At a given steady O-2 consumption ((V)over dotO(2)) in normoxia, cardiac ou
tput ((Q)over dot) is inversely proportional to arterial O-2 concentration
(CaO2), so that O-2 delivery (Q)over dotO(2)=QCaO(2)) is kept constant and
adapted to (V)over dotO(2). The matching between (Q)over dotaO(2) and (V)ov
er dotO(2) keeps O-2 return ((Q)over dot (v) over bar aO(2)=(Q)over dotO(2)
-VO2) constant and independent of (V)over dotO(2) and haemoglobin concentra
tion ([Hb][). This may not be so in hypoxia: in order for (over dot)Q (v) o
ver barO(2) to be independent of the inspired O-2 fractions (FIO2), the slo
pes of the (Q)over dot versus (V)over dotO(2) lines should be greater the l
ower the CaO2, which may not be the case. Thus, we tested the hypothesis of
constant (Q)over dot (v) over barO(2) by determining (Q)over dotaO(2) and
(Q)over dot (v) over barO(2) in acute hypoxia. Thirteen subjects performed
steady-state submaximal exercise on the cycle ergometer at 30, 60, 90 and 1
20 W breathing FIO2 of 0.21, 0.16, 0.13, 0.11 and 0.09. (V)over dotO(2) was
measured by a metabolic cart. (Q)over bot by CO2 rebreathing, [Hb] by a ph
otometric technique and arterial O-2 saturation (SaO(2)) by infrared oximet
ry. CaO2 was calculated from [Hb], SaO(2) and the O-2 binding coefficient o
f haemoglobin. The (V)over dotO(2) versus power relation was independent of
FIO2. The relations between (Q)over dot and (V)over dotO(2) were displaced
upward and had higher slopes in hypoxia than in normoxia. However, the (Q)
over dot changes did not compensate for those in CaO2. The slopes of the (Q
)over dotaO(2) versus (V)over dotO(2) lines tended to decrease in hypoxia.
(Q)over dot (v) over barO(2) was lower the lower the FIO2. A significant re
lationship was found between Q (v) over barO(2) and SaO(2) (Q ($) over barO
(2) = 1.442 SaO(2)+0.107, r=0.871, n=24, P < 10(-7)), which confutes the hy
pothesis of constant (Q)over dotvO(2) in hypoxia.