Abstract
Stimulation of the Beta2 Adrenergic Receptors (B2AR) induces lung fluid clearance through Epithelial Sodium channels (ENaC) on alveolar cells. We previously demonstrated that both albuterol and exercise increase the diffusing capacity of the lung (DLCO), alveolar-capillary membrane conductance (DM), and DM corrected for pulmonary capillary blood volume (Vc)(DM/Vc). The improvement in diffusing capacity with exercise could be a direct result of B2AR stimulation or simply an increase in lymphatic drainage due to augmentations in tidal volume (Vt) and minute ventilation (VE). PURPOSE: To investigate the relationship of the change in DLCO (and components, DM and Vc) with albuterol and the change in DLCO and components with exercise to determine B2AR involvement. METHODS: Healthy participants (N=30) completed a maximal VO2 test for baseline capacity, followed by 2 visits measuring lung diffusing capacity for carbon monoxide and nitric oxide, and functional ventilatory parameters. Measurements were taken at rest and 30-minutes post-albuterol administration or at peak exercise. RESULTS: At rest and at peak exercise there were significant relationships in DLCO, DM, and DM/Vc between the albuterol visit and the exercise visit (DLCO: r=0.90 and 0.78, DM: r=0.77 and 0.67, DM/Vc: r=0.58 and 0.48 for rest and peak exercise, respectively, p<0.05 for all). Exercise resulted in a significant increase in DLCO and DM, when compared to albuterol (DLCO=45±16% vs. 0.78±7.6%, DM=40±24% vs. 2.8±13% for exercise and albuterol, respectively, p<0.05). There was no relationship between changes in DLCO and DM with albuterol when compared to changes with exercise, but the change in DM/Vc under the two conditions was trending towards significance (r=0.35, DM/Vc=11.5±8.3% and DM/Vc=6.4±5.2% for exercise and albuterol, respectively, p=0.06). There was a significant relationship (p<0.05) between the change in Vt and DLCO with exercise, but not with albuterol. CONCLUSIONS: The relationship between lung diffusion parameters at peak exercise and following beta-agonist stimulation suggest that at least a portion of this increase is mediated by the B2AR. However, DLCO, considered to be a gross measure of the components of lung diffusion, is influenced by changes in ventilation with exercise. Supported by NIH Grant RO1 HL108962-05.
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