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

1 We have studied the effects of single oral doses of 80 mg propranolol and 100 mg metoprolol on the cardiovascular and respiratory responses to progressive exercise in nine healthy men in double-blind, placebo-controlled experiment. As judged by their effects on exercise heart rate and cardiac output the doses of the two drugs used were equivalent. 2 Beta-adrenoceptor blockade reduced oxygen consumption by 3.5% over the whole work range with an increase in the respiratory exchange ratio of 0.056 units. Carbon dioxide production and exercise ventilation were unchanged. The two drugs had similar effects. Possible mechanisms for these observations are discussed. 3 Perceived exertion during exercise was increased by both the beta-adrenoceptor blocking drugs and this may be of relevance to the symptom of fatigue reported by patients on these drugs. Endurance, assessed as either total work done or maximal work achieved, was reduced by 15%.
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PMID:The effect of beta-adrenoceptor blockade on factors affecting exercise tolerance in normal man. 3 85

Digitalis and diuretics constitute conventional therapy of congestive heart failure, but systemic vasodilators offer an innovative approach in acute and chronic heart failure of decreasing increased left ventricular systolic wall tension (ventricular afterload) by reducing aortic impedance and/or by reducing cardiac venous return. Thus, vasodilators increase cardiac output (CO) by diminishing peripheral vascular resistance (PVR) and/or decrease increased left ventricular end-diastolic pressure (LVEDP) (ventricular preload) by diminishing venous tone. Concomitantly, there is reduction of myocardial oxygen demand, thereby reliably reducing angina pectoris in coronary disease, and potentially limiting infarct size and ischemia provided systemic arterial pressure remains normal. The vasodilators produce disparate modifications of cardiac function depending upon their differing alterations of preload versus impedance: nitrates principally cause venodilation (decrease LVEDP); nitroprusside, phentolamine and prazosin produce balanced arterial and venous dilation (decrease LVEDP and increase CO) provided left ventricular filling pressure is maintained at the upper limit of normal; whereas hydralazine predominantly effects arteriolar dilation (increases CO). With depressed CO plus highly increased LVEDP and increased PVR, nitrates also induce some increase of CO by reducing PVR. Combined nitroprusside and dopamine synergistically enhance CO and decrease LVEDP. Mechanical counterpulsation aids nitroprusside in acute myocardial infarction. The 30-minute venodilator action of sublingual nitroglycerin is extended for 4 to 6 hours by cutaneous nitroglycerin ointment, by sublingual and oral isosorbide dintrate, and by oral pentaerythritol tetranitrate and sustained-release nitroglycerin capsules. Ambulatory oral vasodilator therapy is provided by long-acting nitrates (relieve pulmonary congestion); hydralazine (improves fatigue); prazosin alone, combined nitrate-hydralazine combined prazosin-hydralazine (improve both dyspnea and fatigue).
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PMID:Afterload reduction and cardiac performance. Physiologic basis of systemic vasodilators as a new approach in treatment of congestive heart failure. 9 30

Reduction in pH is known to decrease O2 affinity (Bohr effect) and increase the rate of O2 release from blood. It provides a potential mechanism for increasing O2 transport to the myocardium. Fifteen patients with refractory, chronic angina were studied by treadmill exercise tolerance tests and whole blood-oxygen release rate measurements before and 4 days after beginning treatment with oral acetazolamide (10 to 20 mg/kg body weight). Positive treadmill exercise test or myocardial necrosis was present in each case. There was a correlation between an increased O2 release rate from blood and relief of symptoms. The major side effect in 2 patients with pathologic fatigue believed to result from acidosis. Of the 7 patients who obtained relief from angina, in each there was a 27% increase in the rate of release of O2 from their whole blood. Seven patients did not obtain relief; they showed no change in the rate of release. In the 4 patients who became worse the rate of deoxygenation decreased by 22%. All changes in deoxygenation rate coincided with the clinical findings. The treatment of ischemic heart disease with acetazolamide or other acidifying agents should not, however, be attempted until further investigation establishes their clinical value.
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PMID:Effect of acidosis on patients with myocardial ischemia. 24 34

