Chest ACCP Education Calendar
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

Guest Access | Sign In via User Name/Password
This Article
Right arrow Abstract Freely available
Right arrow Full Text (PDF) Free
Right arrow Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Article Archive
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via ISI Web of Science (58)
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Hakala, K.
Right arrow Articles by Sovijärvi, A.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Hakala, K.
Right arrow Articles by Sovijärvi, A.
(Chest. 2000;118:1315-1321.)
© 2000 American College of Chest Physicians

Effects of Weight Loss on Peak Flow Variability, Airways Obstruction, and Lung Volumes in Obese Patients With Asthma*

Katri Hakala, MD; Brita Stenius-Aarniala, MD, PhD and Anssi Sovijärvi, MD, PhD

* From the Department of Medicine (Drs. Hakala and Stenius-Aarniala), Division of Pulmonary Medicine, and the Laboratory Department (Dr. Sovijärvi), Division of Clinical Physiology and Nuclear Medicine, Helsinki University Hospital, Helsinki, Finland.

Correspondence to: Katri Hakala, MD, Kallenkaarre 9, FIN - 14200 Turenki, Finland


   Abstract
TOP
 Abstract
Introduction
 Materials and Methods
 Results
 Discussion
 References
 
Study objectives: To clarify the pathophysiologic features of the relation between asthma and obesity, we measured the effects of weight reduction on peak expiratory flow (PEF) variability and airways obstruction, compared to simultaneous changes in lung volumes and ventilatory mechanics in obese patients with stable asthma.

Methods: Fourteen obese asthma patients (11 women and 3 men; aged 25 to 62 years) were studied before and after a very-low-calorie-diet period of 8 weeks. PEF variability was determined as diurnal and day-to-day variations. FEV1 and maximal expiratory flow values were measured with a flow-volume spirometer. Lung volumes, airways resistance (Raw), and specific airways conductance were measured using a constant-volume body plethysmograph. Minute ventilation was monitored in patients in supine and standing positions.

Results: As patients decreased their body mass index (SD) from 37.2 (3.7) to 32.1(4.2) kg/m2 (p < 0.001), diurnal PEF variation declined from 5.5% (2.4) to 4.5% (1.5) (p = 0.01), and day-to-day variation declined from 5.3% (2.6) to 3.1% (1.3) (p < 0.005). The mean morning PEF, FEV1, and FVC increased after weight loss (p = 0.001, p < 0.005, and p < 0.05, respectively). Flow rate at the middle part of FVC (FEF25–75) increased even when related to lung volumes (FEF25–75/FVC; p < 0.05). Functional residual capacity and expiratory reserve volume were significantly higher after weight loss (p < 0.05 and p < 0.005, respectively). A significant reduction in Raw was found (p < 0.01). Resting minute ventilation decreased after weight loss (p = 0.01).

Conclusion: Weight loss reduces airways obstruction as well as PEF variability in obese patients with asthma. The results suggest that obese patients benefit from weight loss by improved pulmonary mechanics and a better control of airways obstruction.

Key Words: airways obstruction • asthma • obesity • peak expiratory flow variation • pulmonary function • weight loss


   Introduction
TOP
 Abstract
 Introduction
Materials and Methods
 Results
 Discussion
 References
 
The prevalence of asthma and obesity has been increasing worldwide in recent years.1 2 Several studies have reported the association between body mass index (BMI) and asthma prevalence.3 4 5 6 Whether asthma patients gain weight as a result of activity limitations or whether obesity increases the risk of developing asthma is uncertain.7 Luder et al8 studied the relationship between asthma symptoms and overweight in children. They found that a higher BMI was associated with more severe asthma symptoms. In adult obese asthmatics, improvement in asthma severity after weight loss has been reported.9 10

It could be assumed that impairment in pulmonary mechanics related to obesity, such as reduction in lung volumes, increased airways resistance (Raw), and impairments in small airways function,11 may contribute to an increase in asthma severity. Although there is evidence that weight loss may improve lung function and oxygenation in obesity,12 very little is known about the effects of weight loss on the severity of asthma in terms of variability of airways obstruction.

