***TASK*** the task is to summarize an input biomedical literature in six sentences 
    ***INPUT*** the input is a biomedical literature 
    ***OUTPUT*** the output is the summary of an input biomedical literature in six sentences 
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    Input: Previous work suggests that exercise-induced arterial hypoxaemia ( EIAH ) , causing only moderate arterial oxygen desaturation ( SaO2 : 92 + /- 1 % ) , does not exaggerate diaphragmatic fatigue exhibited by highly trained endurance athletes . Since changes in arterial O2 tension have a significant effect on the rate of development of locomotor muscle fatigue during strenuous exercise , the present study investigated whether hypoxia superimposed on EIAH exacerbates the exercise-induced diaphragmatic fatigue in these athletes . Eight trained cyclists ( VO2max : 67.0 + /- 2.6 ml kg(-1 ) min(-1 ) ; mean + /- S.E.M. ) completed in balanced order four 5 min exercise tests leading to different levels of end-exercise SaO2 ( 64 + /- 2 , 83 + /- 1 , 91 + /- 1 and 96 + /- 1 % ) via variations in inspired O2 fraction ( FiO2 : 0.13 , 0.17 , 0.21 and 0.26 , respectively ) . Measurements were made at corresponding intensities ( 65 + /- 3 , 80 + /- 3 , 85 + /- 3 and 90 + /- 3 % of normoxic maximal work rate , respectively ) in order to produce the same tidal volume , breathing frequency and respiratory muscle load at each FiO2 . The mean pressure time product of the diaphragm did not differ across the four exercise tests and ranged between 312 + /- 28 and 382 + /- 22 cmH2O s min(-1 ) . Ten minutes into recovery , twitch transdiaphragmatic pressure ( P(di , tw ) ) determined by bilateral phrenic nerve stimulation , was significantly ( P = 0.0001 ) reduced after all tests . After both hypoxic tests ( FiO2 : 0.13 , 0.17 ) the degree of fall in P(di , tw ) ( by 26.9 + /- 2.7 and 27.4 + /- 2.6 % , respectively ) was significantly greater ( P < 0.05 ) than after the normoxic test ( by 20.1 + /- 3.4 % ) . The greater amount of diaphragmatic fatigue in hypoxia at lower leg work rates ( presumably requiring smaller leg blood flow compared with normoxia at higher leg work rates ) , suggests that when ventilatory muscle load is similar between normoxia and hypoxia , hypoxia exaggerates diaphragmatic fatigue in spite of potentially greater respiratory muscle blood flow availability While sustaining a load that leads to task failure , it is unclear whether diaphragmatic fatigue develops progressively or occurs only at task failure . We hypothesized that incremental loading produces a progressive decrease in diaphragmatic contractility ever before task failure . Ten subjects generated 60 % of maximal transdiaphragmatic pressure ( Pdimax ) for 2 min , 4 min , and until task failure . Before loading , 20 min after each period of loading , and approximately 20 h after the last period of loading , Pdimax , nonpotentiated and potentiated Pdi twitch pressure ( Pditw ) , and the pattern of respiratory muscle recruitment during a CO2 challenge were recorded . Sensation of inspiratory effort at the 4th min of the task-failure protocol was greater than at the same time in the preceding 4-min protocol . Surprisingly , potentiated Pditw and Pdimax were reduced after 2 min of loading and decreased further after 4 min of loading and after task failure ; nonpotentiated Pditw was reduced after 4 min of loading and after task failure . The gastric pressure contribution to tidal breathing during a CO2 challenge decreased progressively in relation to duration of the preceding loading period , whereas expiratory muscle recruitment progressively increased . A rest period of approximately 20 h after task failure was not sufficient to normalize these alterations in respiratory muscle recruitment or fatigue-induced changes in diaphragmatic contractility . In conclusion , while sustaining a mechanical load , the diaphragm progressively fatigued , ever before task failure , and when challenged the rib cage-to-diaphragmatic contribution to tidal breathing and recruitment of the expiratory muscles increased pari passu with duration of the preceding loading Background Greater diaphragm fatigue has been reported after hypoxic versus normoxic exercise , but whether this is due to increased ventilation and therefore work of breathing or reduced blood oxygenation per se remains unclear . Hence , we assessed the effect of