Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0015672 (fatigue)
 51,768 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

An outbreak of complaints consisting primarily of eye and respiratory tract irritation accompanied by headache, dizziness, fatigue, and nausea occurred among the operating room personnel of a large metropolitan hospital. This initially was attributed to infiltration of diesel exhaust emissions into the ventilation system. However, following correction of this problem and subsequent unrevealing air monitoring, symptoms persisted and were noted in personnel in adjacent areas of the hospital as well. An industrial hygiene and medical evaluation was undertaken. Monitoring for carbon monoxide, formaldehyde, and anesthetic gases and review of medical records and patient examinations were unrevealing, and the problem resolved gradually over several weeks. This outbreak represents a case of building-associated illness among health professionals in a hospital setting that was triggered by a single, identifiable noxious exposure but was sustained despite any apparent ongoing noxious exposures.
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PMID:Sick-hospital syndrome. 186 55

1. Single, intact muscle fibres from the flexor brevis foot muscle of the mouse have been fatigued at 25 degrees C by 350 ms, 70 Hz stimulation trains, initially delivered every 3.8 s and then at stepwise decreasing intervals until tension was down to about 30% of the original (Po). Rested fibres generated a specific force of 372 +/- 8.4 kPa (mean +/- S.E.M., n = 25). 2. Endurance, defined as time to attain 0.5 Po, varied from 2.5 to 24 min, with the majority of fibres falling in the range 4-8 min, corresponding to 70-160 tetani. In all fibres where it was followed, tension recovery after cessation of stimulation was 90% or better. 3. Tetanic force declined in a characteristic way during fatiguing stimulation: initially tension fell to about 0.85 Po during eight to fourteen tetani (phase 1), then followed a long period of nearly steady tension generation (phase 2) and finally there was a rapid force decline (phase 3). 4. Caffeine (15 or 25 mM) caused a slight potentiation of tetanic force in the rested state (4.7 +/- 0.9%, n = 21) and slowed relaxation. No change in resting tension was seen with caffeine at concentrations up to 25 mM. 5. Caffeine (15-25 mM) caused a rapid and dramatic increase in tetanic force when applied to severely fatigued fibres: force output rose from 29.8 +/- 1.5 to 82.5 +/- 1.2% (n = 13) of Po. During phase 2 force potentiation with caffeine was much smaller. 6. A 10 s pause resulted in a large, transient force increase when imposed during phase 3 but had little effect on force production during phase 2. 7. Intracellular acidosis, induced by superfusion with Tyrode solution gassed with 30% CO2 instead of the normal 5% (extracellular pH 6.5 vs. 7.3), resulted in a fall in tetanic tension to about 0.85 Po (n = 7). This depression could to some extent be counteracted by 15 mM-caffeine, which brought tension back to about 0.90 Po. 8. It is concluded that there are at least two mechanisms for force decline during fatiguing stimulation: one which manifests itself early and is likely to be related to cross-bridge function and another representing deficient Ca2+ handling which becomes prominent at a later stage. For severe fatigue (0.3 Po) the latter mechanism is dominant.
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PMID:Force decline due to fatigue and intracellular acidification in isolated fibres from mouse skeletal muscle. 190 15

1. In the preceding paper we analysed the force decline in fatigue of isolated mouse muscle fibres. Using the same preparation and stimulation scheme we have now examined another aspect of muscle fatigue, namely slowing of relaxation. 2. Relaxation at the end of a tetanic contraction can usually be divided into two phases, an initial nearly linear force decline, followed by an exponential phase. We have analysed the initial phase in terms of decline rate and duration. In rested fibres the decline rate after a 350 ms tetanus was not affected by a 30% reduction of tetanic tension (obtained by decreasing the stimulation frequency). 3. Relaxation became gradually slower during fatiguing stimulation with a maximum reduction at the time when tetanic tension was reduced to about 75% of the original (end of phase 2, see preceding paper). At this time the decline rate of the linear phase had fallen to 55.2 +/- 2.9% (mean +/- S.E.M., n = 25) and its duration had increased to 151.3 +/- 14.2% of the control (unfatigued 350 ms, 70 Hz tetanus). 4. Short rest periods (duration = 10s), given at various times during fatiguing stimulation, resulted in a clear, but partial, normalization of the relaxation parameters; at the time of maximum slowing the mean decline rate increased from 50.3 to 58.7% and the duration decreased from 167.9 to 144.0% of the control (n = 14). 5. The influence of intracellular acidosis on relaxation was studied by exposing rested fibres to 30% CO2 instead of the normal 5%. This resulted in a decline rate of 43.0 +/- 2.6% and a duration of 221.1 +/- 13.1% of the control (n = 7). 6. In amphibian muscle relaxation is known to become gradually slower during a single, prolonged tetanus. The existence of such an effect also in the present preparation was studied by giving 'interrupted' tetani with a total duration of about 2 s. In rested fibres the mean rate of relaxation was found to fall from 140.9 to 71.8% (n = 11) of the control (end of 350 ms stimulation) with a time constant of about 0.5 s. Thus, a marked slowing during a long tetanus occurs also in mammalian muscle. 7. A distinct slowing of relaxation during prolonged tetani was observed also in the fatigued and in the acidified state. Under these two conditions the mean rate of relaxation fell from 87.0 to 34.0% (n = 3) and from 74.0 to 23.0% (n = 5) of the control, respectively, with time constants similar to that in the rested state.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Slowing of relaxation during fatigue in single mouse muscle fibres. 190 16