Nine patients on intermittent mandatory ventilation (IMV) and continuous positive airway pressure (CPAP) were allowed to breathe spontaneously at varying end expiratory pressure-end inspiratory pressure (EEP-EIP) gradients up to 10 cm H2O. There was no change in the mean cardiac output and oxygen delivery despite a lowered mean airway pressure (MAWP) when the gradient was increased. Three patients were uncomfortable at the higher gradients and another manifested evidence of fatigue of the muscles of respiration by raising her arterial PCO2 (PaCO2) and intrapulmonary shunt (Qs/Qt). In view of the difficulty experienced by some patients and lack of improvement in cardiac outputs (CO) during spontaneous inspiration when the EEP-EIP gradient is raised from zero to 5 and 10 cm H2O, it is recommended that the variation in airway pressure during spontaneous breaths while a patient is on CPAP be minimized.
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PMID:Hemodynamic and respiratory response to varying gradients between end-expiratory pressure and end-inspiratory pressure in patients breathing on continuous positive airway pressure. 35 Dec 5

Performance characteristics of the central nervous, cardiovascular, respiratory and muscular systems in man postoperatively have received little investigative attention, despite the well known syndrome of postoperative fatigue. The impairmen in perception and psychomotor skills that has been shown to result from caloric restriction, bedrest, sedation and sleep deprivation suggests that a similar deficit may occur after surgical procedures. After a simple elective surgical procedure, maximal oxygen uptake decreases and the adaptability of heart rate to submaximal workloads is impaired. Similar deleterious effects on cardiorespiratory performance have been documented with starvation and bedrest; an understanding of cardiorespiratory performance postoperatively awaits further investigation. Maximal muscular force of contraction is also impaired by caloric restriction and bedrest, suggesting that similar effects may be seen in the postoperative state, although this has not been studied. A better understanding of the syndrome of postoperative fatigue could be achieved by a descriptive analysis of physiologic performance postoperatively. Such descriptive data could form the basis for objective evaluation of therapeutic measures intended to improve performance, such as nutritional supplementation and pharmacologic intervention. The observation that exercise with the patient in the supine position may decrease the impairment in maximal aerobic power otherwise expected in immobilized patients suggests that controlled exercise therapy may be of value in reducing physiologic impairment postoperatively.
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PMID:Understanding postoperative fatigue. 35 38

An extended period of recovery of vascular resistance, far outlasting the recovery period of oxygen consumption, follows exercise of dog skeletal muscle when flow is restricted relative to the intensity of the exercise pattern. The duration of this postexercise prolonged vasodilation is graded and is related to the blood flow, duration of muscle stimulation, fatigue of the muscles, and total muscle tension development. To test whether prolonged vasodilation is mediated by prostaglandins or histamine, the prostaglandin synthetase inhibitors indomethacin or meclofenamate and the antihistamine tripelennamine were administered intravenously to anesthetized dogs between two 20-min exercise bouts of the anterior calf muscles at 4 twitches/s. Blood flow was held constant at approximately 20 ml 100 g-1 min-1, typically resulting in a venous O2 content below 2.0 ml/100 ml during exercise. The duration of vascular resistance recovery was evaluated by measuring the time at which vascular resistance returned to 90% (t90) of the recovery level (mean +/- SE). All the drugs caused a significant decline in the t90, but none reduced the recovery time to that following free-flow exercise, where the t90 is less than 1 min and the return of vascular resistance parallels the return of oxygen consumption to control. Thus, prostaglandin and/or histamine release may be at least partially responsible for prolonged vasodilation.
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PMID:Prostaglandin and histaminergic mediation of prolonged vasodilation after exercise. 40 1

Ozone (O3) at near ambient smog alert levels has previously been shown to cause alterations in pulmonary function and exercise response in humans. The present study was designed to investigate the effects of O3 administered during graded bicycle exercise to volitional fatigue on work performance and maximal oxygen uptake (VO2max). Nine subjects performed three tests each while breathing either 0.00, 0.15, or 0.30 ppm O3. Forced vital capacity, residual volume, maximal midexpiratory flow rate, and forced expiratory volume in 1 s were assessed before, immediately after, and 4 h after exercise. O3 exposure resulted in no significant effect on maximal work rate, anaerobic threshold, or any pulmonary function parameter. However, maximal expired minute ventilation was decreased (P less than 0.05) in a dose dependent fashion. Thus, exercise ventilation during maximal work was a more sensitive indicator of the effects of O2 exposure than were standard pulmonary function tests. Although subjective symptoms of discomfort were reported more frequently with increased O2 level, it was concluded that exposure of healthy young men to as much as 0.30 ppm O2 for no more than 30 min of progressively incremented exercise to volitional fatigue, is insufficient to cause a significant decrease in work capacity or V02 max.
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PMID:Effects of oxone inhalation on work performance and VO2 max. 42 46

