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

All exercise draws first on intramuscular stores of ATP and creatine phosphate; initially these are replenished by anaerobic glycolysis. The lactic acid produced contributes to the rapid development of fatigue in high intensity exercise. Aerobic metabolism (at first mainly of glycogen, later increasingly of fat) is the principal route of ATP resynthesis in activities lasting longer than 2 min, but can only maintain work-rates about 1/4 of those possible in very brief bursts. Blood lactate rises at the higher aerobic work rates. 'Lactate threshold' (LT: approximately 2 mmol/l) is almost exactly the speed at which endurance races are won, and close to those apparently providing optimal aerobic training. This training, predominantly of muscle aerobic capacity, elevates LT more than maximum oxygen consumption. LT is not now thought to indicate oxygen-deprivation, but intracellular adjustments driving oxidative phosphorylation faster. Ventilatory breakpoints, formerly considered to indicate LT, correlate more closely with the accumulation of potassium than lactate.
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PMID:Aerobic exercise, anaerobic exercise and the lactate threshold. 145 Aug 85

Recently, there have been many reports on the role of serum concentration of potassium as a potential limiting factor during exercise. K+ is known to induce muscle fatigue and to increase ventilation by direct stimulation of peripheral chemoreceptors. These two K(+)-mediated effects are considered to be the factors that limit exercise capacity. This effect seems to be exacerbated in hypoxemic states. The occurrence of hypoxemia in chronic pulmonary disease patients during exercise is believed to cause the excessive efflux of potassium to the extracellular space from skeletal muscles. The present study evaluated the relationship between the changes in arterial concentration of K+ and hypoxemia during exercise in 37 chronic pulmonary patients and 9 healthy controls. The study was carried out after obtaining formal and written consent of the patients in accordance with the stipulations of the Helsinki Declaration. Patients were divided into two groups according to PaO2 level at maximum exercise capacity; group I: PaO2 less than 55 torr, group II: PaO2 greater than or equal to 55 torr. The arterial concentration of K+ in group I patients tended to be higher than that in group II and controls. In group II, K+ concentration was significantly elevated (p less than 0.05) compared to controls. In group II, PaO2 values were inversely correlated with K+ (r = 0.3026; p less than 0.025), whereas in controls and group II they were unrelated. These results suggest that the augmented serum level of potassium in patients with chronic pulmonary disease is an important limiting factor during exercise.
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PMID:[The effect of oxygen administration on serum concentration of potassium during exercise]. 150 85

To investigate the effect of moderate to high intensity exercise of up to 6 min duration on plasma potassium and lactate concentrations, 6 Thoroughbred horses were studied using a treadmill at a 5 degree incline. Each test consisted of an 8-min standardised warm-up followed by an exercise bout at 8, 9, 10 or 12 m/sec. The horses were galloped at each speed for up to a maximum of 6 min or until signs of fatigue were present. The horses were then walked at 0 degree incline. Carotid arterial blood samples were taken during and after the exercise. At 8, 9 and 10 m/sec there was a general pattern of an initial rise in potassium to a peak around 1.5 min of exercise with the concentration then slowly decreasing. At 12 m/sec there was a continuous rise to a peak at the end of exercise in all horses. Immediately after exercise there was a rapid return (within 3-4 min) to the potassium concentrations recorded at the end of the warm-up period. Plasma lactate peaked around the end of exercise at all speeds. At the highest intensity of exercise the mechanisms for the re-uptake of potassium did not appear to be able to match the rate of efflux. In contrast, at less intense work loads, the rate of re-uptake appeared to be similar to or slightly greater than the rate of efflux. It is possible that a disturbance in this balance between efflux and re-uptake could result in a disturbance in normal neuromuscular function during exercise.
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PMID:Plasma potassium and lactate concentrations in thoroughbred horses during exercise of varying intensity. 160 36

A 49-year-old woman who had noted increasing fatigue and found it difficult to concentrate became confused and uncoordinated with rapid speech. Anxious and suffering from insomnia she had for 6 weeks taken a prescription-free bromide-containing drug mixture (daily 0.09 g potassium bromide and 1.8 g sodium bromide), to a total bromide intake of 60 g. The admission diagnosis of chronic bromism was confirmed by a markedly increased serum bromide concentration (325 mg/l). Once she had stopped taking the drug and had increased her salt intake she became symptom-free within 8 days. The case demonstrates that, while chronic bromism has become rare, it should still be included in the differential diagnosis, even after intake of supposedly harmless medication.
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PMID:[Chronic bromide intoxication caused by bromide-containing combination drugs]. 161 20

