epithelial integrity in athletes with exercise-induced hypoxemia. J Appl Physiol 89: [1537][1538][1539][1540][1541][1542] 2000.-The effect of incremental exercise to exhaustion on the change in pulmonary clearance rate (k) of aerosolized 99m Tc-labeled diethylenetriaminepentaacetic acid ( 99m Tc-DTPA) and the relationship between k and arterial PO 2 (Pa O 2 ) during heavy work were investigated. Ten male cyclists (age ϭ 25 Ϯ 2 yr, height ϭ 180.9 Ϯ 4.0 cm, mass ϭ 80.1 Ϯ 9.5 kg, maximal O 2

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... ϭ 5.25 Ϯ 0.35 l/min, mean Ϯ SD) completed a pulmonary clearance test shortly (39 Ϯ 8 min) after a maximal O 2 uptake test. Resting pulmonary clearance was completed Ն24 h before or after the exercise test. Arterial blood was sampled at rest and at 1-min intervals during exercise. Minimum Pa O 2 values and maximum alveolar-arterial PO 2 difference ranged from 73 to 92 Torr and from 30 to 55 Torr, respectively. No significant difference between resting k and postexercise k for the total lung (0.55 Ϯ 0.20 vs. 0.57 Ϯ 0.17 %/min, P Ͼ 0.05) was observed. Pearson product-moment correlation indicated no significant linear relationship between change in k for the total lung and minimum Pa O 2 (r ϭ Ϫ0.26, P Ͼ 0.05). These results indicate that, averaged over subjects, pulmonary clearance of 99m Tc-DTPA after incremental maximal exercise to exhaustion in highly trained male cyclists is unchanged, although the sampling time may have eliminated a transient effect. Lack of a linear relationship between k and minimum Pa O 2 during exercise suggests that exercise-induced hypoxemia occurs despite maintenance of alveolar epithelial integrity. pulmonary clearance of technetium-99m-diethylenetriaminepentaacetic acid; alveolar epithelium; gas exchange EXERCISE-INDUCED HYPOXEMIA (EIH), defined as the inability to maintain arterial PO 2 (Pa O 2 ) and arterial oxyhemoglobin saturation (Sa O 2 ) during exercise, occurs in some high-aerobic-power athletes and is associated with a widened alveolar-arterial PO 2 gradient (A-aPO 2 ) (3, 4, 12, 29). The precise etiology of EIH and the widened A-aPO 2 remains unclear but is likely the result of, or an interaction among, relative alveolar hypoventilation, ventila-