To clarify pathophysiologic features of the relation between asthma and obesity, we measured the effects of weight loss on peak expiratory flow (PEF) variability and airways obstruction, compared to simultaneous changes in lung volumes and ventilatory mechanics in obese patients with stable asthma.


   Materials and Methods
TOP
 Abstract
 Introduction
 Materials and Methods
Results
 Discussion
 References
 
Fourteen patients (11 women and 3 men; aged 25 to 62 years) with a clinical diagnosis of asthma and moderate to morbid obesity BMI (range, 32.5 to 42.5 kg/m2) were recruited for the study. Characteristics of the patients and antiasthmatic medications are presented in Table 1 . Prior to our study, all patients participated as a control group in another study.10 Their spirometric and serial PEF values were carefully followed up every 2 months for 1 year before starting in our study. Because they were control patients, they underwent no interventions other than education concerning asthma and allergy.10 Medical therapy included regular use of inhaled corticosteroids in all 14 patients, sustained-release theophylline compounds in 2 patients, and regular long-acting inhaled ß2-agonists in 3 patients. All patients were nonsmokers or ex-smokers who had stopped smoking for >= 2 years (Table 1) . Patients gave informed consent to participate in the study, which was approved by the Ethical Committee of the Department of Pulmonary Medicine of Helsinki University Hospital.


View this table:
[in this window]
[in a new window]

  		Table 1. Baseline Characteristics of the Patients*

 
Study Protocol
All patients participated in a weight reduction program starting with a very-low-calorie-diet (VLCD) period of 8 weeks. The VLCD preparation used was Nutrilett (Nycomed Pharma AS; Oslo, Norway). The daily dose gives 1,760 kJ/d, and contains daily allowances of all essential nutrients. The principles of this weight reduction program are described by Pekkarinen et al.13

Before weight loss and after the VLCD period, PEF measurements for 2 weeks, pulmonary function tests (see below), and arterial blood gas analyses were evaluated. The symptoms (ie, dyspnea and cough) were recorded on a 100-mm visual analogue scale (VAS), where 0 mm represented best possible and 100 mm represented worst possible. The use of rescue medication was recorded. Patients had been advised not to change their antiasthmatic treatment other than short-acting ß2-agonists during the study if the stability of asthma was clinically acceptable. Patients with allergy to pollen were studied out of season. The dose and timing of long-acting ß2-agonists and sustained-release theophylline compounds were identical at study visits before and after weight loss. Patients did not consume any caffeinated beverages or short-acting bronchodilators for 4 h before pulmonary function tests.

Pulmonary Function and Arterial Blood Gas Measurements
Flow-volume spirometry was performed using a rolling seal spirometer (CPI 220; Cardio Pulmonary Instruments; Houston, TX) connected to a microcomputer system (Medikro 202; Medikro Oy; Kuopio, Finland) according to European recommendations.14 The results from the envelope curve of at least three superimposed forced expiratory flow-volume curves were recorded. FEV1, FVC, flow rate at the middle part of FVC (FEF25–75), and area under the expiratory flow volume curve (AFV) were determined with the patient in the sitting position. Vital capacity (VC), total lung capacity (TLC), residual volume (RV), functional residual capacity (FRC), Raw, and specific airways conductance (SGaw) were measured using a constant-volume body plethysmograph (Bodyscreen; Erich Jaeger; Wurtzburg, Germany) during tidal breathing timed with a metronome (30/min). The mean value of 3 to 5 determinations was recorded for analysis. A single-breath diffusing capacity test (Master Lab; Erich Jaeger) was used for measuring diffusing capacity of the lung for carbon monoxide (DLCO). TLC was also measured using the single-breath helium dilution method (TLC-He). The value of nonventilated lung compartment was calculated as the TLC measured using body plethysmograph (TLC-B) minus the TLC-He.

Minute ventilation (E), tidal volume (VT), and respiratory rate (RR) were continuously monitored and recorded over a 30-s interval in patients in supine and standing positions. A face mask (Rudolph series 7910; Hans Rudolph; Kansas City, MO) was tightly attached and connected to an automatic gas exchange analyzer with a mixing chamber (Ergo-Oxyscreen; Erich Jaeger). The mask and the valve system had a dead space of 185 mL. The mean values of 10 consecutive measurements of 30 s in both body positions were calculated for further analyses.

