Role of exercise-induced potassium fluxes underlying muscle fatigue: a brief review

1991 ◽  
Vol 69 (2) ◽  
pp. 238-245 ◽  
Author(s):  
Gisela Sjøgaard
Keyword(s):  
Membrane Potential ◽  
Muscle Fatigue ◽  
Atp Depletion ◽  
Whole Body ◽  
Muscle Membrane ◽  
Tension Development ◽  
Intracellular Space ◽  
Safety Mechanism ◽  
Intracellular Ca ◽  
Exercise Induced

The site of exercise-induced muscle fatigue is suggested to be the muscle membrane, which includes the sarcolemma and T-tubule membrane; the excitability of the membrane is dependent on the membrane potential. Significant potassium flux from the intracellular space of contracting muscle may decrease the membrane potential to half its resting value. This is true for isolated muscle preparations as well as for the whole body exercise in humans. Specific K+ channels have been identified, that may account for the intracellular K+ loss. Calcium-sensitive K+ channels open when intracellular Ca2+ concentrations increase, as during excitation. ATP-sensitive K+ channels may be involved but may open only at ATP concentrations well below those attained at exhaustion. However, ATP may be compartmentalized and only the membrane-bound ATP concentration may be of significance. Ca2+ accumulation and ATP depletion cause cell destruction; these changes induce an increased K+ conductance, which may inactivate the membrane and consequently prevent tension development. It is hypothesized that such a safety mechanism is identical to the fatigue mechanism.Key words: muscle fatigue, electrolyte fluxes, Na+–K+ pump.

Cyclopiazonic acid decreases spontaneous transient depolarizations in guinea pig mesenteric lymphatic vessels in endothelium-dependent and -independent manners

2004 ◽  
Vol 286 (6) ◽  
pp. H2287-H2295 ◽  
Author(s):  
Ilia Ferrusi ◽  
Jun Zhao ◽  
Dirk van Helden ◽  
Pierre-Yves von der Weid
Keyword(s):  
Smooth Muscle ◽  
Membrane Potential ◽  
Guinea Pig ◽  
Lymphatic Vessels ◽  
Cyclopiazonic Acid ◽  
Muscle Membrane ◽  
Pacemaker Activity ◽  
Smooth Muscle Membrane ◽  
Intracellular Ca

Guinea pig mesenteric lymphatic vessels exhibit vasomotion through a pacemaker mechanism that involves intracellular Ca2+ release and resultant spontaneous transient depolarizations (STDs) of the smooth muscle membrane potential. This study presents a detailed characterization of the effects of cyclopiazonic acid (CPA) on this pacemaker activity. Microelectrode recordings from smooth muscle in vessel segments revealed that application of CPA (1–10 μM) caused a hyperpolarization accompanied by a decrease in the frequency and amplitude of STDs. The CPA-induced hyperpolarization was abolished after destruction of the endothelium and in the presence of NG-nitro-l-arginine (100 μM) or 1 H-[1,2,4]oxadiazolol-[4,3- a]quinoxaline-1-one (10 μM), which suggests a contribution of endothelium-derived nitric oxide (EDNO) in this response. In the absence of EDNO-induced effects, CPA decreased the frequency and amplitude of STDs recorded before and in the presence of the thromboxane A2 mimetic U-46619, norepinephrine, or thimerosal. CPA abolished U-46619-induced vasomotion as determined by measurement of constriction-associated intracellular Ca2+ concentration using the ratiometric Ca2+ indicator fura-2. The endothelial actions of CPA were compared with those of ACh, which is known to cause EDNO release in this preparation. Although CPA and ACh both increased endothelial intracellular Ca2+ concentration and depolarized the membrane potential, the kinetics of action for both parameters were markedly slower for CPA than ACh. These results suggest that CPA first hyperpolarizes the lymphatic smooth muscle and decreases STD frequency and amplitude through endothelial release of EDNO, and second, consistent with the action of CPA to inhibit sarcoplasmic reticulum Ca2+-ATPase and deplete Ca2+ stores, it further reduces STD activity. Inhibition of the lymphatic smooth muscle pacemaker mechanism is thought to abolish agonist-induced vasomotion.