different blood oxygenation level on isolated hyperpnoea-induced inspiratory and expiratory muscle fatigue . Methods Twelve healthy males performed three 15-min isocapnic hyperpnoea tests ( 85 % of maximum voluntary ventilation with controlled breathing pattern ) in normoxic , hypoxic ( SpO2 = 80 % ) and hyperoxic ( FiO2 = 0.60 ) conditions , in a r and om order . Before , immediately after and 30 min after hyperpnoea , transdiaphragmatic pressure ( Pdi , tw ) was measured during cervical magnetic stimulation to assess diaphragm contractility , and gastric pressure ( Pga , tw ) was measured during thoracic magnetic stimulation to assess abdominal muscle contractility . Two-way analysis of variance ( time x condition ) was used to compare hyperpnoea-induced respiratory muscle fatigue between conditions . Results Hypoxia enhanced hyperpnoea-induced Pdi , tw and Pga , tw reductions both immediately after hyperpnoea ( Pdi , tw : normoxia -22 ± 7 % vs hypoxia -34 ± 8 % vs hyperoxia -21 ± 8 % ; Pga , tw : normoxia -17 ± 7 % vs hypoxia -26 ± 10 % vs hyperoxia -16 ± 11 % ; all P < 0.05 ) and after 30 min of recovery ( Pdi , tw : normoxia -10 ± 7 % vs hypoxia -16 ± 8 % vs hyperoxia -8 ± 7 % ; Pga , tw : normoxia -13 ± 6 % vs hypoxia -21 ± 9 % vs hyperoxia -12 ± 12 % ; all P < 0.05 ) . No significant difference in Pdi , tw or Pga , tw reductions was observed between normoxic and hyperoxic conditions . Also , heart rate and blood lactate concentration during hyperpnoea were higher in hypoxia compared to normoxia and hyperoxia . Conclusions These results demonstrate that hypoxia exacerbates both diaphragm and abdominal muscle fatigability . These results emphasize the potential role of respiratory muscle fatigue in exercise performance limitation under conditions coupling increased work of breathing and reduced O2 transport as during exercise in altitude or in hypoxemic patients Inspiratory muscle fatigue may occur in as little as 6 min during high-intensity spontaneously breathing exercise . The aims of this study were to determine whether inspiratory muscle fatigue occurs during swimming exercise and whether inspiratory muscle strength differs between the supine and st and ing body positions . Seven competitive swimmers were recruited to perform a single 200 m front-crawl swim , corresponding to 90 - 95 % of race pace . Inspiratory muscle strength was measured at residual volume using a h and -held mouth pressure meter that measured maximal inspiratory pressure in the upright and supine positions . At baseline , maximal inspiratory pressure in the supine position was significantly lower than maximal inspiratory pressure in the upright position ( 112±20.4 and 133±16.7 cmH2O , respectively ; P⩽0.01 ) . Post-exercise maximal inspiratory pressure in the supine position ( 80±15.7 cmH2O ) was significantly lower than baseline maximal inspiratory pressure in the supine position ( P⩽0.01 ) . The results indicate that a single 200 m front-crawl swim corresponding to 90 - 95 % of race pace was sufficient to induce inspiratory muscle fatigue in less than 2.7 min . Furthermore , although diaphragm muscle length is optimized when supine , our results indicate that the force output of the diaphragm and inspiratory accessory muscles is greater when upright than when supine The use of noninvasive techniques to measure respiratory muscle performance after different types of endurance exercise has not been entirely successful , as the results have not consistently indicated diminished performance for similar types of exercise . The aim of the present study was 1 ) to compare different , noninvasive methods to assess respiratory muscle performance before and after an exhaustive cycling endurance test ( which has previously been shown to induce diaphragmatic fatigue ) and 2 ) to determine which of the tests best reflect published results of measurements of diaphragmatic fatigue . Twelve healthy subjects participated in the study and performed three different test series in a r and om order on three different days . These tests were performed before , and 5 , 40 and 75 min after an exhausting task ( a cycling endurance run at 85 % of maximal oxygen uptake ( V'O2,max ) ) . The tests of the three test series were 1 ) breathing against a constant inspiratory resistance to task failure , 2 ) determination of 12-min sustained ventilatory capacity , and 3 ) spirometric and maximal inspiratory