Abstract
PURPOSE: Due to force coupling between lung parenchyma and intrapulmonary airways, lung volume (VL) has a marked impact on airway caliber. Increased VL has also been shown to disrupt airway smooth muscle actomyosin cross-bridge formation in healthy and asthmatic persons. We hypothesized that elevated operating VL and regular deep lung inflations following an asthmogenic exercise bout would decrease the severity of exercise-induced bronchoconstriction (EIB) in asthmatic adults. METHODS: Nine asthmatic adults completed three experimental trials. During all three trials, subjects completed six minutes of cycling exercise at 85% of the peak workrate reached during a graded exercise test. Following exercise, subjects remained on the ergometer with the mouthpiece in place, and performed a maximal volitional flow-volume maneuver every even minute following exercise for a total of 20 minutes. During the first trial, subjects breathed spontaneously during the 20 minute period following exercise (SPON). The second and third trials were randomized and balanced. During one of the trials, minute ventilation was gradually decreased in a stepwise manner during the first ten minutes following exercise (GRAD); during the other trial, subjects performed an inspiratory capacity every odd minute during the recovery period (IC). Forced expiratory volume 1.0 second (FEV1.0) was compared among the three trials. RESULTS: Nadir post-exercise FEV1.0 (% change baseline) was similar among the three trials (SPON, -27.7 ± 5.3%; GRAD, -22.5 ± 5.2%; IC, -23.3 ± 5.1%; P=0.52). Nadir FEV1.0 also occurred at a similar time after exercise during the three trials (SPON, 11.1 ± 1.8 min; GRAD, 12.9 ± 1.5 min; IC, 9.1 ± 1.6 min, P=0.10). Area under the curve for FEV1.0 was the same during the three trials (SPON, 47.9 ± 15.1 min·l; GRAD, 50.5 ± 12.7 min·l; IC, 50.5 ± 13.8 min·l; P=0.49). CONCLUSIONS:Contrary to our hypothesis, these data suggest that increased VL and regular deep lung inflations after exercise do not attenuate EIB in asthmatic patients. Thus, maintenance of the bronchodilatory influence of increased VL after exercise cessation does not override the opposing stimuli that cause airway narrowing in the asthmatic. FUNDING: Vermont Genetics Network, P20 RR16462 from the INBRE Program of the National Center for Research Resources, NIH.
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