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

It has recently been postulated that diaphragm fatigue may be due, at least in part, to a form of low-grade injury to subcellular organelles. Moreover, several studies have shown that thiol-containing compounds can protect cardiac and striated skeletal muscle organelles from the deleterious effects of a number of physiological stresses. The purpose of the present study was to determine whether pretreatment with N-acetylcysteine (NAC), a thiol-containing compound, would attenuate the rate of development of diaphragmatic fatigue. Studies were performed with the use of an in situ rabbit diaphragm strip preparation that permitted direct and continuous measurement of diaphragm tension development. Diaphragm fatigue was induced by rhythmically stimulating strips to contract at 30/min (20-Hz trains) for 20 min. The diaphragm force-frequency relationship (10-, 20-, 50-, and 100-Hz stimuli) was assessed immediately before and after fatigue trials and then again 20 min into the period of recovery. Half the animals were treated with intravenous NAC before fatigue, whereas the remaining animals were given intravenous saline. The rate of development of fatigue was markedly greater in saline-treated control than in NAC-treated animals, with reductions in tension of 55 +/- 3 and 34 +/- 3%, respectively, in these two groups of animals over 20 min (P less than 0.001). Although rhythmic stimulation resulted in a downward shift in the force-frequency relationship in both NAC- and saline-treated animals, the magnitude of this shift was substantially greater in saline-treated animals (P less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of N-acetylcysteine on diaphragm fatigue. 236 12

The influence of prolonged nutritional deprivation on the succinate dehydrogenase (SDH) activity and cross-sectional areas of individual fibers in the rat diaphragm and deep portion of the medial gastrocnemius (MGr) muscles was determined. Fatigue resistance of the diaphragm was measured by means of an in vitro nerve-muscle strip preparation. Fiber SDH activity and cross-sectional area were quantified by means of an image processing system. Diaphragm fatigue resistance was significantly improved in the nutritionally deprived (ND) group. In both muscles, nutritional deprivation resulted in a significant decrease in fiber cross-sectional area (both type I and II), type II fibers showing greater atrophy. The SDH activities of type I and II fibers in the diaphragm were not affected by nutritional deprivation. This contrasted with a significant decrease in the SDH activity of both type I and II fibers in the MGr of ND animals. An assessment of the interrelationships between fiber atrophy and fiber SDH activity revealed a greater effect of malnutrition on those diaphragm type II fibers that had the lowest relative SDH activities and the largest cross-sectional areas. By comparison, the effect of malnutrition on type I and II fibers in the MGr was nonselective with regard to fiber SDH activity. We conclude that the enhanced diaphragm fatigue resistance in the ND animals does not result from an increase in the oxidative capacity of muscle fibers and is best explained by the pattern of diaphragm muscle fiber atrophy.
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PMID:Effects of undernutrition on diaphragm fiber size, SDH activity, and fatigue resistance. 274 85

The effect of high-intensity trained (6 X 4.5 min at 40 m/min, 15% grade, 2.5-min rest between bouts, 5 days/wk, for 6 wk) on contractile, biochemical, and fatigue properties of the rat diaphragm were examined. The exercise program produced significant elevations in the mitochondrial marker enzyme citrate synthase (mumol X g-1 X min-1) in the soleus (SOL) (27.2 +/- 1.5 vs. 46.7 +/- 2.4; mean +/- SE), deep vastus lateralis (DVL) (40.8 +/- 2.6 vs. 58.3 +/- 2.8), and superficial vastus lateralis (SVL) (8.5 +/- 0.6 vs. 11.4 +/- 0.7). No significant differences were observed in the crural (CRU) (45.9 +/- 2.0 vs. 44.0 +/- 2.3) or ventral costal (VEN) (41.5 +/- 2.0 vs. 45.8 +/- 2.6) diaphragmatic regions. Phosphofructokinase, the rate-limiting enzyme of glycolysis, significantly increased in the SOL (19.0 +/- 0.8 vs. 23.3 +/- 1.3 mumol X g-1 X min-1) and DVL (69.3 +/- 6.0 vs. 86.6 +/- 5.0), but no alterations were seen in the SVL (98.6 +/- 5.7 vs. 106.1 +/- 9.0), CRU (54.4 +/- 2.8 vs. 53.8 +/- 1.5), or VEN (44.7 +/- 2.4 vs. 46.4 +/- 1.4) posttraining. Diaphragm contractile properties, with the exception of an increased rate of fall in twitch tension, remained unchanged after training. Glycogen values were significantly higher in trained diaphragms at rest (6.54 +/- 0.39 vs. 4.86 +/- 0.41 mg/g) and during 1, 5, and 10 min of fatiguing stimulation. During fatigue no differences were observed in force, rate of rise in force, rate of fall in force, muscle lactate, ATP, or creatine phosphate in trained vs. control.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Contractile and biochemical properties of diaphragm: effects of exercise training and fatigue. 294 Feb 18

