Background: Some reports claim that ventilation (VE) is greater in hum
an subjects in normobaric hypoxia than at altitude following an equiva
lent drop in inspired PO2 (PIO2) It has been suggested that reduced ba
rometric pressure (PB) may decrease chemoreceptor sensitivity and acco
unt for these results. In this pilot study we tested the hypothesis th
at VE and hypoxic chemoresponsiveness would not be different after 30
min of normobaric hypoxia and altitude. Methods: We exposed three male
and three female subjects to four conditions in an environmental cham
ber, varying the order. The four conditions were: air (PB = 640, FIO2
= 0.204), hypobaria (434, 0.298), hypoxia (640, 0.14l)and altitude (43
4, 0.203). We measured VE, end-tidal O-2 and CO2 and arterial O-2 satu
ration (SpO(2)) after 30 min in each environment, and while breathing
100% O-2 for 1 min immediately thereafter. Results: The mean increase
in VE relative to air was 14%, 20% and 26% for hypobaria, hypoxia and
altitude, respectively, with corresponding reductions in PETCO(2) in t
he three conditions. The reduction in VE with 100% O-2 was inversely p
roportional to the rise in SpO(2) in all cases, indicating that chemor
esponsiveness was unchanged by PB. When hypobaria preceded altitude, t
he VE at altitude increased less, relative to air, than when altitude
was given first (not significant). Conclusions:The VE and chemosensiti
vity are about the same after 30 min of altitude and equivalent hypoxi
a. However, when the drop in PIO2 is not synchronous with the drop in
PB, like at altitude, the VE values may be altered. Air density, hypox
ic pulmonary vasoconstriction and circulating microbubbles may interac
t to account for the observed findings.