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Query: UMLS:C0015672 (fatigue)
51,768 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of twitch trains on the contractility of succeeding tetani were investigated in the frog toe muscle. The changes in isometric tension and its first derivative were analyzed. Tetani of 1 sec duration were induced every 5 min and trains of twitches (less than 250) with 0.1 to 3 Hz were interposed between two successive tetani. A twitch train which clearly shows an ascending staircase exerted at least three different effects on the following tetani. These were a rapidly decaying potentiation (P1), a slowly decaying potentiation (P2), and an inhibitory effect (I) which was regarded as fatigue. These after-effects were modified by various interventions. Increasing of the twitch frequency at a constant number of stimuli augmented both the potentiating and the inhibiting effects. When the bath temperature was lowered to 4 degrees C, the potentiation was masked by a marked inhibition. At a higher temperature (28 degrees C) the potentiating effect was facilitated. Prolonged perfusion of low concentration (0.5 mM) of caffeine mimicked the effects of low temperature. Effects of twitch train on the contracture induced by 5 mM caffeine were examined and it was found that the repetitive twitches had no effect on the following caffeine contracture. Although the exact mechanism for these after-effects was not clear, it was assumed that the intracellular calcium turnover may play some role in the observed phenomena.
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PMID:Effects of twitch train on the tetanic contractility of the frog skeletal muscle. 660 37

Mg2+-selective microelectrodes have been used to measure the intracellular free Mg2+ concentration in frog skeletal muscle fibers. Glass capillaries with a tip diameter of less than 0.4 micron were backfilled with the Mg2+ sensor, ETH 1117. In the absence of interfering ions, they gave Nernstian responses between 1 and 10 mM free Mg2+. In the presence of an ionic environment resembling the myoplasm, the microelectrode response was sub Nernstian (18-24 mV) but still useful. The electrodes were calibrated before and after muscle-fiber impalements . In quiescent fibers from sartorius muscle (Rana pipiens), with resting membrane potentials not less than -82 mV, the intracellular free Mg2+ concentration was 3.8 +/- 0.41 (S.E.) mM (n = 58) at 22 degrees C. No significant change in the intracellular free Mg2+ was observed following extensive (approx. 6 h) incubation in Mg2+-free media. Increasing the external concentration of magnesium from 4 to 20 mM (approx. 15 min) produced a slow and small enhancement (1.8 mM) of [Mg2+]i, which was fully reverted when the divalent cation was removed from the bathing solution. No change in ionic magnesium resting concentration was observed when the muscle fibers were treated either with caffeine 3 mM or with Na+-free solutions. In depolarized muscle fibers (-23 +/- 2.7 mV) treated with 100 mM K+, the myoplasmic [Mg2+] was 3.7 +/- 0.45 (S.E.) mM, n = 6, immediately after the spontaneous relaxation of the contracture. Similar determinations in muscle fibers during stimulation at low frequency (5 Hz), and after fatigue development, showed no changes in the concentration of free cytosolic Mg2+. These results point out that [Mg2+]i is not modified under these three different experimental conditions.
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PMID:Direct measurement of intracellular free magnesium in frog skeletal muscle using magnesium-selective microelectrodes. 660 20

The properties of caffeine contracture and potassium contracture in fatigued single fibers were examined in detail using frog semitendinosus muscle, Rana japonica. Fatigue was caused by repetitive stimulation at 2 Hz. The dose-response curve of caffeine contracture in the fatigued fibers was shifted toward the right; the threshold concentration of caffeine for the contracture in normal fibers was 1.5 mM, whereas that in fatigued fibers was 5 mM. However, in the presence of 25 mM K+ or 0.01% Triton X-100, caffeine contractures occurred sufficiently at the lower concentrations (3-5 mM) even in the fatigued fibers. Furthermore, in the fatigued fibers, the peak tension of the initial component of biphasic potassium contracture with 60 or 80 mM KC1 (C1 constant; 120 mM) was slightly inhibited, whereas the secondary component of the contracture was markedly inhibited. These results indicate that the permeability to caffeine of the transverse tubular membrane (T-membrane) of the fibers and the Ca influx in response to the direct depolarization of T-membrane with K+ are markedly inhibited in the fatigued fibers.
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PMID:Properties of caffeine- and potassium-contractures in fatigued frog single twitch muscle fibers. 667 57

