Gas Exchange During Exercise In Habitually Active Asthmatic Subjects

PURPOSE The first aim of this study was to characterize the gas exchange and breathing mechanics responses to high-intensity exercise in habitually active asthmatics. We also sought to determine the relationships between breathing mechanics, airway inflammation, gas exchange, and arterial blood gas status during the exercise. METHODS Twenty-one habitually active (maximal oxygen uptake [VO2max], 48.2±7.0 ml.kg−1·min−1; 119% predicted), mild-to-moderate asthmatics performed treadmill exercise to exhaustion (11.2±.15 min) at ∼90% VO2max. Arterial blood was collected and multiple measures of breathing mechanics were assessed during the exercise, and inflammatory cells and mediators were measured in the induced sputum before and after exercise. RESULTS Arterial O2 saturation (SaO2) decreased to less than 94% during the exercise in 8/21 subjects (DESAT), due in large part to a decreased arterial PO2 ([PaO2] 93.0±7.7 to 79.7±4.0 Torr). In the DESAT group, a widened alveolar-to-arterial PO2 (AaDO2) and the magnitude of the ventilatory response accounted for 54 and 46% of the decrease in PaO2, respectively, at end exercise. Furthermore, in several subjects, the decreased SaO2 occurred at lower exercise metabolic rates than normally required to elicit desaturation in healthy subjects (n = 4, exercise VO2 = 36.1±3.8 ml.kg−1·min−1). Baseline pulmonary function and airway inflammation at baseline did not correlate with arterial blood gases or the AaDO2 during exercise. However, sputum histamine increased after exercise in the DESAT group (37.8±27.1 to 61.4±47.3 ng.ml−1, P < 0.05), and the absolute post-exercise values, as well as the change in histamine, correlated with the exercise PaO2 and AaDO2 (P < 0.05). Mean pulmonary resistance was high during exercise (3.4±1.2 cmH2O.L−1.s−1) but did not increase over time during the exercise bout. Expiratory flow-limitation occurred in 19/21 subjects during at least one time point during the exercise, and averaged 60±26% (range, 15 to 85%) of tidal volume near end exercise, and end expiratory lung volume (EELV) rose progressively so that at exhaustion it was 0.27 L greater than resting EELV (P < 0.05). These mechanical constraints to ventilation contributed to a highly heterogeneous and often insufficient ventilatory response; arterial PCO2 ranged from 29.8 to 46.6 Torr at end exercise. CONCLUSIONS We conclude that pulmonary gas exchange is impaired during high intensity exercise in a significant number of habitually active asthmatic subjects due to narrowed, high resistance airways and possibly to a deleterious effect of exercise-induced airway inflammation on gas exchange efficiency.