Gas exchange during exercise in habitually active asthmatic subjects

We determined the relations among gas exchange, breathing mechanics, and airway inflammation during moderate- to maximum-intensity exercise in asthmatic subjects. Twenty-one habitually active (48.2 ± 7.0 ml· kg ^-1·min^-1 maximal O₂ uptake) mildly to moderately asthmatic subjects (94 ± 13% predicted forced expiratory volume in 1.0 s) performed treadmill exercise to exhaustion (11.2 ± 0.15 min) at ∼90% of maximal O₂ uptake. Arterial O₂ saturation decreased to ≤94% during the exercise in 8 of 21 subjects, in large part as a result of a decrease in arterial Po₂ (Pao ₂): from 93.0 ± 7.7 to 79.7 ± 4.0 Torr. A widened alveolar-to-arterial Po₂ difference and the magnitude of the ventilatory response contributed approximately equally to the decrease in PaO₂, during exercise. Airflow limitation and airway inflammation at baseline did not correlate with exercise gas exchange, but an exercise-induced increase in sputum histamine levels correlated with exercise Pao₂ (negatively) and alveolar-to-arterial Po₂ difference (positively). Mean pulmonary resistance was high during exercise (3.4 ± 1.2 CmH ₂O·I^-1·S) and did not increase throughout exercise. Expiratory flow limitation occurred in 19 of 21 subjects, averaging 43 ± 35% of tidal volume near end exercise, and end-expiratory lung volume rose progressively to 0.25 ± 0.47 liter greater than resting end-expiratory lung volume at exhaustion. These mechanical constraints to ventilation contributed to a heterogeneous and frequently insufficient ventilatory response; arterial PcO₂ was 30-47 Torr at end exercise. Thus pulmonary gas exchange is impaired during high-intensity exercise in a significant number of habitually active asthmatic subjects because of high airway resistance and, possibly, a deleterious effect of exercise-induced airway inflammation on gas exchange efficiency.