***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 
    ***DOCUMENTATION*** 
    ***EXAMPLES*** 
    Input: Assessment of individual susceptibility to altitude illnesses and more particularly to  acute mountain sickness ( AMS ) by means of tests performed in normobaric hypoxia ( NH ) or in hypobaric hypoxia ( HH ) is still debated . Eighteen subjects were su bmi tted to  HH and  NH tests ( PIO2=120 hPa , 30 min ) before an expedition . Maximal and mean acute mountain sickness scores ( AMSmax and mean ) were determined using the self-report Lake Louise question naire scored daily .  Cardio-ventilatory ( f , VT , PetO2 and PetCO2 , HR and finger pulse oxymetry SpO2 )  were measured at times 5 and 30 min of the tests . Arterial ( PaO2 , PaCO2 , pH , SaO2 ) and capillary haemoglobin ( Hb ) measurements  were performed at times 30 min . Hypoxic ventilatory ( HVR ) and cardiac ( HCR ) responses , peripheral O2 blood content ( CpO2 ) were calculated . A significant time effect is found for ΔSpO2 ( P = 0.04 ) . Lower PaCO2 ( P = 0.005 ) , SaO2 ( P = 0.07 ) and higher pH ( P = 0.02 ) are observed in HH compared to NH . AMSmax varied from 3 to12 and AMSmean between 0.6 and 3.5 . In NH at 30 min , AMSmax is related to PetO2 ( R = 0.61 , P = 0.03 ) , CpO2 ( R = −0.53 , P = 0.02 ) and in HH to CpO2 ( R = −0.57 , P = 0.01 ) . In NH , AMSmean is related to Δf ( R = 0.46 , P = 0.05 ) , HCR ( R = 0.49 , P = 0.04 ) , CpO2 ( R = −0.51 , P = 0.03 ) and , in HH at 30 min , to VT ( R = 0.69 , P = 0.01 ) and a tendency for CpO2 ( R = −0.43 , P = 0.07 ) . We conclude that HH and NH tests are physiologically different and they must last 30 min . CpO2 is an important variable to predict AMS . For practical considerations , NH test is proposed to quantify AMS individual susceptibility using the formulas : AMSmax = 9.47 + 0.104PetO2(hPa)–0.68CpO2 ( % ) , ( R = 0.77 , P = 0.001 ) ; and AMSmean = 3.91 + 0.059Δf + 0.438HCR–0.135CpO2 ( R = 0.71 , P = 0.017 ) Objectives : To compare a range of physiological responses to acute sea level hypoxia at simulated altitudes with the same physiological responses and acute mountain sickness ( AMS ) scores measured at altitude ( similar to the simulated altitudes ) during a 17 day trek in the Himalayas . Methods : Twenty men and women aged 18–54 years took part in the study .  End tidal CO2 tension ( Petco2 ) and saturated oxygen ( Sao2 ) were measured using a capnograph . Observations made at sea level and some simulated altitudes were compared with those in the Himalayas . Pairwise correlations were used to examine the correlation between variables and regression , with 95 % prediction intervals providing information on how well one variable could be predicted from another for a given subject . Results : There was only a significant correlation for a few comparisons . The 95 % prediction intervals for individual Sao2 values at a range of simulated altitudes were fairly wide going from ± 4 % to ± 5 % . All of the correlations between laboratory and Himalayan Petco2 values were not statistically significant . There was a significant correlation for the relation between Sao2 and Petco2 at sea level for the laboratory data ( r=−0.51 ; p=0.05 ) . For the Himalayan data , there were significant correlations at Namche Bazaar ( 3450 m ; day 3 ) ( r=−0.56 ; p=0.01 ) and Dingboche ( 4300 m ; day 6 ) ( r=−0.48 ; p=0.03 ) . The correlation between Sao2 and Petco2 and AMS was generally poor . Conclusions : The results indicate that limited information can be gained on a subject 's response to altitude by assessing physiological variables at sea level and a range of simulated altitudes before the subject carries out a trek at altitude Since Bert ( 1878 ) and Barcroft ( 1925 ) , studies on hypoxia are realized by lowering ambient O2 partial pressure ( PO2 ) either by barometric pressure reduction ( hypobaric hypoxia HH ) or by lowering the O2 fraction ( normobaric hypoxia NH ) . Today , a question is still debated : " are there any physiological differences between HH and NH for the same ambient PO2 ? " Since published studies are scarce and controversial , we su bmi tted 18 subjects in a r and om order to a 40-min HH test and to a 40-min NH test  at an ambient PO2  equal to 120 hPa ( 4500 m ) . Cardioventilatory variables [ breathing frequency ( f ) , tidal volume ( Vt ) , minute ventilation ( V̇E ) , O2 and CO2 end-tidal fractions or pressures ( FETO2 and FETCO2 or PETO2 and PETCO2 respectively ) , heart rate ( HR ) and O2 arterial saturation by pulse oxymetry ( SpO2 ) ] were measured throughout the tests . At the end of the tests , arterial