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

In sports, vitamins along with minerals, particularly iron, and the energy nutrients such as carbohydrates, are considered especially important. Frequently single or multiple vitamins in combination with other active substances such as iron, other minerals or carbohydrates are administered. In sports, vitamins are added to carbohydrate mixtures or electrolytes enriched with vitamins are offered and frequently used. There is no doubt that due to the numerous effects of vitamins, a connection must exist between the vitamin status and athletic performance capability. It can be concluded that vitamin deficiencies have a negative effect on physical and mental performance. The release of energy can only attain its maximum output when the organism has the required substances at its disposal. Iron is of central importance among these active substances, since its presence in haemoglobin is essential for the transport of oxygen and carbon dioxide, makes it possible for myoglobin to function as an oxygen supply depot and guarantees the functioning of internal respiration in the respiratory chain and various key enzymes. Muscle training increases not only the respiratory chain but also several other iron-rich enzymes. This makes even more astonishing the fact that a variety of recently published articles report on iron deficiency among athletes. The effect of the iron deficiency with anaemia (sports anaemia) is manifest in a reduction of aerobic capacity with an increase in lactate acidosis, greater fatigue, loss of appetite, muscular cramps and vasomotor disturbances.
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PMID:[Effect of vitamins and iron on performance and recovery in humans and in sports anemia]. 360 97

A national registry was begun in 1981 to collect data from 32 centers on patients diagnosed by uniform criteria as having primary pulmonary hypertension. Entered into the registry were 187 patients with a mean age (+/- SD) of 36 +/- 15 years (range, 1 to 81), and a female-to-male ratio of 1.7:1 overall. The mean interval from onset of symptoms to diagnosis was 2 years. The most frequent presenting symptoms included dyspnea (60%), fatigue (19%), and syncope (or near syncope) (13%). Raynaud phenomenon was present in 10% (95% of whom were female) and a positive antinuclear antibody test, in 29% (69% female). Pulmonary function studies showed mild restriction (forced vital capacity [FVC], 82% of predicted) with a reduced diffusing capacity for carbon monoxide (DLCO), and hypoxemia with hypocapnia. The mean (+/- SD) right atrial pressure was 9.7 +/- 6 mm Hg; mean pulmonary artery pressure, 60 +/- 18 mm Hg; cardiac index, 2.3 +/- 0.9 L/min X m2; and pulmonary vascular resistance index, 26 +/- 14 mm Hg/L/min X m2 for the group. Although no deaths or sustained morbid events occurred during the diagnostic evaluation of the patients, the typically long interval from initial symptoms to diagnosis emphasizes the need to develop strategies to make the diagnosis earlier.
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PMID:Primary pulmonary hypertension. A national prospective study. 360

Oxygen utilization, arterial and venous blood gas levels, hemodynamic values and exercise tolerance were compared before and after administration of propranolol and verapamil in 10 patients with stable angina pectoris. During exercise, propranolol decreased cardiac output (CO) by 22%; O2 extraction was increased and O2 consumption (VO2) did not change. With verapamil treatment, CO modestly increased (7%), O2 extraction decreased and VO2 did not change. In contrast to O2 utilization, the drugs produced opposite changes in mixed venous and arterial blood gas levels. Propranolol decreased mixed venous pH, increased CO2 tension and decreased the pH of arterial blood. Verapamil increased venous pH and decreased CO2 tension; pH of arterial blood did not change. The drugs yielded similar levels of antianginal efficacy, but patients exercised longer during verapamil therapy and were less fatigued. The hemodynamic and metabolic differences suggest that muscle perfusion during exercise influences the onset of fatigue and may help determine the choice of therapy.
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PMID:Effect of propranolol and verapamil on oxygen utilization, acidosis and fatigue during exercise in stable angina pectoris. 361 85

