Asthma is a common affliction that is often mild and intermittent but may be debilitating or even fatal. A key component of the asthma phenotype is airways hyperresponsiveness (AHR) characterized by excessive derangements in mechanical lung function in response to standardized doses of airway smooth muscle agonist. Understanding AHR is a multi-scale problem. At the microscopic scale, dynamic interactions between myosin cross-bridges and actin filaments within the ASM cell are ultimately responsible for force generation. The Huxley model of skeletal muscle contraction has been used to account for these interactions, but a coarse-grained version of the model can be derived that acknowledges the much more haphazard arrangement of the contractile proteins in ASM compared to skeletal muscle. At the mesoscopic scale, differential equation models describe airway narrowing due to force generation by the ASM when the pulmonary airways are embedded in viscoelastic parenchymal tissue. Such models recapitulate the strong dependence of narrowing on lung volume due to the forces of airway-parenchymal interdependence. At the macroscopic scale, models explain how distributions of constricting airways in the pulmonary airway tree collectively give rise to the changes in lung mechanical impedance seen, for example, following airway challenge with methacholine aerosol.