Impact of Insulin Resistance on Asthma: Is There Truly No Role of “Obesity”?

Obesity reduces FRC and expiratory reserve volume, with implications for airway closure and inequalities, especially during stress, such as exercise, when many asthmatics report distressing symptoms. Obesity-related reduced FRC may offer a mechanism for increased airway hyperresponsiveness because airway-parenchymal tethering is reduced at lower lung volumes, making it easier for the airways to constrict in response to stimuli. Obesity-related chest wall compression is also implicated in increased lung de-recruitment, either by small airway closure or alveolar atelectasis, manifesting as a reduced FVC. Although similar degrees of lung de-recruitment have been found between obese adults without asthma and obese adults with late-onset nonallergic (LONA) asthma, there is lower FVC and increased difficulty in recruiting closed alveolar units with a deep breath as well as higher airway hyperresponsiveness among obese individuals with LONA asthma. Mechanisms for differences in airway hyperresponsiveness between obese and nonobese individuals with LONA asthma are not fully defined. Still, they include increased airway compliance predisposing to greater airway collapse under a higher chest wall load. Thus, through excess adipose tissue around the chest wall, breathing at lower lung volumes and lung de-recruitment could be factored in physiological changes, such as airway hyperresponsiveness or collapse, and contribute to asthma symptoms and severity.