Arterial blood samples for blood gas analysis were taken from a brachial artery after a rest of 10 min with the patients in supine position.

Histamine Challenge
A rapid dosimetric method with controlled tidal breathing was used for histamine challenge of the airways.15 Patients with an FEV1 of <= 70% predicted were excluded from histamine provocation testing. If FEV1 decreased from the baseline by >= 15% after any dose, further administration of histamine was discontinued. The provocative dose causing a 15% fall in FEV1 (PD15) was calculated from logarithmically transformed histamine doses.

PEF Variability
The highest of three measurements of PEF by mini-Wright peak flowmeter was recorded by the patients themselves every morning and evening during 14 successive days before and after the weight loss period. If patients were receiving bronchodilator, PEF values were measured before its use. PEF variability was expressed in three ways: as the diurnal PEF variation (highest PEF - lowest PEF/mean value of the two, x 100%), the mean difference between the highest and lowest morning PEF values measured over a follow-up period of 14 days, and the day-to-day PEF variation (SD percent mean morning PEF).

Statistical Analysis
Pulmonary function data are expressed as mean (SD). PD15 values were analyzed after log10 conversion. Wilcoxon signed-rank test was used in statistical comparisons of lung function variables between baseline and after treatment. The relations between two variables were calculated with Spearman’s correlation test. A p value < 0.05 was considered to indicate statistical significance.


   Results
TOP
 Abstract
 Introduction
 Materials and Methods
 Results
Discussion
 References
 
The effects of weight reduction on BMI and symptom scores as well as use of rescue medication are shown in Table 2 . The mean weight loss was 13.7 kg (range, 8 to 18 kg). The mean BMI decreased by 5.1 kg/m2 (range, 3.0 to 7.4 kg/m2). Symptoms were recorded on a VAS scale from 0 to 100 mm. A significant reduction in dyspnea was demonstrated; the change in cough score was not statistically significant (NS). The use of rescue sympathomimetics was < 1 dose per day at baseline, and it did not change by the end of the weight reduction period.


View this table:
[in this window]
[in a new window]

  		Table 2. Weight, BMI, Asthma Symptoms, and PEF Indexes Before and After VLCD Period of 8 Weeks in Obese Patients With Asthma*

 
A significant improvement in the mean morning and evening PEF values with weight loss was found. The difference between the daily highest and lowest PEF did not change. Before weight loss, it was 24 L/min (range, 10 to 59 L/min), and after weight loss, it was 20 L/min (range, 8 to 41 L/min). Diurnal PEF variation declined from 5.5% (2.4) to 4.5% (1.5) (p = 0.01). PEF indexes over a follow-up period of 14 days are presented in Table 2 . Calculated from the serial morning PEF values over 2 weeks, the mean difference between the highest and lowest morning PEF values fell by 38% with weight reduction (Table 2) . Day-to-day PEF variation decreased from 5.3% (2.6) to 3.1% (1.3) (p < 0.005). Individual changes in diurnal and day-to-day PEF variations are shown in Figure 1 .



View larger version (19K):
[in this window]
[in a new window]
[Download PPT slide]
  		Figure 1. The individual changes in (top, a) diurnal and (bottom, b) day-to-day PEF variations before and after weight loss in obese patients with asthma (n = 14). The bars present the mean values. The p values refer to Wilcoxon signed rank test.

 
Seven patients met the inclusion criteria for the histamine challenge test. The mean PD15 was 0.20 mg (range, 0.015 to 1.6 mg) before weight loss and 0.30 mg (range, 0.043 to 1.6 mg) after weight loss. The change was NS.

