Skeletal Muscle Action Potentials Research Articles

Hydrogen peroxide decelerates recovery of action potential after high-frequency fatigue in skeletal muscle.

Effects of reactive oxygen species (ROS), especially hydrogen peroxide (H(2)O(2)), on recovery of action potential by resting for 30 min after high-frequency fatigue were studied using frog skeletal muscle fibers. After stimulation at a frequency of 50 HZ for 2 min, the action potential amplitude was decreased by 14.5 mV from controls, and resting membrane was depolarized by 15.4 mV. Action potential duration was also prolonged by high-frequency stimulation (1.5 ms in controls to 2.6 ms). The high-frequency stimulation used here caused no muscle damage. The action potential was partially improved after a 30-min rest. Addition of catalase at 500 units/ml or H(2)O(2) at 0.5 mM to sartorius muscle did not alter any of the parameters of the action potential after high-frequency stimulation. Treatment with catalase accelerated post-fatigue recovery of the action potential. Application of H(2)O(2) delayed post-fatigue recovery of resting and action potentials. When added to detubulated toe muscle fibers, catalase no longer improved the attenuation of action potential induced by high-frequency stimulation, even after a 30-min rest. These findings suggest that removal of H(2)O(2) from transverse tubules is effective for post-fatigue recovery of action potential in skeletal muscle.

The variation of action potential and impedance in human skeletal muscle during voluntary contraction.

We used an insulated acupuncture needle to deliver a 20 kHz alternative current to detect the changes on the electromyogram (EMG) and deep muscle impedance. We found that impedance increased (with a duration of 224.1 +/- 75.3 msec) and then decreased (with a duration of 293.4 +/- 97.3 msec) after motor unit action potential (MUAP) firing during isometric voluntary contraction (VC) of the tibialis anterior muscle (TAM). We divided the positive peak into pattern I (with a latency range of > or = 30 msec and < or = 75 msec) and pattern II (with a latency range of > 75 msec and < or = 140 msec). These patterns of change corresponded to the contraction times of tension caused by the electrical stimulation and VC. These impedance changes may be caused by a change in the extracellular and intracellular fractions, and may reflect the variance of tension intensity in the muscle tissue.

A reconstruction of charge movement during the action potential in frog skeletal muscle

The transfer of intramembrane charge during an action potential at 4 degrees C was reconstructed for a model representing the electrical properties of frog skeletal muscle by a cylindrical surface membrane and 16 concentric annuli ("shells") of transverse tubular membrane of equal radial thickness. The lumina of the transverse tubules were separated from extracellular fluid by a fixed series resistance. The quantity, geometrical distribution and steady-state and kinetic properties of charge movement components were described by equations incorporating earlier experimental results. Introducing such nonlinear charge into the distributed model for muscle membrane diminished the maximum amplitude of the action potential within the transverse tubules by 2 mV but increased the maximum size of the after-depolarization by 3-5 mV and also its duration. However, these changes were small in comparison to the 135-mV deflection represented by the action potential. They therefore did not justify altering the values of the electrical parameters adopted by Adrian R.H., and L.D. Peachey (1973. J. Physiol. [Lond.]. 235:103-131.) and used in the present calculations. Cable properties significantly affected the time course and extent of charge movement in each shell during action potential propagation into the tubular system. Q beta charge moved relatively rapidly in all annuli, and did so without significant latency (approximately 0.3 ms) after the surface action potential upstroke. Its peak displacement varied between 53 and 58% (the range representing the difference fiber edge/fiber axis) of the total Q beta charge. This was attained at 5.4-7.3 ms after the stimulus, depending on depth within the tubules. In contrast, q gamma moved after a 1.7-2.9 ms latency and achieved a peak displacement of up to 22-34% of available charge. Both charge movement species could be driven by repetitive (47.7 Hz) action potentials without buildup of charge transfer. Such stimulus frequencies would normally cause tetanus. Latencies in q gamma charge movement in response to an action potential were resolved into (a) propagation of tubular depolarization required to gain the "threshold" of q gamma charge (0.8-1.5 ms) and (b) dielectric loss processes. The latter took consistently around 1.5 ms throughout the tubular system. Taken with (c) the earlier reports of a minimal latency in delta [Ca2+] signals attributed to tubulo-cisternal coupling following voltage sensing (approximately 2 ms: Zhu, P.H., I. Parker, and R. Miledi., 1986. Proc. R. Soc. Lond. B. Biol. Sci. 229:39-46.). these times can be reconciled to the latency (~ 4-5 ms) reported between the onset of the surface action potential and that of delta [Ca2+] signals (Vergara, J., and M. Delay. 1986. Proc. R. Soc. Lond. B. Biol. Sci. 229:97-110.). This is consistent with a relationship between the q gamma system and excitation-contraction coupling whether as an independent event (e.g.,Adrian, R.H., and C.L.-H. Huang. 1984. J. Physiol. (Lond.). 353:419-434.) or as an end reaction following earlier (q beta) transfers of charge (e.g., Horowicz, P., and M.F. Schneider. 1981. J. Physiol. (Lond.). 314:565-593.; Melzer, W., M.F. Schneider, B.J. Simon,and G. Szucs. 1986. J. Physiol. (Lond.). 373:481-512.)

