Airway hyperresponsiveness in asthma. Not just a problem of smooth muscle relaxation with inspiration

Am J Respir Crit Care Med. 1998 Jul;158(1):203-6. doi: 10.1164/ajrccm.158.1.9707125.


Airway hyperresponsiveness in asthma has been attributed to impaired ability of deep inspiration (DI) to stretch airway smooth muscle. We have retested this hypothesis by comparing the responses to methacholine of 10 asthmatic and 10 control subjects. After each dose subjects breathed tidally without deep inspiration for 4 min, followed by a forced partial expiration from which flow was measured at a constant volume, 35% baseline VC (Vp 35). This index is independent of both DI and increases in end-inspiratory lung volume (EILV). EILV increased significantly more in the asthmatic group than in the control group (15.0 versus 2.5% of baseline VC, p = 0. 019), a factor that if not taken into account would tend to mask the difference in the two responses. Comparisons were made after a cumulative dose of 50 microg methacholine, which was the highest dose common to all subjects. The asthmatic response was significantly greater than that seen in the control group, with reductions to 25.9 and 72.1% of baseline Vp 35, respectively (p = 0. 0007). We conclude that the sensitivity of asthmatic airways to methacholine is greater than that of normal airways even when DI is prohibited. Therefore, the hyperresponsiveness of asthmatic airways is not attributable simply to an inability of DI to stretch airway smooth muscle.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Asthma / physiopathology*
  • Bronchial Hyperreactivity / physiopathology*
  • Bronchial Provocation Tests
  • Bronchoconstrictor Agents* / pharmacology
  • Forced Expiratory Volume
  • Humans
  • Methacholine Chloride* / pharmacology
  • Muscle Relaxation / drug effects
  • Muscle, Smooth / drug effects
  • Muscle, Smooth / physiopathology*
  • Respiratory Function Tests


  • Bronchoconstrictor Agents
  • Methacholine Chloride