Airway Dysfunction in Obesity: Response to Voluntary Restoration of End Expiratory Lung Volume

INTRODUCTION: Abnormality in distal lung function may occur in obesity due to reduction in resting lung volume; however, airway inflammation, vascular congestion and/or concomitant intrinsic airway disease may also be present. The goal of this study is to 1) describe the phenotype of lung function in obese subjects utilizing spirometry, plethysmography and oscillometry; and 2) evaluate residual abnormality when the effect of mass loading is removed by voluntary elevation of end expiratory lung volume (EELV) to predicted FRC. METHODS: 100 non-smoking obese subjects without cardio-pulmonary disease and with normal airflow on spirometry underwent impulse oscillometry (IOS) at baseline and at the elevated EELV. RESULTS: FRC and ERV were reduced (44±22, 62±14% predicted) with normal RV/TLC (29±9%). IOS demonstrated elevated resistance at 20 Hz (R(20), 4.65±1.07 cmH(2)O/L/s); however, specific conductance was normal (0.14±0.04). Resistance at 5–20 Hz (R(5−20), 1.86±1.11 cmH(2)O/L/s) and reactance at 5 Hz (X(5), −2.70±1.44 cmH(2)O/L/s) were abnormal. During elevation of EELV, IOS abnormalities reversed to or towards normal. Residual abnormality in R(5−20) was observed in some subjects despite elevation of EELV (1.16±0.8 cmH(2)O/L/s). R(5−20) responded to bronchodilator at baseline but not during elevation of EELV. CONCLUSIONS: This study describes the phenotype of lung dysfunction in obesity as reduction in FRC with airway narrowing, distal respiratory dysfunction and bronchodilator responsiveness. When R(5−20) normalized during voluntary inflation, mass loading was considered the predominant mechanism. In contrast, when residual abnormality in R(5−20) was demonstrable despite return of EELV to predicted FRC, mechanisms for airway dysfunction in addition to mass loading could be invoked.