1 The accumulation of glucose in the brain produced by the administration of phosphatidylserine liposomes into mice has been studied by measurement of the cerebral contents of glycolytic intermediates and high-energy compounds. 2 With a normal supply of oxygen to the brain, inhibition of glycolysis is indicated mainly at the phosphofructokinase step. The ratio of glucose-6-phosphate to fructose-1,6-diphosphate increased, whereas the levels of pyruvate and especially lactate decreased. 3 Under conditions of cerebral ischaemia, the administration of phosphatidylserine delays glycogen mobilization and ATP use. As a consequence of decreased energy utilization, the brain adenylate energy charge remains at a high level. 4 It is concluded that the phosphatidylserine-induced glucose accumulation in the brain is due to reduced energy expenditure and therefore to a decrease in carbohydrate consumption. The inhibition of glycolysis by the high level of adenylate energy charge is probably the control mechanism explaining the decreased carbohydrate utilization.
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PMID:Pharmacological effects of phosphatidylserine liposomes: regulation of gylcolysis and energy level in brain. 46 67

Field tests are used in many occupations to screen and classify personnel for cardiorespiratory fitness. Presumably these tests yield predictive results which correlate well with maximal oxygen uptake (VO2 max), the most widely-accepted criterion of cardiorespiratory fitness. The purpose of this study was to validate one of the most popular field tests, the modified Kasch Pulse Recovery Step Test (KPRST), used by several emergency service agencies in Southern California. One hundred fourteen male state traffic officers from the California Highway Patrol, ranging in age from 24 to 56 years, performed treadmill VO2 max tests to volitional fatigue and the modified KPRST. Heart rates taken during the first and last 10 seconds of the one-minute recovery period for the modified KPRST compared against treadmill VO2 max values yielded correlations of --0.25 and --0.27, respectively, indicating that the modified KPRST is a poor predictor of cardiorespiratory fitness for the population studied. These results suggest that agencies should carefully validate any predictive measure of cardiorespiratory health and performance before adopting that measure for screening purposes and cardiorespiratory classification.
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PMID:Validation of a bench stepping test for cardiorespiratory fitness classification of emergency service personnel. 50 56

Dyspnea is the medical term for the patient's or subject's complaint of shortness of breath. It encompasses the respiratory discomfort experienced in many different diease states as well as the shortness of breath felt by a normal subject during or after strenuous exercise. Several parameters which have been shown to correlate with the onset or severity of dyspnea are described, including reduced vital capacity, the ratio of minute ventilation to vital capacity, reduced breathing reserve, the work of breathing, and the oxygen cost of breathing. Attempts at quantitation of dyspnea have usually consisted of measuring physiological parameters associated with the sensation, such as the "dyspneic index". The direct measurement of respiratory sensations using modern psycho-physical methods is at an early stage of development. Since the observation that the existence of dyspnea is often unrelated to any disturbance of arterial blood gas composition, it has been generally held that the mechanism of dyspnea is primarily neurophysiological. The neural pathways may conceptually be divided into those which transmit the "dyspnea message" from the respiratory apparatus to integrating centers in the brain, and those concerned with subsequently bringing the sensation to the level of consciousness. It seems likely that there is no single sensing mechanism and neural pathway which will be able to explain dyspnea in the diverse populations of patients and subjects who experience unpleasant respiratory sensations. Three theories concerning mechanisms of dyspnea are briefly described: "length-tension inappropriateness", vagal afferent activity especially from the J-receptors, and the recent concept of diaphragmatic fatigue. Some specific characteristics of the shortness of breath experienced in certain disease states are described, including chronic bronchitis and emphysema, bronchial asthma, pulmonary fibrosis and congestive heart disease.
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PMID:Dyspnea. 50 81


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