Airway hyperresponsiveness in asthma may not be a problem of too much airwa
y smooth muscle strength. Rather, it may be a problem of too little of the
factors that oppose muscle shortening. The weight of available evidence see
ms to support the idea that loss of the dilating response to a deep inspira
tion may play a central role in this process, and that the locus of the res
ponse is within the airway smooth muscle cell. Bridge dynamics and plastic
reorganization of the smooth muscle cytoskeleton are the focus of this comm
entary; how these factors interact and details about underlying mechanisms
remain unclear.