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doi: 10.3810/psm.2010.12.1826
The Physician and Sportsmedicine: Volume 38: No.4
Effect of Body Mass Index on Self-Reported Exercise-Triggered Asthma
Alicia Wright, MSc; Kim L. Lavoie, PhD; Ariane Jacob, BSc; Amanda Rizk, MSc; And Simon L. Bacon, PhD
Copyright 2010 All rights reserved. Cover and contents may not be reproduced in whole or in part without prior written permission. The Physician and Sportsmedicine is a registered trademark of JTE Multimedia, LLC. Sending and distribution of any document from this site is strictly prohibited either for free and or a service fee, and will be sited as a violation of copyright under the laws of THE UNITED STATES OF AMERICA

Abstract: Introduction Exercise-induced asthma (EIA) is common in individuals diagnosed with asthma, with 80% to 90% experiencing asthma symptoms during moderate exercise. Asthma has been linked to obesity such that obesity may be a risk factor for adult-onset asthma. Adults with asthma disclose comorbid obesity as one of the most common barriers to exercise. Physical inactivity has been linked to increases in body mass index (BMI). Few studies have explicitly examined the relationship between BMI and reporting exercise as an asthma trigger. It was hypothesized that individuals with asthma who have an increased BMI will also have increased reports of exercise as an asthma trigger. Methods In total, 673 adult outpatients with asthma at Hôpital du Sacré-Cœur de Montréal in Montréal, Quebec, Canada underwent a brief sociodemographic and medical history interview. Patients provided information on their height, weight (used to calculate BMI), and triggers that generally provoked an asthma exacerbation (though it should be noted that a formal EIA test was not performed). Results When individuals were classified as normal, overweight, or obese, logistic regression analysis revealed that those who were overweight had a 95% increase in the likelihood of reporting exercise-triggered asthma (odds ratio [OR], 1.95; 95% confidence interval [CI], 1.30–2.94) compared with those of normal weight, and this likelihood was more than doubled if the individuals were obese (OR, 2.34; 95% CI, 1.44–3.82). Assessing BMI as a continuous variable revealed that every 1-point increase in BMI was associated with a 9% increase in patients reporting exercise as a trigger (OR, 1.09; 95% CI, 1.04–1.14). All analyses were conducted adjusting for age, sex, asthma severity, and asthma control. Conclusion Results suggest that BMI influences the likelihood of reporting exercise as an asthma trigger, such that individuals with higher BMIs report exercise as an asthma trigger more often than those with a lower BMI. Given that the current study is cross-sectional, further prospective research is needed to define the causal pathway of this relationship.

Keywords: asthma; exercise; body mass index; obesity

Introduction

Asthma is a chronic inflammatory respiratory disorder of the airways, and its prevalence is increasing. In 2009, according to Statistics Canada, 8% of the population aged > 12 years (> 2.3 million individuals) was diagnosed with asthma.1 Similar to the increased prevalence of asthma, the prevalence of obesity in the Western world has also increased drastically in the past 3 decades.2 Obesity may be a risk factor for adult-onset asthma,3 and individuals who are obese and have asthma have been shown to have worse asthma than normal-weight counterparts. In addition, an increased body mass index (BMI) score may be related to decreased asthma control2,4 and increased asthma severity.5 Although few cases of obesity may be the result of more constitutional (ie, genetic) factors, the rapid increase in obesity is generally believed to be due to poor dietary habits and physical inactivity.6-8

Exercise-induced asthma (EIA), defined as a 10% reduction in pulmonary function following moderate exercise, is experienced by 80% to 90% of patients with asthma.9 For individuals with asthma, EIA may be a strong deterrent to engaging in physical activity. The deconditioned state of obese individuals further complicates matters by putting an added strain on the respiratory system: their decreased maximum oxygen consumption (VO2 max) causes this system to work much harder for an equivalent level of physical activity, even at low levels. This added strain likely plays a role in reporting exercise-triggered asthma (ETA). We are unaware of any studies to date that have examined the influence of body weight (assessed via BMI), which may reflect a largely sedentary lifestyle, on the reporting of exercise as a trigger for asthma. As such, the present study examined the effects of high BMI on reporting ETA. We hypothesized that patients with higher BMIs would be more likely to report ETA than those with lower BMIs.

