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PubMed1988

Response of arteriolar network of skeletal muscle to sympathetic nerve stimulation.

The influence of vessel location on arteriolar responses to sympathetic nerve stimulation was systematically studied in a skeletal muscle arteriolar network under normal and altered tissue O2 levels. The exteriorized cat sartorius muscle was exposed to 0, 5, and 10% ambient O2 during sympathetic chain stimulation at 8 pulses/s. Under 0% O2, stimulation initially caused a 25-45% constriction that was faster and more pronounced in distal arterioles. Ninety-one percent of vessels showed a secondary dilation (sympathetic escape), which was largest in distal arterioles. Escape had little effect on calculated volume flow, which, after a large initial fall, showed a modest secondary increase. Under 5 and 10% O2, resting arteriolar diameter was reduced by 12 and 17%, respectively, and escape was reduced by 60 and 73%. Escape was not attenuated in proximal arterioles preconstricted with vasopressin, suggesting that O2 did not attenuate escape through increased vascular tone. Therefore, the arteriolar response to sympathetic stimulation depends largely on location within the network and is modulated to varying degrees by metabolic influences.

Animals↗

PubMed1985

Effects of acute bleeding on oxygen supply to the skeletal muscle in dogs.

To study the effect of acute bleeding on the oxygen supply to the skeletal muscle, heparinized dogs were bled via an arterial cannula until mean arterial pressures of 25 and 50 mm Hg below initial value were reached. The shed blood was retransfused in reverse (50, 25 mm Hg) after correction of the acid-base imbalance in the dogs. Oxygen supply to the skeletal muscle was measured by means of a multiwire polarographic electrode placed on the sartorius muscle and was evaluated by means of ptO2 histograms. The ptO2 histograms showed that the oxygen supply to the skeletal muscle is severely impaired after a decrease in mean arterial pressure of 25 mm Hg. Further impairment was seen after a decrease in pressure of 50 mm Hg. During retransfusion tissue oxygenation was normalized only after all shed blood was retransfused and the initial mean arterial pressure was reached.

Animals↗

PubMed1991

Response of chloride efflux from skeletal muscle of Rana pipiens to changes of temperature and membrane potential and diethylpyrocarbonate treatment.

Efflux of 36Cl- from frog sartorius muscles equilibrated in two depolarizing solutions was measured. Cl- efflux consists of a component present at low pH and a pH-dependent component which increases as external pH increases. For temperatures between 0 and 20 degrees C, the measured activation energy is 7.5 kcal/mol for Cl- efflux at pH 5 and 12.6 kcal/mol for the pH-dependent Cl- efflux. The pH-dependent Cl-efflux can be described by the relation mu = 1/(1 + 10n(pK alpha-pH], where mu is the Cl- efflux increment obtained on stepping from pH 5 to the test pH, normalized with respect to the increment obtained on stepping from pH 5 to 8.5 or 9.0. For muscles equilibrated in solutions containing 150 mM KCl plus 120 mM NaCl (internal potential about -15 mV), the apparent pK alpha is 6.5 at both 0 and 20 degrees C, and n = 2.5 for 0 degrees C and 1.5 for 20 degrees C. For muscles equilibrated in solutions containing 7.5 mM KCl plus 120 mM NaCl (internal potential about -65 mV), the apparent pK alpha at 0 degrees C is 6.9 and n is 1.5. The voltage dependence of the apparent pK alpha suggests that the critical pH-sensitive moiety producing the pH-dependent Cl- efflux is sensitive to the membrane electric field, while the insensitivity to temperature suggests that the apparent heat of ionization of this moiety is zero. The fact that n is greater than 1 suggests that cooperativity between pH-sensitive moieties is involved in determining the Cl- efflux increment on raising external pH. The histidine-modifying reagent diethylpyrocarbonate (DEPC) applied at pH 6 reduces the pH-dependent Cl- efflux according to the relation, efflux = exp(-k.[DEPC].t), where t is the exposure time (min) to DEPC at a prepared initial concentration of [DEPC] (mM). At 17 degrees C, k-1 = 188 mM . min. For temperatures between 10 and 23 degrees C, k has an apparent Q10 of 2.5. The Cl- efflux inhibitor SCN- at a concentration of 20 mM substantially retards the reduction of the pH-dependent Cl- efflux by DEPC. The findings that the apparent pK alpha is 6.5 in depolarized muscles, that DEPC eliminates the pH-dependent Cl- efflux, and that this action is retarded by SCN- supports the notion that protonation of histidine groups associated with Cl- channels is the controlling reaction for the pH-dependent Cl- efflux.

