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 (G_aw) 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 (BMI = weight·height⁻²) andG_aw(after adjustment for FRC) by multiple linear regression, separately for females and males.For males and females, BMI (±95% confidence interval) was 27.0±4.6 kg·m⁻²and 25.6±6.0 kg·m⁻²respectively,G_awwas 0.64±0.04 L·s⁻¹·cmH₂O⁻¹and 0.57±0.03 L·s⁻¹·cmH₂O⁻¹, 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 withG_awin 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.

In epidemiologic studies of asthma there is a group with recent wheeze, but with no airway hyperresponsiveness (AHR), in whom it is unclear whether any significant airway abnormality exists. Exhaled nitric oxide (NO) has been proposed as a measure of airway inflammation. We measured exhaled NO in a population sample of 306 young adults who also underwent bronchial challenge with histamine or a bronchodilator test. Subjects blew into a 3-L Tedlar bag against a 2-mm-diameter resistance to close the soft palate and exclude nasal air. The NO content of expired gas from a single breath was analyzed by chemiluminescent analyzer. Exhaled NO was log-normally distributed in the population sample and duplicate measurements were highly reproducible (intraclass correlation coefficient = 0.98). Exhaled NO correlated significantly with airway responsiveness, measured as the dose-response ratio to histamine (r = 0.39, p < 0.001) and with peripheral blood eosinophils (r = 0.35, p < 0.001). Exhaled NO was significantly greater in asthmatic subjects (geometric mean, 22.2; 95% confidence intervals, 16.1 to 30.7 ppb) than in normal subjects (7.8, 7.1 to 8.4, p < 0.001) or in subjects with wheeze but no AHR (8.8, 7.5 to 10.3, p < 0.001). We conclude that exhaled NO is log-normally distributed, is highly reproducible and discriminates well among subjects, suggesting that it is both a feasible and useful measurement for epidemiologic studies of asthma. The findings suggest that wheeze in the absence of AHR is unlikely to be associated with airway inflammation.

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 (R_rs) during tidal breathing.In 25 asthmatic and 18 nonasthmatic subjects the forced oscillation technique was used to measureR_rsat 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 inR_rsbetween end tidal inspiration and TLC, re-narrowing asR_rsat FRC immediately after DI, as per centR_rsat end-tidal expiration, and volume dependent tidal fluctuation as the difference between meanR_rsat 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.

Rationale: Reduced airway distensibility in subjects with asthma compared with control subjects may be related to differences in lung elastic recoil and bronchomotor tone. Objectives: To examine the contribution of lung elastic recoil and bronchomotor tone to airway distensibility. Methods: We compared airway distensibility in 18 subjects with asthma with 19 control subjects before and after bronchodilator administration and, in a subgroup of 7 subjects with asthma and 8 control subjects, correlated distensibility with pressure–volume parameters. Measurements and Main Results: Distensibility was measured, using the forced oscillation technique, as the linear slope of conductance versus volume between total lung capacity (TLC) and 75% TLC and between 75% TLC and FRC. Transpulmonary pressure was recorded concurrently with distensibility, using an esophageal balloon. Pressure–conductance data were described using linear regressions and pressure–volume data were described using exponential equations. Subjects with asthma had lower baseline FEV1 (p = 0.0003) and conductance (p = 0.002) than did control subjects. Distensibility above 75% TLC was less in subjects with asthma than in control subjects (p < 0.0001), but there was no difference below 75% TLC. Bronchodilator administration did not alter distensibility despite increases in FEV1 (p = 0.0002) and conductance (p < 0.0001) in subjects with asthma, and conductance (p = 0.0004) in control subjects. After bronchodilator administration, subjects with asthma had reduced lung elastic recoil compared with control subjects (p = 0.03) and a reduced pressure–conductance slope (p = 0.01), but there were no correlations between pressure–volume characteristics and airway distensibility. Conclusions: 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.