Chronic obstructive pulmonary disease (COPD) and obesity are common and disabling chronic health conditions with increasing prevalence worldwide. A relationship between COPD and obesity is increasingly recognised, although the nature of this association remains unknown. This review focuses on the epidemiology of obesity in COPD and the impact of excessive fat mass on lung function, exercise capacity and prognosis. The evidence for altered adipose tissue functions in obesity-including reduced lipid storage capacity, altered expression and secretion of inflammatory factors, adipose tissue hypoxia and macrophage infiltration in adipose tissue-is also reviewed. The interrelationship between these factors and their contribution to the development of insulin resistance in obesity is considered. It is proposed that, in patients with COPD,

Healthy subjects with normal nasal resistance breathe almost exclusively through the nose during sleep. This study tested the hypothesis that a mechanical advantage might explain this preponderance of nasal over oral breathing during sleep.A randomised, single-blind, crossover design was used to compare upper airway resistance during sleep in the nasal and oral breathing conditions in 12 (seven male) healthy subjects with normal nasal resistance, aged 30¡4 (mean¡SEM) yrs, and with a body mass index of 23¡1 kg?m 2 . During wakefulness, upper airway resistance was similar between the oral and nasal breathing routes. However, during sleep (supine, stage two) upper airway resistance was much higher while breathing orally (median 12.4 In a recent publication the authors described, for the first time, partitioning of inhaled ventilation between the nose and mouth during sleep in healthy subjects with normal nasal resistance [1]. The main finding of the latter study was that the oral fraction of inhaled ventilation during sleep was very small, averaging only 4% for the group of 10 subjects, and several subjects did not breathe through their mouth at all during sleep. Furthermore, the inhaled oral fraction did not change significantly between different non-rapid eye movement sleep stages or between rapid eye movement (REM) and non-REM sleep.The physiological explanation for the marked predominance of nasal ventilation over oral ventilation during sleep in normal subjects is unknown. Since total airway resistance while awake and breathing through the mouth is typically 2-4 cmH 2 O?L -1 ?s -1 [2] and the normal nasal resistance alone is of similar magnitude [3], it is not intuitively obvious why healthy subjects should choose to breathe almost exclusively through the nasal route during sleep. Specifically, there are no published measurements describing the effect of oral versus nasal breathing on upper airway resistance during sleep.It is important to understand the influence of the breathing route (oral or nasal) on upper airway resistance during sleep from the perspective of understanding normal respiratory physiology during sleep, but this information may also provide an insight into the relationship between the breathing route and upper airway obstruction during sleep. The authors hypothesised that the observed preponderance of nasal over oral ventilation in normal subjects during sleep would reflect a mechanical advantage of the nasal breathing route. To test this hypothesis, the authors compared upper airway resistance during nasal breathing and during oral breathing in healthy sleeping subjects with normal nasal resistance. Methods Study designA randomised, single blind, crossover study was conducted to compare upper airway resistance during sleep when nose breathing with that when mouth breathing. Subjects underwent a single overnight polysomnogram at Kingston General Hospital Sleep Laboratory, Ontario. The night was divided into two parts, oral breathing and nasal breathing, the order being randomised...

Most subjects with COPD in Canada remain undiagnosed. These subjects are less symptomatic and impaired, which may partly explain lack of diagnosis. Although patients with undiagnosed COPD experience fewer exacerbations than those with diagnosed COPD, they use a similar amount of health services for exacerbation events; thus, the overall health system burden of exacerbations in those with undiagnosed COPD is considerable.

