The obesity epidemic is causing a rise in asthma incidence due to the appearance of an obesity-specific late-onset nonallergic (LONA) phenotype. We investigated why only a subset of obese participants develop LONA asthma by determining how obesity, both alone and in combination with LONA asthma, affects the volume dependence of respiratory system impedance. We also determined how obesity and asthma affect impedance during and following challenge with the PC dose of methacholine. We found during passive exhalation that all obese participants, in contrast to lean controls and lean asthmatics, experienced similarly profound elevations in lung elastance as they approached functional residual capacity. We also found, however, that the LONA asthmatics had a greater negative dependence of airway resistance on lung volume over the middle of the volume range compared with the other groups. Methacholine challenge with the PC dose led to comparable changes in respiratory system impedance in the four study groups, but the doses themselves were substantially lower in both obese and lean asthmatic participants compared with obese and lean controls. Also, the obese LONA asthmatics had higher breathing frequencies and lower tidal volumes postchallenge compared with the other participants. Taken together, these results suggest that all obese individuals experience substantial lung collapse as they approach functional residual capacity, presumably due to the weight of the chest wall. It remains unclear why obese LONA asthmatics are hyperresponsive to methacholine while obese nonasthmatic individuals are not. Why only a subset of severely obese subjects develop late-onset nonallergic (LONA) asthma remains unknown, although it is widely assumed that compression of the lungs by the chest wall is somehow involved. We show that lung compression is common to obese individuals both without asthma and with LONA asthma but that those with LONA asthma may have increased airway wall compliance and possibly also a reduced ability to recruit collapsed lung.
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http://dx.doi.org/10.1152/japplphysiol.00666.2020 | DOI Listing |
Int J Environ Res Public Health
January 2022
Department of Pharmacotherapy and Pharmaceutics, Faculté de Pharmacie, Université Libre de Bruxelles (ULB), 1050 Brussels, Belgium.
(1) Asthma is one of the most common chronic diseases in the world among children. The main purpose of this study was to analyze the consumption of asthma medications in order to investigate asthma in children (2-18 years) and the association with health care consumption; (2) a retrospective study using anonymized administrative data for 2013-2018 from the third largest Belgian health insurer was conducted; (3) in 2018, 12.9% of children received at least one asthma medication and 4.
View Article and Find Full Text PDFJ Appl Physiol (1985)
December 2021
Pulmonary Disease and Critical Care Medicine, University of Vermont College of Medicine, Burlington, Vermont.
J Appl Physiol (1985)
January 2021
Department of Medicine, Larner College of Medicine, University of Vermont, Burlington, Vermont.
ERJ Open Res
July 2020
Dept of Medicine, Larner College of Medicine, University of Vermont, Burlington, VT, USA.
Am J Respir Cell Mol Biol
May 2016
Department of Medicine, University of Vermont College of Medicine, Burlington, Vermont.
Obesity affects the incidence and severity of asthma in at least two major phenotypes: an early-onset allergic (EOA) form that is complicated by obesity and a late-onset nonallergic (LONA) form that occurs only in the setting of obesity. Both groups exhibit airway hyperresponsiveness to methacholine challenge but exhibit differential effects of weight loss. Measurements of lung function in patients with LONA obese asthma suggest that this group of individuals may simply be those unlucky enough to have airways that are more compliant than average, and that this leads to airway hyperresponsiveness at the reduced lung volumes caused by excess adipose tissue around the chest wall.
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