Animals↗

PubMed1980

Frequency-domain study of the mechanical response of living striated muscle.

Small-amplitude sinusoidal displacements, in the frequency range 4-100 Hz, were applied to intact whole frog sartorius muscle whilst in a state of tetanus. At low frequencies the muscle was observed to do oscillatory work, while at higher frequencies it tended towards elastic behaviour. Frequency-response plots obtained were compared with those from other muscle preparations. Results were interpreted in terms of mechano-chemical transduction properties of muscle.

Adenosine Triphosphatases↗

PubMed2006

Alterations in calcium homeostasis reduce membrane excitability in amphibian skeletal muscle.

The effects of alterations in intracellular calcium homeostasis on surface membrane excitability were investigated in resting Rana temporaria sartorius muscle. This was prompted by initial results from a fatiguing stimulation protocol study that demonstrated a fibre subpopulation in which action potential generation in response to a standard 1.5 V electrical stimulus failed despite mean membrane potentials [E (m), -69+/-2.3 mV (n=14)] compatible with spike firing in a control set of quiescent muscle fibres. Intracellular micro-electrode recordings showed a similar reversible loss of excitability, attributable to an increased threshold, despite only small (7.1+/-1.8 mV) positive changes in E (m) after approximately 60-min exposures to nominally 0 Ca(2+) Ringer solutions in which Ca(2+) was replaced by Mg(2+). This effect was not reproduced by addition of Mg(2+) to the Ringer solution and persisted under conditions of Cl(-) deprivation. The effects of three pharmacological agents, cyclopiazonic acid (CPA), caffeine and 4-chloro-m-cresol (4-CmC), each known to deplete store Ca(2+) and increase cytosolic Ca(2+) through contrasting mechanisms without influencing E (m), were then investigated. All three agents produced a more rapid, but nevertheless still reversible, loss of membrane excitability than in 0 Ca(2+) Ringer solution alone. This reduction in membrane excitability persisted in fibres studied in solutions containing a normal [Ca(2+)] following prior depletion of store Ca(2+) using CPA- and 4-CmC-containing solutions. These novel findings suggest that sarcoplasmic reticulum Ca(2+) content profoundly influences surface membrane excitability, thereby providing a potential mechanism by which spike firing fails in well-polarised fibres during fatigue.

Action Potentials↗

PubMed1966

Muscle volume changes.

Measurements have been made of the volume changes accompanying single isometric and isotonic twitches of frog sartorius muscle. The volume change consists of a rapid increase, a subsequent decrease, and a return to the initial volume; the order of magnitude of increase and decrease is 10(-5) cc/g of muscle. This volume change is length-dependent: the initial increase becomes more pronounced as the initial length of the muscle is decreased, while the volume decrease is greatest at reference length and is diminished for longer and shorter initial lengths. Muscle volume changes are also dependent upon temperature and amount of shortening: the return phase is prolonged as the temperature is lowered; and, in an isotonic twitch, a volume increase accompanying muscle shortening is superimposed upon the volume change described for an isometric twitch. These "shortening volume changes" may correspond to the volume decrease observed in frog muscle under a passive stretch. If the active state is prolonged by the use of a frog Ringer solution in which iodide ions have been substituted for chloride ions, the time course of the volume decrease is likewise prolonged; this suggests a relationship between the volume decrease and the active state of the muscle.