Materials and Methods
Study Participants

All participants were recruited from the asthma outpatient clinic at Hôpital du Sacré-Cœur de Montréal (HSCM) between June 2003 and April 2004.2 The data collected for this study were part of a large-scale study evaluating the frequency and impact of psychiatric disorders among adults with asthma.10 Patients were eligible for this study if they were aged 18 to 75 years, had physician-diagnosed asthma, had no other condition that conferred greater morbidity than asthma, and were fluent in English or French. Participant screening was done from the 1723 patients who presented to the HSCM asthma clinic during this period. A total of 869 (50.4%) patients were excluded for failing to meet the eligibility criteria; 53 (3.1%) patients refused to participate because of lack of time or interest, resulting in 801 (46.5%) patients who participated in the main study. Of the 801 patients, 128 (16%) had missing or incomplete data. In total, data from 673 (84%) adults were analyzed in the current study.

Study Design

All patients were screened for eligibility, which took place on the same day they presented for their appointment with their pneumologist. Recruited participants completed a brief sociodemographic and medical history questionnaire, including detailed information on their asthma, and the Juniper Asthma Control Questionnaire,11 which assessed asthma control. The asthma diagnosis was verified by the physician based on metacholine challenge and/or bronchodilator reversibility, and confirmed by chart review and medication prescription. As part of their regular visit, patients underwent standard pulmonary function testing, which included spirometry. The study was approved by the HSCM research ethics board, and all patients provided written informed consent to participate in the study.

Asthma Severity

Asthma severity classifications respected the 2002 Global Initiation for Asthma (GINA) asthma severity guidelines on classification. The guidelines included 4 categories of asthma severity: intermittent, mild persistent, moderate persistent, and severe persistent.12

Obesity Assessment

Patients’ self-reported height and weight were used to calculate BMI (kg/m2). Previous population-based studies have found that self-reported height and weight have a high correlation with measured height and weight, especially in the age range of the current participants.5 This method of data collection was used because the larger study focused more on psychological assessments, which were extremely time-consuming. Patients were classified as normal if they had a BMI of < 25 kg/m2; overweight if they had a BMI of ≥ 25 kg/m2 and < 30 kg/m2; and obese if they had a BMI of ≥ 30 kg/m2. These classifications were based on the international standard definition of obesity.13,14

Triggers Assessment

Part of the sociodemographic interview included questions related to the triggers that generally caused asthma exacerbations. Patients indicated which factors could trigger their asthma (eg, exercise, animals, dust/pollen, aspirin, stress and emotions, cold air). In total, 13 triggers were included, and space was provided for patients to indicate other triggers. Previous research has shown that self-reported measures are generally related to more formal skin prick testing.15,16 It should be noted that a formal test of EIA was not completed as part of the study.

Data Analysis

To assess the potential association of BMI with ETA reporting, 2 logistic regression analyses were conducted. The first used BMI, divided into categories, and the second used BMI in its continuous form.17 Both analyses used age, sex, asthma severity, and asthma control as a priori-defined covariates, and were chosen for their potential impact on BMI.2,4,5,18 Additional analyses assessed the association of BMI with cold- and allergy-induced asthma. These triggers were as prevalent as exercise, and the analyses were run to provide comparative data. Statistical analysis was performed using SAS version 9.2 (SAS Institute, Cary, NC).

