Obesity produces
decreased tidal volume and functional residual capacity,
both of which reduce the tidal stretch of smooth muscle thus,
the ability to respond to natural stress such as exercise is hampered
by small tidal volumes [45]. Also, Obesity increased
gastro-esophageal reflux due to accompanied esophageal
sphincter relaxation, resulting in esophageal acid reflux passing
into the trachea and airways. The direct contact of gastric acid
with the airways causes bronchoconstriction owing to the
resulting micro-aspiration or to the vagal reflex [46]. Leptin
plasma levels have been positively correlated with body fat,
stimulating the release of tumor necrosis factor (TNF-a) by
adipocytes and act on the sympathetic nervous system which
is crucial in controlling airway tone and diameter; important
factors in asthma [47]. TNF-a is elevated in asthma and is
related to the production of T helper-2 cytokines as IL-4
[48]. There are common genes, playing a role in both asthma
and obesity as chromosomes 5q, 6, 11q13, and 12q [45].
Adipose tissue contains the enzyme aromatase, which is
responsible for converting androgens into estrogens causing
airway hyper-reactivity and greater severity of irreversible airflow
obstruction [49].