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

Laboratory examination of all birds that were culled or died during an eight-month period in two commerical laying flocks was performed to reveal the causes of disease and their prevalence. The average weekly total of diseased birds was greater in one flock (60-69) than the other (27-37). This resulted mainly from a high incidence in the former flock of leucoses and sarcomas, although losses due to fatty liver syndrome, prolapse and cannibalism and cage layer fatigue were also marginally greater in this flock than the second. Haemangiomas occurred more frequently in the flock with the higher disease level. A total of 273 hens of the 2,000 examined from this flock had single or multiple haemangiomas. Special features of the major causes of disease were outlined and discussed. A conclusion made from this study was that histopathological examination is necessary for accurate diagnosis of avian tumours.
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PMID:Causes of disease in two commercial flocks of laying hens. 118 Jul 72

To clarify the effect of respiratory muscle fatigue on ventilatory response to carbon dioxide, we performed CO2 rebreathing study before and after diaphragmatic fatigue in nine healthy males. Diaphragmatic fatigue was induced by inspiratory resistor loading and confirmed by the increase in Tension Time Index and the decrease in Pdi max at FRC. The effects of diaphragmatic fatigue were as follows: 1) S and B value of VE-CO2 curve did not change. 2) P1-CO2 curve shifted to the left but the slope of the curve did not change. 3) delta Ppl response to CO2 decreased, but delta Pdi response to CO2 did not change. 4) The increase in respiratory accessory muscle EMG was more prominent, compared to diaphragmatic EMG. 5) Rib cage movement became more marked. In conclusion, diaphragmatic fatigue (with 60 percent decrease in Pdi max at FRC) does not affect on ventilatory response to carbon dioxide. To maintain the homeostasis of the chemical ventilatory feedback system, diaphragmatic dysfunction is compensated by the increased activity of respiratory accessory muscles with possible increase in neural drive.
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PMID:[Effect of diaphragmatic fatigue on ventilatory response to carbon dioxide]. 130 16

This study was carried out to test the hypothesis that neuroleptic-induced within-session response decrements reflect a fatigue process, resulting from dopamine depletion, that is present before the session begins but is masked briefly by activational cues present at the start of the session. Response decrementing effects of pimozide were examined in rats lever pressing on random interval schedules of food reinforcement. An initial experiment was carried out to rule out a pharmacokinetic explanation of the response decrement. In a second experiment, the response decrement was not exacerbated by an immediately preceding period of intense forced motor activity (wheel running). Experiments 3 and 4 tested two further predictions: that the pimozide-induced response decrement should be overcome by removing the animal to its home cage and then replacing it in the apparatus (thereby reinstating the activational cues present at the start of the session); and that response impairments should be present from the outset if the animal is confined in the apparatus prior to the start of the session (thereby allowing activational cues to dissipate). Neither prediction was confirmed. Overall, the results provide no support for the dopamine depletion hypothesis.
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PMID:Behavioural tests of the dopamine depletion hypothesis of neuroleptic-induced response decrement. 134 55

The inspiratory muscles can be fatigued by repetitive contractions characterized by high force (inspiratory resistive loads) or high velocities of shortening (hyperpnea). The effects of fatigue induced by inspiratory resistive loaded breathing (pressure tasks) or by eucapnic hyperpnea (flow tasks) on maximal inspiratory pressure-flow capacity and rib cage and diaphragm strength were examined in five healthy adult subjects. Tasks consisted of sustaining an assigned breathing frequency, duty cycle, and either a "pressure-time product" of esophageal pressure (for the pressure tasks) or peak inspiratory flow rate (for the flow tasks). Esophageal pressure was measured during maximal inspiratory efforts against a closed glottis (Pesmax), maximal transdiaphragmatic pressure was measured during open-glottis expulsive maneuvers (Pdimax), and maximal inspiratory flow (VImax) was measured during maximal inspiratory efforts with no added external resistance before and after fatiguing pressure and flow tasks. The reduction in Pesmax) with pressure fatigue (-25 +/- 7%) was significantly greater than the change in Pesmax with flow fatigue (-8 +/- 8%, P less than 0.01). In contrast, the reductions in Pdimax (-11 +/- 8%) and VImax (-16 +/- 3%) with flow fatigue were greater than the changes in Pdimax (-0.6 +/- 4%, P less than 0.05) or VImax (-3 +/- 4%, P less than 0.05) with pressure fatigue. We conclude that respiratory muscle performance is dependent not only on the presence of fatigue but whether fatigue was induced by pressure tasks or flow tasks. The specific impairment of Pesmax and not of Pdimax or flow with pressure fatigue may reflect selective fatigue of the rib cage muscles.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of fatigue on maximal inspiratory pressure-flow capacity. 150 91

Data from the present study indicate a change in the pattern of chest wall muscle recruitment and improved ventilation with pursed-lip breathing (PLB) in COPD. Pursed lip breathing led to increased rib cage and accessory muscle recruitment during inspiration and expiration, increased abdominal muscle recruitment during expiration, decreased duty cycle of the inspiratory muscles and respiratory rate, and improved SaO2. In addition, PLB resulted in no change in pressure across the diaphragm and a less fatiguing breathing pattern of the diaphragm. Changes in chest wall muscle recruitment and respiratory temporal parameters concomitant with the increased SaO2 indicate a mechanism of improving ventilation with PLB while protecting the diaphragm from fatigue in COPD. Alterations in the pattern of respiratory muscle recruitment with PLB may be associated also with the amelioration of dyspnea. Further investigation is necessary to explore the relationship between the pattern of respiratory muscle recruitment during PLB and dyspnea.
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PMID:The pattern of respiratory muscle recruitment during pursed-lip breathing. 172 14