Results
Patient Demographics

The participant demographics are shown according to BMI category in Table 1. Of the 673 eligible patients, 462 (71%) reported exercise as a trigger of their asthma. The sample consisted of 389 (58%) women and 284 (42%) men. For the group, the mean ± standard deviation (SD) age was 49 ± 14 years, with a BMI of 27. 3 ± 4.8 kg/m2. The mean ± SD score for the Juniper’s Asthma Control Questionnaire was 1.7 ± 1.1. Less than 1% of the population had intermittent asthma, compared with 13.1%, 55.9%, and 30.2% of individuals with mild persistent, moderate, and severe asthma, respectively. In addition, 503 (75%) of individuals reported cold as a trigger, and 454 (68%) reported allergies as a trigger.

View: (Table 1 ) - Population Characteristics Classified by BMI Category
Body Mass Index and ETA

There was a significant relationship between BMI category and ETA reporting. Compared with normal-weight participants, patients who were overweight (odds ratio [OR], 1.95; 95% confidence interval [CI], 1.30–2.94) or obese (OR, 2.34; 95% CI, 1.44–3.82) were more likely to report ETA. In addition, when analyzed as a continuous variable, every 1-point increase in BMI score was associated with a 9% increase in the probability of reporting ETA (OR, 1.09; 95% CI, 1.04–1.14). In contrast, BMI was not related to allergy-induced asthma, nor cold-induced asthma (Table 2).

View: (Table 2 ) - Impact of BMI on Exercise, Allergy, and Cold as Asthma Triggers
Discussion

The results of the current study show that there is a relationship between BMI and ETA reporting in adult patients with asthma. Participants who were in a higher BMI category had more than double the chance of reporting ETA, and similarly, each 1-point increase in BMI score was associated with a 9% increase in ETA reporting. Understanding this relationship is important because it may deter patients with asthma from exercising, which can negatively impact their weight and asthma management.2,4,5,19 In contrast to these findings, we did not find a relationship between BMI and cold- or allergy-induced asthma. Given that the prevalence of these triggers was similar to that of exercise, this suggests there may be some degree of specificity between BMI and ETA. To our knowledge, there are no studies that have explored this relationship, and so we can examine 2 potential mechanisms for our findings: a heightened perception of dyspnea and physiological changes related to being overweight/obese.

Dyspnea Perception

When individuals report ETA, they indicate that exercise provokes their asthma symptoms. Dyspnea is an asthma symptom that is commonly reported in obese people, even without the presence of a lung disorder.20,21 Dyspnea may also worsen with deconditioning and increased weight,20 although this relationship is not clearly understood. Increased weight in an individual who does not have asthma results in a greater amount of work needed to breathe (ie, higher oxygen cost), which also contributes to the increased dyspnea sensitivity in overweight and obese individuals.22 Babb et al23 found that there was a strong correlation between oxygen cost of breathing and ratings of perceived breathlessness in obese, nonasthmatic women, during 60-W cycling.23 Goyal et al24 found that obesity was associated with higher perceived symptom score when compared with overweight and normal-weight cardiac patients during the different stages of a Bruce protocol treadmill exercise test, and in a study conducted by Sin et al,21 those who were classified as obese were 2.5 times more likely to have dyspnea due to walking up a hill when compared with those classified in the normal-weight category.21 In terms of dyspnea intensity, Salome et al25 found that obese, nonasthmatic patients had more severe dyspnea than nonobese, nonasthmatic patients during metacholine challenge, which could be partly explained by greater changes in reactance and higher stiffness of the respiratory system at baseline in the obese group.25

The summation of these studies indicates that individuals who are overweight/obese have a heightened perception of dyspnea for many reasons. With dyspnea being one of the most common asthma symptoms, the high ETA reporting among our overweight and obese asthma patients may just represent a reporting bias.

