings should negatively affect exercise tolerance in obese adolescents and suggest an impairment of skeletal muscle oxidative metabolism. Also in obese adolescents, exercise evaluation and prescription at submaximal loads should be done with respect to GET and not at a given percentage of V̇o2max.
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Barstow, Thomas J., Andrew M. Jones, Paul H. Nguyen i Richard Casaburi. "Influence of muscle fiber type and pedal frequency on oxygen uptake kinetics of heavy exercise". Journal of Applied Physiology 81, nr 4 (1.10.1996): 1642–50. http://dx.doi.org/10.1152/jappl.1996.81.4.1642.
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Barstow, Thomas J., Andrew M. Jones, Paul H. Nguyen, and Richard Casaburi. Influence of muscle fiber type and pedal frequency on oxygen uptake kinetics of heavy exercise. J. Appl. Physiol. 81(4): 1642–1650, 1996.—We tested the hypothesis that the amplitude of the additional slow component of O2 uptake (V˙o 2) during heavy exercise is correlated with the percentage of type II (fast-twitch) fibers in the contracting muscles. Ten subjects performed transitions to a work rate calculated to require aV˙o 2 equal to 50% between the estimated lactate (Lac) threshold and maximalV˙o 2 (50%Δ). Nine subjects consented to a muscle biopsy of the vastus lateralis. To enhance the influence of differences in fiber type among subjects, transitions were made while subjects were pedaling at 45, 60, 75, and 90 rpm in different trials. BaselineV˙o 2 was designed to be similar at the different pedal rates by adjusting baseline work rate while the absolute increase in work rate above the baseline was the same. The V˙o 2 response after the onset of exercise was described by a three-exponential model. The relative magnitude of the slow component at the end of 8-min exercise was significantly negatively correlated with %type I fibers at every pedal rate ( r = 0.64 to 0.83, P < 0.05–0.01). Furthermore, the gain of the fast component forV˙o 2 (as ml ⋅ min−1 ⋅ W−1) was positively correlated with the %type I fibers across pedal rates ( r = 0.69–0.83). Increase in pedal rate was associated with decreased relative stress of the exercise but did not affect the relationships between %fiber type and V˙o 2parameters. The relative contribution of the slow component was also significantly negatively correlated with maximalV˙o 2( r = −0.65), whereas the gain for the fast component was positively associated ( r = 0.68–0.71 across rpm). The amplitude of the slow component was significantly correlated with net end-exercise Lac at all four pedal rates ( r = 0.64–0.84), but Lac was not correlated with %type I ( P > 0.05). We conclude that fiber type distribution significantly affects both the fast and slow components ofV˙o 2 during heavy exercise and that fiber type and fitness may have both codependent and independent influences on the metabolic and gas-exchange responses to heavy exercise.
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Malysz, John, David Richardsons, Laura Farraway, Jan D. Huizinga i Marie-Odile Christen. "Generation of slow wave type action potentials in the mouse small intestine involves a non-L-type calcium channel". Canadian Journal of Physiology and Pharmacology 73, nr 10 (1.10.1995): 1502–11. http://dx.doi.org/10.1139/y95-208.
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Intrinsic electrical activities in various isolated segments of the mouse small intestine were recorded (i) to characterize action potential generation and (ii) to obtain a profile on the ion channels involved in initiating the slow wave type action potentials (slow waves). Gradients in slow wave frequency, resting membrane potential, and occurrence of spiking activity were found, with the proximal intestine exhibiting the highest frequency, the most hyperpolarized cell membrane, and the greatest occurrence of spikes. The slow waves were only partially sensitive to L-type calcium channel blockers. Nifedipine, verapamil, and pinaverium bromide abolished spikes that occurred on the plateau phase of the slow waves in all tissues. The activity that remained in the presence of L-type calcium channel blockers, the upstroke potential, retained a similar amplitude to the original slow wave and was of identical frequency. The upstroke potential was not sensitive to a reduction in extracellular chloride or to the sodium channel blockers tetrodotoxin and mexiletine. Abolishment of the Na+ gradient by removal of 120 mM extracellular Na+ reduced the upstroke potential frequency by 13–18% and its amplitude by 50–70% in the ileum. The amplitude was similarly reduced by Ni2+ (up to 5 mM), and by flufenamic acid (100 μM), a nonspecific cation and chloride channel blocker. Gadolinium, a nonspecific blocker of cation and stretch-activated channels, had no effect. Throughout these pharmacological manipulations, a robust oscillation remained at 5–10 mV. This oscillation likely reflects pacemaker activity. It was rapidly abolished by removal of extracellular calcium but not affected by L-type calcium channel blockers. In summary, the mouse small intestine has been established as a model for research into slow wave generation and electrical pacemaker activity. The upstroke part of the slow wave has two components, the pacemaker component involves a non-L-type calcium channel.Key words: slow wave, pacemaker, calcium channel, pinaverium, smooth muscle.
