Effects of nitric oxide inhalation on pulmonary gas exchange during exercise in highly trained athletes

The pathophysiology of exercise-induced hypoxaemia in elite athletes is sti ll unclear but several studies indicate that a diffusion limitation, which could be explained by an interstitial pulmonary oedema, is a major contribu ting factor. Stress failure would induce a haemodynamical interstitial oede ma with inflammatory reaction and release of mediators like histamine. Hist amine release was found to be correlated with the hypoxaemia in elite athle tes. if stress failure is involved, inhalation of pulmonary vasodilatators such as nitric oxide during exercise in athletes should induce an inhibitio n of the histamine release and a reversal of the hypoxaemia. Nine male endu rance-trained young athletes performed two randomized exercise tests: one w ithout and the other with 15 p.p.m. of inhaled NO. Measurements of histamin e release and arterial blood gas analysis were performed at rest and at 50, 75 and 100% (V)over dot O-2max. At rest, inhaled NO induced a decrease in PaO2 and an increase in (Ai-a)DO2 suggesting increased perfusion of units w ith low (V)over dot (A)/(Q)over dot. During exercise, NO inhalation suppres sed the histamine release observed without NO and induced a moderation in t he decrease in PaO2 and the increase in (Ai-a)DO2 observed between 75 and 1 00% of (V)over dot O-2max (P < 0.005). In conclusion, this study showed tha t NO inhalation inhibited exercise-induced histamine release in highly trai ned athletes, but we were unable to confirm the suppression of exercise-ind uced hypoxaemia (EIH). An unexpected result was that inhaled NO seemed to h ave a marked effect on arterial oxygenation in highly trained-athletes, by disturbing gas exchanges.