Animals↗

PubMed1995

Characteristics of Na(+)-Ca2+ exchange in frog skeletal muscle.

1. Fluxes studies were carried out to investigate the Na(+)-dependent outward movement of Ca2+ in intact frog sartorius muscle from Leptodactylus ocellatus, a preparation for which published data on the subject are sparse. 2. Under normal resting conditions the Na(+)-Ca2+ exchange was not readily detectable. 3. When muscles were exposed to 4 mM caffeine, the rate of fractional loss of Ca2+ (kCa,o) increased by about 50%. Most of this increase exhibits characteristics typical of the Na(+)-Ca2+ antiport working in the forward mode found in other cells. 4. The increase in kCa,o promoted by caffeine was decreased by: (a) 72% in the absence of external Na+ (Nao+); (b) 73% in Na(+)-loaded muscles ([Na+]i = 98 mM); (c) 70% when fibres were depolarized to -27 mV ([K+]o = 50 mM); and (d) 80% in the presence of 5 mM amiloride. 5. Ni2+ (5 mM), an inhibitor of the Na(+)-Ca2+ exchanger current, unexpectedly increased the caffeine-promoted rise in kCa,o. This effect of Ni2+ was associated with a concomitant caffeine-stimulated Ni2+ influx. In the absence of caffeine Ni2+ did not affect kCa,o. 6. It was concluded that: (a) under resting conditions the sarcolemmal Ca2+ pump suffices to handle the cytosolic calcium concentration ([Ca2+]i); (b) Na(+)-Ca2+ activity becomes apparent when [Ca2+]i is substantially increased by caffeine-induced Ca2+ release from the sarcoplasmic reticulum; and (c) the blocking effect of Ni2+ on the current generated by a Na(+)-Ca2+ exchange with a coupling ratio > 2 might actually represent a shift of the antiport mode toward an electroneutral 1 Ni(2+)-1Ca2+ exchange.

Amiloride↗

PubMed1976

Concentration dependence of the veratrine effect on inducing depolarization and membrane potential oscillation in skeletal muscle.

The concentration dependence of the effect of veratrine in inducing depolarization and membrane potential oscillation in the frog sartorius muscle has been studied. (1) On increasing the veratrine concentration from 0.025 to 1 mM, the latency period of the development of membrane potential oscillation and depolarization is proportionally shortened. (2) On changing the veratrine concentration from 0.025 to 1 mM, the magnitude of depolarization is raised logarithmically. (3) When the veratrine concentration reaches 0.05-0.1 mM, both the amplitude and the frequency of the membrane potential oscillation increase. On rising to 1 mM, a further increase in frequency to eight-fold occurs especially in the later phase of oscillation. At this concentration range, the amplitude of oscillation inversely proportional to the concentration of veratrine. (4) On increasing the veratrine concentration above 0.1 mM, the membrane potential oscillation ceases after a temporary rise of frequency. This inhibitory effect of veratrine is, however, reversible, and oscillations appear again, despite the absence of veratrine in Ringer's solution. This also proves the persistance of the veratrine effect.

Animals↗

PubMed1986

[Release of beta-alanine from the frog skeletal muscle determined by thin-layer chromatography].

The release of beta-alanine from the resting and contracting frog sartorius muscles was demonstrated by the two-dimensional thin-layer chromatography. The release of beta-alanine from indirectly stimulated muscles of frogs in winter was about 230% higher than at rest. When synaptic transmission was blocked by d-tubocurarine the release of beta-alanine from directly stimulated muscles did not exceed the release at rest. Thus, activation of neuromuscular synapse leads to increased beta-alanine release from contracting muscle.

