Deep inspiration avoidance and airway response to methacholine: Influence of body mass index

Unité de recherche en pneumologie, Institut de cardiologie et de pneumologie de l'Université Laval, Hôpital Laval, Québec City.
Canadian respiratory journal: journal of the Canadian Thoracic Society (Impact Factor: 1.16). 10/2005; 12(7):371-6.
Source: PubMed

ABSTRACT To evaluate the effects of deep inspiration avoidance response to methacholine inhalation in 23 nonobese (body mass index between 18 kg/m2 and 30 kg/m2) and 27 obese (body mass index 30 kg/m2 or greater), nonatopic, nonasthmatic normal subjects.
Each subject had four methacholine challenges. In tests A and B, the first postmethacholine forced expiratory volume in 1 s (FEV1) was measured at 30 s and 3 min postinhalation, respectively; tests C and D were single-dose tests (using the final dose of test B), with the first postmethacholine FEV1 being obtained at 3 min, without (test C) or with (test D) 20 min of deep inspiration avoidance before inhalation.
The mean provocative concentrations inducing a 20% fall in FEV1 on tests A and B were 80.6 mg/mL and 28.5 mg/mL (P<0.0001) in nonobese subjects, respectively, and 56.3 mg/mL and 21.5 mg/mL (P<0.0001) in obese subjects, respectively. No significant differences were observed in test A or B between control and obese subjects. Mean falls in FEV1 for tests C and D were 20.3% and 40.0% (P=0.0003) in nonobese subjects, respectively, and 18.5% and 23.6% (P>0.05) in obese subjects, respectively.
As previously observed in patients with asthma, the present study found that nonasthmatic obese subjects had no increase in the fall in FEV1 after deep inspiration avoidance before methacholine, whereas nonobese subjects did, suggesting that obesity alters airway function. No significant changes were found between groups for symptom perception.

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    • "This may result in airway narrowing and increased airway resistance. However, it is also important to mention that in mild-moderate obesity tidal volumes and frequency of deep inspiration remain in normal range [100, 113–115]. Therefore there is a possibility that lung functions may not be altered until late obesity in some cases. "
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    ABSTRACT: Obesity induces some pertinent physiological changes which are conducive to either development of asthma or cause of poorly controlled asthma state. Obesity related mechanical stress forces induced by abdominal and thoracic fat generate stiffening of the lungs and diaphragmatic movements to result in reduction of resting lung volumes such as functional residual capacity (FRC). Reduced FRC is primarily an outcome of decreased expiratory reserve volume, which pushes the tidal breathing more towards smaller high resistance airways, and consequentially results in expiratory flow limitation during normal breathing in obesity. Reduced FRC also induces plastic alteration in the small collapsible airways, which may generate smooth muscle contraction resulting in increased small airway resistance, which, however, is not picked up by spirometric lung volumes. There is also a possibility that chronically reduced FRC may generate permanent adaptation in the very small airways; therefore, the airway calibres may not change despite weight reduction. Obesity may also induce bronchodilator reversibility and diurnal lung functional variability. Obesity is also associated with airway hyperresponsiveness; however, the mechanism of this is not clear. Thus, obesity has effects on lung function that can generate respiratory distress similar to asthma and may also exaggerate the effects of preexisting asthma.
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