Effects of exhaustive endurance exercise on pulmonary gas exchange and airway function in women

Seventeen fit women ran to exhaustion (14 +/-4 min) at a constant speed and grade, reaching 95 +/-3% of maximal O-2 consumption. Pre- and postexercise lung function, including airway resistance [total respiratory resistance (Rrs)] across a range of oscillation frequencies, was measured, and, on a separate day, airway reactivity was assessed via methacholine challenge. Arterial O-2 saturation decreased from 97.6 +/-0.5% at rest to 95.1 +/-1.9% at 1 min and to 92.5 +/-2.6% at exhaustion. alveolar-arterial O-2 difference (A-aDO(2)) widened to 27 +/-7 Torr after 1 min and was maintained at this level until exhaustion. Arterial PO2 (PaO2) fell to 80 +/-8 Torr at 1 min and then increased to 86 +/-9 Torr at exhaustion. This increase in PaO2 over the exercise duration occurred due to a hyperventilation-induced increase in alveolar PO2 in the presence of a constant A-aDO(2). Arterial O-2 saturation fell with time because of increasing temperature (+2.6 +/-0.5 degreesC) and progressive metabolic acidosis (arterial pH: 7.39 +/-0.04 at 1 min to 7.26 +/-0.07 at exhaustion). Plasma histamine increased throughout exercise but was inversely correlated with the fall in PaO2 at end exercise. Neither pre- nor postexercise Rrs, frequency dependence of Rrs, nor diffusing capacity for CO correlated with the exercise A-aDO(2) or PaO2. Although several subjects had a positive or borderline hyperresponsiveness to methacholine, this reactivity did not correlate with exercise-induced changes in Rrs or exercise-induced arterial hypoxemia. In conclusion, regardless of the degree of exercise-induced arterial hypoxemia at the onset of high-intensity exercise, prolonging exercise to exhaustion had no further deleterious effects on A-aDO(2), and the degree of gas exchange impairment was not related to individual differences in small or large airway function or reactivity.