In some people with asthma, expiratory airflow limitation, premature closure of small airways, activity of inspiratory muscles at the
end of expiration and reduced pulmonary compliance may lead to lung hyperinflation. With the increase in lung volume, chest wall
geometry is modified, shortening the inspiratory muscles and leaving them at a sub-optimal position in their length-tension relationship.
Thus, the capacity of these muscles to generate tension is reduced. An increase in cross-sectional area of the inspiratory muscles caused
by hypertrophy could offset the functional weakening induced by hyperinflation. Previous studies have shown that inspiratory muscle
training promotes diaphragm hypertrophy in healthy people and patients with chronic heart failure, and increases the proportion of
type I fibres and the size of type II fibres of the external intercostal muscles in patients with chronic obstructive pulmonary disease.
However, its effects on clinical outcomes in patients with asthma are unclear.