The concentrations of extracellular and intracellular potassium (K+) in skeletal muscle influence muscle cell function and are also important determinants of cardiovascular and respiratory function. Several studies over the years have shown that exercise results in a release of K+ ions from contracting muscles which produces a decrease in intracellular K+ concentrations and an increase in plasma K+ concentrations. Following exercise there is a recovery of intracellular K+ concentrations in previously contracting muscle and plasma K+ concentrations rapidly return to resting values. The cardiovascular and respiratory responses to K+ released by contracting muscle produce some changes which aid exercise performance. Increases in the interstitial K+ concentrations of contracting muscles stimulate CIII and CIV afferents to directly stimulate heart rate and the rate of ventilation. Localised K+ release causes a vasodilatation of the vascular bed within contracting muscle. This, together with the increase in cardiac output (through increased heart rate), results in an increase in blood flow to isometrically contracted muscle upon cessation of contraction and to dynamically contracting muscle. This exercise hyperaemia aids in the delivery of metabolic substrates to, and in the removal of metabolic endproducts from, contracting and recovering muscle tissues. In contrast to the beneficial respiratory and cardiovascular effects of elevations in interstitial and plasma K+ concentrations, the responses of contracting muscle to decreases in intracellular K+ concentrations and increases in intracellular Na+ concentrations and extracellular K+ concentrations contribute to a reduction in the strength of muscular contraction. Muscle K+ loss has thus been cited as a major factor associated with or contributing to muscle fatigue. The sarcolemma, because of changes in intracellular and extracellular K+ concentrations and Na+ concentrations on the membrane potential and cell excitability, contributes to a fatigue 'safety mechanism'. The purpose of this safety mechanism would be to prevent the muscle cell from the self-destruction which is evident upon overload (metabolic insufficiency) of the tissues. The net loss of K+ and associated net gain of Na+ by contracting muscles may contribute to the pain and degenerative changes seen with prolonged exercise. During exercise, mechanisms are brought into play which serve to regulate cellular and whole body K+ homeostasis. Increased rates of uptake of K+ by contracting muscles and inactive tissues through activation of the Na(+)-K+ pump serve to restore active muscle intracellular K+ concentrations towards precontraction levels and to prevent plasma K+ concentrations from rising to toxic levels. These effects are at least partially mediated by exercise-induced increases in plasma catecholamines, particularly adrenaline.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Potassium regulation during exercise and recovery. 165 9

A total of 930 patients have been evaluated for safety in a programme of clinical trials for lisinopril-hydrochlorothiazide combination treatment. Combination therapy with these two agents is generally well tolerated. In clinical trials, adverse experiences in patients treated with a lisinopril-hydrochlorothiazide combination were dizziness (7.5%), headache (5.2%), cough (3.9%), fatigue (3.7%), orthostatic effects (3.2%), diarrhoea (2.5%), nausea (2.2%) and upper respiratory tract infection (2.2%). Withdrawals from treatment have been relatively infrequent comprising dizziness (0.8%), headache (0.3%), cough (0.6%), fatigue (0.4%), diarrhoea (0.2%), orthostatic effects and nausea (0.1% each). The most common laboratory adverse experiences in patients on therapy with the lisinopril-hydrochlorothiazide combination are: increases in serum glucose, triglycerides, uric acid, serum creatinine, blood urea nitrogen and blood urea; and decreases in serum potassium. However, in individual controlled studies, the addition of lisinopril to treatment with hydrochlorothiazide results in attenuation of some of the potentially adverse metabolic affects of the diuretic. Adverse experiences in the patients treated for periods of 50 weeks or more, the elderly and the renally impaired are similar to those seen in the total population. Overall the available data indicate that a fixed dose combination of lisinopril-hydrochlorothiazide is a well-tolerated therapeutic option in patients with mild-to-moderate hypertension.
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PMID:Review of international safety data for lisinopril-hydrochlorothiazide combination treatment. 166 80

1. The differential effects of beta-adrenoceptor subtypes on potassium fluxes and exercise capacity were compared in eight healthy young men using single oral doses of the selective beta 2-adrenoceptor antagonist ICI-118551, the selective beta 1-adrenoceptor antagonist atenolol or the non-selective beta-adrenoceptor antagonist propranolol. The study was randomized, double-blind and placebo controlled. 2. Potassium in the venous effluent from the exercising muscles increased progressively with increasing exercise intensity. This response was augmented by propranolol, whereas neither atenolol nor ICI-118551 modified the response. After exercise potassium concentration fell exponentially with no difference between the treatment regimens. 3. Cumulative work was significantly reduced by ICI-118551 (6.4%, P = 0.04) and by propranolol (12.4%, P less than 0.01), whereas the reduction with atenolol (5.6%) did not reach statistical significance. 4. Atenolol and propranolol reduced peak heart rate by 23% and 29%, and peak systolic blood pressure by 9% and 11% respectively during maximal exercise. ICI-118551 caused a non-significant reduction in heart rate during submaximal exercise, with a significant reduction at maximum exercise (6% reduction), whereas systolic blood pressure was not different from placebo. Diastolic blood pressures were similar across all treatment regimens. 5. Similar glucose concentrations were obtained at baseline and at exhaustion during all treatment regimens. Lactate concentrations were comparable for any given exercise intensity irrespective of treatment regimens. Propranolol reduced lactate concentrations from the exercising muscles at maximum exercise in proportion to the reduction of maximal exercise capacity. 6. The subjective perception of fatigue was not affected by either beta 1- or beta 2-adrenoceptor blockade.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of selective beta 2-adrenoceptor blockade on serum potassium and exercise performance in normal men. 168 47

