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

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

We quantified the mechanical work of breathing in six normal subjects during assisted mechanical ventilation. Using two volume-cycled ventilators of different design, we investigated the influence of minute ventilation (VE) and machine settings of trigger sensitivity and flow during CO2-driven hyperventilation to moderate and high levels (12-24 L/min). Work estimates were derived from plots of esophageal and airway pressure against inflation volume. Peak flow and trigger sensitivity were important determinants of the energy expended, and for each combination of machine settings the work done by the subject per liter of ventilation increased with VE. During assisted ventilation the subject expended energy equivalent to 33-50 percent of the work of passive inflation, even under the most favorable conditions of VE, sensitivity and flow. Under the least favorable conditions of VE, sensitivity and flow, the subject's inspiratory work of breathing substantially exceeded the energy needed by the ventilator to inflate the passive thorax. These observations imply that exertion of the respiratory muscles continues throughout inflation during assisted mechanical ventilation and call attention to the possibility that inappropriate selection of ventilatory mode or machine settings may contribute to respiratory muscle fatigue and dyspnea.
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PMID:The inspiratory work of breathing during assisted mechanical ventilation. 398 73

The purpose of this study was to compare the methods used to identify abrupt changes in ventilation or plasma lactate (LA) during exercise. Ten males randomly performed a 1-, 3-, and 5-min, 30-W incremental cycle ergometer test to fatigue. The first change in VE and VCO2 relative to VO2 (ventilation threshold, VT1) was determined from plots of VE, VE X VO2-1, and excess CO2 vs VO2. Data were also analyzed for a second change in VE (VT2) relative to both VCO2 and VO2 using plots of VE and VE X VCO2(-1) vs VO2 and semi-log plots of VE X VO2(-1) and VE X VCO2(-1) vs VO2. Arterialized blood samples were taken each 1.0, 1.5, or 2.5 min for the 1-, 3-, and 5-min tests, respectively, to determine the LA threshold (LT) and the onset of blood lactate accumulation (4 mM, OBLA) and 1, 2, 5, 7.5, and 10 min after all tests to calculate the individual anaerobic threshold (IAT). At weekly intervals, subjects also exercised for 10 min at eight different power outputs (W) to define the onset of plasma lactate accumulation (OPLA). Results showed that VO2max was significantly higher for the 1-min (3.88 l X min-1)vs the 3- or 5-min tests (3.65 l X min-1). With increasing W duration, VT1 from either VE or VE X VO2-1 vs VO2 were similar (1.77 vs 1.72 l X min-1) but significantly lower using excess CO2 (1.23 l X min-1) . VO2 at LT (1.62 l X min-1) and OPLA (1.73 l X min-1) were similar to VT1.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Ventilatory and plasma lactate response with different exercise protocols: a comparison of methods. 398 12

Our aim was to determine whether inspiratory muscle fatigue changes breathing pattern and whether any changes seen occur before mechanical fatigue develops. Nine normal subjects breathed through a variable inspiratory resistance with a predetermined mouth pressure (Pm) during inspiration and a fixed ratio of inspiratory time to total breath duration. Breathing pattern after resistive breathing (recovery breathing pattern) was compared with breathing pattern at rest and during CO2 rebreathing (control breathing pattern) for each subject. Relative rapid shallow breathing was seen after mechanical fatigue and also in experiments with electromyogram evidence of diaphragmatic fatigue where Pm was maintained at the predetermined level during the period of resistive breathing. In contrast there was no significant difference between recovery and control breathing patterns when neither mechanical nor electromyogram fatigue was seen. It is suggested that breathing pattern after inspiratory muscle fatigue changes in order to minimize respiratory sensation.
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PMID:Effect of inspiratory muscle fatigue on breathing pattern. 405 95

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 (Pa CO2), increases and hypercapnic respiratory failure ensues. It has also been suggested that such a dysfunction of the respiratory muscles contributes to the pathogenesis of dyspnoea. 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, including the study of pressures created by muscular contraction, and electromyography.
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PMID:[Fatigue of the respiratory muscles]. 623 98

Several reports have suggested that the nervous system can be affected by exposure to electric fields and that these effects may have detrimental health consequences for the exposed organism. The purpose of this study was to investigate the effects of chronic (30-day) exposure of rats to a 60Hz, 100-kV/m electric field on synaptic transmission and peripheral-nerve function. One hundred forty-four rats, housed in individual polycarbonate cages were exposed to uniform, vertical, 60-Hz electric fields in a system free of corona discharge and ozone formation and in which the animals did not receive spark discharges or other shocks during exposure. Following 30 days of exposure to the electric field, superior cervical sympathetic ganglia, vagus and sciatic nerves were removed from rats anesthetized with urethan, placed in a temperature-controlled chamber, and superfused with a modified mammalian Ringer's solution equilibrated with 95% O2 and 5% CO2. Several measures and tests were used to characterize synaptic transmission and peripheral-nerve function. These included amplitude, area, and configuration of the postsynaptic or whole-nerve compound-action potential; conduction velocity; accommodation; refractory period; strength-duration curves; conditioning-test (C-T) response, frequency response; post-tetanic response; and high-frequency-induced fatigue. The results of a series of neurophysiologic tests and measurements indicate that only synaptic transmission is significantly and consistently affected by chronic (30-day) exposure to a 60-Hz, 100-kV/m electric field. Specifically, and increase in synaptic excitability was detected in replicated measurements of the C-T response ratio. In addition, there are trends in other data that can be interpreted to suggest a generalized increase in neuronal excitability in exposed animals.
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PMID:Chronic exposure to a 60-Hz electric field: effects on synaptic transmission and peripheral nerve function in the rat. 626 52

