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The effect of repeat exercise on pulmonary diffusing capacity and EIH in trained athletes. Med. Sci. Sports Exerc., Vol. 31, No. 1, pp. 99-104, 1999.

Purpose: The purpose of this study was to determine the effects of repeated heavy exercise on postexercise pulmonary diffusing capacity (DL) and the development of exercise induced arterial hypoxemia (EIH).

Methods: 13 endurance-trained, male athletes (age = 27 /- 3 yr, height = 179.6 /- 5.0 cm, weight = 71.8 /- 6.9 kg, V[spacing dot above]O2max = 67.0 /- 3.6 mL[middle dot]kg-1[middle dot]min-1) performed two consecutive, continuous exercise tests on a cycle ergometer to V[spacing dot above]O2max, separated by 60 min of recovery. Arterial oxygen saturation (%SaO2) was measured via ear oximetry, and resting DL was measured and partitioned by the single-breath method, before exercise and 60 min after each exercise bout.

Results: No significant differences resulted in V[spacing dot above]O2max, V[spacing dot above]E, peak heart rate (HR), or breathing frequency between exercise bouts (P > 0.05). There was a small but significant decrease (454-446 W; P < 0.05) in peak power output in the second test. %SaO2 decreased from resting values during both exercise tasks, but there was no difference between the minimum saturation achieved in test 1 (91.4) or test 2 (91.6; P > 0.05). After the initial exercise bout, significant decreases (P < 0.05) occurred in DL (11%), membrane diffusing capacity (DM) (11%) and pulmonary capillary volume (VC) (10%). Further decreases occurred in DL (6%; P < 0.05), DM (2%; P > 0.05), and VC (10%; P < 0.05) after the second exercise bout.

Conclusions: These observations question the meaning of post exercise measurements of pulmonary diffusion capacity, and its components, relative to pulmonary gas exchange and pulmonary fluid accumulation during exercise. The fact that there was no further change in %SaO2 after the second test suggests that if any interstitial edema developed, it was of no clinical significance; alternatively, the changes in DLCO may be related more to redistribution of blood than the development of pulmonary edema.

(C) 1999 Lippincott Williams & Wilkins, Inc.