Effect of low chloride on relaxation in hamster diaphragm muscle

1986 ◽  
Vol 61 (1) ◽  
pp. 180-184 ◽  
Author(s):  
S. A. Esau ◽  
N. Sperelakis
Keyword(s):  
Membrane Potential ◽  
Muscle Fatigue ◽  
Time Constant ◽  
Diaphragm Muscle ◽  
Resting Membrane Potential ◽  
Krebs Solution ◽  
Sarcolemmal Membrane ◽  
Cl Conductance

With muscle fatigue the chloride (Cl-) conductance of the sarcolemmal membrane decreases. The role of lowered Cl- conductance in the prolongation of relaxation seen with fatigue was studied in isolated hamster diaphragm strips. The muscles were studied in either a Krebs solution or a low Cl- solution in which half of the NaCl was replaced by Na-gluconate. Short tetanic contractions were produced by a 160-ms train of 0.2-ms pulses at 60 Hz from which tension (T) and the time constant of relaxation were measured. Resting membrane potential (Em) was measured using KCl-filled microelectrodes with resistances of 15–20 M omega. Mild fatigue (20% fall in tension) was induced by 24–25 tetanic contractions at the rate of 2/s. There was no difference in Em or T in the two solutions, either initially or with fatigue. The time constant of relaxation was greater in low Cl- solution, both initially (22 +/- 3 vs. 18 +/- 5 ms, mean +/- SD, P less than 0.05) and with fatigue (51 +/- 18 vs. 26 +/- 7 ms, P less than 0.005). Lowering of sarcolemmal membrane Cl- conductance appears to play a role in the slowing of relaxation of hamster diaphragm muscle seen with fatigue.

Regulation of intracellular calcium in N1E-115 neuroblastoma cells: the role of Na+/Ca2+exchange

2002 ◽  
Vol 282 (5) ◽  
pp. C1000-C1008 ◽  
Author(s):  
Kara L. Kopper ◽  
Joseph S. Adorante
Keyword(s):  
Membrane Potential ◽  
Intracellular Calcium ◽  
Normal Cell ◽  
Buffer Capacity ◽  
Neuroblastoma Cells ◽  
Fold Increase ◽  
Scorpion Venom ◽  
Reverse Mode ◽  
Intracellular Ca

In fura 2-loaded N1E-115 cells, regulation of intracellular Ca2+ concentration ([Ca2+]i) following a Ca2+ load induced by 1 μM thapsigargin and 10 μM carbonylcyanide p-trifluoromethyoxyphenylhydrazone (FCCP) was Na+ dependent and inhibited by 5 mM Ni2+. In cells with normal intracellular Na+ concentration ([Na+]i), removal of bath Na+, which should result in reversal of Na+/Ca2+exchange, did not increase [Ca2+]i unless cell Ca2+ buffer capacity was reduced. When N1E-115 cells were Na+ loaded using 100 μM veratridine and 4 μg/ml scorpion venom, the rate of the reverse mode of the Na+/Ca2+ exchanger was apparently enhanced, since an ∼4- to 6-fold increase in [Ca2+]ioccurred despite normal cell Ca2+ buffering. In SBFI-loaded cells, we were able to demonstrate forward operation of the Na+/Ca2+ exchanger (net efflux of Ca2+) by observing increases (∼ 6 mM) in [Na+]i. These Ni2+ (5 mM)-inhibited increases in [Na+]i could only be observed when a continuous ionomycin-induced influx of Ca2+ occurred. The voltage-sensitive dye bis-(1,3-diethylthiobarbituric acid) trimethine oxonol was used to measure changes in membrane potential. Ionomycin (1 μM) depolarized N1E-115 cells (∼25 mV). This depolarization was Na+dependent and blocked by 5 mM Ni2+ and 250–500 μM benzamil. These data provide evidence for the presence of an electrogenic Na+/Ca2+ exchanger that is capable of regulating [Ca2+]i after release of Ca2+ from cell stores.

Exercise and MEF2–HDAC interactions

2007 ◽  
Vol 32 (5) ◽  
pp. 852-856 ◽  
Author(s):  
Sean L. McGee
Keyword(s):  
Skeletal Muscle ◽  
Protein Kinase ◽  
Nuclear Export ◽  
Energy Homeostasis ◽  
Whole Body ◽  
Positive Health ◽  
Exercise Induced ◽  
Amp Activated Protein Kinase ◽  
Body Energy ◽  
Skeletal Muscle Adaptations

Exercise increases the metabolic capacity of skeletal muscle, which improves whole-body energy homeostasis and contributes to the positive health benefits of exercise. This is, in part, mediated by increases in the expression of a number of metabolic enzymes, regulated largely at the level of transcription. At a molecular level, many of these genes are regulated by the class II histone deacetylase (HDAC) family of transcriptional repressors, in particular HDAC5, through their interaction with myocyte enhancer factor 2 transcription factors. HDAC5 kinases, including 5′-AMP-activated protein kinase and protein kinase D, appear to regulate skeletal muscle metabolic gene transcription by inactivating HDAC5 and inducing HDAC5 nuclear export. These mechanisms appear to participate in exercise-induced gene expression and could be important for skeletal muscle adaptations to exercise.

The resting membrane potential of white muscle from brown trout (Salmo trutta) exposed to copper in soft, acidic water

2000 ◽  
Vol 203 (14) ◽  
pp. 2229-2236 ◽  
Author(s):  
M.W. Beaumont ◽  
E.W. Taylor ◽  
P.J. Butler
Keyword(s):  
Membrane Potential ◽  
Brown Trout ◽  
Salmo Trutta ◽  
White Muscle ◽  
Low Ph ◽  
Ammonium Ion ◽  
Muscle Membrane ◽  
Resting Membrane Potential ◽  
Muscle Fibres ◽  
Brown Trout Salmo Trutta

Previously, the distribution of ammonia between the intracellular and extracellular compartments has been used to predict a significant depolarisation of the resting membrane potential (E(M)) of white muscle from brown trout (Salmo trutta) exposed to a sub-lethal combination of copper and low pH. However, this prediction is based upon two assumptions (i) a relatively high membrane permeability for the ammonium ion with respect to that for ammonia gas and (ii) that this is unaltered by exposure to copper and low pH. Since there is conflicting evidence in the literature of the validity of these assumptions, in the present study E(M) was directly measured in white muscle fibres of trout exposed to copper and low pH (E(M)=−52.2+/−4.9 mV) and compared with that of unexposed, control animals (E(M)=−86.5+/−2.9 mV) (means +/− s.e.m., N=6). In confirming the predicted depolarisation, these data support the hypothesis of electrophysiological impairment as a factor in the reduction in the swimming performance of trout exposed to these pollutants. In addition, the results of this study support the role of a significant permeability of the muscle membrane to NH(4)(+) in determining the distribution of ammonia in fish.

The Effect of Lanthanum on Excitation–Contraction Coupling in Frog Skeletal Muscle

1974 ◽  
Vol 52 (6) ◽  
pp. 1126-1135 ◽  
Author(s):  
D. J. Parry ◽  
A. Kover ◽  
G. B. Frank
Keyword(s):  
Skeletal Muscle ◽  
Action Potential ◽  
Muscle Membrane ◽  
Frog Skeletal Muscle ◽  
Tension Development ◽  
Excitation Contraction Coupling ◽  
Contraction Coupling ◽  
Reduced Rate ◽  
Caffeine Contractures

Exposure of frog toe muscles to 1 mM La3+ results in a decrease in amplitude and rate of tension development of potassium contractures and twitches. At this concentration La3+ also inhibits the uptake of calcium, both in the resting condition and during stimulation. Caffeine contractures are unaffected even after a 5-min pre-exposure to La3+. The depolarization induced by various concentrations of K+ is reduced by about 10 mV as is the amplitude of the action potential. The rate of rise of the action potential is reduced by about 40% after 1 min in La3+ Ringer. Neither the decreased amplitude nor the reduced rate of depolarization is considered to be sufficient to explain the inhibition of tension development. It is suggested that La3+ partially uncouples excitation from contraction by preventing the release of a trigger-Ca2+ fraction from some site on the muscle membrane. This fraction normally plays a role in excitation–contraction coupling, although some tension may still be developed in the absence of a trigger-Ca2+ influx.

Voltage dependence of chloride current through Xenopus muscle membrane in alkaline solutions

1980 ◽  
Vol 58 (9) ◽  
pp. 999-1010 ◽  
Author(s):  
Peter C. Vaughan ◽  
James G. McLarnon ◽  
Donald D. F. Loo
Keyword(s):  
Steady State ◽  
Membrane Potential ◽  
Chloride Conductance ◽  
Resting Potential ◽  
Muscle Membrane ◽  
Alkaline Solutions ◽  
Constant Field ◽  
Confined Space ◽  
Initial Current ◽  
Test Current

