Increased wheeze and asthma diagnosis in obesity may be due to reduced lung volume with subsequent airway narrowing.Asthma (wheeze and airway hyperresponsiveness), functional residual capacity (FRC) and airway conductance (Gaw) were measured in 276 randomly selected subjects aged 28-30 yrs. Data were initially adjusted for smoking and asthma before examining relationships between weight and FRC (after adjustment for height), and between body mass index (BMI5 weight?height -2 ) and Gaw (after adjustment for FRC) by multiple linear regression, separately for females and males.For males and females, BMI (¡95% confidence interval) was 27. , and FRC was 85.3¡3.4 and 84.0¡2.9% of predicted. Weight correlated independently with FRC in males and females. BMI correlated independently and inversely with Gaw in males, but only weakly in females.In conclusion, obesity is associated with reduced lung volume, which is linked with airway narrowing. However, in males, airway narrowing is greater than that due to reduced lung volume alone. The mechanisms causing airway narrowing and sex differences in obesity are unknown.

Airway distensibility measured by forced oscillation technique is reduced in subjects with asthma compared with subjects without asthma, is not related to lung elastic recoil, and is unchanged by bronchodilator administration. Airway wall remodeling remains the most likely cause of reduced airway distensibility in asthma.

In a previous study (J. H. T. Bates, A. M. Lauzon, G. S. Dechman, G. N. Makaym, and T. F. Schuessler. J. Appl. Physiol. 76: 616-626, 1994), we investigated the acute changes in isovolume lung mechanics immediately after a bolus injection of histamine. We found that dynamic resistance and elastance increased progressively in the 80-s period after injection, whereas the estimated tissue hysteresivity reached a stable plateau after approximately 25 s. In the present study, we developed a computer model of the lung to investigate the mechanisms responsible for these observations. The model conforms to Horsfield's morphometry, with the addition of compliant airways and structural damping tissue units. Using this model, we simulated the time course of acute bronchoconstriction after intravenous administration of a bolus of bronchial agonist. Heterogeneity was induced by randomly varying the values of the maximal airway smooth muscle contraction and the tissue response to the agonist. Our results demonstrate that much of the increase in lung impedance observed in our previous study can be produced purely by the effects of airway heterogeneity. However, we were only able to reproduce the plateauing of hysteresivity by assigning a minimum radius to each airway, beyond which it would immediately snap completely shut. We propose that airway closure played an important role in our experimental observations.

After bronchoconstriction, deep inspiration (DI) causes dilatation followed by airway re-narrowing. Re-narrowing may be faster in asthmatic than nonasthmatic subjects. This study investigated the relationship between re-narrowing and the magnitude of both DI-induced dilatation and the volume-dependence of respiratory system resistance (Rrs) during tidal breathing.In 25 asthmatic and 18 nonasthmatic subjects the forced oscillation technique was used to measure Rrs at baseline and after methacholine challenge, during 1 min of tidal breathing, followed by DI to total lung capacity (TLC) and passive return to functional residual capacity (FRC). Dilatation was measured as the decrease in Rrs between end tidal inspiration and TLC, re-narrowing as Rrs at FRC immediately after DI, as per cent Rrs at end-tidal expiration, and volume dependent tidal fluctuation as the difference between mean Rrs at end-expiration and end-inspiration.Asthmatic subjects had greater re-narrowing, less dilatation, and greater tidal fluctuations both at baseline and after challenge. Re-narrowing correlated with baseline tidal fluctuation and inversely with dilatation. Both baseline tidal fluctuation and dilatation were significant independent predictors of re-narrowing.Following deep inspiration-induced dilatation, faster airway re-narrowing in asthmatic than nonasthmatic subjects is associated not only with reduced deep inspiration-induced dilatation but also with some property of the airways that is detectable prior to challenge as an increased volume dependence of resistance. It is well recognised that the response of the airways to deep inspiration (DI) differs in asthmatic and nonasthmatic subjects. Following airway narrowing induced by inhaled methacholine, DI causes dilatation of the airways in both asthmatic and nonasthmatic subjects. However, the magnitude of the dilatation is usually less in asthmatic than in nonasthmatic subjects [1,2]. It has been suggested that the inability of DI to overcome bronchoconstriction is a fundamental abnormality of asthma, and could contribute to airway hyperresponsiveness [1].The amount of residual dilatation measured after a DI is likely to be determined both by the degree to which the airways distend in response to the inflationary pressure of a DI and by the rate at which they re-narrow following the release of the distending force. After a single DI, it can take more than a minute for the airways of a healthy subject to renarrow to pre-DI calibre [3]. Using the forced oscillation technique to measure airway resistance continuously throughout a DI, JENSEN et al.[4] measured the extent of both dilatation and re-narrowing, and found that asthmatic subjects both dilated less and re-narrowed more than healthy subjects. They concluded that these differences were attributable to differences in the behaviour of airway smooth muscle (ASM), most likely due to an increase in the stiffness of asthmatic ASM making it unresponsive to stretch. These findings imply that there is an inverse correlation b...