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Asthma phenotyping and endotyping has emerged as a novel approach to asthma classification inspired by precision medicine which separates the clinical presentations of asthma, or asthma phenotypes, from their underlying causes, or asthma endotypes. The best-supported endotypic distinction is the type 2-high/type 2-low distinction.
Bronchial hyperresponsiveness is a hallmark of asthma but also occurs frequently in people with chronic obstructive pulmonary disease (COPD). [2] In the Lung Health Study, bronchial hyperresponsiveness was present in approximately two-thirds of patients with non-severe COPD, and this predicted lung function decline independently of other ...
Bronchial thermoplasty is the only treatment modality designed to combat a hallmark of airway remodelling; airway smooth muscle hypertrophy. The effects of bronchial thermoplasty on smooth muscle mass are seen up to at least 12 months post-treatment; however, the procedure does not seem to impact other features of airway remodelling. [4]
During an asthma episode, inflamed airways react to environmental triggers such as smoke, dust, or pollen. The airways narrow and produce excess mucus, making it difficult to breathe. In essence, asthma is the result of an immune response in the bronchial airways. [3]
The bronchial spasm is due to the activation of parasympathetic nervous system. Postganglionic parasympathetic fibers will release acetylcholine causing the constriction of the smooth muscle layer surrounding the bronchi. These smooth muscle cells have muscarinic M 3 receptors on their membrane.
There is, of course, no reason why asthma and exercise-induced bronchoconstriction should not co-exist but the distinction is important because without successful treatment of underlying asthma, treatment of an exercise component will likely be unsuccessful.
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