1. We questioned whether exercise-induced arterial hypoxaemia (EIAH) o
ccurs in healthy active women, who have smaller lungs, reduced lung di
ffusion, and lower maximal O-2, consumption rate (V(over dot)(O?2,max)
) than age-and height-matched men. 2. Twenty-nine healthy young women
with widely varying fitness levels (V(over dot)(O?2,max), 57 +/- 6 ml
kg(-1) min(-1); range, 35-70 ml kg(-1) min(-1); or 148 +/- 5%; range,
93-188% predicted) and normal resting lung function underwent an incre
mental treadmill test to V(over dot)(O?2,max) during the follicular ph
ase of their menstrual cycle. Arterial blood samples were taken at res
t and near the end of each workload. 3. Arterial P-O?2 (P-a,P-O?2) dec
reased > 10 mmHg below rest in twenty-two of twenty-nine subjects at V
(over dot)(O?2,max) (P-a,P-O?2 77.5 +/- 0.9 mmHg; range, 67-84mmHg; ar
terial O-2 saturation (S-a,S-O?2)) 92.3 +/- 0.2%; range, 87-94%). The
remaining seven subjects maintained P-a,P-O?2 within 10 mmHg of rest P
-a,P-O?2 at V(over dot)(O?2,max) was inversely related to the alveolar
to arterial O-2, difference (A-aDO(2)) (r = -0.93; 35-52 mmHg) and to
arterial P-CO?2 (P-a,P-CO?2) (r = 0.62; 26-39 mmHg). 4. EIAH was inve
rsely related to V(over dot )(O?2,max) (r = 0.49); however, there were
many exceptions. Almost half of the women with significant EIAH had V
(over dot)(O?2,max) within 15% of predicted normal values (V(over dot)
(O?2,max) 40-55 ml kg(-1)min(-1)); among subjects with very high V(ove
r dot)(O?2,max), (55-70 ml kg(-1)min(-1)), the degree of excessive A-a
DO(2) and EIAH varied markedly (e.g. A-aDO(2), 30-50 mmHg; P-a,P-O?2 6
8-91 mmHg). 5. In the women with EIAH at V(over dot)(O?2,max) many beg
an to experience an excessive widening of of their A-aDO(2), during mo
derate intensity exercise, which when combined with a weak ventilatory
response, led to a progressive hypoxaemia. Inactive, less fit subject
s had no EIAH and narrower A-aDO(2) when compared with active, fitter
subjects at the same V(over dot)(O?2) (40-50 ml kg(-1) min(-1)). 6. Th
ese data demonstrate that many active healthy young women experience s
ignificant EIAH, and at a V(over dot)(O?2,max), that is substantially
less than those in their active male contemporaries. The onset of EIAH
during submaximal exercise, and/or its occurrence at a relatively low
V(over dot)(O?2,max), implies that lung structure/function subserving
alveolar to arterial O-2 transport is abnormally compromised in many
of these habitually active subjects.