Obesity and upper airway control during sleep

Abstract

Mechanisms linking obesity with upper airway dysfunction in obstructive sleep apnea are reviewed. Obstructive sleep apnea is due to alterations in upper airway anatomy and neuromuscular control. Upper airway structural alterations in obesity are related to adipose deposition around the pharynx, which can increase its collapsibility or critical pressure (P(crit)). In addition, obesity and, particularly, central adiposity lead to reductions in resting lung volume, resulting in loss of caudal traction on upper airway structures and parallel increases in pharyngeal collapsibility. Metabolic and humoral factors that promote central adiposity may contribute to these alterations in upper airway mechanical function and increase sleep apnea susceptibility. In contrast, neural responses to upper airway obstruction can mitigate these mechanical loads and restore pharyngeal patency during sleep. Current evidence suggests that these responses can improve with weight loss. Improvements in these neural responses with weight loss may be related to a decline in systemic and local pharyngeal concentrations of specific inflammatory mediators with somnogenic effects.

Figures

Fig. 1.

Scheme relating obesity, body fat distribution, upper airway collapsibility [critical pressure (Pcrit)], and sleep apnea pathogenesis. Mechanical loads and neuromuscular responses sum (∑) to increase (+) and decrease (−) Pcrit, respectively. Mechanical and humoral effects of regional adipose depots can modulate these components, which can mediate differences in sleep apnea susceptibility between men and women.