We describe the cases of three women with pulmonary involvement in the eosinophilia-myalgia syndrome. The illness was characterized by elevated peripheral blood eosinophil counts, myalgias, fatigue, and dyspnea. Two of three patients had bilateral infiltrates on chest roentgenograms. All three had markedly decreased carbon monoxide diffusing capacities and pulmonary hypertension. High-dose prednisone therapy provided only partial resolution of the pulmonary symptoms. Open lung biopsy specimens showed chronic interstitial and perivascular infiltrates in two of the patients and moderate fibrointimal hyperplasia of pulmonary vasculature in the third. High-dose prednisone therapy prior to the biopsies may have modified the original histologic features.
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PMID:Pulmonary involvement in the eosinophilia-myalgia syndrome. 198 90

A prospective evaluation of the prevalence of CO2 retention and its relationship to lung mechanics and inspiratory muscle strength was carried out in 311 clinically stable patients with chronic obstructive pulmonary disease (COPD). Of these patients 32.8% had hypercapnia (PaCO2 greater than or equal to 43 mm Hg). PaCO2 was directly related to lung resistance (RL; r = 0.53) and inversely related to FEV1 (r = 0.53) and to an expression of the dead space/tidal volume ratio (1 - VD/VT) (r = 0.48). RL was found to be a major determinant of the mean intrathoracic pressure swing developed during inspiration (PI) at rest (r = 0.85). Maximal inspiratory pressure (PImax) was found to improve the predictive value for PaCO2 of several mechanical loads, with RL/PImax the best predictor (r = 0.57). The prevalence of hypercapnia increased from virtually 0 to 100% with increases in the RL/PImax value and was higher in the obese subjects at intermediate RL/PImax values, probably because of the burden placed on the respiratory muscles by chest wall mass loading. Our results show that chronic alveolar hypoventilation is likely to develop in COPD patients who have a combination of high inspiratory loads and inspiratory muscle weakness. hypercapnia may be one strategy available to avoid overloading of the inspiratory muscles leading to fatigue and possible irreversible failure.
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PMID:Inspiratory muscle dysfunction and chronic hypercapnia in chronic obstructive pulmonary disease. 202 40

Hypoxic, hypercapnic acidosis (HHA) decreases tension and enhances fatigue in hamster diaphragm in vitro. We hypothesized that theophylline would decrease the harmful effect of HHA. Hamster diaphragm strips were studied in Krebs solution aerated with 21% O2 and 12% CO2. The force-frequency responses and the tension and relaxation of brief, submaximal contractions were studied. Mild fatigue was produced by a series of 45 submaximal contractions, after which recovery of force was followed for 15 min. Theophylline (0.55 mM) was added at the time of exposure to HHA (early theophylline) in half the strips and at the end of the fatigue run (late theophylline) in the others. In contrast to our hypothesis, early theophylline had a limited effect on force production in unfatigued HHA diaphragm strips and resulted in lower force production in the recovery period. Late theophylline improved force in the recovery period for low-frequency contractions. Thus the effect of theophylline in the setting of HHA depended on the time it was added and was beneficial only if added after the muscle stopped contracting.
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PMID:The effect of theophylline on hypoxic, hypercapnic hamster diaphragm muscle in vitro. 202 50

