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

Theophylline enhances the force of diaphragmatic contraction and delays fatigue. The mechanism is not known, but recent evidence suggests it may act at the cell membrane. To test this hypothesis, we studied the effect of theophylline on resting membrane potential and tension in hamster diaphragm cells. Muscle strips were obtained from five adult hamsters and placed in Krebs solution, aerated with 95% O2, 5% CO2. Resting membrane potential was measured using 3-M KCl-filled glass microelectrodes; 15-22 fibers in each strip were sampled. Force frequency curves (twitch to 100 Hz) were obtained. The muscle bath was then changed to one containing 100 mg/liter (0.55) theophylline. Resting membrane potential was -76 +/- 3 mV (mean +/- S.D.) in Krebs solution and increased to -85 +/- 3 mV (P less than 0.01) with added theophylline. Tension increased from 5% (at 100 Hz) to 20% (at 10 Hz) with theophylline. Hyperpolarization indicates an increase in intracellular to extracellular potassium concentration. Net potassium outflow occurs with each contraction, causing the cell membrane to become depolarized with repeated contractions, ultimately leading to fatigue. The hyperpolarization of the skeletal muscle cell membrane observed with theophylline may play an important role in prolonging time to fatigue.
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PMID:Effect of theophylline on membrane potential and contractile force in hamster diaphragm muscle in vitro. 394 72

The effect of selective and nonselective beta-adrenoceptor blockade on the thermoregulatory responses of 11 physically active, healthy, young adult men was studied during 2-hour block-stepping in heat. The trial consisted of 3 periods of 6 days each during which propranolol (160 mg/day), atenolol (100 mg) or matching placebo was administered in a randomized, double-blind crossover fashion. Propranolol and atenolol induced similar, significant (p less than 0.001) increases in subjective ratings of perceived exertion. The mechanism of this increased fatigue was not evident from the documented alterations in serum electrolyte, blood glucose and blood lactate levels or ventilatory parameters. Propranolol did, however, induce a postexercise delayed serum-potassium reversion. Although rectal and mean skin temperature responses were essentially unaltered by beta-adrenoceptor blockade during block-stepping, an increased total sweat loss was observed with propranolol (p less than 0.01 versus placebo) and to a lesser degree with atenolol (p = not significant versus placebo). This indicates that persons receiving beta-adrenoceptor blockers have an increased need to adhere to a strict fluid-replacement regimen during exercise. This potentially adverse response was minimal with atenolol in contrast to propranolol, and this in turn suggests the use of beta1-selective adrenoceptor blockers during prolonged exercise when adequate fluid replacement is not possible.
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PMID:Effect of selective and nonselective beta-adrenoceptor blockade on thermoregulation during prolonged exercise in heat. 399 52

It has been postulated that the power spectral shift in the surface EMG during fatigue is due to accumulation of muscle lactate. This hypothesis has been directly tested by measuring such shift in 3 patients with myophosphorylase deficiency who performed sustained isometric contractions of the quadriceps muscle. It was found that the spectral shift in these patients was greater than that in normal subjects, rendering lactate as a cause of this phenomenon very unlikely. The mechanism of excessive fatiguability in myophosphorylase deficiency is thought to be due to failure of excitation of the muscle membrane; further support for this postulate is provided and it is contended that accumulation of extracellular potassium ions may explain the phenomena of spectral shift in normals and myophosphorylase deficient patients and the excessive fatiguability in the latter.
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PMID:Muscle fatigue in myophosphorylase deficiency: power spectral analysis of the electromyogram. 620 Feb 96

Microelectrode measurements of tissue oxygen tension (PtO2) and extracellular potassium ion concentration ([K+]o) and dual wavelength spectrophotometric measurements of the reduction/oxidation state of cytochrome aa3 were used to compare the resistance of turtle and rat brain to anoxia in vivo. In both species, respiration with 100% N2 resulted in a decrease of tissue oxygen tension to near 0 mmHg and reduction of cytochrome aa3. However, N2 respiration resulted in only moderate elevation of [K+]o in turtle bran while [K+]o in rat brain was elevated to levels greater than 50 mM. In addition, N2 respiration in turtles had no effect on the rate of recovery of [K+]o, which was elevated by direct electrical stimulation of the brain. Electrocorticographic activity (ECoG) of the turtle brain was only moderately depressed during N2 respiration for up to 4 h whereas the ECoG of rat brain became isoelectric within 1 min. Inhibition of glycolysis with iodoacetate (IAA) resulted in rapid elevation of [K+]o in turtle brain during anoxia, but IAA had little effect on [K+]o during normoxia. These results indicate that the remarkable resistance of the diving turtle to anoxia does not result from continued provision of oxygen to the brain either by redistribution of systemic blood flow or from blood O2 storage. In addition, the turtle brain does not rely on cellular stores of high-energy compounds for maintenance of ionic homeostasis. We conclude that potassium ion homeostasis in the anoxic turtle brain must result from increased glycolytic ATP production and from decreased energy utilization.
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PMID:Brain potassium ion homeostasis, anoxia, and metabolic inhibition in turtles and rats. 628 69