Pulmonary function data are shown in Table 3 . The mean FEV1 was low before weight loss (77% of predicted; range, 50 to 105%), while the mean FVC was within normal range (93% of predicted; range, 71 to 114%). Weight reduction induced a significant increase in FEV1 (percent predicted; p < 0.01) and FVC (percent predicted; p < 0.05). Also, AFV increased with weight loss (p < 0.005). FEV1/FVC ratio did not change. Flow rates at low lung volumes (FEF25–75) were slightly reduced and showed a significant rise after weight loss (percent predicted; p = 0.01) also when related to FVC (FEF25–75/FVC percent; p < 0.05; Table 3 ). DLCO was within normal range in all patients before and after weight loss. The mean baseline DLCO was 102.5% of predicted (range, 84 to 121% of predicted).


View this table:
[in this window]
[in a new window]

  		Table 3. Pulmonary Function Data

 
The mean values of FRC, VC, and TLC were within normal range before weight loss, but still a significant increase in lung volumes was demonstrated with weight reduction. RV or RV/TLC did not change. The most significant improvement in lung volumes was the increase in expiratory reserve volume (ERV) from 0.43 L (0.22) to 0.72 L (0.50). The rise in ERV also mainly accounts for the increase in FRC, because RV did not change. TLC-He and TLC-B are presented in Table 3 . Nonventilated gas compartment (TLC-B - TLC-He) was 0.43 L before and 0.61 L after weight loss; the change was NS. The mean Raw was high before weight loss (329% predicted; range, 161 to 579% predicted; Table 3 ). In response to weight reduction, Raw decreased toward the normal level (p < 0.05), but the mean value was still after weight reduction 252% of predicted (range, 67 to 473% predicted). The change in BMI expressed as a percent baseline value correlated with the increase in SGaw (1/Raw; r = 0.59; p < 0.05).

The mean baseline arterial oxygen tension (PaO2 = 11.4 [0.9] kPa) and the mean carbon dioxide tension (PaCO2 = 5.2 [0.3] kPa) were within normal range. Weight loss did not alter the values. The effects of weight loss on E are shown in Table 4 . E measured in patients in supine and standing positions fell after weight loss by 16% (p < 0.01) and by 14% (p = 0.01), respectively. VT also showed slight decrease (p = 0.07 supine; p < 0.05 standing) while RR did not change.


View this table:
[in this window]
[in a new window]

  		Table 4. The Effects of Weight Loss on E, VT, and RR Measured with Patients in Supine and Standing Positions*

 

   Discussion
TOP
 Abstract
 Introduction
 Materials and Methods
 Results
 Discussion
References
 
The results of our study indicate improved pulmonary function after weight reduction in obese patients with asthma, suggesting that these patients benefit from even modest weight loss. The increase in FEV1 with no change in FEV1/FVC ratio may rather reflect improvement in lung volumes, a well-known effect of weight loss in obesity,12 16 17 than decrease in airways obstruction. However, increased FEF25–75 even when related to volume (FEF25–75/FVC) may suggest a relief in peripheral airways obstruction. Furthermore, increased FVC and VC may indicate improvement in small airways obstruction. However, the decrease in PEF variability after weight loss found in the present study refers to an attenuated variability of bronchial obstruction in larger airways. Also the decline in Raw may reflect the decrease in airways obstruction more in large than in small airways.

In obesity, increased volumes after weight loss, especially ERV or FRC, have been reported in several studies.12 16 17 RV usually remains unchanged.12 In chronic asthma, RV and FRC can be elevated because of hyperinflation.18 In obese asthmatics, weight reduction and a decrease in asthma severity with lessened hyperinflation may change FRC values to opposite directions. The results of the present study demonstrated a significant increase in the mean FRC after weight reduction, although the individual changes in FRC varied within a wide range. The increase in ERV was more constant. In this respect, changes in ERV may better than FRC reflect the effects of obesity or weight loss on lung volumes in this study.

