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

The use of non-invasive resistive breathing to task failure to assess inspiratory muscle performance remains a matter of debate. CO2 retention rather than diaphragmatic fatigue was suggested to limit endurance during inspiratory resistive breathing. Cervical magnetic stimulation (CMS) allows discrimination between diaphragmatic and rib cage muscle fatigue. We tested a new protocol with respect to the extent and the partitioning of inspiratory muscle fatigue at task failure. Nine healthy subjects performed two runs of inspiratory resistive breathing at 67 (12)% of their maximal inspiratory mouth pressure, respiratory rate (fR), paced at 18 min(-1), with a 15-min pause between runs. Diaphragm and rib cage muscle contractility were assessed from CMS-induced esophageal (P(es,tw)), gastric (P(ga,tw)), and transdiaphragmatic (P(di,tw)) twitch pressures. Average endurance times of the first and second runs were similar [9.1 (6.7) and 8.4 (3.5) min]. P(di,tw) significantly decreased from 33.1 to 25.9 cmH2O in the first run, partially recovered (27.6 cmH2O), and decreased further in the second run (23.4 cmH2O). P(es,tw) also decreased significantly (-5.1 and -2.4 cmH2O), while P(ga,tw) did not change significantly (-2.0 and -1.9 cmH2O), indicating more pronounced rib cage rather than diaphragmatic fatigue. End-tidal partial pressure of CO2 ( PETCO2) rose from 37.2 to 44.0 and 45.3 mmHg, and arterial oxygen saturation (SaO2) decreased in both runs from 98% to 94%. Thus, task failure in mouth-pressure-targeted, inspiratory resistive breathing is associated with both diaphragmatic and rib cage muscle fatigue. Similar endurance times despite different degrees of muscle fatigue at the start of the runs indicate that other factors, e.g. increases in PETCO2, and/or decreases in SaO2, probably contributed to task-failure.
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PMID:Task failure from inspiratory resistive loaded breathing: a role for inspiratory muscle fatigue? 1282 67

Lung hyperinflation is a consequence of airway obstruction, increased airway resistance and compliance in patients with chronic obstructive pulmonary disease (COPD) which may result in respiratory muscle fatigue and deterioration of gas transfer. The aim of this study was to investigate the influence of hyperinflation on respiratory muscles, gas transfer and breathing pattern and compare the differences between mild and severe COPD. Twenty-eight COPD patients with radiological and tomographic evidence of emphysema were included in the study and they were divided into two groups according to the severity of COPD. Group I= FEV(1) < or = 49% (n= 16). Group II= FEV(1) > or = 50% (n= 12). Airflow rates were decreased and airway resistance was increased significantly in Group I. Maximal inspiratory pressure (MIP) was significantly reduced in Group I. FRC, RV and RV/TLC ratio were increased above 120% in both groups with more significant increase in Group I. Group I showed moderate hypoxemia (PaO(2) = 54.02 mmHg) with hypercapnia (PaCO(2)= 46.65 mmHg) whereas Group II patients were mildly hypoxemic (PaO(2)= 63.78 mmHg) with normocapnia. Parameters of breathing pattern were similar in both groups. Diaphragm height index (DHI) didn't showed significant difference between groups. But there were significant correlations between DHI and RV, FRC. MIP showed significant positive correlation with airflow rates and DLCO, negative correlation with lung volumes, positive correlation with PaO(2) and negative correlation with PaCO(2). FRC also negatively correlated with Ti and Ti/Ttot. In conclusion, hyperinflation present even in the mild forms of COPD causes inspiratory muscle weakness which in return results in impairment in gas transfer.
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PMID:[The effect of hyperinflation on respiratory muscles and breathing pattern in COPD]. 1514 1