Physiological Response

It is also possible that the relationship between body weight and ETA may be due to underlying physiological mechanisms. For example, patients with asthma and higher BMI are susceptible to increased airway hyperreactivity (AHR),19,26,27 thus making them more likely to experience an asthma exacerbation. However, others have proposed a U-shaped relationship between body weight and AHR.26 Alternatively, Wang and Cerny28 used a chest mass loading model to evaluate effects of upper body fat distribution on ventilatory responses. The weight placed in the vest was calculated so that participants would have a BMI of 32 kg/m2. Healthy nonobese participants wore the weighted vest during exercise testing on a cycle ergometer and compared this with cycling without the weighted vest. They found that chest loading decreased peak work rates, altered breathing patterns, and decreased baseline pulmonary function (forced expiratory volume in 1 second [FEV1], forced vital capacity [FVC], and expiratory reserve volume [ERV]), which supports the decreased lung volumes found in obese patients. Another study in healthy individuals ranging from normal weight to obese demonstrated that functional residual capacity (FRC) and ERV were markedly decreased with increasing body weight.29 For a 10-point increase in BMI (20–30 kg/m2), there was a decrease in FRC from 112% to 84% of predicted values, and a decrease in ERV from 118% to 55% of predicted values. The study showed that with just a modest increase in BMI, there was a rapid decrease in FRC and ERV.29

Similar findings have also been replicated in patients with asthma. Deesomchok et al30 reported that obese individuals with asthma had reduced ERV and end-expiratory lung volume compared with normal-weight patients with asthma, and these reductions were inversely correlated with BMI. Inspiratory capacity was significantly increased in obese patients when compared with normal-weight patients with asthma.30

Another potential physiological mechanism linking BMI and ETA is inflammation. A number of studies have shown that obese patients with asthma have metabolic and inflammatory abnormalities in comparison with normal weight patients with asthma.31 It has been suggested that this is due to the fact that adipose tissue can promote a state of systemic inflammation via the release of leptin.32 This increased level of systematic inflammation may increase the underlying potential for patients to be responsive to triggers. However, it is unclear how this hypothesis would relate to exercise specifically, as seen in the current study, and further research is needed to elucidate this.

Collectively, these studies indicate that exercise tolerance may be lower, lung capacity may be compromised, and inflammation upregulated in overweight/obese individuals with asthma when compared with normal-weight individuals. These physiological changes may also be the mechanism linking increased BMI with patients who are more likely to report ETA.

The results of this study should be considered in the light of several limitations. Of particular note is the fact that the presence of EIA was not formally confirmed in the patients who reported ETA. As such, it is possible that the current results reflect some form of reporting bias. However, the fact that other triggers of similar prevalence were not related to BMI suggests some specificity to exercise. Due to the cross-sectional nature of this study, we are not able to disentangle the temporal relationship between increased BMI and greater ETA reporting, though it is of note that this relationship is specific to ETA and not other forms of asthma-triggered events. In addition, participants may not have had the ability to discern the difference between shortness of breath, normally occurring with exercise, or true asthma symptoms provoked by exercise, and we did not collect data to be able to assess this. Demographically, most of our participants were white, thus limiting our external validity. In contrast, there were also several strengths of this study. We had a large sample size, and all participants had physician-diagnosed asthma, rather than self-reported. Also, participants’ BMIs were analyzed both as a continuous variable and by BMI category. This allowed us to look at the relationship between BMI and ETA reporting by BMI category, as well as show the impact of gaining smaller amounts of weight, represented by a 1- or 2-point BMI, and how it can also affect ETA.

Conclusion

Results of this cross-sectional study suggest that BMI may influence the likelihood of reporting ETA, such that people with higher BMIs report exercise as an asthma trigger more often than those with lower BMIs. However, without having conducted exercise testing, it is not possible to quantify EIA. This relationship is of clinical importance because those who are overweight or obese and report ETA are likely to be deterred from engaging in exercise or general physical activity. This issue may lead these patients to maintain a sedentary lifestyle, resulting in increasing weight, thus further fueling the downward spiral leading to worsened health. Given the importance of exercise and regular physical activity in weight management, greater care should be taken when working with these patients to refer them to appropriate weight management specialists to help them control and safely reduce their weight. Also, proper patient education informing this particular subset of asthma patients on how to safely start exercise could serve as additional encouragement to lead a more active lifestyle.

