Relationship between decreased oxyhaemoglobin saturation and exhaled nitric oxide during exercise

Decreases in oxyhaemoglobin saturation (S(a)o(2)) are frequently observed i n highly trained male endurance athletes during heavy work and has been ter med exercise-induced hypoxaemia (EIH). Ventilation perfusion (V-A/Q) mismat ching and diffusion limitations are thought to be responsible. Nitric oxide (NO), a potent vasodilator, is present in the exhaled air of resting and e xercising humans. Endogenously produced NO is thought to play a role in V-A /O matching and maintenance of low pulmonary vascular resistance. The purpo se of this study was to determine the relationship between exhaled NO and E IH. It was hypothesized that athletes with EIH would have lower NO levels c ompared with non-EIH athletes. Eighteen highly trained male cyclists (Vo(2m ax) = 67.7 +/- 5.2 mL kg(-1) min(-1), mean +/- SD) were divided into normal (NORM, n = 12, S(a)o(2) = 93.9 +/- 0.8) or low (LOW, n = 6, S(a)o(2) = 90. 3 +/- 1.0) group, based on significantly different peak exercise S(a)o(2) v alues (P < 0.05). All other descriptive and physiological characteristics w ere similar between the groups. Subjects performed a ramped cycle test to e xhaustion breathing NO-free gas. The concentration (C-NO) and production ra te (V-NO) of NO were determined from mixed gas samples at rest and during e xercise at 100, 200, 250, 300, 350. 400 and 450 W using a chemiluminescent analyser. C-NO remained unchanged from resting Values in all subjects. V-NO increased significantly during exercise in all subjects but was not differ ent between LOW and NORM groups. The correlation between change in S(a)o(2) and V-NO 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 S(a)o(2) during heavy exercise in highly trained male cyclists.