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Departments of 1Population Health Sciences and 2Pediatrics, University of Wisconsin-Madison, Madison, Wisconsin
Submitted 21 December 2004 ; accepted in final form 14 July 2005
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·l1·s1] 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 9
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-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.
exercise-induced bronchospasm; pulmonary resistance; airway inflammation; bronchodilation; alveolar-to-arterial oxygen difference
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