We studied O-2 transport in the leg to determine if hyperoxia will inc
rease the maximal rate of O-2, uptake (VO2max) in exercising muscle. A
n increase in inspired O-2 fraction (FIO2) from 0.21 to 1.00 was postu
lated to have the following effects: 1) increase the leg VO2max by sim
ilar to 5-10%, 2) increase the maximal O-2 delivery [arterial O-2 conc
entration.flow (Ca-O2.Q)] by similar to 10%, and 3) raise the leg VO2m
ax in proportion to both the femoral venous PO2 and mean leg capillary
PO2. To test these hypotheses, 11 men performed cycle exercise to the
highest work rates (WR(max)) they could achieve while breathing 100%
O-2 (hyperoxia), 21% O-2 (normoxia), and 12% O-2 (hypoxia). Leg VO2, w
as derived from duplicate measurements of femoral venous blood flow an
d Ca-O2 and femoral venous blood O-2, concentrations (Cv(O2)) at 20, 3
5, 50, 92, and 100% WR(max) in each FIO2. Femoral venous leg Q (Q(leg)
) was measured by the constant-infusion thermodilution technique, and
leg O-2 uptake (VO2) was determined by the Fick principle [V-O2 = Q(le
g)(CaO2 - Cv(O2))]. Leg VO2max was the mean of duplicate values of VO2
at 100% WR(max) for each FIO2. Hyperoxia increased leg VO2max by 8.1%
(P = 0.016) and maximal O-2 delivery by 10.9% (P = 0.005) without cha
nging Q(leg). There was a significant increase in femoral venous PO2 (
P <0.001) that was proportionally greater than the increase in leg VO2
max. The results support our first and second maw hypotheses, providin
g direct evidence that in normal subjects leg VO2max is limited by O-2
supply during normoxia. Contrary to the third hypothesis, leg VO2max
did not increase in proportion to either the femoral venous PO2 or mea
n leg capillary PO2 during hyperoxia.