The influence of clinical doses of drugs that affect beta-adrenoceptors has been examined on heart rate, blood pressure, duration of exercise, and on electrolyte concentrations (Na, K, Ca and Mg) during recovery from exercise in healthy volunteers. The drugs used were a beta 1-adrenoceptor antagonist atenolol, a nonselective beta-adrenoceptor antagonist propranolol, and a cardioselective, partial beta 1-adrenoceptor agonist with 43% ISA activity, xamoterol. The duration of exercise was smaller on propranolol. Maximum exercise heart rate and blood pressure were reduced significantly by propranolol and atenolol. Xamoterol reduced maximum exercise heart rate and had no effect on blood pressure. The degree of breathlessness and fatigue revealed no differences between treatments. Recent evidence has suggested an association between hyperkalaemia and hypomagnesaemia with an increase in the occurrence of arrythmias following acute myocardial infarction. Exercise-induced hyperkalaemia has been suggested as a factor in sudden death. The results confirmed a rise in serum potassium during exercise and attenuation of the fall during recovery under beta-adrenoceptor blockade. Xamoterol was no different from placebo in these respects. Exercise also produced a rise in magnesium levels and during recovery the level fell below baseline. Both these effects were attenuated by propranolol. Calcium levels were not affected by any of the treatments.
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PMID:Comparison of the effects of xamoterol, atenolol and propranolol on breathlessness, fatigue and plasma electrolytes during exercise in healthy volunteers. 168 93

1. Heptaminol stopped or delayed the progressive decline in tension which characterizes the phenomenon of fatigue in frog isolated twitch muscle fibre. 2. Heptaminol had no action on the sodium, potassium and calcium voltage-dependent ionic conductances. 3. The hypothesis of an action via an internal alkalinization was tested by comparison with the action of NH4Cl. Both substances increased the tension. 4. The action of heptaminol was suppressed in sodium-free (TRIS) solution or in the presence of amiloride while the action of NH4Cl was always observed. 5. These results could be explained by a stimulation of the Na/H antiport by heptaminol.
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PMID:Action of heptaminol hydrochloride on contractile properties in frog isolated twitch muscle fibre. 172 30

Rates of performing work that engender a sustained lactic acidosis evidence a slow component of pulmonary O2 uptake (VO2) kinetics. This slow component delays or obviates the attainment of a stable VO2 and elevates VO2 above that predicted from considerations of work rate. The mechanistic basis for this slow component is obscure. Competing hypotheses depend on its origin within either the exercising limbs or the rest of the body. To resolve this question, six healthy males performed light nonfatiguing [approximately 50% maximal O2 uptake (VO2max)] and severe fatiguing cycle ergometry, and simultaneous measurements were made of pulmonary VO2 and leg blood flow by thermodilution. Blood was sampled 1) from the femoral vein for O2 and CO2 pressures and O2 content, lactate, pH, epinephrine, norepinephrine, and potassium concentrations, and temperature and 2) from the radial artery for O2 and CO2 pressures, O2 content, lactate concentration, and pH. Two-leg VO2 was thus calculated as the product of 2 X blood flow and arteriovenous O2 difference. Blood pressure was measured in the radial artery and femoral vein. During light exercise, both pulmonary and leg VO2 remained stable from minute 3 to the end of exercise (26 min). In contrast, during severe exercise [295 +/- 10 (SE) W], pulmonary VO2 increased 19.8 +/- 2.4% (P less than 0.05) from minute 3 to fatigue (occurring on average at 20.8 min). Over the same period, leg VO2 increased by 24.2 +/- 5.2% (P less than 0.05). Increases of leg and pulmonary VO2 were highly correlated (r = 0.911), and augmented leg VO2 could account for 86% of the rise in pulmonary VO2.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Contribution of exercising legs to the slow component of oxygen uptake kinetics in humans. 175 46


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