Mechanisms how higher lung volumes affect pulmonary mechanics and work of breathing in asthma are not clear. Based on previous data concerning pulmonary function in asthma or obesity, several mechanisms could be postulated. Firstly, increase in FRC may contribute to a decrease in Raw that further reduces work of breathing.19 Secondly, in acute asthma with bronchoconstriction, a certain degree of hyperinflation with increased FRC may decrease work of breathing.20 It could be hypothesized that in this respect, low FRC could be unfavorable in obese asthmatics. Thirdly, low FRC with further decrease in FRC in supine position and concomitant increase in Raw may worsen nocturnal airways obstruction and increase diurnal variation of obstruction in asthma.21

Both obesity and asthma can cause an excessive small airway closure and increase in gas trapping.11 12 22 Of parameters that reflect small airways obstruction, our data showed reduced FEF25–75 that increased after weight loss as well as FEF25–75/FVC. Also, an increase in FVC and VC may reflect decreased small airway obstruction. However, only slight, if any, gas trapping was observed based on our TLC-B - TLC-He data.

Rapid shallow breathing pattern with low VT has been reported in morbid obesity.11 However, our data showed higher E and VT before than after weight loss. Tobin et al23 have suggested that symptomatic patients with chronic asthma may display increased E in association with an elevated respiratory center drive. They have reported increased VT in patients with asthma while breathing frequency may be normal. Our findings are in keeping with this, suggesting that tendency to increase VT in asthma patients may counteract the effects of obesity on breathing pattern.

There are increasing data available on the relation between obesity and bronchial hyperresponsiveness (BHR). It has been postulated that the lower VT of obese patients results in less tidal stretching of airways smooth muscle and could promote airway narrowing and possibly airway hyperreactivity.24 Kaplan and Montana25 have studied exercise-induced bronchospasm in obese nonasthmatic children. They demonstrated that the frequency and degree of exercise-induced bronchospasm was higher in obese children. Huang and colleagues26 have studied the relation between BMI and BHR in adolescents in Taiwan. They found that BMI was a significant predictor of BHR in teenage girls but not in boys. If obesity is associated with an increased risk of BHR, one would expect a decrease in bronchial responsiveness with weight loss. FEF25–75/FVC ratio has been reported to be associated with airways responsiveness.27 The results of the present study showed increase in FEF25–75/FVC, which may indicate decreased BHR after weight loss. In this study, the small number of patients tested may partly explain why we did not find a significant change in BHR measured using a histamine challenge test.

To our knowledge, there are no previous studies concerning the effects of weight loss on PEF variability in obese asthma patients. The results of the present study indicated that PEF variability decreased with weight loss. The mechanism is not clear, but the increase in PEF values could partly explain the reduction in diurnal variation, assuming parallel changes in morning and evening PEF values. However, the increase in PEF values may not explain the decline in day-to-day PEF variation reported herein. Our data showed that the difference between highest and lowest morning PEF values decreased with weight reduction. An interesting finding was that the lowest morning PEF values increased significantly while the highest morning PEF remained unchanged. The mechanisms of how weight loss affects PEF variation remain unclear. The decrease in airways obstruction and improved ventilatory mechanics after weight loss may contribute to a better control of airways obstruction.

It is also possible that there are other mechanisms linking weight loss to the decrease in bronchial obstruction and hyperreactivity. Earlier studies have reported changes in serum leptin levels after weight loss.28 According to preliminary results, leptin may have proinflammatory effects in the airways and may affect bronchial reactivity.29 Gene polymorphism may alter adrenergic receptor responsiveness both in asthma and obesity.30 Altered adrenoceptor function could be another common pathway between obesity and asthma. Further studies concerning effects of weight loss on responsiveness of ß2-adrenoceptors in lungs would be of interest.

The results of our study suggest that obese asthmatics benefit from weight loss as all obese patients do in terms of increased lung volumes and improved ventilatory mechanics. Our results also indicate decreased airways obstruction as well as lower PEF variability after weight loss, suggesting that obesity may increase the degree and variability of airways obstruction in asthmatics. Yet, further studies with larger patient groups will be necessary to clarify the relationship between obesity and asthma.


   Footnotes
 
Abbreviations: AFV = area under the expiratory flow volume curve; BHR = bronchial hyperresponsiveness; BMI = body mass index; DLCO = diffusing capacity of the lung for carbon monoxide; ERV = expiratory reserve volume; FEF25–75 = flow rate at the middle part of FVC; FRC = functional residual capacity; NS = not statistically significant; PD15 = provocative dose causing a 15% fall in FEV1; PEF = peak expiratory flow; Raw = airways resistance; RR = respiratory rate; RV = residual volume; SGaw = airways conductance; TLC = total lung capacity; TLC-B = TLC measured using body plethysmograph; TLC-He = TLC measured using the single-breath helium dilution method; VAS = visual analogue scale; E = minute ventilation; VLCD = very-low-calorie-diet; VT = tidal volume

This study was supported by the Finnish Cultural Foundation.