The diseases which are commonly complicated by hypercapnic respiratory failure also compromise the respiratory muscles in several ways. Increased work of breathing, mechanical disadvantage, neuromuscular disease, impaired nutritional status, shock, hypoxemia, acidosis, and deficiency of potassium, magnesium, and inorganic phosphorus are the major non-neurologic factors which contribute to respiratory muscle fatigue and failure. Respiratory muscle fatigue has two components. High frequency fatigue occurs rapidly with intense contractile efforts but is usually not severe. It also recovers rapidly with rest. Low frequency fatigue develops more slowly but is severe and requires hours for recovery. Since the spontaneous rate of neural stimulation is predominantly in the low frequency range, this component of fatigue is of particular clinical importance. Fatigue of the inspiratory muscles leads to acute respiratory acidosis, but before carbon dioxide retention occurs, it can be recognized from characteristic symptoms and signs. These include dyspnea which responds to mechanical ventilation, rapid shallow breathing, and asynchronous movements of the chest and abdomen. Inspiratory muscle fatigue must be treated by putting these muscles to rest, by mechanically supporting ventilation. In addition, underlying metabolic nutritional and circulatory abnormalities must be corrected and infection treated. Aminophylline and isoproterenol can restore inspiratory muscle contractility, but controlled clinical trials remain to be done regarding their application in acute and chronic respiratory failure. Inspiratory muscle training improves strength and endurance in patients with obstructive lung disease, cystic fibrosis, and spinal cord injury, but does not always improve physical exercise performance. Again, more work is needed to develop the indications for inspiratory muscle training and to determine the optimum type and duration of the training regimen.
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PMID:Respiratory muscle failure. 634 27

The effect of the converting enzyme inhibitor captopril as long term treatment was investigated in 14 patients with severe congestive heart failure in a double blind trial. Captopril reduced plasma concentrations of angiotensin II and noradrenaline, with a converse increase in active renin concentration. Effective renal plasma flow increased and renal vascular resistance fell; glomerular filtration rate did not change. Serum urea and creatinine concentrations rose. Both serum and total body potassium contents increased; there were no long term changes in serum concentration or total body content of sodium. Exercise tolerance was appreciably improved, and dyspnoea and fatigue lessened. Left ventricular end systolic and end diastolic dimensions were reduced. There was an appreciable reduction in complex ventricular ectopic rhythms. Adverse effects were few: weight gain and fluid retention were evident in five patients when captopril was introduced and two patients initially experienced mild postural dizziness; rashes in two patients did not recur when the drug was reintroduced at a lower dose; there was a significant reduction in white cell count overall, but the lowest individual white cell count was 4000 X 10(6)/l. Captopril thus seemed to be of considerable value in the long term treatment of severe cardiac failure.
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PMID:Captopril in heart failure. A double blind controlled trial. 638 12

During the past 20 years there have been great developments in the scientific understanding of the role of nutrition in health and physical performance. Epidemiological and physiological studies have provided evidence that certain forms of dietary behaviour may be linked with an increased risk of developing disorders such as high blood pressure, coronary artery disease and some cancers. This has resulted in dietary recommendations that are intended to reduce the incidence of these disorders in the community. The science of nutrition in relation to sports performance has progressed from empirical studies investigating the effects of dietary manipulations, such as restriction and supplementation, to the direct investigation of the physiological basis of the specific nutritional demands of hard physical exercise. This review is based on the premise that it is "what comes out' rather than "what goes in', which provides the clues to ideal nutrition for athletic performance. Various aspects of the physical demands of athletic exercise are viewed as stresses that induce specific biochemical, and hence nutritional, strains in the athlete. Training is the predominant demand in the athletic lifestyle. This is characterised by acute bouts of high power output. During one hour of hard training an athlete may expend 30% of his or her total 24-hour energy output. These high power outputs have important implications for energy substrate and water requirements. Carbohydrate, specifically muscle glycogen, is an obligatory fuel for the high power outputs demanded by athletic sports. Muscle glycogen is a limiting factor in hard exercise because it is held in limited amounts, utilised rapidly by intense exercise, and fatigue occurs when it is depleted to low levels in the active muscles. Liver glycogen may also be exhausted by hard exercise and low blood glucose contributes to fatigue. High sweat rates are demanded during severe exercise and large water deficits commensurate with energy expenditure are incurred during extended periods of hard training and competition. Salt, potassium, and magnesium are lost in nutritionally significant amounts in the sweat, but vitamins and trace elements are not. Adaptive mechanisms protect athletes against electrolyte depletion. Iron loss in sweat may contribute to the iron deficiency seen in some endurance runners. Protein is degraded and amino acids are oxidised during physical exercise. Protein is also retained during muscle building training. Recent investigations indicate that the minimal protein requirements of athletes may be substantially higher than those for sedentary persons.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Nutrition and sports performance. 639 Jun 9