and expiratory mouth pressure measurements . The only measurement that was affected by exhaustive cycling was the time to task failure breathing against inspiratory resistance . It was significantly reduced from ( mean+/-sD ) 364+/-88 s before exercise to 219+/-122 s at 5 min after cessation of exercise . It is concluded that the constant-load resistive breathing test to task failure is the only noninvasive respiratory muscle performance test evaluated in this study which shows a decrease in respiratory muscle performance after exhaustive endurance exercise Exercise-induced inspiratory muscle fatigue ( IMF ) has been reported in males but there are few reports of IMF in females . It is not known if a gender difference exists for inspiratory muscle strength following heavy exercise , as is reported in locomotor muscles . Therefore , the relationship between fatigue and subsequent recovery of maximal inspiratory pressure ( MIP ) following exercise to maximal oxygen consumption $ $ ( \dot V_{{\text{O}}_{{\text{2max}}}})$$ was examined in a group of moderately trained males and females . Eighteen males ( 23±3 years ; mean ± SD ) and 16 females ( 23±2 years ) completed ten MIP and ten maximal h and grip ( HG ) strength maneuvers to establish baseline . Post-exercise MIP and HG were assessed successively immediately following a progressive intensity $ $ \dot V_{{\text{O}}_{{\text{2max } } } } $ $ test on a cycle ergometer and at 1 , 2 , 3 , 4 , 5 , 10 , and 15 min . $ $ \dot V_{{\text{O}}_{{\text{2max } } } } , $ $ relative to fat-free mass was not statistically different between males ( 62±7 ml kg−1 min−1 ) and females ( 60±8 ml kg−1 min−1 ) . Males had higher absolute MIP values than females at all time intervals ( P<0.05 ) . Immediately following exercise , MIP was significantly reduced in both genders ( M=83±16 % ; F=78±15 % of baseline ) but HG values were not different than resting values . MIP values remained depressed for both males and females throughout the 15 min ( P<0.05 ) . Differences for MIP between males and females were not statistically significant at any measurement time ( P>0.05 ) . The findings in this study conclude that IMF , observed immediately following maximal exercise , demonstrated the same pattern of recovery for both genders The purpose of this study was to determine whether the human diaphragm , like limb muscle , has a threshold of force output at which a metaboreflex is activated causing systemic vasoconstriction . We used Doppler ultrasound techniques to quantify leg blood flow ( Q(L ) ) and utilized the changes in mouth twitch pressure ( DeltaP(M)T ) in response to bilateral phrenic nerve stimulation to quantify the onset of diaphragm fatigue . Six healthy male subjects performed four r and omly assigned trials of identical duration ( 8 + /- 2 min ) and breathing pattern [ 20 breaths/min and time spent on inspiration during the duty cycle ( time spent on inspiration/total time of one breathing cycle ) was 0.4 ] during which they inspired primarily with the diaphragm . For trials 1 - 3 , inspiratory resistance and effort was gradually increased [ 30 , 40 , and 50 % maximal inspiratory pressure ( MIP ) ] , diaphragm fatigue did not occur , and Q(L ) , limb vascular resistance ( LVR ) , and mean arterial pressure remained unchanged from control ( P > 0.05 ) . The fourth trial utilized the same breathing pattern with 60 % MIP and caused diaphragm fatigue , as shown by a 30 + /- 12 % reduction in P(M)T with bilateral phrenic nerve stimulation . During the fatigue trial , Q(L ) and LVR were unchanged from baseline at minute 1 , but LVR rose 36 % and Q(L ) fell 25 % at minute 2 and by 52 % and 30 % , respectively , during the final minutes of the trial . Both LVR and Q(L ) returned to control within 30 s of recovery . In summary , voluntary increases in inspiratory muscle effort , in the absence of fatigue , had no effect on LVR and Q(L ) , whereas fatiguing the diaphragm elicited time-dependent increases in LVR and decreases in Q(L ) . We attribute the limb vasoconstriction to a metaboreflex originating in the diaphragm , which reaches its threshold for activation during fatiguing contractions BACKGROUND --Diaphragm strength can be assessed by the measurement of 
    Output:
    
Inspiratory resistive loadings at intensities of 60 - 80 % of maximum , and cycling at 85 % of maximum were found to produce IMF most consistently .