Obesity alters the topographical distribution of ventilation and the regional response to bronchoconstriction

• Published in: Journal of applied physiology (1985) Vol. 128; no. 1; pp. 168 - 177
• Main Authors: Rutting, S., Mahadev, S., Tonga, K. O., Bailey, D. L., Dame Carroll, J. R., Farrow, C. E., Thamrin, C., Chapman, D. G., King, G. G.
• Format: Journal Article
• Language: English
• Published: United States 01.01.2020
• Subjects: Adolescent; Adult; Aged; Bronchial Hyperreactivity - etiology; Bronchial Hyperreactivity - pathology; Bronchial Provocation Tests; Bronchoconstriction; Female; Humans; Lung Volume Measurements; Male; Methacholine Chloride - pharmacology; Middle Aged; Obesity - complications; Obesity - diagnostic imaging; Pulmonary Ventilation; Respiratory Physiological Phenomena; Single Photon Emission Computed Tomography Computed Tomography; Young Adult; bronchoprovocation; ventilation distribution; obesity; single-photon emission computed tomography
• ISSN: 8750-7587; 1522-1601; 1522-1601
• DOI: 10.1152/japplphysiol.00482.2019

Obesity is associated with reduced operating lung volumes that may contribute to increased airway closure during tidal breathing and abnormalities in ventilation distribution. We investigated the effect of obesity on the topographical distribution of ventilation before and after methacholine-induced bronchoconstriction using single-photon emission computed tomography (SPECT)-computed tomography (CT) in healthy subjects. Subjects with obesity ( n = 9) and subjects without obesity ( n = 10) underwent baseline and postbronchoprovocation SPECT-CT imaging, in which Technegas was inhaled upright and followed by supine scanning. Lung regions that were nonventilated (Vent non ), low ventilated (Vent low ), or well ventilated (Vent well ) were calculated using an adaptive threshold method and were expressed as a percentage of total lung volume. To determine regional ventilation, lungs were divided into upper, middle, and lower thirds of axial length, derived from CT. At baseline, Vent non and Vent low for the entire lung were similar in subjects with and without obesity. However, in the upper lung zone, Vent non (17.5 ± 10.6% vs. 34.7 ± 7.8%, P < 0.001) and Vent low (25.7 ± 6.3% vs. 33.6 ± 5.1%, P < 0.05) were decreased in subjects with obesity, with a consequent increase in Vent well (56.8 ± 9.2% vs. 31.7 ± 10.1%, P < 0.001). The greater diversion of ventilation to the upper zone was correlated with body mass index ( r s  = 0.74, P < 0.001), respiratory system resistance ( r s  = 0.72, P < 0.001), and respiratory system reactance ( r s  = −0.64, P = 0.003) but not with lung volumes or basal airway closure. Following bronchoprovocation, overall Vent non increased similarly in both groups; however, in subjects without obesity, Vent non only increased in the lower zone, whereas in subjects with obesity, Vent non increased more evenly across all lung zones. In conclusion, obesity is associated with altered ventilation distribution during baseline and following bronchoprovocation, independent of reduced lung volumes. NEW & NOTEWORTHY Using ventilation SPECT-computed tomography imaging in healthy subjects, we demonstrate that ventilation in obesity is diverted to the upper lung zone and that this is strongly correlated with body mass index but is independent of operating lung volumes and of airway closure. Furthermore, methacholine-induced bronchoconstriction only occurred in the lower lung zone in individuals who were not obese, whereas in subjects who were obese, it occurred more evenly across all lung zones. These findings show that obesity-associated factors alter the topographical distribution of ventilation.