Abnormal physical exhaustion and fatigue are often simply regarded as a natural consequence of pulmonary diseases. Apart from factors not specifically related to pulmonary diseases (e.g. consequences of infections or malignant diseases of the lungs), increased work of breathing due to impaired lung/thoracic cage mechanics, the effects of chronic hypoxia and hypercapnia, the consequences of disturbed sleep and psychosocial factors are mainly responsible for the impaired physical fitness and the fatigue in association with lung diseases. A careful case history including psychosocial aspects and a thorough physical examination are essential for an efficient diagnostic evaluation. Tests of pulmonary function not only in the awake patient at rest, but also during sleep or adequate physical exercise can reveal the causes of impaired physical performance and fatigue related to lung diseases.
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PMID:[Pulmonary causes of abnormal fatigability]. 175 70

A survey was conducted to better understand complaints of fatigue in patients previously diagnosed as having polio. Eighty-six individuals with postpolio syndrome and 20 healthy controls completed a questionnaire about their fatigue, the Beck Depression Inventory, and the CAGE questionnaire. The results showed that fatigue in postpolio syndrome usually occurred on a daily basis and increased in severity as the day progressed. Both the study group and controls described their fatigue as tiredness and a lack of energy. However, physical weakness was reported only in the postpolio group. Minimal physical exercise exacerbated fatigue in 48% of the postpolio group, whereas it diminished fatigue in 70% of the controls and in 15% of the postpolio group. Twenty-seven percent of the postpolio group and none of the controls reported mild to moderate depressive symptoms. However, depression, age, alcohol abuse, and employment status did not significantly affect the differences between groups in reported prevalence or description of chronic fatigue. Criteria to separate psychologic from organic causes of fatigue and treatment interventions are discussed.
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PMID:Fatigue in postpolio syndrome. 199 Oct 11

In COLD, the inspiratory muscles are severely disadvantaged by virtue of the hyperinflation that accompanies this disorder. Such mechanical disadvantage will lead clinically, in the stable patient, to the active recruitment of the accessory muscles of inspiration and to a pattern of rapid, shallow breathing that may be due to either peripheral (muscle) or central (neurogenic) influences thought to be linked to a critical tension-time index of the inspiratory muscles. This pattern appears to be all the more pronounced in the patient with acute respiratory failure and is frequently accompanied by disordered rib cage-abdominal movements. While these movements may reflect the muscles' attempts to stave off fatigue, they may also imply that if the imposed mechanical stress is unrelieved, muscle failure will ensue. In the laboratory, mechanical disadvantage is marked by diminished inspiratory mouth pressures. Because of wide scatter, a low mouth pressure beyond that which can be explained by hyperinflation alone should be confirmed by an assessment of Pesosniff or by the measurement of transdiaphragmatic pressure. Muscle endurance, also compromised in this condition, can be assessed indirectly by the measurement of MVV or MSVC, or more directly by an invasive assessment of the tension-time index and endurance time of the diaphragm or noninvasively by the Endurance Index of McKenzie and Gandevia. And finally, once muscle failure is pending or has been established, a program of muscle rest, either complete or partial, pharmacotherapy, and goal-specific training should be instituted.
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PMID:Assessment of respiratory muscle dysfunction in chronic obstructive lung disease. 218 36

A number of age-related anatomical and physiological factors place the respiratory system of the neonate and young infant in a potentially vulnerable position during disease states. Maintenance of a lung volume necessary for effective gas exchange is compromised by the floppy chest wall, the relatively stiff lungs and the horizontal position of the body. Respiratory muscles are prone to fatigue in case of increased respiratory loads and fail to move the rib cage efficiently. Many signs of lower airway disease, observed during the physical examination of the young infant, can be related to these factors. Awareness of them helps in the interpretation of these symptoms in order to make the correct diagnosis and to initiate treatment.
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PMID:[The dyspneic infant. Interpretation of symptoms of lower airway disorders in the first year of life]. 231 4

This review describes the movements of the parts of the chest wall (rib cage and abdomen) that occur during anaesthesia and operation. Methods of assessing these movements are reviewed and a simple model is used to illustrate the actions of the muscle groups involved, which are: the diaphragm, those of the rib cage, and of the abdomen. The control of these muscle groups, the forces that they generate, and the movements that can result are discussed. It is not possible to infer the action of these muscle groups from surface measurements alone. In particular, rib cage and abdominal movements do not necessarily indicate the separate actions of rib cage muscles and diaphragm. The changes in volume that occur in the chest wall on induction of anaesthesia are reviewed. The pattern of chest wall movement in the conscious subject, during anaesthesia with either spontaneous or artificial ventilation, and after operation is described, and the mechanisms of the changes that occur are discussed. Aspects of movements in respiratory failure and muscle fatigue are introduced.
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PMID:Chest wall movements in anaesthesia. 265 39


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