One of the most important food components for the ability to concentrate is protein because certain amino acids are precursors of neurotransmitters, e.g. serotonin from tryptophan. There is a close relation between tryptophan content in the diet, serotonin biosynthesis in the brain and food intake. While lack of carbohydrates causes a symptomatic hypoglycemia which leeds to decreases in different functions and performances (e.g. memory and concentration, orientation, critical evaluation of environmental influences), glucose load does not mean an increased performance. In this respect dietary fats and minerals have not been investigated, some vitamins, e.g. thiamin, influence the functions of the nervous system. With coffee and caffeine containing beverages a drop of performance can be compensated for only a short time at the expense of energy reserves. Under the moderate influence of alcohol the function of nervous cells is markedly affected. In connection with medicine this negative effect is aggravated. After coffee and alcohol consumption events are subjectively experienced on quite a different level than can be objectively measured; misleading estimations are the consequence. A high meal frequency with small meals stimulates the serotonin biosynthesis and seems to reduce fatigue.
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PMID:[Nutrition and capacity for concentration in automobile drivers]. 685 55

We studied the effect of caffeine on voluntary and electrically stimulated contractions of the adductor pollicis muscle in five adult volunteers. Caffeine (500 mg) was administered orally in a double-blind fashion. Electrical stimulation of the ulnar nerve was performed at 10, 20, 30, 50, and 100 Hz before and after a sustained voluntary contraction held at 50% of the maximal voluntary contraction (MVC). A brief tetanus at 30 Hz was also performed to calculate relaxation rate in the fresh muscle. Contractile properties, relaxation rate, and endurance were then assessed after caffeine and placebo, as well as the response of the fatigued muscle to different frequencies of stimulation. There was no difference in the maximal tension obtained with electrical stimulation (T100) or in the MVC between placebo and caffeine. The tensions developed with electrical stimulation at lower frequencies increased significantly with caffeine ingestion, shifting the frequency-force curve to the left, both before and after fatigue. Mean plasma caffeine concentration associated with these responses was 12.2 +/- 4.9 mg/l. We conclude that caffeine has a direct effect on skeletal muscle contractile properties both before and after fatigue as demonstrated by electrical stimulation.
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PMID:Effect of caffeine on skeletal muscle function before and after fatigue. 686 91

Tension and metabolite concentrations were measured in single frog muscle fibers at 15 degrees C in vitro, in response to electrical stimulation or to immersion in caffeine- or potassium chloride-Ringer. Sarcomere length equaled 2.3 micrometers. Interrupted stimulation for 150 s at 20 Hz or stimulation for 7.5 min at 1 Hz was followed by at least 20 min of fatigue, evidenced by a reduced 200-ms test contraction. Fatigued fibers contracted maximally in potassium chloride- or caffeine-Ringer. They had high lactate and glucose 6-phosphate concentrations and a reduced phosphocreatine (PCr) concentration. Adenosine 5'-triphosphate (ATP) concentration was approximately normal but was markedly reduced by a caffeine contracture. A plot of PCr consumption against the tension-time integral at different stimulation frequencies (25, 35, or 50 Hz) and durations had an intercept of 25.5 nmol PCr/mg protein at time zero and a corrected slope of 0.65 nmol approximately P/mg protein per kg . s . cm-2. Prolonged fatigue is not due to energy exhaustion or to the inability of muscle fibers to consume residual ATP but probably arises from long-lasting interference in excitation-contraction coupling, which can be reversed by KCl- or caffeine-induced release of Ca2+ from intracellular stores.
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PMID:Fatigue and metabolism of frog muscle fibers during stimulation and in response to caffeine. 697 5

