Proceedings of the American Thoracic Society
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The Proceedings of the American Thoracic Society 6:663-667 (2009)
© 2009 The American Thoracic Society
doi: 10.1513/pats.200907-070DP
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Physical Inactivity and Obesity

Relation to Asthma and Chronic Obstructive Pulmonary Disease?

Nick H. T. ten Hacken1

1 Department of Pulmonology, University Medical Center Groningen, University of Groningen, The Netherlands

Correspondence and requests for reprints should be addressed to N.H.T. ten Hacken, M.D., Ph.D., Dept. of Pulmonology, UMCG, PO Box 30001, 9700 RB Groningen, The Netherlands. E-mail: n.h.t.ten.hacken{at}int.umcg.nl

ABSTRACT

Physical inactivity and obesity are modifiable risk factors for many chronic diseases, including cardiovascular disease, diabetes mellitus, osteoporosis, osteoarthritis, and depression. Both physical inactivity and obesity are associated with low-grade systemic inflammation that may contribute to the inflammatory processes present in many chronic diseases. In asthma, almost no studies are available in which physical inactivity has been studied using performance-based instruments. In contrast, the association between obesity and a higher prevalence of asthma has often been suggested in a large number of studies. In chronic obstructive pulmonary disease (COPD) physical inactivity has been demonstrated in a few studies that used performance-based instruments; this was associated with the higher COPD Global Initiative on Obstructive Lung Disease (GOLD) stages and a higher degree of systemic inflammation, independent of body mass index. In contrast to physical inactivity, obesity in COPD is associated with the lower GOLD stages. Additionally, obesity is associated with the chronic obstructive phenotype and features of the metabolic syndrome. To elucidate the independent relation of physical inactivity and obesity with systemic inflammation, performance-based studies of physical inactivity in asthma and COPD are highly needed.

Key Words: physical activity • obesity • asthma • chronic obstructive pulmonary disease • systemic inflammation

Physical activity can be defined as any bodily movement produced by the skeletal muscles that requires energy expenditure (http://www.who.int/dietphysicalactivity/factsheet_recommendations/en/). Physical (in)activity can be investigated by direct observation, assessment of energy expenditure (calorimetry, doubly labeled water), use of self-reported questionnaires, and motion sensors (pedometers, accelerometers) (1). The level of physical activity can be arbitrarily categorized by counting the number of steps per day: sedentary (<5,000), low-active (5,000–7,499), somewhat active (7,500–9,999), active (≥10,000), and very active (>12,500) (2). Physical inactivity is an independent risk factor for many chronic diseases, such as obesity, coronary heart disease, stroke, type II diabetes, and colon and breast cancer (3). An intriguing finding from the well-known European Community Respiratory Health Survey II (ECRHS-II) study suggests that physical inactivity is a strong and independent risk factor for bronchial hyperresponsiveness in adults from the general population (4).

Obesity is defined arbitrarily as a body mass index (BMI) ≥30. A high BMI is a major risk factor for chronic diseases, such as cardiovascular disease, diabetes, musculoskeletal diseases, and endometrial, breast, and colon cancer (http://www.who.int/mediacentre/factsheets/fs311/en/index.html). Interestingly, a recent large-scale population-based study demonstrated that abdominal obesity, as part of the metabolic syndrome, was the strongest independent predictor of lung function impairment (5).

During the last decade, it has become clear that a low-grade systemic inflammation plays an important role in the pathological processes of many chronic diseases. A low-grade systemic inflammation can be defined as a two- to fourfold elevation in circulating levels of proinflammatory and antiinflammatory cytokines, naturally occurring cytokine antagonists, and acute phase proteins, as well as minor increases in counts of neutrophil and natural killer cells (6). From a pulmonary perspective it is interesting to note that a well-known marker of systemic inflammation, C-reactive protein (CRP), was associated with a lower FEV1 in a number of cross-sectional and longitudinal studies in healthy subjects with a wide range of age (7–12). In addition, CRP levels were strongly and independently associated with a higher frequency of bronchial hyperresponsiveness to methacholine in the ECRHS-II study (10).