Acknowledgments
We would like to thank the Social Sciences and Humanities Research Council for funding the main study and the Canadian Institute of Health Research (AW and SLB) and Fonds de la Recherche en Santé du Québec (KLL and SLB) for student scholarships and new investigator funding. We would also like to thank Guillaume Lacoste (Research Manager) for his efforts in recruiting the participants for the study.

Conflict of Interest Statement
Alicia Wright, MSc, Kim L. Lavoie, PhD, Ariane Jacob, BSc, Amanda Rizk, MSc, and Simon L. Bacon, PhD disclose no conflicts of interest.
References
  1. Statistic Canada. Asthma, by sex, by provinces and territories. https://www40.statcan.ca/l01/cst01/health50a.htm. Accessed October 14, 2010.

  2. Lavoie KL, Bacon SL, Labrecque M, Cartier A, Ditto B. Higher BMI is associated with worse asthma control and quality of life but not asthma severity. Respir Med. 2006;100(4):648–657.

  3. Nystad W, Meyer HE, Nafstad P, Tverdal A, Engeland A. Body mass index in relation to adult asthma among 135,000 Norwegian men and women. Am J Epidemiol. 2004;160(10):969–976.

  4. Saint-Pierre P, Bourdin A, Chanez P, Daures JP, Godard P. Are overweight asthmatics more difficult to control? Allergy. 2006;61(1):79–84.

  5. Varraso R, Siroux V, Maccario J, Pin I, Kauffmann F; Epidemiological Study on the Genetics and Environment of Asthma. Asthma severity is associated with body mass index and early menarche in women. Am J Respir Crit Care Med. 2022;171(4):334–339.

  6. French SA, Story M, Jeffery RW. Environmental influences on eating and physical activity. Annu Rev Public Health. 2001;22:309–335.

  7. Bell CG, Walley AJ, Froguel P. The genetics of human obesity. Nat Rev Genet. 2005;6(3):221–234.

  8. Bouchard C. Current understanding of the etiology of obesity: genetic and nongenetic factors. Am J Clin Nutr. 1991;53(6 suppl):1561S–1565S.

  9. Gotshall RW. Exercise-induced bronchoconstriction. Drugs. 2002;62(12):1725–1739.

  10. Lavoie KL, Cartier A, Labrecque M, et al. Are psychiatric disorders associated with worse asthma control and quality of life in asthma patients? Respir Med. 2005;99(10):1249–1257.

  11. Juniper EF, O’Byrne PM, Guyatt GH, Ferrie PJ, King DR. Development and validation of a questionnaire to measure asthma control. Eur Respir J. 1999;14(4):902–907.

  12. Global Initiative for Asthma. https://www.ginasthma.com/. Accessed November 3, 2010.

  13. Clinical guidelines on the identification, evaluation, and treatment of overweight and obesity in adults—the evidence report. National Institutes of Health. Obes Res. 1998;6(suppl 2):51S–209S.

  14. Obesity: preventing and managing the global epidemic. Report of a WHO consultation. World Health Organ Tech Rep Ser. 2000;894:i–xii, 1–253.

  15. Weiss ST, Horner A, Shapiro G, Sternberg AL; Childhood Asthma Management Program (CAMP) Research Group. The prevalence of environmental exposure to perceived asthma triggers in children with mild-to-moderate asthma: data from the Childhood Asthma Management Program (CAMP). J Allergy Clin Immunol. 2001;107(4):634–640.

  16. Ritz T, Steptoe A, Bobb C, Harris AH, Edwards M. The asthma trigger inventory: validation of a questionnaire for perceived triggers of asthma. Psychosom Med. 2006;68(6):956–965.

  17. MacCallum RC, Zhang S, Preacher KJ, Rucker DD. On the practice of dichotomization of quantitative variables. Psychol Methods. 2002;7(1):19–40.

