Repeat exercise normalizes the gas-exchange impairment induced by a previous exercise bout in asthmatic subjects

Abstract

Twenty-one subjects with asthma underwent treadmill exercise to exhaustion at a workload that elicited ∼90% of each subject's maximal O2 uptake (EX1). After EX1, 12 subjects experienced significant exercise-induced bronchospasm [(EIB+), %decrease in forced expiratory volume in 1.0 s = −24.0 ± 11.5%; pulmonary resistance at rest vs. postexercise = 3.2 ± 1.5 vs. 8.1 ± 4.5 cmH2O·l−1·s−1] and nine did not (EIB−). The alveolar-to-arterial Po2 difference (A-aDo2) was widened from rest (9.1 ± 6.7 Torr) to 23.1 ± 10.4 and 18.1 ± 9.1 Torr at 35 min after EX1 in subjects with and without EIB, respectively ( P < 0.05). Arterial Po2 (PaO2) was reduced in both groups during recovery (EIB+, −16.0 ± −13.0 Torr vs. baseline; EIB−, −11.0 ± 9.4 Torr vs. baseline, P ≤ 0.05). Forty minutes after EX1, a second exercise bout was completed at maximal O2 uptake. During the second exercise bout, pulmonary resistance decreased to baseline levels in the EIB+ group and the A-aDo2 and PaO2 returned to match the values seen during EX1 in both groups. Sputum histamine (34.6 ± 25.9 vs. 61.2 ± 42.0 ng/ml, pre- vs. postexercise) and urinary 9α,11β-prostaglandin F2 (74.5 ± 38.6 vs. 164.6 ± 84.2 ng/mmol creatinine, pre- vs. postexercise) were increased after exercise only in the EIB+ group ( P < 0.05), and postexercise sputum histamine was significantly correlated with the exercise PaO2 and A-aDo2 in the EIB+ subjects. Thus exercise causes gas-exchange impairment during the postexercise period in asthmatic subjects independent of decreases in forced expiratory flow rates after the exercise; however, a subsequent exercise bout normalizes this impairment secondary in part to a fast acting, robust exercise-induced bronchodilatory response.