Alanine↗

PubMed1993

Adenosine and adenine nucleotides are independently released from both the nerve terminals and the muscle fibres upon electrical stimulation of the innervated skeletal muscle of the frog.

The independent release of adenosine and adenine nucleotides upon electrical stimulation was studied in the innervated sartorius muscle of the frog after blockade of the extracellular catabolism of adenosine monophosphate (AMP) through exo-AMP deaminase and ecto-5'-nucleotidase. Nerve stimulation (30 min, 0.2Hz) induced the release of both adenosine (19 +/- 3 pmol) and adenine nucleotides (101 +/- 7 pmol). Experiments performed in the presence of tubocurarine (5 microM) to prevent purine release due to nerve-evoked muscle twitching, or under direct stimulation of the muscle in low calcium solutions to prevent pre-synaptic release of purines, showed that there was an evoked release of adenosine and adenine nucleotides both from the nerve endings and from the twitching muscle fibres. Removal of ecto-5'-nucleotidase inhibition shows that the catabolism of adenine nucleotides released during stimulation contributes in about 50% to the amount of endogenous extracellular adenosine. When only one of the enzymes catabolizing AMP (ecto-5'-nucleotidase or exo-AMP deaminase) was inhibited, the evoked release of adenine nucleotides was undetectable, suggesting that each enzyme is able to catabolize all the AMP formed from adenine nucleotides released upon stimulation. It is concluded that the concentration of endogenous extracellular adenosine is under the control of the relative activities of exo-AMP deaminase and ecto-5'-nucleotidase.

AMP Deaminase↗

PubMed1990

Calcium release modulated by inositol trisphosphate in ruptured fibers from frog skeletal muscle.

To investigate the effect of inositol 1,4,5-trisphosphate on calcium release, we used fiber bundles of frog sartorius muscle mechanically permeabilized by a scratching procedure, and we detected increments in calcium concentration by measuring aqueorin light signals. Submicromolar concentrations of inositol 1,4,5-trisphosphate induced fast calcium-release signals, with a half time to peak of 60 ms or less. Similar responses were elicited by caffeine. The calcium-release signal induced by inositol 1,4,5-trisphosphate occurred at pCa values of 7 or lower, and the dose-response curve depended on the ionic composition of the incubation solution. Lower inositol 1,4,5-trisphosphate concentrations were needed to induce release when incubation solutions of ionic composition expected to depolarize the transverse tubule membrane were used. Inositol 1,4,5-trisphosphate was more effective than inositol 1,3,4-trisphosphate, inositol 1,4,5,6-tetrakisphosphate, and inositol 1,4-bisphosphate. The effect of inositol 1,4,5-trisphosphate was synergistic with that of caffeine, and was not inhibited by heparin. These results, by showing directly that at resting calcium levels inositol 1,4,5-trisphosphate elicited calcium release, are consistent with a role for inositol 1,4,5-trisphosphate as a chemical modulator in excitation/contraction coupling in skeletal muscle.

Aequorin↗

PubMed1984

Caffeine contractures in denervated frog muscle.

Caffeine contracture tension, effect of caffeine on the resting membrane potential, and caffeine influx in normal and denervated frog sartorius muscle have been investigated. Peak caffeine contracture tension is increased after denervation at all caffeine concentrations. The percentage increases in tension are highest for lower caffeine concentrations. The caffeine concentration required for half maximum tension is decreased from about 3.6 mM in control muscles to 2.6 mM in denervated muscles. Caffeine at 3.5 mM produces a depolarization of about 6 mV in control muscles and 16mV in denervated muscles. The large contracture tensions observed in denervated muscles are not due to the greater depolarization produced by the drug in denervated muscles since innervated muscles depolarized to the same level by external K+ do not enhance caffeine contracture tension. Both control and denervated muscles are highly permeable to caffeine. The increases in sarcoplasmic reticulum development ( Moscatello et al. 1965) and calcium content ( Picken and Kirby 1976) promoted by denervation may explain the larger tension elicited by caffeine in denervated muscles.