Background: Clinical trials measure exacerbations of chronic obstructive pulmonary disease (COPD) inconsistently. A study was undertaken to determine if different methods for ascertaining and analysing COPD exacerbations lead to biased estimates of treatment effects. Methods: Information on the methods used to count, analyse and report COPD exacerbation rates was abstracted from clinical trials of long-acting bronchodilators or long-acting bronchodilator/inhaled steroid combination products published between 2000 and 2006. Data from the Canadian Optimal Therapy of COPD Trial was used to illustrate how different analytical approaches can affect the estimate of exacerbation rates and their confidence intervals. Results: 22 trials (17 156 patients) met the inclusion criteria and were reviewed. None of the trials adjudicated exacerbations or determined independence of events. 14/22 studies (64%) introduced selection bias by not analysing outcome data for subjects who prematurely stopped study medications. Only 31% of trials used timeweighted analyses to calculate the mean number of exacerbations/patient-year and only 15% accounted for between-subject variation. In the Canadian Optimal Therapy of COPD Trial the rate ratio for exacerbations/ patient-year was 0.85 when all data were included in a time-weighted analysis, but was overestimated as 0.79 when data for those who prematurely stopped study medications were excluded and was further overestimated as 0.46 when a time-weighted analysis was not conducted; p values ranged from 0.03 to 0.24 depending on how exacerbations were determined and analysed. Conclusions: Clinical trials have used widely different methods to define and analyse COPD exacerbations and this can lead to biased estimates of treatment effects. Future trials should strive to include blinded adjudication and assessment of the independence of exacerbation events, and trials should report time-weighted intentionto-treat analyses with adjustments for between-subject variation in COPD exacerbations.Patients with chronic obstructive pulmonary disease (COPD) exhibit slow progressive deterioration in airflow and respiratory status that can be punctuated by acute episodes of clinical deterioration known as COPD exacerbations. Acute exacerbations of COPD are characterised clinically by acute or subacute worsening of respiratory symptoms and may include abrupt increases in cough, sputum production, sputum purulence and breathlessness. 1COPD exacerbations have an important negative impact on health-related quality of life 2-4 and generate considerable economic costs. 5 The prevention of exacerbations is now recognised as a primary goal of COPD therapy. 6 Earlier trials of COPD therapy considered lung function as the primary outcome and analysed exacerbations as secondary outcomes.7 8 More recently, many clinical trials of maintenance medications for COPD have evaluated COPD exacerbation rates as a primary outcome. Unfortunately, clinical trials have not been consistent in how they count, record or anal...

To cope with the increased ventilatory demands of exercise, patients with severe expiratory flow limitation adopt strategies that ultimately place greater demands on their inspiratory muscles. Increased inspiratory muscle work may contribute to dyspnea causation and exercise limitation in such patients even before their ventilatory ceiling is attained. In this setting, continuous positive airway pressure (CPAP) should, by favorably affecting inspiratory muscle function and respiratory sensation, improve exercise performance. Six patients with chronic airflow limitation (CAL) (FEV1 +/- SD = 35 +/- 12% predicted) undertook constant-load, submaximal, cycle exercise at 50% of their predetermined maximal oxygen consumption: CPAP of 4 to 5 cm H2O was delivered during one exercise session and bracketed by one or two unassisted control sessions. In four patients, CPAP-assisted (4 to 5 cm H2O) exercise was bracketed by two unassisted control exercise sessions; two remaining patients undertook CPAP-assisted exercise and one unassisted control session. CPAP resulted in a significant increase in exercise endurance time (TLIM) (by 48%: CPAP TLIM (mean +/- SE) = 8.82 +/- 1.90 min; averaged control TLIM = 5.98 +/- 1.23 min (p less than 0.01). CPAP effectively ameliorated exertional dyspnea in the majority of patients; selected dyspnea ratings (Borg scale) during control (final minute) and CPAP at isotime, at comparable levels of ventilation, were (mean +/- SD) 7.83 +/- 2.25 and 5.5 +/- 2.2, respectively (p less than 0.025). Breathing frequency fell significantly during CPAP application (at isotime) by 17% (p less than 0.02); other steady-state ventilatory variables and end-expiratory lung volumes were not significantly different during CPAP and control.(ABSTRACT TRUNCATED AT 250 WORDS)