The results from this large scale population‐based study show a negative association between physical activity and BHR. This association was consistent across several subgroups and was independent of potential confounders for BHR and physical activity. To the best of our knowledge, this is the first study to investigate the association between physical activity and BHR in adults from the general population. The study shows that the cut‐off point for the frequency (or duration) of physical activity at which BHR would be significantly reduced is relatively low. This suggests that, if causal, even modest physical activity can have a beneficial effect on BHR.
The participation rate at ECRHS II was 58.2% (7648 of 13
130) which is comparable to several recent population studies and higher than that of the one population study of change in BHR.21
Eligible men were slightly more likely to respond to the main questionnaire at ECRHS II than women. Responders were slightly older than non‐responders at baseline (mean age 34.1 years vs 33.8 years). No significant difference in baseline lung function was observed between responders and non‐responders (mean FEV1
3.90 l vs 3.86 l). Subjects lost to follow‐up were more frequently smokers at baseline. These small differences were unlikely to bias the reported relations between physical activity and BHR substantially. Of the 7648 participants, 16% completed the questionnaire only and did not perform lung function tests. Of the 6413 with an acceptable FEV1
measurement, 519 (8.1%) had contraindications for the methacholine test and bronchial responsiveness was measured in 5158 (80.4%); thus only 39% of the original population were included in the present analysis. The distributions of smoking and atopy status were comparable between subjects with and without bronchial responsiveness data. Subjects who were tested for BHR had slightly greater BMI and slightly greater FEV1
than those not tested. Asthma and asthma‐like symptoms were more common in subjects who did not perform a methacholine challenge than in those with BHR data. Inadequately active subjects were over‐represented in those without BHR data. It therefore seems likely that the association between physical activity and BHR is underestimated in our study.
Some studies have investigated the relationship between inactivity and increased levels of BHR in children. In a cross‐sectional study, a negative relationship between physical activity and BHR was shown in children currently with asthma but this relationship was not observed in children without asthma.25
A longitudinal study of 757 previously asymptomatic children found a weak association between physical fitness in childhood and the response of the airways to methacholine at follow‐up, and physical fitness tended to be correlated with a reduced risk of developing adolescent asthma.26
Another prospective study of 262 twin pairs showed that the twin who participated in conditioning exercise had a lower risk of asthma than the sedentary twin.3
Previous studies of the relationship between physical activity and BHR in adults have focused on athletes and showed positive associations between BHR and intense exercise.27,28,29
In such populations, this positive relationship may be related to thermal stimuli—heat loss that leads to vascular engorgement as the airways warm back up after intense exercise, initiating bronchoconstriction. Alternatively, it may be related to osmotic stimuli—water loss that leads to a change in airway osmolarity, initiating epithelial and mast cell activation and resulting in the release of inflammatory mediators in the airways that cause bronchoconstriction.30
However, these studies carried out in high level sportsmen cannot be compared with our study of subjects from the general population.
Two outcome definitions of bronchial responsiveness were used—the dichotomous BHR variable and the logarithmically transformed slope, as suggested by Chinn et al
Whichever outcome was used, the results were similar.
The validity of the physical activity data may be questionable because there is no gold standard for assessment of physical activity. Although physical activity was assessed by a standardised interviewer‐administrated questionnaire, as in most epidemiological studies,31
the responses reflect self‐assessment of physical activity level or frequency. However, the questions used in the ECRHS have been validated previously.32,33,34
Moreover, assessing physical activity by questionnaire may be the only practical method of collecting data in large epidemiological studies with intensive respiratory tests such as the ECRHS. Given that self‐reported physical activity may not reveal the real levels of physical activity, which may be overestimated,35
the results may be influenced by some misclassification. However, it was possible to categorise the subjects and misclassification is likely to be random as the physical activity data were collected before the BHR test was carried out. Such a bias, if any, would therefore lead to an underestimation of the true association.
The mechanisms linking physical activity to BHR are not clear. Moderate and vigorous physical activity may be one component of a healthy lifestyle or may be a marker of a generally better constitution. We therefore adjusted for possible confounding influences of age, smoking status, BMI and educational levels, and still observed the independent associations between BHR and physical activity. Moreover, some over‐adjustment may have occurred for BMI. Obesity and being overweight may partly be a result of low physical activity,36,37
and adjusting for BMI would lead to underestimation of the associations between physical activity and BHR. Some subjects with asthma or respiratory symptoms may refrain from vigorous physical activity to avoid unpleasant respiratory effects. However, when we adjusted for asthma and respiratory symptoms and, more importantly, stratified for these variables, the results did not change (results not shown). Also, the exclusion of subjects who avoided taking vigorous exercise because of wheezing or asthma had no effect on the results. We further reduced the potential for reverse causation, that is, serious disease causing low physical activity rather than vice versa, by asking subjects whether they were disabled from walking due to their diseases. The exclusion of these subjects (n
361) also had almost no effect on the observed association (results available from authors).
A more plausible hypothesis is that physical activity might influence airway physiology and BHR. A deep inspiration, as in exercise, seems to be the first line of defence against bronchospasm (bronchoprotective effect) and can partially reverse it once bronchoconstriction is established (bronchodilatory effect) because of its effect on the constriction of smooth airway muscles.38,39,40,41
It has therefore been suggested that a decrease in the amount of these sighs or periodic expansions of the lungs while sedentary may contribute to non‐specific BHR in children.42
Another possible explanation is that moderate physical activity might be associated with a reduction in systemic inflammation. Physical activity has been shown to be associated with an improvement in the lipoprotein profile and a reduction in the level of some inflammatory markers (such as plasma fibrinogen and C‐reactive protein).43,44,45,46
On the other hand, chronic systemic inflammation has recently been shown to be associated with BHR.47
The strengths of the present study are its large size, the use of high quality data from a random general population sample, the use of a standardised questionnaire and the strictly standardised assessment of BHR in all participating countries. The percentage of BHR (13%) observed in our study was comparable to that obtained in other population‐based studies by different methods.48
The present study confirmed previous findings that sex, BMI, smoking, atopy, asthma‐like symptoms and asthma are associated with an increased risk of BHR. The observed associations of physical activity with age, BMI, smoking habits and education level are also consistent with previously published results.49
However, our findings should be considered in the context of the study limitations. First, a cause‐and‐effect relationship cannot be established between exercise and BHR because of the cross‐sectional design of the study. Second, despite controlling for a large number of potentially confounding variables in our multivariable analyses, we are unable to completely exclude residual confounders due to unknown factors.
In conclusion, this study shows a strong and consistent negative relationship between physical activity and BHR in adults. If causal, our findings suggest that relatively small amounts of physical activity would markedly reduce BHR in the general population. This implies that another beneficial effect of physical activity may be added to the already known benefits. Further data are needed to clarify the relationship between physical activity and BHR and to determine the optimal amount (frequency and duration) and type of physical activity required. If confirmed, our results may contribute to the development of primary prevention programmes for pulmonary diseases.