Animals↗

PubMed1975

Influence of the membrane stabilizer diphenylhydantoin on potassium and sodium movements in skeletal muscle.

The membrane stabilizer diphenylhydantoin (DPH) did not alter the net content of Na, K, Ca or Mg in frog sartorius muscle freshly incubated or actively transporting Na and K following Na-loading and K-depletion. Resting influx of K from normal Ringer was significantly reduced by DPH, and this inhibition occurred in the ouabain-insensitive K-uptake. Inhibition of K-influx by DPH was overcome when [K]0 was raised to 10 mM, and Rb-influx was not sensitive to the inhibitor in 2.5 mM Rb-Ringer. Efflux of tracer K was reduced by DPH in the presence and absence of ouabain. Exchange of muscle Na was not affected under conditions in which K-exchange was significantly reduced, but DPH appeared to cause increased net loss of Na from muscles washed in Na-free medium. The inhibition of DPH of resting K-exchange was not sensitive to wide variations in [Na]0 or in [Ca]0. The results suggest that the effect of DPH on frog skeletal muscle in normal ionic environment is to reduce the resting, passive component of K-exchange across the fibre membrane. This effect is discussed in relation to the membrane stabilizing actions of diphenylhydantoin.

Animals↗

PubMed1985

First-order kinetics of muscle oxygen consumption, and an equivalent proportionality between QO2 and phosphorylcreatine level. Implications for the control of respiration.

In frog sartorius muscle, after a tetanus at 20 degrees C, during which an impulse-like increase occurs in the rate of ATP hydrolysis, the rate of O2 consumption (QO2) reaches a peak relatively quickly and then declines monoexponentially, with a time constant not dependent on the tetanus duration (tau = 2.6 min in Rana pipiens and 2.1 min in Rana temporaria). To a good approximation, these kinetics are those of a first-order impulse response, and the scheme of reactions that couple O2 consumption to extramitochondrial ATP hydrolysis thus behaves as a first-order system. It is first deduced and then demonstrated directly that while QO2(t) is monoexponential, it changes in parallel with the levels of creatine and phosphorylcreatine, with proportionality constants +/- 1/tau p, where p is the P/O2 ratio in vivo. From this, it is further deduced that the mitochondrial creatine kinase (CK) reaction is pseudo-first order in vivo. The relationship between [creatine] and QO2 predicted by published models of the control of respiration is markedly different from that actually observed. As shown here, the first-order kinetics of QO2 are consistent with the hypothesis that respiration is rate-limited by the mitochondrial CK reaction; this has as a corollary the "creatine shuttle" hypothesis.

Adenosine Triphosphate↗

PubMed2004

Gold sodium thiomalate improves membrane potential impaired by high-frequency stimulation.

Effects of gold sodium thiomalate (GSTM) on membrane potential and tetanus tension were examined to elucidate whether the gold compound improves mechanical and electrical muscle dysfunction produced by continuous repeated stimulation of frog skeletal muscles. Continuous stimulation (50 Hz for 2 min, 0.05 ms pulse duration) to the sartorius muscle depolarized the membrane, decreased action potential amplitude, and prolonged action potential duration. GSTM (0.1 mM), unlike thiomalic acid (0.1 mM), markedly decreased impairment of these electrical parameters produced during the stimulation period. In the presence of 500 units/mL of catalase, fatigue stimulation still lengthened by 1.5-fold the half-duration of the action potential after a 5-min rest. The prolongation was, however, smaller than that in controls (no catalase). Application of both catalase and GSTM led to no further changes in action potential compared with the application of catalase alone. GSTM did not affect resting tension of single toe muscle fibers though it suppressed the maximum tension after continuous stimulation. These findings suggest that GSTM can inhibit excitable dysfunction of skeletal muscles subjected to continuous stimulation and that such protective effects of GSTM may be partially mediated by H2O2.