The metabolic and ventilatory responses to steady state submaximal exercise on the cycle ergometer were compared at four intensities in 8 healthy subjects. The trials were performed so that, after a 10 min adaptation period, power output was adjusted to maintain steady state VO2 for 30 min at values equivalent to: (1) the aerobic threshold (AeT); (2) between the aerobic and the anaerobic threshold (AeTAnT); (3) the anaerobic threshold (AnT); and (4) between the anaerobic threshold and VO2max (AnTmax). Blood lactate concentration and ventilatory equivalents for O2 and CO2 demonstrated steady state values during the last 20 min of exercise at the AeT, AeAnT and AnT intensities, but increased progressively until fatigue in the AnTmax trial (mean time = 16 min). Serum glycerol levels were significantly higher at 40 min of exercise on the AeAnT and the AnT when compared to AeT, while the respiratory exchange ratios were not significantly different from each other. Thus, metabolic and ventilatory steady state can be maintained during prolonged exercise at intensities up to and including the AnT, and fat continues to be a major fuel source when exercise intensities are increased from the AeT to the AnT in steady state conditions. The blood lactate response to exercise suggests that, for the organism as a whole, anaerobic glycolysis plays a minor role in the energy release system at exercise intensities upt to and including the AnT during steady state conditions.
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PMID:Metabolic and ventilatory responses to steady state exercise relative to lactate thresholds. 369 10

These experiments were conducted to determine whether changes in arterial O2 tension are related to changes in muscle metabolism during fatiguing contractions. Arterial and venous circulation to the gastrocnemius muscle (n = 8) was isolated, and the Achilles tendon was attached to a force transducer. Each muscle was electrically stimulated through the sciatic nerve for three 2-min periods of fatiguing contractions separated by 8 min of rest. The arterial O2 tensions were altered for each work period (mean PO2 = 44, 72, 391 Torr). Arterial and venous samples were drawn to measure lactate, O2 and CO2 concentrations (Van Slyke analysis), and [H+]. Muscle biopsies were taken to measure muscle [H+] (homogenate method) and lactate. Fatigue was evaluated as the decline in tension from peak initial tension. At the end of the contraction periods, values were significantly different (P less than 0.05) between the low arterial O2 tension and the high for flow [84 +/- 6 (mean +/- SE) vs. 70 +/- 8 ml X 100 g-1 X min-1], muscle lactate contraction (44 +/- 10 vs. 26 +/- 4 mmol/kg dry wt), and lactate release (122 +/- 12 vs. 57 +/- 14 mumol X 100 g-1 X min-1). O2 uptake and the rate of fatigue were not different among treatments during contractions. Muscle [H+] increased (work [H+] minus rest [H+]) to a significantly greater extent during low arterial O2 tensions compared with high (P less than 0.05). We conclude that alterations in arterial O2 tension during fatiguing contractions induce changes in blood and muscle acid-base status and in muscle metabolism that are independent of O2 uptake.
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PMID:Effect of altered arterial O2 tensions on muscle metabolism in dog skeletal muscle during fatiguing work. 374 Feb 52

Albino rats, Wistar family, have been raised since birth in normobaric hypoxic environment (10-12% O2). This hypoxic animal group and a normoxic animal group were subjected to muscular fatigue by forced march within revolving room. Normoxic animals were subjected to 3 spaced trials: in normoxic environment; in hypoxic normobaric environment; in the same hypoxic normobaric environment with about 2% CO2 added. Hypoxic animals were subjected to 2 spaced trials: in hypoxic normobaric environment; in the same hypoxic environment with about 2% CO2 added. At the end of every single trial, lactatemia, blood pyruvate, acid-base balance and the erythrocytic number were examined. Albino rats raised in hypoxic environment since birth, subjected to muscular work in hypoxic environment showed a smaller increase of lactatemia and a moderate variation of the acid-base balance, compared to normoxic animals in the same conditions. CO2 added to the respired hypoxic mixture during muscular work, attenuated in both animal groups, the observed modifications. Finally we found that the erythrocytes per mm3 of blood increased from the second drawing of blood.
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PMID:Acid-base balance and blood lactate and pyruvate levels in albino rats bred under normobaric hypoxia or normoxia, after muscular work in a hypoxic or hypoxic-hypercapnic environment. 380 71