Received for publication December 29, 1999. Accepted for publication May 3, 2000.


   References
TOP
 Abstract
 Introduction
 Materials and Methods
 Results
 Discussion
 References
 

  1. Huovinen, E, Kaprio, J, Laitinen, LA, et al (1999) Incidence and prevalence of asthma among adult Finnish men and women of the Finnish twin cohort from 1975 to 1990, and their relation to hay fever and chronic bronchitis. Chest 115,928-936[Abstract/Free Full Text]
  2. Must, A, Spadano, J, Coakley, EH, et al (1999) The disease burden associated with overweight and obesity. JAMA 282,1523-1529[Abstract/Free Full Text]
  3. Gennuso, J, Epstein, LH, Paluch, RA, et al (1998) The relationship between asthma and obesity in urban minority children and adolescents. Arch Pediatr Adolesc Med 152,1197-1200[Abstract/Free Full Text]
  4. Shaheen, SO, Sterne, JAC, Montgomery, SM, et al (1999) Birth weight, body mass index and asthma in young adults. Thorax 54,396-402[Abstract/Free Full Text]
  5. Chen, Y, Dales, R, Krewski, D, et al (1999) Increased effects of smoking and obesity on asthma among female Canadians: the National Population Health Survey, 1994–1995. Am J Epidemiol 150,255-262[Abstract/Free Full Text]
  6. Camargo, CA, Weiss, ST, Zhang, S, et al (1999) Prospective study of body mass index, weight change, and risk of adult-onset asthma in women. Arch Intern Med 159,2582-2588[Abstract/Free Full Text]
  7. Shaheen, SO (1999) Obesity and asthma: cause for concern? Clin Exp Allergy 29,291-293[CrossRef][ISI][Medline]
  8. Luder, E, Melnik, TA, DiMaio, M (1998) Association of being overweight with greater asthma symptoms in inner city black and Hispanic children. J Pediatr 132,699-703[CrossRef][ISI][Medline]
  9. Dixon, JB, Chapman, L, O’Brien, P (1999) Marked improvement in asthma after Lap-Band surgery for morbid obesity. Obes Surg 9,385-389[CrossRef][ISI][Medline]
  10. Stenius-Aarniala, B, Poussa, T, Kvarnström, J, et al (2000) Immediate and long term effects of weight reduction in obese people with asthma: randomised controlled study. BMJ 320,827-832[Abstract/Free Full Text]
  11. Luce, JM (1980) Respiratory complications of obesity. Chest 78,626-631[Free Full Text]
  12. Hakala, K, Mustajoki, M, Aittomäki, J, et al (1995) The effect of weight loss and body position on pulmonary function and gas exchange abnormalities in morbid obesity. Int J Obes 19,343-346[ISI][Medline]
  13. Pekkarinen, T, Takala, I, Mustajoki, P (1996) Two year maintenance of weight loss after a VLCD and behavioral therapy for obesity: correlation to the scores of questionnaires measuring eating behavior. Int J Obes Relat Metab Disord 20,332-337[ISI][Medline]
  14. Quanjer, PH, Tammeling, GJ, Cotes, JE, et al (1993) Lung volumes and forced ventilatory flows: official statement of the European Respiratory Society. Eur Respir J 6(suppl 16),5-40[Medline]
