title: 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 approximately 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 < or = 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 9alpha,11beta-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.
authors.affiliation: Department of Population Health Sciences, University of Wisconsin-Madison, Madison, Wisconsin, USA. hans.haverkamp@med.uvm.edu
authors.forename: H C
authors.initials: HC
authors.lastname: Haverkamp
authors.forename: J A
authors.initials: JA
authors.lastname: Dempsey
authors.forename: J D
authors.initials: JD
authors.lastname: Miller
authors.forename: L M
authors.initials: LM
authors.lastname: Romer
authors.forename: D F
authors.initials: DF
authors.lastname: Pegelow
authors.forename: A T
authors.initials: AT
authors.lastname: Lovering
authors.forename: M W
authors.initials: MW
authors.lastname: Eldridge
mesh_terms: D000136:Acid-Base Equilibrium / Q000502:physiology; D000328:Adult; D000403:Airway Resistance / Q000502:physiology; D001249:Asthma / Q000503:physiopathology*; D001250:Asthma, Exercise-Induced / Q000503:physiopathology*; D002245:Carbon Dioxide / Q000097:blood; D015444:Exercise / Q000502:physiology*; D005260:Female; D006801:Humans; D018836:Inflammation Mediators / Q000502:physiology; D008297:Male; D010100:Oxygen / Q000097:blood; D010313:Partial Pressure; D011650:Pulmonary Alveoli / Q000502:physiology; D011659:Pulmonary Gas Exchange / Q000502:physiology*; D015656:Respiratory Mechanics / Q000502:physiology
chemical_list: D018836:Inflammation Mediators; D002245:Carbon Dioxide; D010100:Oxygen