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

When respiratory muscle demands for energy exceed supplies, the energy stored within the muscles is depleted and the force of contraction diminishes. This state is called inspiratory muscle fatigue. When it occurs alveolar ventilation decreases, arterial carbon dioxide tension (PaCO2) increases and hypercapnic respiratory failure ensues. It has also been suggested that such a dysfunction of the respiratory muscles contributes to the pathogenesis of acute respiratory failure. The purpose of this article is to review those factors that predispose to respiratory muscle fatigue and determine energy demand and supply and the principal means of investigation available to detect respiratory muscle fatigue in the clinical setting.
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PMID:Respiratory muscle fatigue. 265 11

Hypoxia and hypercapnic acidosis have been shown to have a negative inotropic effect on diaphragmatic contractility. The effect of combined hypercapnia and hypoxia was studied in vitro using hamster diaphragm strips. A 12% CO2, 21% O2, and 67% N2 gas mixture was used to produce hypoxic, hypercapnic acidosis. Force-frequency curves were generated using twitches and maximal tetanic contractions produced by stimulating with 0.2-ms pulses at 10 to 120 Hz for 300 to 500 ms. Moderate fatigue was then induced by repeated submaximal contractions (25 Hz, 160 ms, at the rate of 1/s for 45 contractions). Muscle strips exposed to hypoxic, hypercapnic acidosis had a decreased force response at all frequencies. The decrease in force was not different from that seen with hypoxia alone but was significantly worse than with hypercapnia alone. In the combined hypercapnic, hypoxia solution, tension produced by stimulating at 25 Hz for 160 ms was decreased to 52 +/- 11% of control (p less than 0.001). For these submaximal contractions, hypercapnic acidosis had a greater negative inotropic effect than did hypoxia alone. With repeated contractions, tension declined at a faster rate than in control, hypoxia alone, or hypercapnia alone. In the combined hypoxic, hypercapnic solution, the time constant of relaxation (tau) was increased prior to the start of the fatigue run compared to the control (tau = 35 +/- 6 versus 45 +/- 5 ms; p less than 0.001), and the tau increased at a faster rate than in control. These studies suggest that hypoxic, hypercapnic acidosis has a greater detrimental effect on the muscle than either abnormality alone and makes the muscle more susceptible to fatigue.
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PMID:Hypoxic, hypercapnic acidosis decreases tension and increases fatigue in hamster diaphragm muscle in vitro. 265 1

New technologies for the noninvasive assessment of oxygen and carbon dioxide are transforming clinical practice. Transcutaneous monitoring of PO2 (PtcO2) and PCO2 (PtCO2) provides an approximation of PaO2 and PaCO2 values in hemodynamically normal individuals, but both PtcO2 and PtcCO2 diverge from the corresponding arterial values when cardiac output is reduced, even in the absence of hypotension. Transcutaneous monitors also have relatively slow equilibration and response times. Pulse oximeters rapidly assess arterial O2 saturation, but give spurious results when dyshemoglobins (for example, carboxyhemoglobin, methemoglobin) are present in significant quantity. End-tidal CO2 (PetCO2) monitoring tracks breath-by-breath changes in ventilation, and PetCO2 approximates PaCO2 when significant physiologic dead-space is not present. Respiratory inductive plethysmography provides a semiquantitative assessment of tidal volume and the relative contribution of the thorax and abdomen to ventilation; among other uses, this technology may allow for the early detection of respiratory muscle fatigue prior to the onset of respiratory failure.
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PMID:Noninvasive monitoring of oxygen and carbon dioxide. 266 Nov 21

Regional cerebral blood flow (CBF), mood states and somatic symptoms were measured before and after inhalation of amyl nitrite in 10 physically healthy volunteers with a prior history of using volatile nitrites for recreational purposes. CBF was measured with the same technique, under identical laboratory conditions, in an equal number of normal volunteers. During CBF measurements, blood pressure, pulse rate, respiratory rate and end-tidal levels of carbon dioxide were monitored. The amyl nitrite group and the control group were compared on CBF, rating scale scores and physiological indices via analysis of variance. Amyl nitrite inhalation was associated with significant global increases in CBF, while the control group did not show any change. Pulse rate increase was the only physiological change associated with administration of the drug. Subjects who received the drug reported significant decrease in anger, fatigue and depression and increased palpitation, breathing difficulty, dizziness and headache. Changes in the rating scale scores, physiological indices, and somatic symptoms after amyl nitrite did not correlate with regional CBF change.
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PMID:Regional cerebral blood flow changes associated with amyl nitrite inhalation. 270 85

