Rationale: We have previously reported that regular physical activity reduces risk of chronic obstructive pulmonary disease (COPD) exacerbation. We hypothesized that higher levels of regular physical activity could reduce the risk of COPD by modifying smoking-related lung function decline. Objective: To estimate the longitudinal association between regular physical activity and FEV1 and FVC decline and COPD risk. Methods: A population-based sample (n = 6,790) was recruited and assessed with respect to physical activity, smoking, lung function, and other covariates, in Copenhagen in 1981–1983, and followed until 1991–1994. Mean level of physical activity between baseline and follow-up was classified into “low,” “moderate,” and “high.” FEV1 and FVC decline rates were expressed as milliliters per year. COPD was defined as FEV1/FVC ⩽ 70%. Adjusted associations between physical activity and FEV1 and FVC decline, and COPD incidence, were obtained using linear and logistic regression, respectively. Results: Active smokers with moderate and high physical activity had a reduced FEV1 and FVC decline compared with those with low physical activity (relative change of +2.6 and +4.8 ml/yr of FEV1, P-for-trend = 0.006, and +2.6 and +7.7 ml/yr of FVC, P-for-trend < 0.0001, for the moderate and high physical activity group, respectively), after adjusting for all potential confounders and risk factors of lung function decline. Active smokers with moderate to high physical activity had a reduced risk of developing COPD as compared with the low physical activity group (odds ratio, 0.77; p = 0.027). Conclusions: This prospective study shows that moderate to high levels of regular physical activity are associated with reduced lung function decline and COPD risk among smokers.

Background Chronic obstructive pulmonary disease (COPD) is increasingly considered a heterogeneous condition. It was hypothesised that COPD, as currently defined, includes different clinically relevant subtypes. Methods To identify and validate COPD subtypes, 342 subjects hospitalised for the first time because of a COPD exacerbation were recruited. Three months after discharge, when clinically stable, symptoms and quality of life, lung function, exercise capacity, nutritional status, biomarkers of systemic and bronchial inflammation, sputum microbiology, CT of the thorax and echocardiography were assessed. COPD groups were identified by partitioning cluster analysis and validated prospectively against cause-specific hospitalisations and all-cause mortality during a 4 year follow-up. Results Three COPD groups were identified: group 1 (n=126, 67 years) was characterised by severe airflow limitation (postbronchodilator forced expiratory volume in 1 s (FEV₁) 38% predicted) and worse performance in most of the respiratory domains of the disease; group 2 (n=125, 69 years) showed milder airflow limitation (FEV₁ 63% predicted); and group 3 (n=91, 67 years) combined a similarly milder airflow limitation (FEV₁ 58% predicted) with a high proportion of obesity, cardiovascular disorders, diabetes and systemic inflammation. During follow-up, group 1 had more frequent hospitalisations due to COPD (HR 3.28, p<0.001) and higher all-cause mortality (HR 2.36, p=0.018) than the other two groups, whereas group 3 had more admissions due to cardiovascular disease (HR 2.87, p=0.014). Conclusions In patients with COPD recruited at their first hospitalisation, three different COPD subtypes were identified and prospectively validated: ‘severe respiratory COPD’, ‘moderate respiratory COPD’, and ‘systemic COPD’.

Little is known about changes in physical activity in subjects with chronic obstructive pulmonary disease (COPD) and its impact on mortality. Therefore, we aimed to study changes in physical activity in subjects with and without COPD and the impact of physical activity on mortality risk.Subjects from the Copenhagen City Heart Study with at least two consecutive examinations were selected. Each examination included a self-administered questionnaire and clinical examination.1270 COPD subjects and 8734 subjects without COPD (forced expiratory volume in 1 s 67±18 and 91±15% predicted, respectively) were included. COPD subjects with moderate or high baseline physical activity who reported low physical activity level at follow-up had the highest hazard ratios of mortality (1.73 and 2.35, respectively; both p<0.001). In COPD subjects with low baseline physical activity, no differences were found in survival between unchanged or increased physical activity at follow-up. In addition, subjects without COPD with low physical activity at follow-up had the highest hazard ratio of mortality, irrespective of baseline physical activity level (p≤0.05).A decline to low physical activity at follow-up was associated with an increased mortality risk in subjects with and without COPD. These observational data suggest that it is important to assess and encourage physical activity in the earliest stages of COPD in order to maintain a physical activity level that is as high as possible, as this is associated with better prognosis.

The origin(s) of systemic inflammation in patients with chronic obstructive pulmonary disease (COPD) is unclear. We investigated the impact of exposure to ambient air pollution on systemic biomarkers of inflammation (C-reactive protein (CRP), tumour necrosis factor-α, interleukin (IL)-6, IL-8 and fibrinogen) and tissue repair (hepatocyte growth factor (HGF)) in 242 clinically stable COPD patients (mean age 67.8 years and forced expiratory volume in 1 s 71.3% predicted) in Barcelona, Spain, in 2004–2006.A spatiotemporal exposure assessment framework was applied to predict ambient nitrogen dioxide (NO₂) and levels of particles with a 50% cut-off aerodynamic diameter of 2.5 μm (PM_2.5) at each participant’s home address during 10 periods of 24 h (lags 1–10) and 1 year prior to the blood sampling date. We used linear regression models to estimate associations between biomarkers and exposure levels.An interquartile range (IQR) increase in NO₂exposure in lag 5 was associated with 51%, 10% and 9% increases in CRP, fibrinogen and HGF levels respectively. We also observed 12% and 8% increases in IL-8 associated with an IQR increase in NO₂exposure in lag 3 and over the year before sampling, respectively. These increases were larger in former smokers. The results for PM_2.5were not conclusive.These results show that exposure to ambient NO₂increases systemic inflammation in COPD patients, especially in former smokers.