  18. Chiriboga DE, Ma Y, Li W, et al. Gender differences in predictors of body weight and body weight change in healthy adults. Obesity (Silver Spring). 2008;16(1):137–145.

  19. Jang AS, Lee JH, Park SW, Shin MY, Kim DJ, Park CS. Severe airway hyperresponsiveness in school-aged boys with a high body mass index. Korean J Intern Med. 2006;21(1):10–14.

  20. El-Gamal H, Khayat A, Shikora S, Unterborn JN. Relationship of dyspnea to respiratory drive and pulmonary function tests in obese patients before and after weight loss. Chest. 2005;128(6):3870–3874.

  21. Sin DD, Jones RL, Man SF. Obesity is a risk factor for dyspnea but not for airflow obstruction. Arch Intern Med. 2002;162(13):1477–1481.

  22. Parameswaran K, Todd DC, Soth M. Altered respiratory physiology in obesity. Can Respir J. 2006;13(4):203–210.

  23. Babb TG, Ranasinghe KG, Comeau LA, Semon TL, Schwartz B. Dyspnea on exertion in obese women: association with an increased oxygen cost of breathing. Am J Respir Crit Care Med. 2008;178(2):116–123.

  24. Goyal D, Logie IM, Nadar SK, Lip GY, Macfadyen RJ. Generalized obesity but not that characterized by raised waist-hip ratio is associated with increased perceived breathlessness during treadmill exercise testing. Cardiovasc Ther. 2009;27(1):10–16.

  25. Salome CM, Munoz PA, Berend N, Thorpe CW, Schachter LM, King GG. Effect of obesity on breathlessness and airway responsiveness to methacholine in non-asthmatic subjects. Int J Obes (Lond). 2008;32(3):502–509.

  26. Litonjua AA, Sparrow D, Celedon JC, DeMolles D, Weiss ST. Association of body mass index with the development of methacholine airway hyperresponsiveness in men: the Normative Aging Study. Thorax. 2002;57(7):581–585.

  27. Chinn S, Jarvis D, Burney P; European Community Respiratory Health Survey. Relation of bronchial responsiveness to body mass index in the ECRHS. European Community Respiratory Health Survey. Thorax. 2002;57(12):1028–1033.

  28. Wang LY, Cerny FJ. Ventilatory response to exercise in simulated obesity by chest loading. Med Sci Sports Exerc. 2004;36(5):780–786.

  29. Jones RL, Nzekwu MM. The effects of body mass index on lung volumes. Chest. 2006;130(3):827–833.

  30. Deesomchok A, Fisher T, Webb KA, et al. Effects of obesity on perceptual and mechanical responses to bronchoconstriction in asthma. Am J Respir Crit Care Med. 2010;181(2):125–133.

  31. Poulain M, Doucet M, Major GC, et al. The effect of obesity on chronic respiratory diseases: pathophysiology and therapeutic strategies. CMAJ. 2006;174(9):1293–1299.

  32. Shore SA. Obesity, airway hyperresponsiveness, and inflammation. J Appl Physiol. 2010;108(3):735–743.

Alicia Wright, MSc 1
Kim L. Lavoie, PhD 1
Ariane Jacob, BSc 1
Amanda Rizk, MSc 1
Simon L. Bacon, PhD 1

1Montreal Behavioural Medicine Centre, Hôpital du Sacré-Cœur de Montréal – a University of Montreal affiliated hospital, Montreal, Quebec, Canada 2Department of Psychology, University of Quebec at Montreal, Montreal, Quebec, Canada 3Research Centre, Montréal Heart Institute – a University of Montreal affiliated hospital, Montreal, Quebec, Canada 4Department of Exercise Science, Concordia University, Montreal, Quebec, Canada

Correspondence: Simon L. Bacon, PhD, Montreal Behavioural Medicine Centre, Department of Exercise Science, Concordia University, Montreal, Quebec, H4B 1R6, Canada.
Tel: 514-848-2424 ext 5750
E-mail: [email protected]
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