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

In biotin-deficient rats, a decreased intestinal transport of Na+, H2O and L-phenylalanine, and no transport differences of 3-O-methyl-D-glucose were observed. The lower Na+ and L-phenylalanine transport appears to be referable to a decreased energy availability and probably not to the lack of a carrier.
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PMID:Transport of sodium, water, 3-O-methyl-glucose and L-phenylalanine in vitro in biotin-deficient rats intestine. 89 71

The anti-fatigue effect of phosphoserine, L-serine and a mixture of sodium phosphate and L-serine has been studied in rats. Phosphoserine orally administered induced a statistically significant anti-fatigue effect in rats of both sexes submitted to a training test by rotarod, with 14 sessions in 3 days. Furthermore, phosphoserine was utilized better than the mixture of sodium phosphate and L-serine, whereas L-serine alone induced no effect. Therefore the effect of phosphoserine seems to be due to the phosphoryl bond.
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PMID:Influence of phosphoserine on the performance of rats on the rotarod. 95 8

A decrease in amplitude and conduction speed in the compound action potential is observed with time in gar olfactory and rabbit vagus nerve when it is stimulated between 4 and 15 Hz at 26 degrees C in vitro. The amplitude decays exponentially for 1-3 min before reaching a steady state. Recs 15 s for gar olfactory nerve and 50 s for rabbit vagus nerve. The steady state values are 14% and 36% of the original amplitude, respectively, and conduction speeds are reduced by 25 % in both nerves. The effect results from completion between ion flow during the action potential and active transport. The accumulation of K+ions and depletion of Na+ ions in the restricted extracellular space contributes to the amplitude fatigue while the depletion of Na+ ions alone causes the decrease in conduction speed. Ouabain increases the fatigue rate in both preparations, but more so for gar. The fatigue and recovery measurements may provide a useful method to investigate active pumping, including both the total pumping rate and the electrogenic component.
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PMID:Action potential fatigue in nonmyelinated nerve fibers: garfish olfactory and rabbit vagus nerve. 97 77

A small-for-gestational-age infant, found to have analbuminemia in the neonatal period, is reported and the twelve cases recorded in the world literature are reviewed. Patients lacking this serum protein are essentially asymptomatic, apart from minimal ankle edema and ease of fatigue. Apparent compensatory mechanisms which come into play when serum albumin is low include prolonged half-life of albumin and transferrin, an increase in serum globulins, beta lipoprotein, and glycoproteins, arterial hypotension with reduced capillary hydrostatic pressure, and the ability to respond with rapid sodium and chloride diuresis in response to small volume changes. Examination of plasma amino acids, an investigation not previously reported, revealed an extremely low plasma tryptophan level, a finding which may be important in view of the role of tryptophan in albumin synthesis.
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PMID:Analbuminemia in a neonate. 112 26

The addition of carbohydrate and sodium to sport drinks has been recommended to enhance fluid intake and absorption and to delay fatigue. Other electrolytes (E) which are lost through sweating are also commonly added. However, too many E may lead to increased serum E and osmolality levels, which may negatively influence thermoregulation, depress sweating, and cause gastrointestinal distress. On the other hand, drinking large amounts of plain water to compensate sweat loss may induce hyponatremia. Therefore, literature describing sweat E losses was examined in order to estimate average whole-body E loss and to determine an upper limit for replacement of E with sport drinks. Mean E loss was determined from 13 studies, with +/- 1 SD resulting in a hypothetical range for E losses. Correction for net absorption resulted in an upper limit fo electrolyte replacement. It is suggested that the E levels in sport rehydration drinks should not exceed the upper limit of the range given.
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PMID:Rationale for upper limits of electrolyte replacement during exercise. 129 95

There is considerable debate regarding the ergogenic effects of sodium bicarbonate (NaHCO3) on racing performance in horses. Anecdotal evidence suggests that NaHCO3 improves performance by increasing the buffering capacity of the blood and delaying the onset of hydrogen ion-induced fatigue. In a cross-over study, 16 Thoroughbred racehorses were given an aqueous solution of NaHCO3 (0.4 g/kg in 1 litre H2O) or a control treatment (1 litre H2O) before a 1600-m race. Treatments were administered 3 h before the race, which was the time to peak buffering capacity (2.5-3.0 h) determined in a separate study. Before the race, there was a significant increase in venous HCO3- and pH in the NaHCO3-treated horses. After the race, there was a significant increase in venous blood pH and lactate in the NaHCO3-treated horses. Collectively, the data suggest an improved buffering capacity of the blood after NaHCO3 treatment. However, there was no change in race times or venous partial pressure of carbon dioxide. Therefore, the administration of NaHCO3 provided no ergogenic benefit to horses competing in a 1,600-m race.
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PMID:Effects of induced alkalosis on performance in thoroughbreds during a 1,600-m race. 131 65