12 Brazilian men were treated with gossypol for 1 year. The treatment schedule consisted of oral administration of 20 mg gossypol daily for 4 months, followed by a maintenance dose of 20 mg on alternate days (o days/week), totaling 60 mg weekly for 8 months. 10 men became azoospermic at the end of the 4th month of treatment, and the other 2 developed marked oligospermia with necrospermia. Except for 1 man who complained of transient listlessness and fatigue, the subjects reported no side effects during treatment. No changes in libido or potency were reported, and plasma testosterone remained unchanged. Blood chemistry values, which included complete blood cell count, cholesterol, glucose, triglycerides, acid phosphatase, urea, transaminases, sodium, and potassium, were not changed significantly during treatment. The response of the pituitary to gonadotropin-releasing hormone stimulation and the response of the testis to gonadotropin stimulation appeared normal in men treated with gossypol. After treatment, sperm counts reverted to essentially normal levels in 8 of 12 men. In 4 men, azoospermia continued 1 year after gossypol treatment discontinuation. Retrograde phlebography carried out in 3 of 4 men who remained azoospermic after therapy discontinuation revealed subclinical varicocele.
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PMID:Antispermatogenic action of gossypol in men. 646 76

We have compared the nature of the enkephalin-like material derived from proenkephalin present in the intact cat adrenal gland with the material co-released with catecholamines from the perfused adrenal in response to splanchnic nerve stimulation and to perfusions with solutions containing acetylcholine (ACh) or high potassium chloride (KCl). In cat adrenals most of the enkephalin-like material was in the form of large enkephalin-containing peptides. Free (met)enkephalin immunoreactivity represented only 25% of the total (met)enkephalin immunoreactivity as determined by enzymatic digestion of large enkephalin-containing fragments. Electrical stimulation (15 Hz) of the splanchnic nerve or perfusion of the gland with ACh (0.1 mM) or KCl (50 mM), applied for 10 min, induced an immediate release of free (met)enkephalin immunoreactivity, (met)enkephalyl-arg-phe immunoreactivity, and of large (met)enkephalin-containing peptides. The release by all three modes of stimulation followed a pattern that paralleled the output of catecholamines. A rapid fatigue of all secretory processes developed during the stimulation periods, similar to that observed for catecholamines. During splanchnic nerve stimulation, each nanomole of catecholamine output was accompanied by the output of 0.4 pmol free (met)enkephalin immunoreactivity, of 1.1 pmol total (met)enkephalin immunoreactivity and of 0.1 pmol (met)enkephalyl-arg-phe immunoreactivity. Analysis of the perfusate by high-pressure liquid chromatography revealed that (met)enkephalin, (met)enkephalyl-arg-phe and (met)enkephalyl-arg-gly-leu were released in molar ratios of 4 to 1 to 1 which is similar to the ratio found in the precursor, proenkephalin. The ratio of total (met)enkephalin immunoreactivity to free (met)enkephalin immunoreactivity in the perfusate was the same (approximately 2.7) during two successive periods of splanchnic nerve stimulation separated by 10 min. When release was evoked by increasing the K+ concentration to 50 mM-KCl, this ratio was increased more than twofold compared with that obtained by electrical stimulation of the splanchnic nerve. Analysis of the perfusate by gel filtration showed that, during splanchnic nerve stimulation, 47% of the total (met)enkephalin immunoreactivity eluted in fractions containing fragments of low molecular weight. When KCl was used as stimulus only 12% of total (met)enkephalin immunoreactivity eluted in these fractions. The results indicate that the nature of the released peptides depends on the type of stimulus used to evoke release.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Co-release of enkephalins and precursors with catecholamines from the perfused cat adrenal gland in situ. 648 22

To evaluate the degree of physical activity in hemodialysis patients, working capacity was assessed by bicycle ergometry in 16 hemodialysis patients (mean age 47 +/- 12 [SD] years). The mean length of dialysis treatment was 21 +/- 17 months. The laboratory and clinical findings were as follows (mean values +/- SD): urea 34 +/- 6 mmol/l; creatinine 1127 +/- 169 mumol/l; potassium 5.7 +/- 0.63 mmol/l; calcium 2.25 +/- 0.22 mmol/l; phosphate 1.76 +/- 0.54 mmol/l; hemoglobin 8.54 +/- 1.02 g/dl; hematocrit 26.1 +/- 2.9%; blood pressure 140 +/- 18/86 +/- 9 mm Hg; nerve conduction velocity 39.5 +/- 6.5 m/sec. Mean working capacity was 58 +/- 31 W (41 +/- 24% of normal values) and the specific working capacity (watts/kg body weight) was 0.79 +/- 0.54. The duration of exercise testing was 4.9 +/- 2 min. The ergometry had to be discontinued because of the following reasons: leg fatigue (10 patients); general fatigue (3); dyspnea (1); attainment of maximal heart rate (2). The maximal blood pressure during exercise testing was 149 +/- 21/86 +/- 14 mm Hg and the maximal increase in heart rate 117 +/- 34 beats/min. In patients treated with a beta-blocker agent for hypertension, maximal increase in blood pressure was comparable to normotensive patients. There was a negative correlation between working capacity and the age of the patients (r = 0.77; p less than 0.01). A positive correlation was found between working capacity and the serum creatinine level (r = 0.52; p less than 0.05).
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PMID:[Ergometrically determined work capacity in chronic hemodialysis treatment]. 649 68


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