Recently, there is increasing interest in the possible causes and consequences of the above-described low-grade systemic inflammation. The relationship with obesity has been studied extensively, particularly in the frame of the metabolic syndrome. Figure 1 depicts the central role of visceral abdominal fat in this syndrome (13), demonstrating that adipose tissue is not just an inert tissue but an active secretory organ participating in the regulation of many pathological processes (14). The red arrows in Figure 1 indicate the possible effects of smoking, another important risk factor for low-grade systemic inflammation. The contribution of physical inactivity to this low-grade systemic inflammation in our opinion is rather underestimated in the medical literature. Physical inactivity does not only contribute to a positive energy balance and the induction of (abdominal) obesity; the lack of enough physical activity is also associated with increased markers of systemic inflammation (15–17). Apparently, the skeletal muscles are not just an inert tissue but constitute a large secretory organ that produces antiinflammatory factors in the process of skeletal contractions (18, 19).


Figure 1
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  		Figure 1. Schematic representation of mechanisms linking obesity with low-grade systemic inflammation and cardiovascular disease. The red arrows indicate an effect of smoking. Both abdominal obesity and smoking are associated with insulin resistance, oxidative stress, and increased levels of different (adipo)cytokines and inflammatory markers, all of which lead ultimately to endothelial dysfunction (Reprinted by permission from Reference 13).

 
As physical inactivity, obesity, and systemic inflammation are probably important risk factors for the health and general well-being of patients with asthma and COPD, there is increasing interest in these modifiable risk factors. The primary purpose of this review is to summarize the available literature regarding the potential role of physical inactivity and obesity in asthma and COPD and to examine their contribution to systemic inflammation.

ASTHMA

Physical Inactivity
Children with established asthma seem to have a physical activity level comparable with that of healthy controls. Nevertheless, they frequently develop physical inactivity during the time of maturation from adolescence into adulthood and from adulthood into elderly age (20). Ford and colleagues demonstrated that adults with asthma were less likely to engage in running, basketball, golf, and weightlifting but were more likely to use an exercise bicycle (21). Furthermore, they demonstrated that adult patients with asthma were not meeting the current recommendations for physical activity. Physical inactivity is known to affect many important asthma outcomes. For example, a large United States population-based study on risk factors for asthma demonstrated that physical inactivity was associated with a higher number of emergency room visits, inability to go to work, asthma symptoms, sleep problems, use of medication, and use of inhalers (22). Another study demonstrated that lower physical activity at work and during leisure time associated significantly with lower spirometry values in adult patients with asthma (30–89 years) (23). To our knowledge there is no direct evidence that physical inactivity associates with increased systemic inflammation in established asthma.

There are a number of studies in the general population that suggest that physical inactivity may be an independent risk factor for the induction of asthma. A prospective community-based study in 757 asymptomatic children with an average age of 9.7 years demonstrated that low physical fitness correlated with the development of asthma during adolescence (24). In asymptomatic children at age 3.5 years it was demonstrated that TV watching longer than 2 hours per day was associated with the development of bronchial hyperresponsiveness and the clinical expression of asthma (25). Similarly, the ECRHS-II population-based study demonstrated that decreased physical activity was strongly associated with bronchial hyperresponsiveness in a dose–response manner (4). The authors speculated about the underlying mechanisms that link physical inactivity to increased bronchial hyperresponsiveness and suggested that physical inactivity might be associated with systemic inflammation. Interestingly, the same ECRHS-II study demonstrated a positive association between bronchial hyperresponsiveness and CRP (10).

Obesity
Because the prevalence of obesity and asthma both have increased during the last 2 decades one may hypothesize that the two conditions have a causal relationship (26). In a metaanalysis on seven studies (333,102 subjects total) it was demonstrated that a BMI ≥25 conferred increased odds of incident asthma at 1-year follow-up, with an increased risk of 46% in men, and 68% in women (27). Unfortunately, most epidemiological studies did not take physical inactivity into account, whereas physical inactivity is an important risk factor for obesity. Only the prospective study of Camargo and colleagues did correct for this by including a question about physical activity. This study demonstrated a relative risk for incident asthma with increasing BMI up to 2.7 for obese individuals, independent of physical activity (28). In a systematic review the beneficial effect of weight loss was demonstrated in at least one clinical asthma outcome, regardless of the type of intervention (29). One study investigated systemic and local inflammation in obese and normal-weight subjects with and without asthma and demonstrated that obese versus normal-weight subjects with asthma have higher levels of IL-4, IL-6, high sensitivity–CRP, and leptin, although the differences did not reach the level of significance (30). Indeed, a number of reviews suggest (14, 21, 31–34) that obesity-induced systemic inflammation may play a role in the clinical expression of asthma, but clearly we are just at the beginning of understanding the underlying mechanisms.