A syndrome of headache, fatigue, dizziness, paresthesias, chest pain, palpitations and visual disturbances was associated with chronic occult carbon monoxide exposure in 26 patients in a primary care setting. A causal association was supported by finding a source of carbon monoxide in a patient's home, workplace or vehicle; results of screening tests that ruled out other illnesses; an abnormally high carboxyhemoglobin level in 11 of 14 patients tested, and abatement or resolution of symptoms when the source of carbon monoxide was removed. Exposed household pets provided an important clue to the diagnosis in some cases. Recurrent occult carbon monoxide poisoning may be a frequently overlooked cause of persistent or recurrent headache, fatigue, dizziness, paresthesias, abdominal pain, diarrhea and unusual spells.
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PMID:Occult carbon monoxide poisoning. 382 10

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

Ventilation (VE), CO2 output (VCO2), oxygen uptake (VO2), respiratory exchange ratio (R), and the ventilatory equivalents for VO2 and VCO2 were measured during graded exercise before and after 10 d of continuous bed rest (BR) in the -6 degrees head-down position to determine the effect of deconditioning on the anaerobic threshold (AT), i.e., the highest workrate or VO2 which was achieved without evidence of lactic acidosis, as judged from the profile of ventilatory and gas exchange responses. Ten healthy male subjects performed a supine graded cycle ergometer test before (pre) and after (post) BR which consisted of 4 min of unloaded pedaling at 60 rpm followed by an increased workrate of 15 W X min-1 until volitional fatigue (max). VE, VCO2, VO2, R, VE/VO2 and VE/VCO2 were measured every 30 s and used collectively to identify the AT. Plasma (PV) and blood (BV) volumes were measured pre- and post-BR by T-1824. Following BR, VO2max decreased from 2.42 +/- 0.17 to 2.25 +/- 0.13 L X min-1 (7.0%, p less than 0.05). BR significantly (p less than 0.05) reduced the AT from 1.26 +/- 0.09 to 0.95 +/- 0.05 L X min-1 VO2; from 52.2 +/- 2.0 to 42.6 +/- 1.6% VO2max; and from 93 +/- 9 to 65 +/- 6 W. A correlation coefficient (r) of -0.11 (NS) was found between the change in VO2max and change in AT. A decrease in BV of 8.8% (p less than 0.05) was due to the 11.0% reduction in PV; red cell volume remained constant.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of simulated weightlessness on exercise-induced anaerobic threshold. 396 61

Diaphragmatic fatigue was induced in six normal young men inspiring against a variable alinear resistance. Breathing pattern was rigidly controlled (tidal volume 0.75 liter, 12 breaths . min-1). Fatigue was defined as an inability to continue to generate a target transdiaphragmatic pressure (Pdi = 0.65 - 0.84 Pdimax). Diaphragmatic electromyogram (EMG, esophageal electrode) and perceived effort (PE, open-ended scale) were recorded. Subjects were tested on an identical resistance inspiring air or 100% O2 in random order on different days. They were unaware of the gas mixture inspired. Mean endurance time (tlim) +/- SE for air was 4.1 +/- 1.4 min and for O2 was 8.6 +/- 2.7 min (P less than 0.005). The increased tlim in O2 was associated with a delay in onset of EMG changes heralding diaphragmatic fatigue and a decrease in PE at any time during the study compared with the level of PE in air. Arterial O2 saturation (ear oximeter) remained at the resting level of 99.0 +/- 0.2% in O2 and decreased from the resting level of 97.2 +/- 0.2% by 2.8 +/- 0.7% (P less than 0.01) in air. The end-tidal CO2 fraction increased to a similar degree in air and O2 studies. We conclude that when breathing pattern, minute ventilation, and Pdi are held constant during inspiratory resistive loading, breathing O2 delays the onset of diaphragm fatigue and decreases PE.
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PMID:Diaphragmatic fatigue in normoxia and hyperoxia. 398 Mar 78


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