blood sample s were taken to measure arterial blood gases [ O2 and CO2 arterial partial pressures ( PaO2 and PaCO2 ) , pH and O2 arterial saturation ( SaO2 ) ] . Results show that during HH compared to NH , f is greater ( P≤0.001 ) , Vt and V̇E under BTPS conditions are lower ( P≤0.05 ) , and FETO2 and FETCO2 are higher ( P≤0.05 ) . However , PETO2 does not change during the last 25 min of the tests , and neither does PETCO2 throughout the tests . HR is higher ( P≤0.05 ) and SpO2 lower ( P≤0.05 ) in HH compared to NH . Arterial blood data reveal that hypoxemia , hypocapnia and blood alkalosis are greater in HH compared to NH and that SaO2 is lower ( P≤0.05 ) . It is concluded that the physiological responses of humans su bmi tted to an acute hypoxia at a PO2 equal to 120 hPa differ according to the type of hypoxia . Compared to NH , HH leads to a greater hypoxemia , hypocapnia , blood alkalosis and a lower O2 arterial saturation . These physiological differences could be the consequence of an increase in dead space ventilation , probably related to the barometric pressure reduction , and could be grouped together under the term " the specific response to hypobaric hypoxia " . Knowledge of this specific response could improve the comprehension , prevention and treatment of altitude illnesses in the future PURPOSE Slight differences in physiological responses and nitric oxide ( NO ) have been reported at rest between hypobaric hypoxia  ( HH ) and normobaric hypoxia  ( NH ) during short exposure . Our study reports NO and oxidative stress at rest and physiological responses during moderate exercise in HH versus NH . METHODS Ten subjects were r and omly exposed for 24 h to HH  ( 3000 m ; FIO2 , 20.9 % ; BP , 530 ± 6 mm Hg ) or to NH  ( FIO2 , 14.7 % ; BP , 720 ± 1 mm Hg ) . Before and every 8 h during the hypoxic exposures , pulse oxygen saturation ( SpO2 ) , HR , and gas exchanges were measured during a 6-min submaximal cycling exercise . At rest , the partial pressure of exhaled NO , blood nitrate and nitrite ( NOx ) , plasma levels of oxidative stress , and pH levels were additionally measured . RESULTS During exercise , minute ventilation was lower in HH compared with NH ( -13 % after 8 h , P < 0.05 ) . End-tidal CO2 pressure was lower ( P < 0.01 ) than PRE both in HH and NH but decreased less in HH than that in NH ( -25 % vs. -37 % , P < 0.05).At rest , exhaled NO and NOx decreased in HH ( -46 % and -36 % after 24 h , respectively , P < 0.05 ) whereas stable in NH . By contrast , oxidative stress was higher in HH than that in NH after 24 h ( P < 0.05 ) . The plasma pH level was stable in HH but increased in NH ( P < 0.01 ) . When compared with prenormoxic values , SpO2 , HR , oxygen consumption , breathing frequency , and end-tidal O2 pressure showed similar changes in HH and NH . CONCLUSION Lower ventilatory responses to a similar hypoxic stimulus during rest and exercise in HH versus NH were sustained for 24 h and associated with lower plasma pH level , exaggerated oxidative stress , and impaired NO bioavailability Acute mountain sickness ( AMS ) strikes those in the mountains who go too high too fast . Although AMS has been long assumed to be due solely to the hypoxia of high altitude , recent evidence suggests that hypobaria may also make a significant contribution to the pathophysiology of AMS . We studied nine healthy men exposed to simulated altitude , normobaric hypoxia , and normoxic hypobaria in an environmental chamber for 9 h on separate occasions . To simulate altitude , the barometric pressure was lowered to 432 + /- 2 ( SE ) mmHg ( simulated terrestrial altitude 4,564 m ) . Normobaric hypoxia result ed from adding nitrogen to the chamber ( maintained near normobaric conditions ) to match the inspired PO2 of the altitude exposure . By lowering the barometric pressure and adding oxygen , we achieved normoxic hypobaria with the same inspired PO2 as in our laboratory at normal pressure . AMS symptom scores ( average scores from 6 and 9 h of exposure ) were higher during simulated altitude ( 3.7 + /- 0.8 ) compared with either normobaric hypoxia ( 2.0 + /- 0.8 ; P < 0.01 ) or normoxic hypobaria ( 0.4 + /- 0.2 ; P < 0.01 ) . In conclusion , simulated altitude induces AMS to a greater extent than does either normobaric hypoxia or normoxic hypobaria , although normobaric hypoxia induced some AMS 
    Output:
    
Several studies reported a number of variables ( e.g. minute ventilation and NO levels ) that were different between the two conditions , lending support to the notion that true physiological difference is indeed present .