Animals↗

PubMedDate not supplied

Capillary ultrastructure and functional capillary density.

We briefly summarize our findings on alterations in capillary structure in skeletal muscle and heart in response to up to 30 min of ischemia. In frog sartorius muscle, reactive hyperemia was absent in atrophy. Increased spatial heterogeneity of red cell velocity in individual capillaries was observed, as were increases in the percentage of capillaries with damaged endothelium and white cell volume density in capillaries. Examination of the effect of aging on the response of the vascular bed to 30 min ischemia in extensor digitorum longus muscle of Fisher 344 rats suggested that the lack of postischemic hyperemia and structural alterations in frog muscle were related to disuse rather than aging per se. However, the specific study of disuse in rat extensor digitorum longus muscle after chronic application of tetrodotoxin revealed both capillary damage and a postischemic hyperemic response. It suggested an effect of the degree of tissue deterioration on the hyperemic response after short-term disuse in rat muscle, compared to longer-term atrophy in frog. Morphometric data in isolated rabbit heart suggested a link between microvascular compression as a result of tissue edema and decreased perfusion after 30 min total ischemia.

Aging↗

PubMed1985

Distribution of mass in relaxed frog skeletal muscle and its redistribution upon activation.

Five orders of equatorial reflection were recorded from both relaxed and fully activated intact frog sartorius muscle using synchrotron x-ray radiation. Electron density maps of the myofilament lattice in axial projection were calculated from the integrated intensities by Fourier synthesis, using all possible phase combinations. These maps were evaluated systematically in terms of their compatibility with electron microscopically and biochemically derived properties of the lattice structure and with the minimum wavelength principle. For the relaxed state, one phase combination emerged as most consistent with these constraints: it shows a thick filament with a compact core surrounded by an annular shell of density. The distribution of mass suggests that the S-2 moiety of the myosin molecule is an integral part of the thick-filament backbone and the S-1 moiety makes up the shell and is tilted or slewed around the backbone. For the active state, there are two feasible maps, which differ according to whether or not the activation process is associated with phase inversion in two of the reflections. Both maps represent patterns of redistribution of mass upon activation in which the thick-filament backbone is practically unaffected and there is movement of density from the annular shell towards the thin filaments. In addition to this outward radial flux of density from the thick-filament periphery, the pattern of net mass transfer involves a pronounced azimuthal component in both cases. The total net mass transfer is equivalent to approximately 20% (no phase change) or approximately 40% (with phase change) of the S-1 mass. From the observed systematic increase in peak widths of the higher orders, the size of the crystalline domain in the myofilament lattice in the relaxed sartorius is estimated to be greater than 650 nm and the variations in myofilament lattice spacing among different myofibrils to be about +/- 3%. Furthermore, in the activated state, the equilibrium positions of the myofilaments are no longer well ordered, but are distributed statistically about the lattice points with a standard deviation of approximately 3 nm.

Animals↗

PubMed1994

Ryanodine and theophylline-induced depletion of energy stores in amphibian muscle.

The effects of high and low levels of ryanodine on theophylline-induced energy depletion were studied in isolated frog sartorius muscle. Whereas low concentrations of ryanodine (1-10 microM) did not change high energy phosphate contents (PE) after 60 min, high levels (100 microM) reduced resting energy contents by 60% after 60 min. Subcontracture levels of theophylline (2 mM), in the presence of high ryanodine, produced an 80% PE depletion, suggesting possible additive or synergistic effects of these two agents. In contrast to theophylline-induced depletion, neither the ryanodine-induced depletion nor the theophylline-plus-ryanodine-induced depletion of PE seemed sensitive to inhibition by 1 mM procaine. This suggests that there may be differences in the mechanisms whereby methylxanthines and ryanodine deplete energy stores and evoke contractures in amphibian skeletal muscle.

Adenosine Triphosphate↗