Decreases in oxyhaemoglobin saturation (SaO2) are frequently observed in highly trained male endurance athletes during heavy work and has been termed exercise-induced hypoxaemia (EIH). Ventilation perfusion (VA/Q) mismatching and diffusion limitations are thought to be responsible. Nitric oxide (NO), a potent vasodilator, is present in the exhaled air of resting and exercising humans. Endogenously produced NO is thought to play a role in VA/Q matching and maintenance of low pulmonary vascular resistance. The purpose of this study was to determine the relationship between exhaled NO and EIH. It was hypothesized that athletes with EIH would have lower NO levels compared with non-EIH athletes. Eighteen highly trained male cyclists (VO2max=67.7 +/- 5.2 mL kg-1 min-1, mean +/- SD) were divided into normal (NORM, n=12, SaO2= 93.9 +/- 0.8) or low (LOW, n=6, SaO2=90.3 +/- 1.0) group, based on significantly different peak exercise SaO2 values (P < 0.05). All other descriptive and physiological characteristics were similar between the groups. Subjects performed a ramped cycle test to exhaustion breathing NO-free gas. The concentration (CNO) and production rate (VNO) of NO were determined from mixed gas samples at rest and during exercise at 100, 200, 250, 300, 350, 400 and 450 W using a chemiluminescent analyser. CNO remained unchanged from resting values in all subjects. VNO increased significantly during exercise in all subjects but was not different between LOW and NORM groups. The correlation between change in SaO2 and VNO from rest to maximal exercise was not significant (r=-0.12, P > 0.05). Collectively, these data suggest that exhaled NO is not related to decreased SaO2 during heavy exercise in highly trained male cyclists.