Diaphragm function is thought to depend on the balance between diaphragm blood flow and metabolic demand. If blood flow is inadequate, fatigue should ensue. Likewise, in the presence of fatigue, function should improve when blood flow is increased. To test this hypothesis, we evaluated the effect of increasing blood flow to the fatigued diaphragm. Studies were performed on anesthetized, mechanically ventilated dogs in which strips of costal diaphragm were developed in situ. Strip tension was measured with an isometric tension transducer. The inferior phrenic artery supplying the strip was cannulated and pump perfused at a pressure of 92 +/- 3 mm Hg; phrenic artery flow and pressure were continuously monitored with in-line doppler flow probes and pressure transducers, respectively. Fatigue was produced by electrically stimulating strips to contract 15 times/min (initial tension 80% of maximum, duty cycle 50%). Rhythmic contraction resulted in a downward shift in the diaphragm force-frequency relationship in all strips. In eight strips, stepwise increments in phrenic artery perfusion pressure to 161 +/- 8 and 281 +/- 17 mm Hg were produced by increasing pump speed at 6 and 8 min into rhythmic stimulation; in four strips, phrenic artery perfusion pressure was increased to 152 +/- 20 and 257 +/- 32 mm Hg at 20 and 25 min into rhythmic stimulation, respectively. Each increase in phrenic artery pressure resulted in increases in phrenic artery flow and diaphragm tension and produced an upshift in the diaphragm force-frequency relationship.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Reversibility of diaphragm fatigue by mechanical hyperperfusion. 297 61

An experimental study was performed to determine the main site of fatigue associated with diaphragm pacing. Using 24 mature mongrel dogs, weighing 7.5 to 12.7 kg, direct phrenic nerve pacing was conducted from the right cervical area at three different respiration rates, 37 (Group 1, n = 6), 25 (Group 2, n = 6) and 12 (Group 3, n = 6) times per minute, under fixed stimulation conditions (pulse duration, 200 microseconds; frequency, 25 Hz; pulse train repetition time, 1.2 sec). Diaphragm fatigue was defined as the reduction in transdiaphragmatic pressure (Pdi) to less than or equal to 60% of the initial value. In each animal, tidal volume (Vt), induced muscle action potential (Edi), conduction time (CT) and electrical current (E) between two electrodes were examined at various periods until fatigue. In addition, after fatigue, aminophylline (10 mg/kg) was injected and each parameter was observed for an additional 45 min. In 10 animals, the polarity of stimulation was changed from anodal to cathodal current after fatigue and changes in Pdi and Edi were examined. The time to fatigue was 70 +/- 20 min for Group 1, 149 +/- 48 min for Group 2, and 371 +/- 97 min for Group 3, showing a significant stimulation rate dependency (P less than 0.05). Vt and Edi showed a significant decrease (P less than 0.05) at fatigue in all of the groups. However, no significant differences of CT and E were seen between pre- and postfatigue values. Pdi and Edi did not change even when polarity was changed after fatigue. Following administration of aminophylline, Pdi showed a significant (P less than 0.05) increase over time in all groups: 19.8 +/- 13.5% at 5 min, 23.0 +/- 13.5% at 15 min, and 16.2 +/- 14.9% at 30 min for Group 1; 23.6 +/- 11.6% at 5 min, 27.3 +/- 15.5% at 15 min, and 19.0 +/- 16.1% at 30 min for Group 2; and 29.9 +/- 21.1% at 5 min, 29.5 +/- 18.6% at 15 min, 22.3 +/- 13.8% at 30 min, and 15.5 +/- 13.4% at 45 min for Group 3. In contrast, administration of aminophylline caused no significant changes in Edi. Based upon the finding that aminophylline was significantly effective at the time of diaphragm fatigue, it is concluded that fatigue of the muscle itself constitutes one of the contributing factors for the fatigue phenomenon associated with diaphragm pacing.
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PMID:Experimental study on diaphragm fatigue during diaphragm pacing. 326 19

Thirty years of clinical and technical research have produced a reliable apparatus for diaphragm pacing. This entails electrical stimulation to the phrenic nerve by a remote radio-frequency transmitter. Prerequisites for diaphragm pacing are adequate alveolar gas exchange, an intact phrenic nerve and diaphragm muscle, and a co-operative patient for the prolonged period of rehabilitation. Diaphragm pacing has been used in cases of central alveolar hypoventilation and chronic obstructive airway disease, as well as for lesions of the cervical cord. To avoid fatigue and possible irreversible injury to the muscle, the right and left hemidiaphragms are paced alternately. We demonstrate the effectiveness of diaphragm pacing for long-term artificial respiration in a patient with transection of the cord at C3/4. The decisive benefit of diaphragm pacing for the quadriplegic patient is that it renders him free of dependence on a mechanical ventilator with its associated social and psychological impediments.
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PMID:Diaphragm pacing in the treatment of ventilatory failure. 387 3

