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

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

Of 56 middle-aged male joggers (mean age 43.3 yr), 38 were measured for maximal oxygen uptake (VO2max) and 18 for cardiac output at a heart rate of 170 bpm (Q170). Each Q170 was divided by subject body surface area to yield cardiac index (CI170). A treadmill protocol was used to elicit maximal exercise during measurement of VO2max. The bicycle ergometer was employed when measuring Q170. For maximal exercise, termination was upon subject-declared fatigue. In subjects measured for VO2max, heart rate at 3.5 miles/h and 5% treadmill grade (HRsubmax) as well as heart rate at maximal exercise (HRmax) were noted. Heart rates were monitored electrocardiographically. A modified Douglas bag technique was applied when sampling expired air for determination of VO2max. Carbon dioxide rebreathing was used to estimate Q170. Data were grouped according to age (43 yr and older; 42 yr and younger). There were significant (P less than 0.05) positive relationships between VO2max and HRmax and between HRsubmax and age. Significant negative relationships existed between HRmax and HRsubmax, and between CI170 and 10 km running time. There were no significant differences (P greater than 0.05) between means achieved by the age groups. The overall mean for VO2max was 43.36 ml/kg per min and for Q170 33.53 1/min. Findings suggest that men who remain physically active retain youthful characteristics of cardiorespiratory function.
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PMID:Physical fitness in aging men. 407 25

The endogenous opioids seem likely to be assigned a significant role in the integrated hormonal and metabolic response to exercise. This article reviews the present evidence on exercise and the endogenous opioids, and examines their involvement in a number of widely disparate physiological processes. In considering the role of individual opioid peptides, it is important to remember that many of the tools and techniques now used are still relatively crude. Most studies have demonstrated that serum concentrations of endogenous opioids, in particular beta-endorphin and beta-lipotrophin, increase in response to both acute exercise and training programmes. Elevated serum beta-endorphin concentrations induced by exercise have been linked to several psychological and physiological changes, including mood state changes and 'exercise-induced euphoria', altered pain perception, menstrual disturbances in female athletes, and the stress responses of numerous hormones (growth hormone, ACTH, prolactin, catecholamines and cortisol). Many reports have described a role for the endorphin response as seen during exercise and have used the opioid receptor antagonist, naloxone, to investigate and verify the degree of involvement of the opioids. However, whether the observed increases in peripheral endorphin concentrations are sufficient to cause immediate mood changes, create menstrual cycle dysfunction or alter pain perception is still not resolved. A relatively new implication for the endorphins and associated changes with exercise is in ventilatory regulation. A number of studies have suggested that endogenous opioids depress ventilation and may, therefore, play a role in ventilatory regulation by carbon dioxide, hypoxia and exercise. It may also be possible that during exercise, the perception of fatigue is modulated by an increase of endogenous opioids.
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PMID:Endorphins and exercise. 609 Dec 17

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

The capacity to sustain an increase in ventilation (VE) sufficient to decrease the end-tidal partial pressure of carbon dioxide (PETCO2) by about 10 mm Hg was studied in six hypercapnic patients with moderate to severe chronic airflow limitation (CAL). Patients could continue such an increased VE for a finite time (range 5 to 54 minutes). During hyperventilation (H), ventilation was approximately doubled and represented 77.1 +/- 8.4 (mean +/- SE) percent of maximum voluntary ventilation, mean oxygen consumption (VO2) increased 44 percent (p less than 0.005) and mean inspiratory pleural pressure (Ppl) swings were 43.8 +/- 10.5 percent of maximum Ppl. Four patients achieved reductions of PETCO2 less than 10 mm Hg, and two patients achieved or exceeded the target decrease in PETCO2. The decrease in PaCO2 was correlated with the wasted ventilation ratios (VD/VT) during H, the greatest decrease in PaCO2 being related to the lowest VD/VT (p less than 0.05). Electromyographic (EMG) evidence of inspiratory muscle fatigue developed in four of the six patients during H. Five normal subjects achieved an equal or greater decrease in PETCO2, and none showed EMG evidence of inspiratory muscle fatigue. We conclude that, although impaired gas exchange limits the capacity to voluntarily reduce the PaCO2, the development of respiratory muscle fatigue in some patients with CAL may also contribute by limiting the capacity to sustain the substantial increase in respiratory muscle work done in the attempt.
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PMID:Endurance of hyperventilation in chronic airflow limitation. 640 5

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


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