When muscles contract, airway diameter decreases and bronchus tissue is displaced towards the center. As tissue is incompressible, the thickness of the wall increases. Hence resistance to flow increases on two accounts: smaller diameter and airways mucosa encroaching on the airway lumen. The reverse holds during bronchodilatation.
There is considerable smooth muscle hypertrophy. Note also the pronounced thickening of the basal membrane in this woman, who died of status asthmaticus.
Smooth muscles can contract isometrically, istonically, or in an intermediate fashion between these two extremes, in vivo. Airway smooth muscle does not contract isometrically, since the airway is not rigid. It is likely that airway smooth muscles contract semi-isotonically, becoming shorter until this is limited by opposing forces, e.g. airway wall elastance and lung elastic recoil. The force developed by airway smooth muscles when stimulated depends on their initial length. This relationship is described by the force-length characteristics of the muscle. The force developed is minimal when the muscle is near its minimum or maximum length, and is greatest in between these lengths (optimal length). The smooth muscle can return to its initial length upon relaxation. It is generally assumed that in asthma or COPD exogenous and endogenous substances give rise to smooth muscle stimulation. Hence in these diseases basic smooth muscle stimulation will generally be on a higher level compared to healthy subjects, and potentially greater relaxation can be achieved.Chronic airway inflammation in asthma and COPD may not only be accompanied by increased muscle tone, but also by smooth muscle hypertrophy and hyperplasia. The total smooth muscle mass relative to airway calibre is then larger than in the normal airway.