Muscle chloride channels.

Muscle chloride channels.

Cardiac dysrhythmias in the acute setting: Pathophysiology or anyone can understand cardiac dysrhythmias

Cardiac dysrhythmias are easy. Unlike the lung (which has formidable neuroendocrine, metabolic, and respiratory responsibilities), the heart is simple. It is an innervated muscular pump. A resting Purkinje or ventricular muscle cell membrane maintains a charge of about 90 millivolts. The five phases of a cardiac action potential are similar to the action potential in skeletal muscle, however, the cardiac action potential lasts a hundred times longer. When sodium specific “fast” channels and calcium specific “slow” channels open, positive ions rush into the myocardial cell, thus causing rapid membrane depolarization. In order to produce an action potential, some stimulus must decrease the membrane potential from − 90 millivolts to “threshold” or − 60 millivolts. Purkinje fibers do not have a stable phase for diastolic potential. These fibers continuously depolarize during diastole. Hypoxemia or hypokalemia may exacerbate this diastolic depolarization, thus promoting “hyperexcitability” or “automatic” ectopy. When myocardium is damaged, characteristically with myocardial ischemia, rapid conduction of cardiac impulses may be slowed dramatically. Very slow impulses may course through muscle such that by the time the activation wave front returns to the initiating site, this origin has had a chance to repolarize. This is the basis for re-entrant dysrhythmias. All cardiac dysrhythmias are automatic, re-entrant or both.

Local anaesthesia and immunomodulatory effects of antithyroid drugs

Propylthiouracil (PTU) and propranolol can suppress, while methimazole (MMI) can enhance, mitogenic activation of lymphocytes. The present study investigated whether this effect of PTU, as has been shown for propranolol, relates to local anaesthetic activity. MMI (1 mM) but not PTU (1 mM) reduced the action potential in rat skeletal muscle. Thus, PTU seems to lack local anaesthetic activity. Moreover, the recorded local anaesthetic capacity of MMI hardly explains the stimulatory influence of MMI on lymphocyte activation. Apparently, the interference of MMI and PTU with lymphocyte activation seems to be due to another mechanism than local anaesthetic activity.

Increased membrane permeability to chloride in Duchenne muscular dystrophy fibroblasts and its relationship to muscle function.

Previous studies have suggested an abnormality in Cl- metabolism in Duchenne muscular dystrophy (DMD) fibroblasts. In order to further characterize this abnormality, we have studied 36Cl- distribution and permeability in 11 DMD and 12 normal fibroblast lines. Under steady-state conditions Cl- efflux in fibroblasts is observed to be biphasic, revealing the presence of two major subcellular compartments. Each compartment contains approximately half of the cellular Cl-. The faster of the two observed efflux components is significantly higher in DMD than in control fibroblasts (P less than 0.001). To determine the results of a similar increase in Cl- permeability on skeletal muscle action potentials, we have simulated the effects of increased Cl- conductance on muscle by using a computer model. Effects on the simulated action potential include lower rates of membrane depolarization, lower overpotential, longer duration, and lower input resistance. These effects are similar to those actually observed in DMD muscle.

