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1 Department of Thoracic
Medicine, Royal Adelaide Hospital, Adelaide, South Australia 5000;
2 Department of Medicine,
University of California San Diego, La Jolla, California 92093;
3 Australian Institute of Sport,
The causes of exercise-induced hypoxemia (EIH)
remain unclear. We studied the mechanisms of EIH in highly trained
cyclists. Five subjects had no significant change from resting arterial PO2
(PaO2; 92.1 ± 2.6 Torr)
during maximal exercise (C), and seven subjects (E) had a
>10-Torr reduction in PaO2 (81.7 ± 4.5 Torr). Later, they were studied at rest and during various exercise intensities by using the multiple inert gas elimination technique in normoxia and hypoxia (13.2%
O2). During normoxia at 90%
peak O2 consumption,
PaO2 was lower in E compared with C (87 ± 4 vs. 97 ± 6 Torr, P < 0.001) and alveolar-to-arterial O2
tension difference
(A-aDO2)
was greater (33 ± 4 vs. 23 ± 1 Torr,
P < 0.001). Diffusion limitation
accounted for 23 (E) and 13 Torr (C) of the
A-aDO2
(P < 0.01). There were no
significant differences between groups in arterial
PCO2 (PaCO2) or ventilation-perfusion
(
A/
)
inequality as measured by the log SD of the perfusion distribution
(logSD). Stepwise
multiple linear regression revealed that lung
O2 diffusing capacity
(DLO2),
logSD, and
PaCO2 each accounted for ~30% of the
variance in PaO2
(r = 0.95, P < 0.001). These data suggest that
EIH has a multifactorial etiology related to
DLO2,
A/
inequality, and ventilation.
ventilation-perfusion inequality; pulmonary diffusion limitation; exercise
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