Nocturnal sleep-related ventilatory alterations may occur in dis-proportion to the severity of the neuromuscular disorder. Diaphragm paralysis occurring with a neuromuscular disorder is an overlooked complication. Failure to thrive, daytime tiredness, and incapacitating fatigue may be the result of a correctable sleep-related abnormality, not the result of relentless progression of a neuromuscular condition. Polysomnographic evaluation is recommended for patients who have neuromuscular disorder who develop symptoms and signs of sleep-wake abnormality or nocturnal respiratory failure. Application of noninvasive positive airway ventilation and, in some cases, administration of supple-mental oxygen may improve quality of life and prolong survival of patients who have neuromuscular disorder.
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PMID:Sleep and neuromuscular disorders. 1624 23

Genetic deficiency of the muscle chloride channel CLC-1 leads to myotonia congenita in humans as well as myotonia in mice and goats. The hallmark of myotonia is delayed muscle relaxation due to persistent electrical discharges in the muscle. The present study tested the hypothesis that performance of CLC-1 deficient diaphragm muscle is also altered during the contractile phase of the contraction-relaxation cycle. Diaphragm of CLC-1 deficient and wild type mice underwent in vitro isometric contractility testing. Myotonia was easily demonstrable during contractions elicited by train stimulation, but was not seen during twitch stimulation or during train stimulation preceded by a series of twitch stimulations. Twitch force was reduced from 16.7+/-2.5 N/cm(2) in normal muscle to 7.2+/-1.9 N/cm(2) in CLC-1 deficient muscle (P<0.002). Isometric twitch contraction time was shortened from 19.6+/-0.9 to 15.7+/-1.0 ms (P<0.002). During repetitive 25 Hz stimulation, force/area was lower for diseased than normal muscle, whereas force as a percent of initial values declined at a faster rate for normal than diseased muscle. The latter could be accounted for by a rightward shift in the force-frequency relationship of CLC-1 deficient relative to normal muscle, as use of stimulation frequencies which elicited comparable force levels as a percentage of maximum 100 Hz tetanic force led to similar rates of fatigue. These findings indicate that genetic CLC-1 deficiency not only affects muscle relaxation (myotonia) but also modulates diaphragm performance during the contractile phase of the contraction-relaxation cycle.
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PMID:Genetic CLC-1 chloride channel deficiency modifies diaphragm muscle isometric contractile properties. 1695 50

We investigated whether the inspiratory muscles affect maximal incremental exercise performance using a placebo-controlled, crossover design. Six cyclists each performed six incremental exercise tests. For three trials, subjects exercised with proportional assist ventilation (PAV). For the remaining three trials, subjects underwent sham respiratory muscle unloading (placebo). Inspiratory muscle pressure (P(mus)) was reduced with PAV (-35.9+/-2.3% versus placebo; P<0.05). Furthermore, V(O2) and perceptions of dyspnea and limb discomfort at submaximal exercise intensities were significantly reduced with PAV. Peak power output, however, was not different between placebo and PAV (324+/-4W versus 326+/-4W; P>0.05). Diaphragm fatigue (bilateral phrenic nerve stimulation) did not occur in placebo. In conclusion, substantially unloading the inspiratory muscles did not affect maximal incremental exercise performance. Therefore, our data do not support a role for either inspiratory muscle work or fatigue per se in the limitation of maximal incremental exercise.
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PMID:Inspiratory muscles do not limit maximal incremental exercise performance in healthy subjects. 1713 46

Fatiguing exercise promotes oxidation of intracellular thiols, notably glutathione. Interventions that oppose or reverse thiol oxidation can inhibit fatigue. The reduced cysteine donor l-2-oxothiazolidine-4-carboxylate (OTC) supports glutathione synthesis and is approved for use in humans but has not been evaluated for effects on skeletal muscle. We tested the hypotheses that OTC would 1) increase reduced glutathione (GSH) levels and decrease oxidized glutathione, and 2) inhibit functional indexes of fatigue. Diaphragm fiber bundles from adult male ICR mice were incubated for 1 or 2 h at 37 degrees C with buffer (control, C) or OTC (10 mM). N-acetylcysteine (NAC; 10 mM) was used as a positive control. We measured GSH metabolites and fatigue characteristics. We found that muscle GSH content was increased after 1-h incubation with OTC or NAC but was not altered after 2-h incubation. One-hour treatment with OTC or NAC slowed the decline in force with repetitive stimulation [mean (SD) fatigue index at 300 s: OTC = 34 +/- 6% vs. C = 50 +/- 8%, P < 0.05; NAC = 55 +/- 4% vs. C = 65 +/- 8%, P < 0.05] as did the 2-h OTC treatment (OTC = 38 +/- 9% vs. C = 51 +/- 9%, P < 0.05). These results demonstrate that OTC modulates the muscle GSH pool and opposes fatigue under the current experimental conditions.
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PMID:L-2-Oxothiazolidine-4-carboxylate reverses glutathione oxidation and delays fatigue of skeletal muscle in vitro. 1940 60