The effect of septic shock on skeletal muscle action potentials in the primate

The effect of septic shock on skeletal muscle action potentials in the primate

Partial purification and characterization of neurotrophic substance affecting tetrodotoxin sensitivity of organ-cultured mouse muscle

From mouse spinal cord homogenate, we isolated a trophic substance which reverses the post-denervation decrease in tetrodotoxin sensitivity of action potential in organ-cultured extensor digitorum longus muscle of mouse and characterized its physicochemical properties. The trophic substance was separated from macromolecules in homogenate by gel filtration on Biogel P2 column. The partially purified trophic substance was heat-stable, acid-stable and alkaline-labile. The trophic activity was destroyed by lyophilization at neutral pH but not at acidic pH. The trophic activity was abolished by incubation with pronase or leucine aminopeptidase, but not by trypsin, chymotrypsin, thermolysin or carboxypeptidase A. The trophic substance passed through an ultrafiltration membrane UM10 freely. A small part of the trophic activity passed through a UM2 or UM05, and the rest was retained on the membranes. The trophic substance adsorbed on CM-Sephadex at pH 7.2 but passed through DEAE-Sephadex at pH 8.4. These results suggest that the trophic substance regulating tetrodotoxin sensitivity of action potential in mouse skeletal muscle is a peptide with a rather low molecular weight of less than 10,000 and that while the N-terminus of the peptide is free, the C-terminus is probably blocked. This peptide differs from other trophic substances reported previously by other investigators.

The effect of septic shock on skeletal muscle action potentials in the primate.

Techniques developed for the in vivo study of cellular physiology have been applied to septic shock in primates. Measurements of skeletal muscle transmembrane resting and action potentials were correlated with an analysis of fluid and electrolyte changes in the intracellular and extracellular compartments of skeletal muscle. The data obtained indicated a marked depletion of muscle extracellular water and an increase in intracellular sodium chloride and water content during shock. The significant decrease of resting membrane potential was associated with a decrease in amplitude of the action potential and prolongation of both the repolarization and depolarization time. In addition, there was a decrease of muscle intracellular potassium concentration during shock. This study demonstrates that the alterations in cellular membranes in hemorrhagic shock and septic shock are similar.

Detubulation effects on the action of zinc on frog skeletal muscle action potential

Detubulation of the untreated fiber decreases the time constant of the action potential's foot (tauf) and increases the maximal rate of rise of the spike (Vmax). Zinc at all concentrations, and regardless of whether the fiber is intact or detubulated, increases tauf and decreases Vmax, and thus seems to decrease Na activation of the fiber. Detubulation was used principally to elucidate the localization and mechanism of the Zn2+-induced retardation of the falling phase of the frog sartorius fiber action potential, which evidently results from a general depression of delayed rectification. At 50 to 1000 mum, Zn2+ not only prolongs repolarization of intact fibers (measured by increase in t0.5, the half-time of the spike's fall), but also produces a marked hump early in this phase. Detubulation of zinc-free fibers reduces t0.5 to about 80% of its intact value, and under Zn2+ treatment t0.5 is increased but only to about 80% of that produced in the inus, detubulation decreases t0.5 in Zn2+-treated fibers not only to about 80% of that produced in the intact fiber, and the falling-phase hump is completely obliterated. Thus, detubulation decreases t0.5 in Zn2+-treated fibers not only by generally eliminating T-tubular participation in action potential generation, but also by subtracting a Zn2+-induced retardation of tubular delayed rectification. Tubular delayed rectification must therefore be an intrinsic feature of normal excitation. These results are further analyzed by means of (i) Stanfield's findings about retardation of delayed rectification by Zn2+ and (ii) Adrian-Peachey's theory of T-tubule participation in action potential generation, which suggests that the Zn2+-evoked repolarization hump signals onset of Zn2+-altered active participation of T-tubules in determining the spike's shape.

Trichinella spiralis: Taxes of first-stage migratory larvae

Male albino mice were infected orally with 450 ± 10 excysted Trichinella spiralis larvae. Between Days 6 and 11 after infection, adults were collected from the intestine and incubated in vitro. The females shed first-stage migratory larvae which were collected and placed in a migratory chamber. The larvae showed a definite ability to respond to a microenvironmental stimulus. The taxis was positive ( p < 0.025) to a 120-mV stimulus simulating the skeletal muscle action potential and to a 120-mV polar stimulus ( p < 0.005). There was a negative taxis ( p < 0.005) to a 95-mV stimulus simulating the resting skeletal muscle potential and to a KCl gradient. A significant ( p < 0.05) distribution occurred to a lactic acid gradient, and there were no taxes ( p > 0.05) to either glycogen or phosphocreatine.

