PURPOSE: Exercise capacity is thought to be compromised in asthmatic subjects. This would especially be the case when exercise is preceded by significant airflow limitation in asthmatics who exhibit variable airway function on a day-to-day basis. The strong bronchodilatory effect of exercise, however, might minimize potential for pre-exercise airflow limitation to influence the responses to exercise. METHODS: Mild-to-moderate asthmatic subjects (n=9) completed exercise-to-exhaustion on a cycle ergometer (85% peak power) on three separate occasions: 1) following a eucapnic voluntary hyperpnea challenge (EVH), 2) a sham to the EVH (SHAM), and 3) a control trial of seated relaxation (CON). Pulmonary function was assessed at baseline and following each intervention. Metabolic rate, minute ventilation and its determinants, and spontaneous exercise flow-volume loops were analyzed at regular intervals during exercise. RESULTS: Subjects exhibited a 21% decrease in the forced expiratory volume 1.0 s (FEV1.0) following EVH (p<0.05 vs. CON and SHAM), and pre-exercise FEV1.0 was significantly lower during EVH compared to CON and SHAM (pre-exercise FEV1.0 = 3.8 ± 0.8, 3.8 ± 1.0, 3.2 ± 0.5 L for CON, SHAM, and EVH, respectively; p<0.05). During exercise, partial forced expiratory maneuvers demonstrated increases in expiratory flow rates compared to baseline during all trials, but the increased airflow was most marked during EVH. Exercise time-to-exhaustion was not different among the three trials (5.6 ± 1.6, 5.1 ± 1.5, 5.6 ± 2.4 minutes for CON, SHAM, and EVH). The ventilatory equivalent for metabolic carbon dioxide production (VE/VCO2), tidal volume to inspiratory capacity ratio (VT/IC), and exercise lung volumes (determined by IC maneuvers) were not different among the three trials. CONCLUSIONS: Acute, inflammatory-based airway dysfunction present immediately before exercise does not affect exercise ventilation or the airway mechanical responses to exercise in asthmatic subjects with mild-to-moderate disease. The powerful bronchodilatory response to exercise thus appears to override the airway dysfunction seen prior to exercise. Funding: Vermont Genetics Network, P20 RR16462 from the INBRE Program of the National Center for Research Resources, a component of the National Institutes of Health (NIH).
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