Effect of obesity on breathlessness and airway responsiveness to methacholine in non-asthmatic subjects

Abstract

Background: Obesity is associated with increased prevalence and incidence of asthma, but the mechanism is unknown. Obesity reduces lung volumes, which can increase airway responsiveness, and increases resistive and elastic work of breathing, which can increase dyspnea. Objective: To determine if the intensity of dyspnea due to airway narrowing or if airway responsiveness is increased in obese, non-asthmatic subjects. Subjects: Twenty-three obese (BMI (body mass index) X30 kg m À2 ) and 26 non-obese (BMI o30 kg m À2 ) non-asthmatic subjects, aged between 18 and 70 years. Methods: High-dose methacholine challenge was used to determine the sensitivity and the maximal response to methacholine. Respiratory system resistance (Rrs) and reactance were measured, using the forced oscillation technique, as indicators of resistive and elastic loads during challenge. Perception of dyspnea was measured by the Borg score during challenge. Static lung volumes were measured by body plethysmography. Results: Static lung volumes were reduced in the obese subjects. There were no significant differences in the sensitivity or maximal response to methacholine between obese and non-obese subjects. The magnitude of change in Rrs was similar in both groups, but obese subjects had more negative reactance after challenge (P ¼ 0.002) indicating a greater elastic load. The intensity of dyspnea was greater in obese subjects (P ¼ 0.03). Conclusions: Obesity reduces lung volumes, but does not alter the sensitivity or maximal response to methacholine. However, obese subjects have enhanced perception of dyspnea, associated with greater apparent stiffness of the respiratory system, and may therefore be at greater risk of symptoms.

Does increased baseline ventilation heterogeneity following chest wall strapping predispose to airway hyperresponsiveness?

“…The magnitude of the changes in lung volumes with CWS were consistent with the changes observed in mild-tomoderate obesity, including a slightly reduced TLC, a normal RV, and a ϳ500-ml reduction in FRC (18). CWS has consistently been shown to increase airway responsiveness in healthy subjects; however, evidence of an effect of obesity on airway responsiveness is weak and inconsistent in subjects with asthma (21) and without asthma (25). The present study suggests that a reduction in end-expiratory volume as seen in obesity should lead to AHR, independent of whether obesity, per se, does (17) or does not (16) alter ventilation heterogeneity.…”

Physiological Mechanisms of Airway Hyperresponsiveness in Obese Asthma

“…Something that both those with LONA obese asthma and those with EOA obese asthma have in common is the chronic reduction in lung volume that tends to accompany mass loading of the chest wall by adipose tissue in all individuals with obese asthma (50). Reduced lung volume is a potent mechanism for increasing AHR through the release of airway-parenchymal tethering forces, as discussed above, and thus in some way presumably represents a common pathway for all forms of obese asthma.…”

Obesity enhanced respiratory health effects of ambient air pollution in Chinese children: the Seven Northeastern Cities study

“…54 Breathing at low lung volumes has been shown to enhance development of dyspnea, which is associated with greater stiffness of the respiratory system, and may, therefore, increase risk of other respiratory complications in human subjects. 55 Obese humans have been shown to breathe with relatively smaller tidal volumes than individuals of normal weight, 56 which leads to a reduction in lung tissue stretching that could potentially affect sensitivity to ambient air pollution.…”