flow limitation (1). Obesity does effect respiratory function and a factor take in account is the distribution of the excess adipose tissue in the thorax region (1). Another factor to appreciate is the anatomical postion in which the patient is in. For instance, gas exchange is compromised in severely bese patients in the supine posture(1). Since COPD patients have a lack of exercise as compared to healthy individuals they have an increased chance of developing obesity. Due to constant doses of glucocorticosteroids, COPD patients are at a greater risk for obesity because of its stimulatory effect on intake (1).
Obese patients are already known to have restrictive deficits and with the combination COPD these patients have even worsening symptoms.
Patients with COPD have problems with ventillatory mechanics and obesity would amplify these issues (1). Obese patients with COPD would therefore have higher ventillatory requirements as opposed to a person of normal weight, due to an “increase in chemostimulation that arises from the combination of increased metabolic loading, high fixed physiological dead space and possibly earlier earlier metabolic acidosis due to impairement of oxygen uptake from deconditiong or cardiac dysfunction” (1). Patients with central obesity have an increase in expiratory flow rates due to an increase in recoil to the lung and chest wall as compared with COPD non obese patients. Besides the limitations in ventilation, any alterations in the composition of the body is associated with exercise intolerance in COPD patients. Reduced exercise capacity and muscle weakness are due to loss of FFM, these issues are common in people with COPD. Patients with a combination of early stage COPD, reduction in lean to fat mass ratio, and obesity were seen to have a 6 minute walk test with functional limitation. This limitation and negative impact was due to the accretion of fat mass and not so much the decrease in lean mass
(1).
Patients with COPD not only have pulmonary inflammation but also a level of systemic inflammation. COPD patients with a detrimental health related quality of life and a decreased capacity to exercise had the presence of systemic inflammation. In the circulation of these patients were increased amounts proinfllmatory cells in plasma contains, such as C- Reactive protein (CRP), leuckocytes, TNF alpha, and interleukins- 6,8,10,18 when compared to healthy individuals. COPD Patients with depleted FFMhad increased level of TNFalpha and IL6 as compared with patients with preserved FFM. In muscle wasting related to COPD there is a role of systemic inflammation. Adipose tissue also plays a role in systemic inflammation, it has systemic metabolic effects and proinflmmatory mediators. It can be hypothesized that patients with COPD and obesity or high amount of adipose tissue produces inflammation. Patients with COPD tend to have a loss of skeletal muscle mass, which is associated with systemic inflammation. This may lead to loss of FFM and intensify the changes in composition towards the preservation of fat and depletion of FFM (1).