Isolated extensor digitorum longus muscles from rat were exposed to atmospheres of 30% CO2 (high-CO2 muscles) or 6.5% CO2 (control muscles) in O2 for 95 min. Muscle contraction characteristics were studied before and after the incubation. Tetanic tension decreased in high-CO2 muscles to 55% of initial value but remained unchanged in control muscles. Relaxation time was prolonged in high-CO2 muscles but not in control muscles. Intracellular pH was 6.67 +/- 0.04 (SD) in high-CO2 muscles and 7.01 +/- 0.04 in control muscles. CO2-induced acidosis had a marked influence on the intermediary energy metabolism as shown by a fourfold increase of glucose 6-phosphate, a 14% increase of ADP, and a decrease of phosphocreatine to 44% of the control value. Lactate and pyruvate contents were unchanged. The observed metabolic changes can be explained by an effect of H+ on the activity of phosphofructokinase and on the creatine kinase equilibrium. It can be concluded that H+ concentration causes muscular fatigue. It is, however, uncertain whether this is an effect of increased H+ per se or by high-energy phosphate depletion induced by acidosis.
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PMID:Fatigue and phosphocreatine depletion during carbon dioxide-induced acidosis in rat muscle. 640 27

Previous research indicates that fatiguing static exercise causes hyperventilation and a decrease of end-tidal CO2 partial pressure PETCO2. The objectives of this study were 1) to examine the changes in pattern of breathing during static exercise, and 2) to define the isocapnic ventilatory response. Six healthy males were studied once a week at one of three levels of static handgrip exercise: 15, 25, or 30% maximum voluntary contraction (MVC) was sustained for 5 min while holding PETCO2 constant or allowing it to run free. During 25 and 30% MVC, we observed 1) progressive increases in mean tidal volume (VT), inspiratory ventilation (VI), VT/TI, heart rate (HR), and arterial BP, 2) increased breath-to-breath variability of VT, 3) no significant changes in respiratory frequency (f), and 4) progressive decreases in PETCO2. Keeping PETCO2 constant at preexercise levels did not change the pattern or magnitude of the ventilatory response to exercise. The time course and magnitude of the subjects' perceived effort resembled the time course and magnitude of the ventilatory response. The variability of VT during the response to static exercise suggests an element of control instability. The identical ventilatory responses during hypocapnic and isocapnic conditions may result from the slow response of the central chemoreceptors; an overriding influence of muscle afferents; and/or increased central command arising with fatigue.
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PMID:Ventilatory responses to static handgrip exercise. 640 57

Four normal subjects and 5 patients with chronic obstructive pulmonary disease (COPD) (mean FEV1, 1.03 L) had frequency:force curves of their sternomastoid muscle measured before and 5 min after a 12-min walk on a flat treadmill, a progressive exercise test (normal subjects only), and a 10-min period of sustained maximal voluntary ventilation (SMVV). Before each test, all subjects had a normal frequency:force curve, and the ratio of the force response at 20 Hz to that at 50 Hz was normal. After SMVV, all the normal subjects and 4 of the 5 patients developed a greater than 15% fall in 20:50 ratio, and this was taken to indicate the presence of low frequency fatigue (LFF). During SMVV, all the subjects achieved minute ventilation greater than 70% of predicted maximal breathing capacity (MBC). During the 12-min walk, all the patients exceeded 70% MBC, and 4 developed LFF. The normal subjects performing progressive exercise also exceeded 70% MBC, and all showed LFF. The 12-min walk did not cause LFF in the normal subjects, but no subject reached 70% of MBC. Despite the presence of LFF in the sternomastoid muscle, the patients were all able to walk the same distance during a second 12-min walk. In both the normal and patient groups, the ventilatory response to CO2 was not changed by the presence of LFF. There were no changes in maximal inspiratory and expiratory mouth pressures or spirometry with LFF. High, sustained levels of minute ventilation cause sternomastoid LFF, but the clinical significance of this phenomenon is not yet certain.
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PMID:Sternomastoid muscle function and fatigue in normal subjects and in patients with chronic obstructive pulmonary disease. 642 15


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