Low levels of reactive oxygen species (ROS) production are necessary to optimize muscle force production in unfatigued muscle. In contrast, sustained high levels of ROS production have been linked to impaired muscle force production and contraction-induced skeletal muscle fatigue. Using genetically engineered mice, we tested the hypothesis that the independent transgenic overexpression of catalase (CAT), copper/zinc superoxide dismutase (CuZnSOD; SOD1) or manganese superoxide dismutase (MnSOD; SOD2) antioxidant enzymes would negatively affect force production in unfatigued diaphragm muscle but would delay the development of muscle fatigue and enhance force recovery after fatiguing contractions. Diaphragm muscle from wild-type littermates (WT) and from CAT, SOD1 and SOD2 overexpressing mice were subjected to an in vitro contractile protocol to investigate the force-frequency characteristics, the fatigue properties and the time course of recovery from fatigue. The CAT, SOD1 and SOD2 overexpressors produced less specific force (in N cm(-2)) at stimulation frequencies of 20-300 Hz and produced lower maximal tetanic force than WT littermates. The relative development of muscle fatigue and recovery from fatigue were not influenced by transgenic overexpression of any antioxidant enzyme. Morphologically, the mean cross-sectional area (in microm(2)) of diaphragm myofibres expressing myosin heavy chain type IIA was decreased in both CAT and SOD2 transgenic animals, and the percentage of non-contractile tissue increased in diaphragms from all transgenic mice. In conclusion, our results do not support the hypothesis that overexpression of independent antioxidant enzymes protects diaphragm muscle from contraction-induced fatigue or improves recovery from fatigue. Moreover, our data are consistent with the concept that a basal level of ROS is important to optimize muscle force production, since transgenic overexpression of major cellular antioxidants is associated with contractile dysfunction. Finally, the transgenic overexpression of independent endogenous antioxidants alters diaphragm skeletal muscle morphology, and these changes may also contribute to the diminished specific force production observed in these animals.
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PMID:Overexpression of antioxidant enzymes in diaphragm muscle does not alter contraction-induced fatigue or recovery. 1978 18

There is evidence that female athletes may be more susceptible to exercise-induced arterial hypoxemia and expiratory flow limitation and have greater increases in operational lung volumes during exercise relative to men. These pulmonary limitations may ultimately lead to greater levels of diaphragmatic fatigue in women. Accordingly, the purpose of this study was to determine whether there are sex differences in the prevalence and severity of exercise-induced diaphragmatic fatigue in 38 healthy endurance-trained men (n = 19; maximal aerobic capacity = 64.0 +/- 1.9 ml x kg(-1) x min(-1)) and women (n = 19; maximal aerobic capacity = 57.1 +/- 1.5 ml x kg(-1) x min(-1)). Transdiaphragmatic pressure (Pdi) was calculated as the difference between gastric and esophageal pressures. Inspiratory pressure-time products of the diaphragm and esophagus were calculated as the product of breathing frequency and the Pdi and esophageal pressure time integrals, respectively. Cervical magnetic stimulation was used to measure potentiated Pdi twitches (Pdi,tw) before and 10, 30, and 60 min after a constant-load cycling test performed at 90% of peak work rate until exhaustion. Diaphragm fatigue was considered present if there was a >or=15% reduction in Pdi,tw after exercise. Diaphragm fatigue occurred in 11 of 19 men (58%) and 8 of 19 women (42%). The percent drop in Pdi,tw at 10, 30, and 60 min after exercise in men (n = 11) was 30.6 +/- 2.3, 20.7 +/- 3.2, and 13.3 +/- 4.5%, respectively, whereas results in women (n = 8) were 21.0 +/- 2.1, 11.6 +/- 2.9, and 9.7 +/- 4.2%, respectively, with sex differences occurring at 10 and 30 min (P < 0.05). Men continued to have a reduced contribution of the diaphragm to total inspiratory force output (pressure-time product of the diaphragm/pressure-time product of the esophagus) during exercise, whereas diaphragmatic contribution in women changed very little over time. The findings from this study point to a female diaphragm that is more resistant to fatigue relative to their male counterparts.
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PMID:Sex differences in exercise-induced diaphragmatic fatigue in endurance-trained athletes. 2041 22