Sophisticated techniques for electrical stimulation of excitable tissue to treat neuromuscular disorders rationally have been developed over the past 3 decades. A historical review shows that electricity has been applied to the phrenic nerves to activate the diaphragm for some 200 years. Of the contemporary methods for stimulating the phrenic nerve in cases of ventilatory insufficiency, the authors prefer stimulation of the phrenic nerve in the thorax using a platinum ribbon electrode placed behind the nerve and an attached subcutaneously implanted radiofrequency (RF) receiver inductively coupled to an external RF transmitter. Instructions are given for implanting the electrode-receiver assembly, emphasizing atraumatic handling of the phrenic nerve and strict aseptic techniques. Diaphragm pacing is conducted with low frequency electrical stimulation at a slow repetition (respiratory) rate to condition the diaphragm muscle against fatigue and maintain it fatigue-free. Candidates for diaphragm pacing are those with ventilatory insufficiency due to malfunction of the respiratory control center or interruption of the upper motor neurons of the phrenic nerve. In the Yale series, there were 77 patients treated by diaphragm pacing; 63 (82%) started before 1981 and thus were available for follow-up for at least 5 years; 33 (52%) were paced for 5 to 10 years, and 15 (24%) were paced for 10 to 16. Long term stimulation of the phrenic nerves to pace the diaphragm is an effective method of ventilatory support in selected cases.
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PMID:Diaphragm pacing by electrical stimulation of the phrenic nerve. 390 66

The influence of nutritional deprivation on the contractile and fatigue properties of the diaphragm was studied in adult rats. Food access was restricted to one-third of normal daily intake until the body weight of nutritionally deprived (ND) animals was approximately 50% of controls (CTL). Isometric contractile properties were studied in an in vitro nerve muscle strip preparation. Both twitch (Pt) and tetanic (Po) tensions of diaphragms from the ND animals were markedly reduced compared with CTL; however, Pt/Po was higher for the ND group. The shape of the force-frequency curve (normalized to Po) was generally similar between the two groups, except at 5 and 10 pulses/s stimulation, where greater relative tensions were produced in diaphragms from the ND animals. Diaphragm fatigue was induced by repetitive stimulation at either 20 or 100 pulses/s. Endurance time (defined as the time required for tension to fall to 50% of initial) of diaphragms from ND animals was prolonged at both 20 and 100 pulses/s. Immediately after induction of fatigue, force-frequency curves for both ND and CTL diaphragms were shifted to the right. However, this rightward shift was attenuated in the ND group compared with CTL. Nutritional deprivation had no effect on the proportions of different fiber types within the diaphragm but did result in a significant decrease in the cross-sectional area of both fast-and slow-twitch fibers. This decrease in cross-sectional area was significantly greater for fast-twitch fibers. We conclude that these changes in diaphragm contractile and fatigue properties occur as a result of the influence of malnutrition on muscle fiber cross-sectional area.
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PMID:Effect of nutritional deprivation on diaphragm contractility and muscle fiber size. 394 61

Diaphragm fatigue was studied in innervated diaphragm strips from 63 Sprague-Dawley rats. The experiments examined 1) the effect on the rate of diaphragmatic fatigue of increases in the diaphragm's duty cycle, i.e., the ratio of the period of diaphragmatic contraction (Ti) to the duration of a cycle of contraction and rest (Ttot) and 2) the possibility that impaired neural transmission contributed to the fatigue process. Alterations in the duty cycle of the diaphragm were simulated by varying the pattern of electrical stimuli applied cyclically to the phrenic nerve. Fatigue was assessed from the rate of fall of isometric tension when the muscle was made to contract 90 times/min. The contribution of neural element fatigue was assessed by comparing the tension during phrenic nerve stimulation to the tension developed when the muscle was stimulated directly. Increasing the duty cycle (Ti/Ttot) from 25 to 50 to 75% increased the rate of diaphragmatic fatigue progressively. Holding Ti/Ttot constant at 75%, while varying Ti and Ttot, did not affect the rate of fatigue. Increases in duty cycle appear to increase the rate of fatigue by increasing the number of times the contractile process was activated. In fatigued muscle strips diaphragmatic tension was greater in directly stimulated muscle than in muscle strips activated via the phrenic nerve. The results indicate that 1) when the breathing action of the diaphragm is simulated in vitro, increases in duty cycle accelerate the fatigue process and 2) failure of transmission of phrenic impulses to diaphragmatic muscle cells contributes to the fall in tension during fatigue.
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PMID:Fatigue of the mammalian diaphragm in vitro. 628 38

A single derived index of the power spectrum of the diaphragm electromyogram (EMG) has been used in detecting fatigue. Additional information in the EMG could be used to study diaphragm function in other respiratory conditions. Diaphragm EMGs and calculated power spectra at 12 frequencies were measured in normal subjects and patients with severe chronic obstructive pulmonary disease during several respiratory maneuvers both before and after treadmill exercise to dyspnea. The power spectra were characterized by the first five moments. Changes in the EMG were similar when assessed by multivariate analysis of variance of the spectral estimates or of the moments. Factor analysis provided two latent variables that correlated with the first and second moment respectively. The first moment was found to be the most sensitive single discriminant of fatigue and is only slightly improved by adding other information. It is concluded that the first and second moments of the EMG power spectra provide a concise, parsimonious description of the changes in the EMG.
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PMID:Multivariate analysis of diaphragm EMG power spectral moments. 672 71


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