  15. Sovijärvi, ARA, Malmberg, LP, Reinikainen, K, et al (1993) A rapid dosimetric method with controlled tidal breathing for histamine challenge. Chest 104,164-170[Abstract/Free Full Text]
  16. Thomas, PS, Cowen, ERT, Hulands, G, et al (1989) Respiratory function in morbidly obese before and after weight loss. Thorax 44,382-386[Abstract]
  17. Vaughan, RW, Cork, RC, Hollander, D (1981) The effect of massive weight loss on arterial oxygenation and pulmonary function tests. Anesthesiology 54,325-328[ISI][Medline]
  18. Pellegrino, R, Brusasco, V (1994) Lung volumes and expiratory flow during bronchoconstriction in asthma. Monaldi Arch Chest Dis 49,439-443[Medline]
  19. Zerah, F, Harf, A, Perlemuter, L, et al (1993) Effects of obesity on respiratory resistance. Chest 103,1470-1476[Abstract/Free Full Text]
  20. Wheatly, JR, West, S, Cala, SJ, et al (1990) The effect of hyperinflation on respiratory muscle work in acute induced asthma. Eur Respir J 3,625-632[Abstract]
  21. Ballard, RD, Irvin, CG, Martin, RJ, et al (1990) Influence of sleep on lung volume in asthmatic patients and normal subjects. J Appl Physiol 68,2034-2041[Abstract/Free Full Text]
  22. Evans, DJ, Green, M (1998) Small airways: a time to revisit? Thorax 53,629-630[Free Full Text]
  23. Tobin, MJ, Chadha, TS, Jenouri, G, et al (1983) Breathing patterns: 2. Diseased subjects. Chest 84,286-294[Abstract/Free Full Text]
  24. Fredberg, JJ, Inouye, D, Miller, B, et al (1997) Airway smooth muscle, tidal stretches, and dynamically determined contractile states. Am J Respir Crit Care Med 156,1752-1759[Abstract/Free Full Text]
  25. Kaplan, TA, Montana, E (1993) Exercise-induced bronchospasm in nonasthmatic obese children. Clin Pediatr 32,220-225
  26. Huang, SL, Shiao, G, Chou, P (1999) Association between body mass index and allergy in teenage girls in Taiwan. Clin Exp Allergy 29,323-329[CrossRef][ISI][Medline]
  27. Litonjua, AA, Sparrow, D, Weiss, ST (1999) The FEF25–75/FVC ratio is associated with methacholine airway responsiveness: the normative aging study. Am J Respir Crit Care Med 159,1574-1579[Abstract/Free Full Text]
  28. Wadden, TA, Considine, RV, Foster, GD, et al (1998) Short- and long-term changes in serum leptin dieting obese women: effects of caloric restriction and weight loss. J Clin Endocrinol Metab 83,214-218[Abstract/Free Full Text]
  29. Shore, SA, Abraham, J, Schwartzman, IN, et al (1999) Airway responses to ozone are reduced in leptin deficient mice [abstract]. Am J Respir Crit Care Med 159,A468
  30. Large, V, Hellstrom, L, Reynisdottir, S, et al (1997) Human ß-2 adrenoceptor gene polymorphisms are highly frequent in obesity and associate with altered adipocyte ß-2 adrenoceptor function. J Clin Invest 100,3005-3013[ISI][Medline]
  31. Viljanen, AA, Halttunen, PK, Kreus, KE, et al (1982) Spirometric studies in non-smoking, healthy adults. Scand J Clin Lab Invest Suppl 159,5-20[Medline]