1. A form of skeletal muscle fatigue was examined with isolated animal and human muscle preparations. The possibility that methylxanthines could overcome this was investigated. 2. Prolonged contractile activity resulted in a long-lasting impairment of force generation at low frequencies of stimulation at times when the force at higher frequencies had substantially recovered. This was seen with both fast-twitch and slow-twitch animal muscles and with samples of isolated human muscle. 3. The decrease in low-frequency force was due to a decrease in twitch amplitude, suggesting damage to the processes involved in excitation--contraction coupling. 4. Caffeine and theophylline at concentrations of 1 mmol/l rapidly and completely reversed the effects of this form of fatigue in both animal and human muscle preparations. 5. Agents that potentiate muscle force production could be an effective means of counteracting the effects of an important form of skeletal muscle fatigue, but a clinically useful compound would need to be more potent than the methylxanthines currently in use.
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PMID:Low-frequency fatigue in isolated skeletal muscles and the effects of methylxanthines. 708 77

Sumatriptan is a potent and selective agonist at a vascular serotonin1 (5-hydroxytryptamine1; 5-HT1) receptor subtype (similar to 5-HT1D) and is used in acute treatment of migraine and cluster headache. Following administration of sumatriptan 100mg orally, relief of migraine headache (at 2 hours) was achieved in 50 to 67% of patients compared with 10 to 31% with placebo in controlled clinical trials. In a comparative study, oral administration of sumatriptan 100mg consistently achieved significantly greater response rates than a fixed combination of ergotamine 2mg plus caffeine 200mg during 3 consecutive migraine attacks (66 vs 48% for first attack). Oral sumatriptan 100mg was also more effective than aspirin 900mg plus metoclopramide 10mg orally in a similar study. In the majority of controlled clinical trials, headache relief (at 1 hour after administration) was achieved in 70 to 80% of patients with migraine receiving sumatriptan 6mg subcutaneously compared with 18 to 26% of placebo recipients. Approximately 40% of patients who initially responded to oral or subcutaneous sumatriptan experienced recurrence of their headache, usually within 24 hours, but the majority of these patients responded well to a further dose of sumatriptan. Patients with cluster headache were treated for acute attacks with sumatriptan 6mg subcutaneously or placebo in 2 crossover trials. Headache relief was achieved within 15 minutes in 74 and 75% of patients receiving sumatriptan in these studies compared with 26 and 35%, respectively, with placebo. Patients receiving sumatriptan 12mg had a similar response rate as those receiving 6mg, but the higher dose was associated with an increased incidence of adverse events. Based on extensive safety data pooled from controlled clinical trials, sumatriptan is generally well tolerated and most adverse events are transient. The most frequently reported adverse events following oral administration include nausea, vomiting, malaise, fatigue and dizziness. Injection site reactions (minor pain and redness of brief duration) occur in approximately 40% of patients receiving subcutaneous sumatriptan, although the incidence appears to be markedly reduced when patients self-administer the drug with an auto-injector. Chest symptoms (mainly tightness and pressure) occur in 3 to 5% of sumatriptan recipients, but have not been associated with myocardial ischaemia except in a few isolated cases. Sumatriptan is contraindicated in patients with ischaemic heart disease, angina pectoris including Prinzmetal (variant) angina, previous myocardial infarction and uncontrolled hypertension, but is not contraindicated in patients with migraine and asthma. Data from long term studies in acute treatment of migraine and cluster headache suggest that sumatriptan remains effective and well tolerated over several months.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Sumatriptan. A reappraisal of its pharmacology and therapeutic efficacy in the acute treatment of migraine and cluster headache. 751 61

1. Indirect and direct twitch (0.1-Hz) stimulation of the rat phrenic nerve-diaphragm disclosed that the inhibitory effect of HgCl2, 3.7 x 10(-5) M, on the neuromuscular transmission and in the muscle cell, was accelerated by 10-sec periods of 50-Hz tetanic stimulation every 10 min. This activity-dependent enhancement suggested an inhibitory mechanism of HgCl2 related to the development of fatigue, like membrane depolarization or decreased excitability, decreased availability of transmitter, or interference with the factors controlling excitation-secretion coupling of the nerve terminal, i.e. (Ca2+)0 or (Ca2+)i, and excitation-contraction coupling in the muscle cell, i.e., (Ca2+)i. 2. During both indirect and direct stimulation, HgCl2-induced inhibition was enhanced markedly by pretreatment with caffeine, which releases Ca2+ from endoplasmic and sarcoplasmic reticulum in the nerve terminal and muscle cell, respectively. This caffeine-induced enhancement was completely antagonized by dantrolene, which inhibits the caffeine-induced release. However, dantrolene alone did not antagonize the HgCl2-induced inhibition. 3. Since caffeine depletes the intracellular Ca2+ stores of the smooth endoplasmic reticulum, HgCl2 probably inhibits by binding to SH groups of transport proteins conveying the messenger function of (Ca2+)i. In the muscle cell this leads to inhibition of contraction. In the nerve terminal, an additional enhancement of the HgCl2-induced inhibition, by inhibiting reuptake of choline by TEA and tetanic stimulation, suggested that HgCl2 inhibited a (Ca2+)i signal necessary for this limiting factor in resynthesis of acetylcholine. 4. The (Ca2+)0 signal necessary for stimulus-induced release of acetylcholine was not affected by HgCl2. Hyperpolarization in K(+)-free solution antagonized the inhibitory effect of HgCl2 at indirect stimulation, and Ca(2+)-free solution enhanced the inhibitory effect at direct stimulation. K+ depolarization, membrane electric field increase with high Ca2+, membrane stabilization with lidocaine, and half-threshold stimulation, did not change the inhibitory effect of HgCl CH3HgCl. 1.85 x 10(-5) M, disclosed a synergistic interaction with caffeine during direct, but not during indirect, stimulation.
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PMID:Inhibitory effects of HgCl2 on excitation-secretion coupling at the motor nerve terminal and excitation-contraction coupling in the muscle cell. 754 23

This review summarizes the main cellular mechanisms involved in potassium regulation in plasma and skeletal muscle during exercise. The effects of exercise-induced hyperkalemia and post-exercise hypokalemia on the cardiac action potential are reviewed in light of recent research on Na+ and K+ channel activity. Specific consideration is given to K+ release from contracting skeletal muscle, K+ uptake by contracting skeletal muscle, K+ uptake by non-contracting tissues during the period of exercise, and K+ uptake by skeletal muscle recovering from contractile activity. The onset of exercise is associated with a net release of K+ from contracting skeletal muscle that results in an increase in plasma [K+]. Resultant decreases in intracellular [K+] and increases in interstitial [K+] in contracting skeletal muscle have been implicated in the fatigue process. The rate and magnitude of increase in plasma [K+] is dependent on exercise intensity, trained state of the individual, and on drugs such as beta-adrenoceptor blockers and caffeine. During exercise, the uptake of K+ from the blood by non-contracting tissues may be important in preventing plasma [K+] from rising to excessive levels that will impair skeletal muscle and myocardial excitability and contractility. Cessation of exercise results in a rapid decrease in plasma [K+], often to 3 mEq/l or less with intense exercise, that may be maintained for prolonged periods. The rapid increases and decreases in plasma [K+] with onset and cessation of exercise, respectively, has been implicated in altered myocardial function and sudden cardiac death. Recent studies suggest that increases in catecholamines during exercise are cardioprotective to the arrhythmogenic effects of hyperkalemia.
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PMID:Potassium regulation during exercise and recovery in humans: implications for skeletal and cardiac muscle. 756 98


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