Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0015672 (fatigue)
 51,768 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Maximal voluntary drive to the diaphragm and a non-respiratory muscle group (elbow flexors) was compared in 10 control subjects and 11 asthmatics who were studied when well. The degree of voluntary activation during repeated attempted maximal quasi-static efforts was determined using the twitch interpolation technique in the absence of contractile fatigue under both control conditions and following bronchial challenge with histamine. Diaphragm activation was assessed using bilateral phrenic stimulation at the normal resting end-expiratory lung volume after exhalation from TLC. Asthmatic subjects showed lower and more variable voluntary activation than control subjects for both diaphragm (82.0% +/- 18.4 [SD], vs 87.8% +/- 12.0, P < 0.01) and elbow flexors (91.3% +/- 7.6 vs 95.8% +/- 4.1, P < 0.01). Histamine challenge decreased FEV1 in asthmatic subjects to 50% of the initial value, but had no significant effect on voluntary activation in either subject group. The decreased voluntary drive to the diaphragm observed in some asthmatic subjects may predispose to rapid development of ventilatory failure during severe airway narrowing.
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PMID:Reduced voluntary drive to breathe in asthmatic subjects. 836 14

The effects of vitamin E deficiency on diaphragm function were studied at rest and after resistive breathing (RB) in Sprague-Dawley rats (wt 300-400 g). The animals were pair fed a vitamin E-deficient diet (E-def) or a matched vitamin E-sufficient diet (E-suf). Each diet group was then further subdivided into a group that breathed unimpeded (control) and a second group that breathed through an inspiratory resistor until the animals were unable to sustain 70% of their maximum airway pressure. Diaphragm samples were obtained for analysis of thiobarbituric acid-reactive substances, glutathione (GSH) concentrations, and glutathione disulfide (GSSG) concentrations. In vitro isometric contractile studies were also performed and included twitch (Pt) and maximum tetanic (Po) tensions, force-frequency curves, fatigue index, and recovery index. Pt was significantly reduced in the E-suf RB group as well as both of the E-def groups. Po was also significantly reduced in both E-def groups. The E-def rats subjected to RB showed a significant decrease in tension at both high and low frequencies compared with the E-suf rats. Concentrations of diaphragm thiobarbituric acid-reactive substances were significantly increased in both E-def groups. RB in both E-suf and E-def rats resulted in increases in diaphragm concentrations of GSSG and decreases in the GSH/GSSG ratios. We conclude that reduction of contractile function, lipid peroxidation, and activation of the GSH redox cycle occur with RB and that these effects are significantly increased in the presence of vitamin E deficiency.
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PMID:Diaphragmatic function after resistive breathing in vitamin E-deficient rats. 844 2

The effects of long-term (24- to 28-wk) continuous respiratory resistive loading on diaphragm mass, contractility, fatigue, and fiber types were studied in male rats. Increased respiratory resistance was produced by extratracheal banding, and results were compared with sham-operated pair-fed controls. At the time the animals were killed, banded tracheal segment internal diameter was reduced by 57% of control values. Diaphragm surface area and muscle mass (normalized for body mass) increased by 19% of control values. Isometric diaphragm contractility and fatigue resistance indexes were measured using an in vitro diaphragm costal strip preparation at 37 degrees C. Twitch and tetanic stimulations were evoked using direct stimulation. Compared with controls, baseline tensions (normalized for diaphragm cross-sectional area) were significantly decreased at low frequencies. Fatigue resistance (endurance) indexes were significantly increased at all frequencies. These findings were consistent with observed increases in number and cross-sectional area of type I (low-tension high-endurance) fibers. We conclude that the diaphragm adapts to chronic long-term resistive loads by sacrificing peak tensions for an increase in endurance capacity.
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PMID:Effects of long-term continuous respiratory resistive loading on rat diaphragm function and structure. 848 60