Normal human subjects (n = 7) breathing 21% O2 (normoxia), 13% O2 (hypoxia), or 100% O2 (hyperoxia) performed repeated maximal inspiratory maneuvers (inspiratory duration = 1.5 s, total breath duration = 3.5 s) on an "isoflow" system, which delivered a constant mouth flow (1.25 or 1 l/s) while maintaining normocapnia (5.5% end-tidal CO2). Respective mean arterial O2 saturation values (ear lobe oximetry) were 98 +/- 1, 91 +/- 4 (P less than or equal to 0.01), and 99 +/- 1% (NS). Maximal mouth pressure (Pm) was measured during inspirations at rest and during a 10-min fatigue trial, and the Pm measurements obtained during the fatigue trials were fit to an exponential equation. The parameters of the equation included the time constant (tau), which describes the rate of decay of Pm from the initial pressure (Pi) to the asymptote, or "sustainable" pressure (Ps). The mean fraction of Pm remaining at the end of the fatigue trials (Ps/Pi) was 63 +/- 5%. No significant differences in Pi, Ps, or tau were observed between O2 treatments. This suggests that fatigue of the inspiratory muscles in normal humans occurs by a mechanism that is insensitive to changes in blood O2 content that occur during inspiration of O2 in the range of 13-100%.
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PMID:Hyperoxia and moderate hypoxia fail to affect inspiratory muscle fatigue in humans. 270 19

Exertional muscle pain and fatigue are common complaints; some patients with these symptoms have a metabolic myopathy. We have performed graded exercise testing with analysis of expired ventilation on 13 individuals with various kinds of metabolic myopathies. Their results differed from normal and reflected the underlying biochemical abnormality. Patients with disorders of the mitochondrial electron transport chain demonstrated marked limitations in aerobic metabolism and a greatly reduced maximum oxygen consumption. During intense exertion, normal individuals increase carbon dioxide generation due to buffering of lactic acid. This did not occur in patients with McArdle disease, in whom the respiratory exchange ratio (carbon dioxide production/oxygen consumption) did not rise above 1.0 at maximum exercise. These results indicated a deficit in anaerobic metabolism. Pyruvate dehydrogenase complex allows pyruvate produced from carbohydrate metabolism to enter the citric acid cycle. Patients with this enzyme deficiency showed an initially normal pattern followed by an abrupt cessation in carbohydrate dependent aerobic metabolism at higher work loads. During high-intensity exercise, progressive anaerobic metabolism was not accompanied by additional oxygen consumption. Finally, results from a patient with carnitine palmitoyl transferase deficiency revealed an early dependence on carbohydrate metabolism. The ventilatory threshold occurred at a low percentage of maximal oxygen consumption, reflecting the limited availability of lipid substrates for aerobic metabolism. Detection of some muscle metabolic abnormalities can be made on small biopsy specimens. However, definitive diagnosis of the defect nearly always requires studies on fresh or frozen muscle tissue obtained by an open biopsy. The decision on how the tissue should be processed and which metabolic studies should be performed frequently needs to be made before the biopsy is obtained. Thus, a noninvasive method to initially characterize patients with potential metabolic disorders is useful. Exercise testing with expired gas analysis can indicate the presence of a metabolic myopathy and results can then be used to direct the appropriate biochemical evaluations.
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PMID:Metabolic myopathies: evaluation by graded exercise testing. 271 15

One hundred forty-five male welders from a West Coast shipyard were studied cross-sectionally and across a Monday work shift by pulmonary function tests and a questionnaire. Ten years of welding was associated with chronic bronchitis in 23.3% of nonsmokers compared to 3.3% in male controls, shortness of breath in 31.5% of nonsmokers compared to 1.5% in controls, and chest pain or heaviness in 38.4% compared to 4.4% in controls. Men who welded aluminum but had never smoked had more frequent wheezing, chest tightness, phlegm, feverishness and fatigue than those welding mild (black) or stainless steel. There were no significant cross-shift effects from welding exposure on measurements of pulmonary function. Although baseline expiratory flows were reduced slightly when compared to Caucasian-predicted values, ethnic specific comparisons for the largest subgroup showed only that FEF25-75 was reduced to 92.9 percentage of predicted values. Diffusing capacities for carbon monoxide were significantly reduced as compared to referents. The pulmonary function values of 25 current smokers were indistinguishable from the 41 who had never smoked, which probably reflects their low consumption of cigarettes.
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PMID:Respiratory symptoms and functional impairment from acute (cross-shift) exposure to welding gases and fumes. 281 87

