Moreover, for a given FEV1, IC is higher
in obese subjects [29]. These changes seem beneficial to
COPD subjects, counteracting some of the deleterious effects
of the disease. However, oxygen consumption is higher for a
given workload for obese subjects, leading to higher ventilatory
demand. This increased ventilatory requirement further
stresses the respiratory system whose capacity is already
reduced by the presence of airflow limitation [30]. Adipose tissue
is the main lipid storage depot in the body and is of crucial
importance in buffering the daily influx of dietary fat entering
the circulation. One characteristic of adipose tissue in obesity
is the enlargement of adipocytes which may represent impaired
adipocyte differentiation. The hypertrophic adipocytes of
obese subjects are overloaded with stored triacylglycerol and
it is likely that the buffering capacity for further lipid storage
in these adipocytes is decreased, especially in the postprandial
state. Non-adipose tissues are therefore exposed to an excessive
influx of lipids which could lead to ectopic fat deposition
[31].