The airways of asthmatic subjects undergo complex changes which affect all compartments of the airway wall. The airway smooth muscle (ASM) is particularly affected and is increased in mass. Both hyperplasia and hypertrophy probably contribute to the altered mass of muscle which is a potential cause of airway hyperresponsiveness. The impedance to smooth muscle shortening resulting from the constitutive properties of the airway wall and the elasticity of the parenchyma may be more easily overcome by the excess muscle of the asthmatic airway. The ASM may also undergo important changes in its functional characteristics as a result of allergic sensitization and challenge. Increases in maximal shortening velocity, phospholipase C activity and membrane potential are some of the changes in the characteristics of sensitized ASM. The ASM may also change its phenotype from a contractile to a secretory tissue in response to the stimulus of airway inflammation and in doing so may contribute to the inflammatory process itself. The current therapies for asthma have the potential to counter some of the adverse effects of airway modelling, in particular in so far as the ASM is concerned. These effects should be kept in mind when considering the rationale for effective maintenance therapy for asthma.