期刊
JOURNAL OF APPLIED PHYSIOLOGY
卷 108, 期 2, 页码 430-435出版社
AMER PHYSIOLOGICAL SOC
DOI: 10.1152/japplphysiol.00919.2009
关键词
obstructive sleep apnea; upper airway obstruction; neuromuscular control; pharyngeal neuromechanical function
资金
- National Center for Research Resources (NCRR) [UL1-RR-025005]
- National Heart, Lung, and Blood Institute [HL-50381, HL-37379, HL-077137, HL-072126]
- National Institutes of Health Roadmap for Medical Research.
Schwartz AR, Patil SP, Squier S, Schneider H, Kirkness JP, Smith PL. Obesity and upper airway control during sleep. J Appl Physiol 108: 430-435, 2010. First published October 29, 2009; doi:10.1152/japplphysiol.00919.2009.-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
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