Three-microelectrode voltage-clamp experiments have been conducted on surface fibres of Xenopus laevis sartorius muscles. When potassium and chloride were substituted by rubidium and sulphate, negligibly small currents were observed. In solutions containing rubidium and chloride at pH 8.4–8.8 normally polarized fibres exhibited instantaneous current–voltage relations that were linear over a wide voltage range. Chloride conductance varied widely from fibre to fibre; the mean resting conductance at −80 mV was 7.4 × 10−4 ± 2.6 × 10−4 S/cm2 (mean ± SE). When hyperpolarizing voltage steps were made, conductance declined from the initial to the steady state; inward currents saturated near 14 μA/cm2. In experiments performed on fibres depolarized by immersion in K+-and Rb+-rich solutions it was found that resting conductance did not increase by as much as would be expected from constant field – constant permeability precepts, by comparison with normally polarized fibres. Despite the low chloride transmembrane concentration ratio, rectification in the steady state was similar in depolarized and normally polarized fibres.When a two-pulse protocol was employed to test the availability of chloride conductance after conditioning of the system at some voltage, it was found that the test current, the initial current at the onset of the test voltage step, depended sigmoidally on the conditioning voltage. The sigmoid relationships had asymptotic limits: after hyperpolarizing conditioning the test current was minimal, after depolarizing conditioning, maximal. Normalized sigmoid relations were superimposable, whether from normally polarized or chronically depolarized cells.When the protocol was repeated using different test potentials and initial currents following a particular conditioning voltage were plotted against the test potential, families of straight lines were obtained. The slopes of the members of these families were dependent on the conditioning voltage: the more negative the conditioning step the lower the slope. The lines projected through a mutual intersection at a voltage slightly more positive than the resting potential. This is interpreted as indicating that there is some voltage, slightly positive with respect to the membrane potential, at which the initial current is independent of the conditioning voltage.It is concluded that the state of the chloride conductance mechanism is a function of the deviation of the membrane from the resting potential rather than of the absolute membrane potential and that relaxations from initial to steady states reflect properties of the permeation mechanism rather than accumulation or depletion of chloride in a confined space, although some contribution by a mechanism such as the latter cannot be completely ruled out.

Preparation and Functionality Research of Anion Functional Fabrics

2010 ◽  
Vol 178 ◽  
pp. 216-219
Author(s):  
Qing Shan Li ◽  
Ming Shuang Xu
Keyword(s):  
Muscle Fatigue ◽  
Application Research ◽  
Significant Difference ◽  
Generating Capacity ◽  
Exercise Induced

In order to provide scientific proof to anion functional fabrics application research in textile domain, in this article, anion functional fabrics were prepared, the anion generating capacity was determined and the effect of anion fabrics and mice BLA after exercise were first studied. The anion generating capacity shows that: due to the adding of anion function powders to function fabrics, the anion amount released by function fabrics is apparently higher than common fabrics. Washing can not significantly reduce the anion amount of function fabrics releasing. These can indicate that the function fabrics can release anion stable and lasting. The determination of mice’s BLA after swimming showed that Compared to common fabrics, functional fabrics have significant difference (P<0.05). The anions of functional fabrics releasing can reduce animals BLA after exercise and help to eliminate exercise-induced muscle fatigue.

Catecholaminergic automatic activity in the rat pulmonary vein: electrophysiological differences between cardiac muscle in the left atrium and pulmonary vein

2009 ◽  
Vol 297 (1) ◽  
pp. H102-H108 ◽  
Author(s):  
Nicolas Doisne ◽  
Véronique Maupoil ◽  
Pierre Cosnay ◽  
Ian Findlay
Keyword(s):  
Membrane Potential ◽  
Electrical Activity ◽  
Cardiac Muscle ◽  
Left Atrium ◽  
Pulmonary Vein ◽  
Pulmonary Veins ◽  
Muscle Membrane ◽  
Resting Membrane Potential ◽  
Ectopic Activity ◽  
Automatic Activity

Ectopic activity in cardiac muscle within pulmonary veins (PVs) is associated with the onset and the maintenance of atrial fibrillation in humans. The mechanism underlying this ectopic activity is unknown. Here we investigate automatic activity generated by catecholaminergic stimulation in the rat PV. Intracellular microelectrodes were used to record electrical activity in isolated strips of rat PV and left atrium (LA). The resting cardiac muscle membrane potential was lower in PV [−70 ± 1 (SE) mV, n = 8] than in LA (−85 ± 1 mV, n = 8). No spontaneous activity was recorded in PV or LA under basal conditions. Norepinephrine (10−5 M) induced first a hyperpolarization (−8 ± 1 mV in PV, −3 ± 1 mV in LA, n = 8 for both) then a slowly developing depolarization (+21 ± 2 mV after 15 min in PV, +1 ± 2 mV in LA) of the resting membrane potential. Automatic activity occurred only in PV; it was triggered at approximately −50 mV, and it occurred as repetitive bursts of slow action potentials. The diastolic membrane potential increased during a burst and slowly depolarized between bursts. Automatic activity in the PV was blocked by either atenolol or prazosine, and it could be generated with a mixture of cirazoline and isoprenaline. In both tissues, cirazoline (10−6 M) induced a depolarization (+37 ± 2 mV in PV, n = 5; +5 ± 1 mV in LA, n = 5), and isoprenaline (10−7 M) evoked a hyperpolarization (−11 ± 3 mV in PV, n = 7; −3 ± 1 mV in LA, n = 6). The differences in membrane potential and reaction to adrenergic stimulation lead to automatic electrical activity occurring specifically in cardiac muscle in the PV.

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