Airway hyperresponsiveness is the excessive narrowing of the airway lumen caused by stimuli that would cause little or no narrowing in the normal individual. It is one of the cardinal features of asthma but remains largely unexplained. Sometimes, though, clues to the greatest mysteries are right in front of us but we do not see them, and the role of breathing in airway hyperresponsiveness may be one of these clues.

The smooth muscle surrounding the airway shortens when it is activated, and as the muscle shortens the airway narrows and breathing tends to become difficult. The lung has a potent built-in defence against bronchospasm, however, and this defence works in the opposite direction; the act of breathing makes it difficult for activated muscle to shorten [1–8]. Asthma is an inflammatory disease, but could it be that it is the failure of this particular defence mechanism which is the most telling end-effect of the inflammatory cascade, and therefore the proximal cause of airway hyperresponsiveness in asthma? This idea is not at all new [1], but the emergence of new evidence and new understanding of underlying mechanisms invites reconsideration of this question.