Respiratory muscle fatigue is caused by excessive effort relative to the strength and endurance of the respiratory muscles. It can be manifested by reductions in respiratory drive (central fatigue), by impaired neuromuscular transmission (transmission fatigue), by decreased contractility (contractile fatigue), or by a combination of these factors. Respiratory muscle fatigue probably contributes to the difficulties some patients have with weaning from mechanical ventilation, the symptoms of exercise intolerance and dyspnea in chronic lung disease, and CO2 retention. Therapy depends on a reduction in the required level of respiratory effort and/or an improvement in respiratory muscle strength and endurance.
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PMID:Respiratory muscle fatigue. 283 16

The ferrihaemoglobin (HbFe3+) formation by amyl nitrite (AN) or sodium nitrite (NaNO2) was studied in different species including man, in vivo and in vitro. In in vivo studies AN was administered intravenously (i.v.), intramuscularly (i.m.), by inhalation, or orally. NaNO2 was injected i.v.. AN i.v. produced HbFe3+ much more rapidly than NaNO2 in dogs, cats, rabbits, and rats. In dogs, i.m. injection of AN was followed by a very slow linear increase in the HbFe3+ content. Inhalation of AN did not lead to HbFe3+ formation in dogs unless it was rebreathed in a closed (bag) or not completely open (gas mask) system. HbFe3+ was produced by oral AN in dogs, the effect being enhanced by addition of DMSO. Inhalation of AN by human volunteers in a gas mask and from ampoules crushed close to the nose did not induce haemoglobin oxidation to a practically significant extent, but it was associated with headache, tiredness, dizziness, and a fall in blood pressure. In in vitro studies, in contrast to NaNO2, AN produced HbFe3+ instantaneously in erythrocytes of various species and in purified human haemoglobin. AN 1 mol yielded 2 mol Fe3+. Only 20% of the oxygen released during the oxidation of haemoglobin by AN or NaNO2 was recovered. In 0.2 M phosphate buffer, pH 7.4, 0.01 mol O2/mol AN was consumed. CO2 was released in the presence of AN, but not of NaNO2, from blood, plasma, and 0.02 M NaHCO3 solution. The ratio (lactate)/(pyruvate) decreased when HbFe3+ was formed by AN or NaNO2.
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PMID:Ferrihaemoglobin formation by amyl nitrite and sodium nitrite in different species in vivo and in vitro. 290 49

H+ ions are generated rapidly when muscles are maximally activated. This results in an intracellular proton load. Typical proton loads in active muscles reach a level of 20-25 mumol X g-1, resulting in a fall in intracellular pH of 0.3-0.5 units in mammalian muscle and 0.6-0.8 units in frog muscle. In isolated frog muscles stimulated to fatigue a proton load of this magnitude is developed, and at the same time maximum isometric force is suppressed by 70-80%. Proton loss is slowed when external pH is kept low. This is paralleled by a slow recovery of contractile tension and seems to support the idea that suppression results from intracellular acidosis. Nonfatigued muscles subjected to similar intracellular proton loads by high CO2 levels show a suppression of maximal tension by only about 30%. This indicates that only a part of the suppression during fatigue is normally due to the direct effect of intracellular acidosis. Further evidence for a component of fatigue that is not due to intracellular acidosis is provided by the fact that some muscle preparations (rat diaphragm) can be fatigued with very little lactate accumulation and very low proton loads. Even under these conditions, a low external pH (6.2) can slow recovery of tension development 10-fold compared with normal pH (7.4). We must conclude that there are at least two components to fatigue. One, due to a direct effect of intracellular acidosis, acting directly on the myofibrils, accounts for a part of the suppression of contractile force. A second, which in many cases may be the major component, is not dependent on intracellular acidosis. This component seems to be due to a change of state in one or more of the steps of the excitation-contraction coupling process. Reversal of this state is sensitive to external pH which suggests that this component is accessible from the outside of the cell.
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PMID:The effect of acid-base balance on fatigue of skeletal muscle. 299 67


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