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Kito, Yoshihiko, Sean M. Ward i Kenton M. Sanders. "Pacemaker potentials generated by interstitial cells of Cajal in the murine intestine". American Journal of Physiology-Cell Physiology 288, nr 3 (marzec 2005): C710—C720. http://dx.doi.org/10.1152/ajpcell.00361.2004.
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Pacemaker potentials were recorded in situ from myenteric interstitial cells of Cajal (ICC-MY) in the murine small intestine. The nature of the two components of pacemaker potentials (upstroke and plateau) were investigated and compared with slow waves recorded from circular muscle cells. Pacemaker potentials and slow waves were not blocked by nifedipine (3 μM). In the presence of nifedipine, mibefradil, a voltage-dependent Ca2+ channel blocker, reduced the amplitude, frequency, and rate of rise of upstroke depolarization (d V/d tmax) of pacemaker potentials and slow waves in a dose-dependent manner (1–30 μM). Mibefradil (30 μM) changed the pattern of pacemaker potentials from rapidly rising, high-frequency events to slowly depolarizing, low-frequency events with considerable membrane noise (unitary potentials) between pacemaker potentials. Caffeine (3 mM) abolished pacemaker potentials in the presence of mibefradil. Pinacidil (10 μM), an ATP-sensitive K+ channel opener, hyperpolarized ICC-MY and increased the amplitude and d V/d tmax without affecting frequency. Pinacidil hyperpolarized smooth muscle cells and attenuated the amplitude and d V/d tmax of slow waves without affecting frequency. The effects of pinacidil were blocked by glibenclamide (10 μM). These data suggest that slow waves are electrotonic potentials driven by pacemaker potentials. The upstroke component of pacemaker potentials is due to activation of dihydropyridine-resistant Ca2+ channels, and this depolarization entrains pacemaker activity to create the plateau potential. The plateau potential may be due to summation of unitary potentials generated by individual or small groups of pacemaker units in ICC-MY. Entrainment of unitary potentials appears to depend on Ca2+ entry during upstroke depolarization.
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Vargas-Caballero, Mariana, i Hugh P. C. Robinson. "A Slow Fraction of Mg2+ Unblock of NMDA Receptors Limits Their Contribution to Spike Generation in Cortical Pyramidal Neurons". Journal of Neurophysiology 89, nr 5 (1.05.2003): 2778–83. http://dx.doi.org/10.1152/jn.01038.2002.
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The timing of voltage-dependent removal of Mg2+block of N-methyl-d-aspartate receptors (NMDARs) is potentially critical for determining their nonlinear contribution to excitability. Here, we measure the kinetics of NMDAR unblock in nucleated patch and whole cell recordings of rat cortical pyramidal neurons during depolarizing voltage steps. At room temperature, the unblock showed a very fast component (τ < 1 ms) and a slower component (τ = 14–23 ms in nucleated patches). The slow component accounted for half of the current at +40 mV and its amplitude and time constant showed some voltage dependence. Blocking with hyperpolarization was very fast (τ < 200 μs). Voltage-clamp with action potential waveforms, at both room temperature and at 33°C, showed that the rising phase of single fast action potentials unblocks far less NMDAR current than expected from the stationary voltage dependence, while a large amplitude of current is uncovered during the upstroke of slow calcium action potentials. The repolarization of fast sodium action potentials uncovers an NMDAR tail current, much bigger than the stationary level of current.