Phase-plane analysis of action potentials in uterine smooth muscle.

Action potentials were recorded by microelectrode from narrow strips of pregnant rat uterus in vitro. The phase-plane display (V vs dV/dt) of selected action potentials was analysed by the method of Jenerick (1964) to yield the ionic current. From this membrane current data, various parameters of the action potential were calculated. In comparison to skeletal muscle action potentials, the ionic currents were 30-100 times smaller in the uterus action potential. Epinephrine hyperpolarized the resting potentials and suppressed spontaneous activity, but did not cause any significant changes in the stimulated action potential. The after-potential may have been affected by epinephrine, preventing repetitive firing, but the data were inconclusive. The phase-plane analysis results were similar to the results of the double sucrose gap voltage clamp method on the same tissue (Kao and McCullough, 1975).

Electric and motor activity of innervated and vagally denervated feline esophagus.

Motor and electric activities of the feline esophagus were detected before and after vagotomy by use of intraluminal pressure detectors and chronically implanted platinum electrodes. These were placed in the midesophagus (E1), at the three-quarter point (E2) and in the lower 2 cm (E3). Both inner and outer layers of muscle were skeletal at E1 and smooth at E3, whereas at E2 the outer layer was predominantly skeletal and the inner predominantly smooth. Before vagotomy, contractions of the skeletal muscle fibers of the midesophagus were associated with pressure changes and action potentials of lesser amplitude, briefer duration and faster propagation than those of the smooth muscle fibers of the lower esophagus. The frequency of the skeletal muscle action potentials was greater than 25 cycles per second (cps), and that of the smooth muscle action potentials was less than 25 cps. The first recorded event during peristalsis was orad movement of the electrodes due to contraction of longitudinal fibers. After vagotomy, action potentials occurred with nearly every stimulation, but the incidence of intraluminal pressure increases was reduced. Repetitive responses were common. Action potentials with frequencies faster than 25 cps were eliminated in the lower quarter of the esophagus were orad movement of electrodes was also abolished owing to paralysis of longitudinal muscle fibers. The incidence of peristalsis was reduced during the first month after vagotomy to between 33 and 44% of responses, but thereafter its occurrence improved to 40 to 80% of responses. The predominant electromotor features of the period after vagotomy were persistent weakness, incoordination and repetitive responses in the lower esophagus, which prevented normal emptying of the organ.

Analysis of the membrane capacity in frog muscle.

1. The membrane capacity (C(f)) was determined from the conduction velocity and the time constant of the foot of the action potential in frog's skeletal muscle.2. In normal fibres C(f) was 2.6 muF/cm(2), and the value was almost constant over a range of diameter from 55 to 140 mu.3. In fibres, in which the transverse tubular system was disconnected from the surface by the glycerol treatment, C(f) was 0.9 muF/cm(2) and was fairly constant over a range of diameter from 60 to 130 mu. The low frequency capacity in glycerol-treated fibres was 1.9 muF/cm(2).4. These results as well as those obtained at low frequencies were consistent with the electrical model proposed by Adrian, Chandler & Hodgkin (1969).5. Analysis in terms of the model and of Peachey's (1965) data on tubular dimensions led to the following quantitative conclusions. The capacities of the surface membrane (C(S)) and of the tubular wall (C(W)) are both about 1 muF/cm(2). The conductances of the surface membrane (G(S)) and tubular wall (G(W)) are ca. 0.11 and 0.03 mmho/cm(2), respectively. The conductivity of the luminal fluid in the tubules is ca. 6 mmho/cm.

Changes in frog skeletal muscle action potentials following hypophysectomy and adrenalectomy

Hypophysectomy and adrenalectomy caused changes in skeletal muscle action potentials. Stimulation for 3–5 minutes, or immersion for 60 minutes in Ringer, caused a reduction in the action potential amplitude.