Diaphragm fatigue was studied in isolated phrenic nerve diaphragm strips from 28 Swiss Albino rats. Three procedures were used to estimate the isometric twitch characters and force frequency responses to fatigue of the rat diaphragm at different rates of phrenic nerve stimulation. Diaphragm fatigue was induced by using low frequency stimulation (0.2 ms pulse duration, at 5 Hz frequency, 3 min), high frequency stimulation (0.2 ms pulse duration, at 50 Hz frequency, 3 min), and by production brief submaximal contraction (25 Hz, for 160 ms at the rate of 1/s for 45 contractions). Tension was reduced to 26.67 +/- 5.10% and 6.59 +/- 2.64% and 68.69 +/- 2.45% of the initial value at the end of the low and high frequency and brief submaximal stimulation, respectively. In all the fatigue experiments, twitch tension and tetanic tension decreased, contraction and 1/2 relaxation time prolonged and force-frequency curves shifted to the right. The most significant changes were observed in low frequency fatigue whereas the most moderate ones were recorded in brief submaximal fatigue. It was concluded that fatigue in the rat diaphragm depended on the frequency and duration of stimulation as well as on the number of stimuli delivered to the muscle. Various mechanisms of muscle fatigue are described in the discussion to explain the observations made in the present investigation.
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PMID:Dependence of fatigue properties on the pattern of stimulation in the rat diaphragm muscle. 858 42

The present study tested the hypothesis that growth hormone (GH), an anabolic agent, could prevent the abnormalities of diaphragm structure and function associated with short-term administration of the corticosteroid triamcinolone (TR). During a 10-day period, male rats (n = 33) were assigned to control (CTL), TR (1 mg.kg-1.day-1 im), and TR-GH (2 mg.kg-1.day-1 im) groups. Diaphragm weight was significantly reduced in the TR and TR-GH animals compared with the CTL animals, but there was no difference in the diaphragm-to-body weight ratio. Fiber type (I, IIa, and IIx/b) proportions did not differ among the three groups. However, in TR rats there was a significant reduction in the contribution of type IIx/b fibers to total diaphragm cross-sectional area due to marked atrophy (approximately 42% decrease in mean fiber cross-sectional area). There was no significant reversal of TR-induced type IIx/b fiber atrophy by concomitant GH administration. TR and TR-GH groups both exhibited a left-ward shift of the force-frequency relationship and enhanced in vitro fatigue resistance, whereas maximal specific force was unaltered. We conclude that GH does not prevent corticosteroid-induced effects on the diaphragm under these conditions, possibly as a result of reduced nutritional intake associated with TR administration.
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PMID:Growth hormone does not prevent corticosteroid-induced changes in rat diaphragm structure and function. 859 16

It is controversial whether insulin-like growth factor I (IGF-I), growth hormone (GH), or their combination might enhance body growth and/or tissue anabolism in the well-fed animal with an intact somatotrophic axis. To assess this further, we studied four groups of adolescent rats: 1) control (Ctr), 2) GH, 3) IGF-I, and 4) GH/IGF-I. IGF-I was given via an osmotic minipump, whereas GH was injected subcutaneously for a period of 72 h. Diaphragm (Dia) contractile and fatigue properties were determined in vitro. Quantitative histochemical and morphometric analyses were performed on Dia fibers. Total serum IGF-I levels were significantly increased in the groups receiving growth factors. Although body weight increased to a greater extent in the animals receiving growth factors, a further synergistic effect was noted in the GH/IGF-I animals compared with either GH or IGF-I groups. Costal Dia mass was greater in the groups receiving growth factors. The Dia of GH/IGF-I animals was more fatigue resistant than the Dia in Ctr. The cross-sectional area of types IIa and IIx fibers were increased to a similar extent in all groups receiving growth factors compared with Ctr. Succinate dehydrogenase activity of type IIa fibers was significantly greater in the GH/IGF-I animals compared with the other groups. We conclude that the short-term provision of growth factors to well-nourished, normally growing adolescent rats can accelerate body growth and promote selective hypertrophy of predominantly type II Dia fibers.
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PMID:Anabolic influences of insulin-like growth factor I and/or growth hormone on the diaphragm of young rats. 917 66