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Pringle, Jamie S. M., Jonathan H. Doust, Helen Carter, Keith Tolfrey i Andrew M. Jones. "Effect of pedal rate on primary and slow-component oxygen uptake responses during heavy-cycle exercise". Journal of Applied Physiology 94, nr 4 (1.04.2003): 1501–7. http://dx.doi.org/10.1152/japplphysiol.00456.2002.
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We hypothesized that a higher pedal rate (assumed to result in a greater proportional contribution of type II motor units) would be associated with an increased amplitude of the O2 uptake (V˙o 2) slow component during heavy-cycle exercise. Ten subjects (mean ± SD, age 26 ± 4 yr, body mass 71.5 ± 7.9 kg) completed a series of square-wave transitions to heavy exercise at pedal rates of 35, 75, and 115 rpm. The exercise power output was set at 50% of the difference between the pedal rate-specific ventilatory threshold and peakV˙o 2, and the baseline power output was adjusted to account for differences in the O2 cost of unloaded pedaling. The gain of the V˙o 2primary component was significantly higher at 35 rpm compared with 75 and 115 rpm (mean ± SE, 10.6 ± 0.3, 9.5 ± 0.2, and 8.9 ± 0.4 ml · min−1 · W−1, respectively; P < 0.05). The amplitude of theV˙o 2 slow component was significantly greater at 115 rpm (328 ± 29 ml/min) compared with 35 rpm (109 ± 30 ml/min) and 75 rpm (202 ± 38 ml/min) ( P < 0.05). There were no significant differences in the time constants or time delays associated with the primary and slow components across the pedal rates. The change in blood lactate concentration was significantly greater at 115 rpm (3.7 ± 0.2 mM) and 75 rpm (2.8 ± 0.3 mM) compared with 35 rpm (1.7 ± 0.4 mM) ( P < 0.05). These data indicate that pedal rate influences V˙o 2 kinetics during heavy exercise at the same relative intensity, presumably by altering motor unit recruitment patterns.
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Jones, Andrew M., Daryl P. Wilkerson, Sally Wilmshurst i Iain T. Campbell. "Influence of l-NAME on pulmonary O2 uptake kinetics during heavy-intensity cycle exercise". Journal of Applied Physiology 96, nr 3 (marzec 2004): 1033–38. http://dx.doi.org/10.1152/japplphysiol.00381.2003.
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We hypothesized that inhibition of nitric oxide synthase (NOS) by NG-nitro-l-arginine methyl ester (l-NAME) would alleviate the inhibition of mitochondrial oxygen uptake (V̇o2) by nitric oxide and result in a speeding of phase II pulmonary V̇o2 kinetics at the onset of heavy-intensity exercise. Seven men performed square-wave transitions from unloaded cycling to a work rate requiring 40% of the difference between the gas exchange threshold and peak V̇o2 with and without prior intravenous infusion of l-NAME (4 mg/kg in 50 ml saline over 60 min). Pulmonary gas exchange was measured breath by breath, and V̇o2 kinetics were determined from the averaged response to two exercise bouts performed in each condition. There were no significant differences between the control (C) and l-NAME conditions (L) for baseline V̇o2, the duration of phase I, or the amplitude of the primary V̇o2 response. However, the time constant of the V̇o2 response in phase II was significantly smaller (mean ± SE: C: 25.1 ± 3.0 s; L: 21.8 ± 3.3 s; P < 0.05), and the amplitude of the V̇o2 slow component was significantly greater (C: 240 ± 47 ml/min; L: 363 ± 24 ml/min; P < 0.05) after l-NAME infusion. These data indicate that inhibition of NOS by l-NAME results in a significant (13%) speeding of V̇o2 kinetics and a significant increase in the amplitude of the V̇o2 slow component in the transition to heavy-intensity cycle exercise in men. The speeding of the primary component V̇o2 kinetics after l-NAME infusion indicates that at least part of the intrinsic inertia to oxidative metabolism at the onset of heavy-intensity exercise may result from inhibition of mitochondrial V̇o2 by nitric oxide. The cause of the larger V̇o2 slow-component amplitude with l-NAME requires further investigation but may be related to differences in muscle blood flow early in the rest-to-exercise transition.