Cervical spinal cord injury (CSCI) results in a decrease in the capacity of the lungs and chest wall for pressure, volume, and airflow generation. We asked whether such impairments might increase the potential for exercise-induced diaphragmatic fatigue and mechanical ventilatory constraint in this population. Seven Paralympic wheelchair rugby players (mean + or - SD peak oxygen uptake = 16.9 + or - 4.9 ml x kg(-1) x min(-1)) with traumatic CSCI (C(5)-C(7)) performed arm-crank exercise to the limit of tolerance at 90% of their predetermined peak work rate. Diaphragm function was assessed before and 15 and 30 min after exercise by measuring the twitch transdiaphragmatic pressure (P(di,tw)) response to bilateral anterolateral magnetic stimulation of the phrenic nerves. Ventilatory constraint was assessed by measuring the tidal flow volume responses to exercise in relation to the maximal flow volume envelope. P(di,tw) was not different from baseline at any time after exercise (unpotentiated P(di,tw) = 19.3 + or - 5.6 cmH(2)O at baseline, 19.8 + or - 5.0 cmH(2)O at 15 min after exercise, and 19.4 + or - 5.7 cmH(2)O at 30 min after exercise; P = 0.16). During exercise, there was a sudden, sustained rise in operating lung volumes and an eightfold increase in the work of breathing. However, only two subjects showed expiratory flow limitation, and there was substantial capacity to increase both flow and volume (<50% of maximal breathing reserve). In conclusion, highly trained athletes with CSCI do not develop exercise-induced diaphragmatic fatigue and rarely reach mechanical ventilatory constraint.
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PMID:No effect of arm-crank exercise on diaphragmatic fatigue or ventilatory constraint in Paralympic athletes with cervical spinal cord injury. 2048 38

Respiratory muscle dysfunction is a cardinal feature of acute and chronic respiratory failure in COPD. Diaphragm and accessory inspiratory muscles face increased load due to increased lung resistance and elastance, as well as increased ventilatory demands. Concomitantly, the capacity of the inspiratory muscles to generate pressure is decreased due to mechanical disadvantage imposed by hyperinflation. Additionally, inflammation and oxidative stress impair muscle fiber specific force generation and increase diaphragm susceptibility to sarcomer disruption during acute inspiratory loading. In response to this increased load diaphragm presents unique adaptations in its cellular structure and passive and contractile mechanical properties, and displays a more efficient metabolic armamentarium. A shift of muscle fiber type towards slow-twitch, oxidative type I fibers, which are more fatigue-resistant, increases diaphragmatic endurance but protein degradation and a significant reduction in myosin content decrease its force generating capacity. Furthermore, diaphragm adapts to chronic hyperinflation by sarcomere deletion so that its overall length is shortened, in an attempt to preserve optimum force-length relationship. Adaptation however may not be complete, or may be overwhelmed by pathophysiologic derangements during exercise or acute exacerbations, leading to obvious "dysfunction" of the respiratory muscles, and if sustained, ultimately to muscle fatigue and respiratory pump failure.
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PMID:Respiratory muscle dysfunction in COPD: from muscles to cell. 2119 7


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