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J Appl Physiol 99: 1843-1852, 2005. First published July 21, 2005; doi:10.1152/japplphysiol.01399.2004
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Repeat exercise normalizes the gas-exchange impairment induced by a previous exercise bout in asthmatic subjects

H. C. Haverkamp,1 J. A. Dempsey,1 J. D. Miller,1 L. M. Romer,1 D. F. Pegelow,1 A. T. Lovering,1 and M. W. Eldridge1,2

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·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 9{alpha},11{beta}-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



Address for reprint requests and other correspondence: H. C. Haverkamp, Univ. of Vermont, Vermont Lung Center, 149 Beaumont Ave., HSRF 226, Burlington, VT 05405 (e-mail: hans.haverkamp{at}med.uvm.edu)




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