Free radical injury is believed to be important in diaphragm dysfunction. N-Acetylcysteine (NAC) is a potent free radical scavenger shown in animal models to attenuate diaphragm fatigue; however, its effects on human diaphragm function are unknown. We assessed diaphragm function by electrophrenic twitch stimulation (PdiT) and twitch occlusion (to yield Pdimax) in four healthy subjects 35 +/- 3 yr of age (mean +/- SD). We intravenously administered NAC (150 mg/kg in 250 ml D5W) or placebo (CON) (250 ml D5W) in a randomized manner after subjects were premedicated with antihistamines. There were no significant side effects with the infusion. After infusion, we measured baseline Pdimax and PdiT at FRC. Diaphragm fatigue was then induced by subjects breathing through an inspiratory resistive load. Pdimax and PdiT were then measured at 15 to 30 min and 1, 2, 3, 4, and 20-25 h after fatigue. Times to fatigue were 13 +/- 4 min (CON) and 21 +/- 6 min (NAC) (p = 0.04). At 15 min after fatigue, PdiT was reduced to 40% (CON) compared with 30% (NAC) initial PdiT value (p = 0.05). Other twitch characteristics (maximal rate of relaxation and maximal contraction rate) were reduced to a greater degree after placebo compared with NAC. There were no significant differences in the rate of recovery between CON and NAC. Pdimax at 30 min after fatigue was significantly greater with NAC; however, at 1 h after fatigue, Pdimax for CON and NAC were not different, suggesting similar rates of recovery in high-frequency fatigue. These data suggest that NAC may attenuate low-frequency human diaphragm fatigue.
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PMID:Effect of N-acetylcysteine on human diaphragm strength and fatigability. 937 77

Diaphragm pacing (DP) by electrical stimulation of the phrenic nerve offers important advantages to a highly select group of patients with respiratory paralysis. The patient wears an external radiofrequency (RF) transmitter over an implanted receiver, and a stimulating current is induced without the need for any transcutaneous wires. We review the conditions and requirements of patients who may benefit most from DP. We outline the preoperative evaluation and procedures for surgical implantation. We discuss the risk of diaphragmatic fatigue posed by initiation of DP and the use of gradual conditioning to limit this problem. Other problems encountered by patients in the course of DP can be minimized by well-instructed home caregivers and by systematic medical follow-up. Although a few patients derive considerable benefit from DP, many patients with respiratory paralysis are better treated by less invasive means such as nasal bilevel positive airway pressure or intermittent positive pressure ventilation, which we also review.
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PMID:Diaphragm pacing for respiratory insufficiency. 941 84

The purpose of this study was to determine the relationship between intrathoracic pressure (delta ITP) and diaphragm shortening (DS) during the development of diaphragm fatigue. Fatigue of the diaphragm was produced by having rats breath 15% CO2 in O2. Diaphragm shortening increased significantly to 178% of control during the first 5 min of hypercapnia and then decreased to 86% of control at approximately 80 min. Twenty minutes after terminating hypercapnia, DS increased to 115% of the prehypercapnic value. delta ITP increased to 199% of control following 5 min of hypercapnia and continued to increase, reaching 267% of control at the end of the hypercapnic period. Twenty minutes later, delta ITP was 147% of control. These results illustrate that during increased respiratory work, DS can decrease while intrathoracic pressure remains increased. These findings suggest that intrathoracic pressure may not always reflect the contractile status of the diaphragm. These findings are consistent with other studies indicating that as the diaphragm fatigues, accessory respiratory muscle activity increases to maintain delta ITP.
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PMID:Diaphragm shortening and intrathoracic pressure during hypercapnia in rats. 951 16

Inspiratory muscle fatigue can probably determine hypercapnic respiratory failure. Diaphragm fatigue is detected by electrical phrenic stimulation (ELS), but there is no simple tool to assess rib cage muscle (RCM) fatigue. Cervical magnetic stimulation (CMS) costimulates the phrenic nerves and RCM. We reasoned that changes in transdiaphragmatic pressure twitch (Pdi,tw) with CMS and ELS should be different after selective diaphragm vs. RCM fatigue. Five volunteers performed inspiratory resistive tasks while voluntarily uncoupling diaphragm and RCM. Baseline Pdi,twELS and Pdi,twCMS were 28.57 +/- 1.68 and 32.83 +/- 2.92 cmH2O. After selective diaphragm loading, Pdi,twELS and Pdi,twCMS were reduced by 39 and 26%, with comparable decreases in gastric pressure twitch (Pga,tw). Esophageal pressure twitch (Pes,tw) was better preserved with CMS. Therefore Pes,tw/Pga,tw was lower with ELS than CMS (-1.24 +/- 0.16 vs. -1.73 +/- 0.11, P = 0.05). After selective RCM loading, there was no diaphragm fatigue, but Pes,twCMS was significantly reduced (-30%). These findings support the role of rib cage stiffening by CMS-related RCM contraction in the ELS-CMS differences and suggest that CMS can be used to assess RCM fatigue.
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PMID:Cervical magnetic stimulation as a method to discriminate between diaphragm and rib cage muscle fatigue. 957 19


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