COPD

Physical Inactivity
Few data are available confirming that the physical activity level in COPD is lower than in age-matched controls; the studies that used performance-based instruments are summarized in Table 1. The largest of these studies demonstrated that steps per day, minutes of at least moderate activity, and physical activity levels were significantly reduced from Global Initiative for Obstructive Lung Disease (GOLD) stage II, GOLD stage III, and GOLD stage IV, respectively, as compared with patients with chronic bronchitis (35). In another study, a triaxial accelerometer was used to identify different types of physical (in)activity. During the daytime patients with COPD (GOLD stage II–III) were shown to sit down an average of 374 minutes and lie down 87 minutes per day, whereas healthy controls were shown to sit down for 306 minutes and lie down for 29 minutes (36). Independent predictors of low physical activity, as demonstrated by another study, were older age, female sex, lower socioeconomic status, history of diabetes, health-related quality of life, and long-term oxygen therapy using the Minnesota Leisure Time Physical Activity Questionnaire (37). The same group demonstrated in a large population-based sample that regular physical activity modifies smoking-related lung function decline and development of COPD (38).


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  		TABLE 1. PERFORMANCE-BASED PHYSICAL ACTIVITY: CHRONIC OBSTRUCTIVE PULMONARY DISEASE VS. CONTROLS

 
Only a few reports investigated the association between physical inactivity and low-grade systemic inflammation. Watz and colleagues demonstrated in 170 outpatients with COPD that physical activity gradually declined with higher GOLD and BODE (body mass index, airflow obstruction, dyspnea, and exercise capacity) stages of COPD, whereas fibrinogen and CRP levels demonstrated opposite trends (39). These higher values of systemic inflammation were associated with reduced physical activity independent of the GOLD or the BODE stage. Similarly, Garcia and colleagues demonstrated in 341 patients with COPD that those with the lowest quartile of physical activity had increased risk of increased circulating tumor necrosis factor (TNF) and CRP levels in a multivariate logistic regression analysis (40).

Obesity
A relationship between obesity and COPD is increasingly recognized, although the nature of this association remains unknown (41). The prevalence of obesity in a primary care population of patients with COPD was found to be 18%, which was higher than in the general population (42). Interestingly, as in many other COPD studies, the prevalence of obesity was higher with a lower GOLD stage, in line with the intriguing finding that a higher BMI (and higher fat-free mass) is associated with a lower mortality rate in COPD (43, 44). Another study demonstrated that overweight/obesity in COPD is more prevalent in the chronic obstructive phenotype, whereas underweight is more prevalent in the emphysematous phenotype (45). A small study in 28 patients with COPD demonstrated that obese patients with COPD more frequently had features of the metabolic syndrome, and that TNF, IL-6, and leptin levels were higher and adiponectin levels were lower than in normal-weight controls (46). A larger study in 30 patients with chronic bronchitis and 170 patients with COPD demonstrated that the prevalence of the metabolic syndrome was 47.5% and that this condition was associated with higher levels of CRP and IL-6, but with lower levels of physical activity (47). In multivariate linear regression analysis the metabolic syndrome, physical activity level, and GOLD stage of COPD were independent predictors of CRP and IL-6. Together, these data suggest that systemic inflammation in the early stages of COPD is promoted particularly by obesity and the metabolic syndrome and in the late stages by physical inactivity.

SUMMARY

Physical inactivity and obesity are both associated with a low-grade systemic inflammation in the general population. Because high CRP levels in young healthy adults are associated with a faster decline in lung function, the question arises whether physical inactivity and obesity are independent risk factors for the induction and clinical expression of asthma and COPD (Figure 2). Adult asthma and COPD demonstrate a higher prevalence of physical inactivity, obesity, and low-grade systemic inflammation; however, the exact interaction of these factors has not been studied and is unclear. Interventions that improve physical inactivity and reduce obesity may unravel a possible causal relationship between physical inactivity- and/or obesity-induced systemic inflammation and subsequent decline in lung function. Importantly, such studies should use performance-based instruments to assess physical inactivity.


Figure 2
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  		Figure 2. Simplified hypothetical scheme of the complex relationship between physical (in)activity, obesity, and systemic inflammation, and its consequences for obstructive airway disease. The low-grade systemic inflammation may constitute an important link between well-known risk factors for obstructive lung diseases and their comorbidity. The solid arrows indicate positive effects, whereas the dashed arrows indicate negative effects. BHR = bronchial hyperresponsiveness.

 
FOOTNOTES

Conflict of Interest Statement: N.H.T.t.H. does not have a financial relationship with a commercial entity that has an interest in the subject of this manuscript.

(Received in original form July 22, 2009; accepted in final form October 1, 2009)

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