The clinical and biochemical manifestations of secondary adrenocortical insufficiency are not well defined in the medical literature. This study was designed to determine the clinical and laboratory features suggesting the diagnosis of adrenal insufficiency in 15 chronic ACTH deficiency patients during low and normal cortisol states. Except for fatigue and weakness, the characteristic clinical manifestations of primary adrenal insufficiency occurred rarely. ACTH deficiency did not significantly modify blood glucose, serum calcium, sodium, potassium and differential white blood cell count. However, serum T4 was lower (65 +/- 19 vs 95 +/- 21 nmol/l, p less than 0.001) during cortisol deficiency, while T3 was higher (2.4 +/- 0.67 vs 2.0 +/- 0.60 nmol/l, p less than 0.001). Furthermore, rT3 decreased significantly during hypocorticism (0.27 +/- 0.07 vs 0.18 +/- 0.07 nmol/l, p less than 0.001). The T4/T3 ratio was significantly lower than the normal in 15 out of the 17 episodes of ACTH deficiency (29 +/- 12.5 vs 57 +/- 9.4, p less than 0.0001). We conclude that the increase in T3 and decrease in T4 levels are associated with chronic secondary adrenocortical insufficiency. This laboratory feature could be due, at least in part, to the increased peripheral conversion of T4 to T3 during cortisol deficiency.
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PMID:Increase in T3 levels during hypocorticism in patients with chronic secondary adrenocortical insufficiency. 131 31

Chronic low-frequency stimulation of rabbit fast-twitch muscle induced time-dependent increases in the concentration of the sarcolemmal Na+,K(+)-ATPase and in mitochondrial citrate synthase activity. The almost twofold increase in Na+,K(+)-ATPase preceded the rise in citrate synthase and was complete after 10 days of stimulation. We suggest that the increase in Na+,K(+)-ATPase enhances resistance to fatigue of low-frequency-stimulated muscle prior to elevations in aerobic-oxidative capacity.
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PMID:Time-dependent increases in Na+,K(+)-ATPase content of low-frequency-stimulated rabbit muscle. 132 68

Muscular fatigue is manifested by a decline in force- or power-generating capacity and may be prominent in both submaximal and maximal contractions. Disturbances in muscle electrolytes play an important role in the development of muscular fatigue. Intense muscular contraction is accompanied by an increased muscle water content, distributed in both intracellular and extracellular spaces. This water influx will modify ionic changes in both compartments. Changes in muscle intracellular electrolyte concentrations with intense contraction may be summarised as including decreases in potassium (6 to 20%) and in creatine phosphate (up to 70 to 100%) and increases in lactate (more than 10-fold), sodium (2-fold) and small, variable increases in chloride. The net result of these intracellular ionic concentration changes with exercise will be a reduction in the intracellular strong ion difference, with a consequent marked rise in intracellular hydrogen ion concentration. This intracellular acidosis has been linked with fatigue via impairment of regulatory and contractile protein function, calcium regulation and metabolism. Potassium efflux from the contracting muscle cell dramatically decreases the intracellular to extracellular potassium ratio, leading to depolarisation of sarcolemmal and t-tubular membranes. Surprisingly little research has investigated the effects of intense exercise training on electrolyte regulation and fatigue.
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PMID:The roles of ionic processes in muscular fatigue during intense exercise. 137 45

A 44-year-old female with 16-year history of rheumatoid arthritis visited Akiru Hospital with complaints of a thirst, a dry mouth and a general fatigue. One week prior to admission, the patient manifested excessive thirsty feeling, a body weight loss and a sleepless by the polyuria. She has been given 5-10 mg of prednisolone and 240 mg of lobenzarit disodium (CCA) in a day for 11 months. A hematologic examination showed no abnormality, and the examination of her serum showed the following values: BUN, 9.3 mg/dl; creatinine, 0.9 mg/dl; sodium, 139 mEq/l; chloride, 102 mEq/l; potassium, 3.9 mEq/l; osmolality, 290 mOsm/l. Plasma antidiuretic hormone (ADH) level increased slightly (6.0 pg/ml). Examination of her urine revealed specific gravity, 1.005; no trace of glucose, protein, blood and ketones; normal sediment; and osmolality, 209 mOsm/l. The patient was given exogenous ADH (10 units of vasopressin tannate in oil, intramuscularly) to obtain a diagnosis, and she was found to be unable to concentrate her urine more than 1.008 in the specific gravity. A water restriction, as a test for diabetes insipidus, also failed to concentrate her urine in the specific gravity and in the osmolality. Together with these findings, the patient was diagnosed to be a diabetes insipidus, and CCA was seemed to account for the disease. This unfavorable effect of CCA appeared to be reversible, since the patient recovered her urinary concentrating ability after the medication of CCA was discontinued.
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PMID:[Lobenzarit disodium (CCA)--induced diabetes insipidus in a patient with rheumatoid arthritis]. 141 95


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