Published online June 1, 2007
PEDIATRICS
Vol. 119
No. 6
June 2007, pp.
1247-1248
(doi:10.1542/peds.2007-0422)
Asthma as a Barrier to Children's Physical Activity
Daniel J. Weiner, MD
Division of Pulmonary Medicine
Children's Hospital of Pittsburgh
Pittsburgh, PA 15213
Joe McDonough, MS
Julian Allen, MD
Division of Pulmonary Medicine
Children's Hospital of Philadelphia
Philadelphia, PA 19104
To the Editor.—
We read with interest the recent report from Glazebrook et al.1 They found a high prevalence of obesity (21.4%) in their population of outpatients with asthma and that asthma acted as a barrier to exercise in these children. We performed a retrospective review of a pulmonary-function database maintained at our institution (1988–2005), which we think lends an interesting additional perspective to the findings of Glazebrook et al. Within this database, 1095 children with a diagnosis of asthma were referred for testing. The BMI was calculated and categorized as normal (5th–85th percentile), overweight (85th–95th percentile), or obese (>95th percentile). We found that in this population with a median age of 10.28 years (range: 4.4–25 years), the body composition was normal in 691 patients (63%), overweight in 178 (16%), and obese in 226 (21%). Lung-function testing revealed that the ratio of forced expiratory volume in 1 second to forced vital capacity (FEV1/FVC) was slightly lower in the obese group (median: 79% vs 83% in the normal-BMI group; P = .001), and functional residual capacity (FRC) was significantly lower in the obese group (median: 93% predicted vs 103% predicted in the normal-BMI group; P < .001). There were no differences between BMI groups in the degree of improvement in specific airway conductance after administration of inhaled bronchodilator.
These findings and those of Glazebrook et al raise an important question: are children with asthma less likely to exercise and thus be at high risk of obesity (because they are limited by their asthma symptoms), or does obesity itself cause asthma to be more difficult to control? Or, are both true? Similar to Glazebrook et al, we found a high prevalence of obesity in patients with asthma who were referred for lung-function testing. However, asthma is also more prevalent in overweight children.2 The high prevalence of asthma in overweight and obese children has been attributed to abnormal baseline lung mechanics or to inflammatory mediators produced by adipose tissue.3,4 However, despite earlier studies5,6 that showed airway hyperresponsiveness to exercise and methacholine in obese subjects with asthma, we did not find increased airway responsiveness to bronchodilators in obese children compared with those in other BMI groups.
A relative reduction in bronchodilator responsiveness compared with bronchial hyperreactivity to constricting stimuli in the obese patient with asthma could be a result of airway remodeling (not highly likely at this age), or it may be related to airway/parenchymal/chest-wall interactions7 such as the effect of obesity on slowly cycling latch bridges in airway smooth muscle.8 According to this hypothesis, the ability of airway smooth muscle to relax when exposed to bronchodilators depends on its ability to break and reattach actin-myosin links. Low FRC and tidal-volume states such as obesity, by reducing tidal stretch on airway smooth muscle, reduce the probability of actin-myosin detachment/reattachment, in effect "freezing" the attachments in a "latch state." This could explain less-than-expected bronchodilator responsiveness in obese subjects with asthma. In addition, the airway "compressive" effects of a low FRC may limit the amount that the airways can dilate in an obese subject with asthma.
What are the implications of these findings for the cause-and-effect question posed above? Obese subjects with asthma have asthma symptoms that are more difficult to control.9–11 Increased bronchial lability to exercise unaccompanied by increased bronchodilator responsiveness could likewise make exercise-induced asthma more difficult to control in the obese subject, which leads to less willingness to exercise and, in turn, increases the risk of obesity. We agree with Glazebrook et al that barriers to exercise in obese children with asthma need to be addressed. It would be of interest to study whether intermittent increases in tidal volume in obese subjects, such as those engendered by incentive spirometry, could help increase bronchodilator responsiveness by "unfreezing" the latch state. Our findings suggest that because there is increased bronchial lability with exercise that is not matched by increased bronchodilator responsiveness in obese subjects, more importance needs to be placed on preventative therapy, including appropriate use of antiinflammatory controller medications and control of obesity itself.
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PEDIATRICS (ISSN 1098-4275). ©2007 by the American Academy of Pediatrics