The pattern of oxygen (O2) consumption (VO2), carbon dioxide (CO2) production (VCO2), ventilatory and metabolic responses during and in recovery from supine bicycle exercise was examined in 18 patients with recent myocardial infarction. An increase in VO2 with increasing work load was accomplished by proportional increases in both cardiac output and the arteriovenous O2 difference. During recovery, however, the arteriovenous O2 difference rapidly decreased below levels at rest, whereas VO2 and cardiac output remained elevated, indicating that VO2 during recovery further depended on relatively high cardiac output. The ratio of VCO2 to VO2 further increased after exercise, suggesting that such cardiac output contributed to the remaining high CO2 flow to the lung and therefore enhanced ventilation. Increased arterial catecholamines during exercise remained elevated for the first 5 minutes of recovery. Arterial lactate during this period continued to increase and resulted in profound metabolic acidosis, causing alveolar hyperventilation after exercise. These results suggest that during recovery from exercise, cardiopulmonary responses remain enhanced because of continuing high cardiac output, resulting in subsequent high CO2 flow to the lung and metabolic acidosis, and that this may be associated with profound fatigue or dyspnea after exercise.
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PMID:Oxygen utilization, carbon dioxide elimination and ventilation during recovery from supine bicycle exercise 6 to 8 weeks after acute myocardial infarction. 203 36

The effect of carbon monoxide (CO) exposure on hypothalamic brain-stimulation reward (BSR) was examined. Rats were trained in a procedure that daily determined their stimulus duration threshold (SDT), that is, the shortest electrical stimulus to the posterior lateral hypothalamus that would support discrete-trial leverpress responding for BSR. After a stable SDT baseline was established using a single response lever, rats were exposed to 0, 5, 10, 20, and 40 ml/kg pure CO by IP injection. The SDT was significantly elevated by the 40 ml/kg exposure (corresponding to approximately 65% carboxyhemoglobin in the blood) compared to control exposures of an equal volume. No change was observed in response rate at any dose in this 1-lever task. No tolerance was observed when 40 ml/kg CO exposure was repeated on alternating days for 14 exposures, but a small reduction in response rate was observed in this procedure. When rats of a second group were required to alternate responses on two levers some distance apart, SDT was elevated by the highest exposure (40 ml/kg) as before. Additionally, response rate was also significantly suppressed by the highest exposure in this 2-lever task. The results support the view that CO has a direct effect on brain reward systems assessed by the SDT task. Response rate changes due to CO exposure may be due to both direct effects on brain reward systems and other effects such as hypoxia-induced fatigue.
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PMID:Carbon monoxide exposure reduces the rewarding quality of brain-stimulation reward in rats. 204 37

The force-velocity relation of frog sartorius muscle was observed during slow stretch and during shortening in solutions with and without CO2 at extracellular pH (pHo) 6.9 and pHo 7.5 (5 degrees C). Less force was produced with CO2 than without CO2 during stretch, during shortening, and under isometric conditions. Compared with pHo 7.5, the effects were greater at pHo 6.9, where the concentration of CO2, a permeant acid, was greater and would cause a greater acidification of intracellular pH (pHi). The reduction of force caused by CO2 was smaller during stretch than during shortening or isometric contraction. This result indicates that the crossbridge states specific to stretch retain their ability to produce force better under acidic conditions than those characteristic of shortening and isometric conditions. This difference between stretch and shortening suggests that there may be compensating changes in the pattern of motor unit activity during fatigue in vivo.
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PMID:Force during stretch and shortening of frog sartorius muscle: effects of intracellular acidification due to increased carbon dioxide. 211 94

In ten lightly anaesthetized dogs breathing spontaneously, we studied diaphragmatic force generation (Pdi 10, 30, 100 Hz and single twitch) and ventilatory control (P 0, 1, Vt/Ti and respiratory frequency). We found CO2 retention proportional to hypothermia (Fig. 3). The TP was not changed while VMxA and VMxD decreased (Table 1). High frequency fatigue and low frequency potentiation were found (Fig. 1, 2). These changes do not explain CO2 retention which correlated with fall in central drive (P 0, 1, Vt/Ti, Fig. 3, 4) and respiratory timing (respiratory frequency, Fig. 4).
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PMID:[Diaphragmatic strength and ventilatory control in experimental hypothermia]. 213 Feb 40


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