This article has been cited by other articles:


Home page
 ChestHome page
J. A. Fiz, J. Gnitecki, S. S. Kraman, G. R. Wodicka, and H. Pasterkamp
Effect of Body Position on Lung Sounds in Healthy Young Men
Chest, March 1, 2008; 133(3): 729 - 736.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Lung Cell. Mol. Physiol.Home page
F. L. Lu, R. A. Johnston, L. Flynt, T. A. Theman, R. D. Terry, I. N. Schwartzman, A. Lee, and S. A. Shore
Increased pulmonary responses to acute ozone exposure in obese db/db mice
Am J Physiol Lung Cell Mol Physiol, May 1, 2006; 290(5): L856 - L865.
[Abstract] [Full Text] [PDF]

Home page
 CMAJHome page
M. Poulain, M. Doucet, G. C. Major, V. Drapeau, F. Series, L.-P. Boulet, A. Tremblay, and F. Maltais
The effect of obesity on chronic respiratory diseases: pathophysiology and therapeutic strategies.
Can. Med. Assoc. J., April 25, 2006; 174(9): 1293 - 1299.
[Abstract] [Full Text] [PDF]

Home page
 Eur Respir JHome page
M. Peters-Golden, A. Swern, S. S. Bird, C. M. Hustad, E. Grant, and J. M. Edelman
Influence of body mass index on the response to asthma controller agents.
Eur. Respir. J., March 1, 2006; 27(3): 495 - 503.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Regul. Integr. Comp. Physiol.Home page
R. A. Johnston, T. A. Theman, and S. A. Shore
Augmented responses to ozone in obese carboxypeptidase E-deficient mice
Am J Physiol Regulatory Integrative Comp Physiol, January 1, 2006; 290(1): R126 - R133.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Respir. Crit. Care Med.Home page
S. Wenzel
Severe Asthma in Adults
Am. J. Respir. Crit. Care Med., July 15, 2005; 172(2): 149 - 160.
[Abstract] [Full Text] [PDF]

Home page
 ThoraxHome page
I S Olafsdottir, T Gislason, B Thjodleifsson, I Olafsson, D Gislason, R Jogi, and C Janson
C reactive protein levels are increased in non-allergic but not allergic asthma: a multicentre epidemiological study
Thorax, June 1, 2005; 60(6): 451 - 454.
[Abstract] [Full Text] [PDF]

Home page
 ThoraxHome page
K Wickens, D Barry, A Friezema, R Rhodius, N Bone, G Purdie, and J Crane
Obesity and asthma in 11-12 year old New Zealand children in 1989 and 2000
Thorax, January 1, 2005; 60(1): 7 - 12.
[Abstract] [Full Text] [PDF]

Home page
 Eur Respir JHome page
E.S. Ford, D.M. Mannino, S.C. Redd, A.H. Mokdad, and J.A. Mott
Body mass index and asthma incidence among USA adults
Eur. Respir. J., November 1, 2004; 24(5): 740 - 744.
[Abstract] [Full Text] [PDF]

Home page
 JAMAHome page
D. D. Sin, J. Man, H. Sharpe, W. Q. Gan, and S. F. P. Man
Pharmacological Management to Reduce Exacerbations in Adults With Asthma: A Systematic Review and Meta-analysis
JAMA, July 21, 2004; 292(3): 367 - 376.
[Abstract] [Full Text] [PDF]

Home page
 Eur Respir JHome page
M.I. Gunnbjornsdottir, E. Omenaas, T. Gislason, E. Norrman, A-C. Olin, R. Jogi, E.J. Jensen, E. Lindberg, E. Bjornsson, K. Franklin, et al.
Obesity and nocturnal gastro-oesophageal reflux are related to onset of asthma and respiratory symptoms
Eur. Respir. J., July 1, 2004; 24(1): 116 - 121.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Respir. Crit. Care Med.Home page
S. Guerra, A. L. Wright, W. J. Morgan, D. L. Sherrill, C. J. Holberg, and F. D. Martinez
Persistence of Asthma Symptoms during Adolescence: Role of Obesity and Age at the Onset of Puberty
Am. J. Respir. Crit. Care Med., July 1, 2004; 170(1): 78 - 85.
[Abstract] [Full Text] [PDF]

Home page
 BMJHome page
Minerva
BMJ, October 6, 2003; 327(7418): E6 - 6.
[Full Text] [PDF]

Home page
 ChestHome page
W. J. Calhoun
Nocturnal Asthma
Chest, March 1, 2003; 123(2007): 399S - 405S.
[Abstract] [Full Text] [PDF]

Home page
 ThoraxHome page
K G Tantisira and S T Weiss
Complex interactions in complex traits: obesity and asthma
Thorax, September 1, 2001; 56(90002): ii64 - 74.
[Full Text] [PDF]

This Article
Right arrow Abstract Freely available
Right arrow Full Text (PDF) Free
Right arrow Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Article Archive
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via ISI Web of Science (58)
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Hakala, K.
Right arrow Articles by Sovijärvi, A.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Hakala, K.
Right arrow Articles by Sovijärvi, A.

HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS