Neuromechanical control of upper airway patency during sleep
Department of Medicine, Division of Pulmonary and Critical Care Medicine, Johns Hopkins University, Baltimore, Maryland Submitted 6 March 2006 ; accepted in final form 26 September 2006 Obstructive sleep apnea is caused by pharyngeal occlusion due to alterations in upper airway mechanical properties...
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creator | Patil, Susheel P Schneider, Hartmut Marx, Jason J Gladmon, Elizabeth Schwartz, Alan R Smith, Philip L |
description | Department of Medicine, Division of Pulmonary and Critical Care Medicine, Johns Hopkins University, Baltimore, Maryland
Submitted 6 March 2006
; accepted in final form 26 September 2006
Obstructive sleep apnea is caused by pharyngeal occlusion due to alterations in upper airway mechanical properties and/or disturbances in neuromuscular control. The objective of the study was to determine the relative contribution of mechanical loads and dynamic neuromuscular responses to pharyngeal collapse during sleep. Sixteen obstructive sleep apnea patients and sixteen normal subjects were matched on age, sex, and body mass index. Pharyngeal collapsibility, defined by the critical pressure, was measured during sleep. The critical pressure was partitioned between its passive mechanical properties (passive critical pressure) and active dynamic responses to upper airway obstruction (active critical pressure). Compared with normal subjects, sleep apnea patients demonstrated elevated mechanical loads as demonstrated by higher passive critical pressures [0.05 (SD 2.4) vs. 4.5 cmH 2 O (SD 3.0), P = 0.0003]. Dynamic responses were depressed in sleep apnea patients, as suggested by failure to lower their active critical pressures [1.6 (SD 3.5) vs. 11.1 cmH 2 O (SD 5.3), P < 0.0001] in response to upper airway obstruction. Moreover, elevated mechanical loads placed some normal individuals at risk for sleep apnea. In this subset, dynamic responses to upper airway obstruction compensated for mechanical loads and maintained airway patency by lowering the active critical pressure. The present study suggests that increased mechanical loads and blunted neuromuscular responses are both required for the development of obstructive sleep apnea.
obstructive sleep apnea; critical pressure; mechanical properties; neuromuscular control
Address for reprint requests and other correspondence: S. P. Patil, Johns Hopkins Sleep Disorders Center, Asthma and Allergy Bldg., 5501 Hopkins Bayview Circle, Rm. 4B30A, Baltimore, MD 21224 (e-mail: spatil{at}jhmi.edu ) |
doi_str_mv | 10.1152/japplphysiol.00282.2006 |
format | Article |
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Submitted 6 March 2006
; accepted in final form 26 September 2006
Obstructive sleep apnea is caused by pharyngeal occlusion due to alterations in upper airway mechanical properties and/or disturbances in neuromuscular control. The objective of the study was to determine the relative contribution of mechanical loads and dynamic neuromuscular responses to pharyngeal collapse during sleep. Sixteen obstructive sleep apnea patients and sixteen normal subjects were matched on age, sex, and body mass index. Pharyngeal collapsibility, defined by the critical pressure, was measured during sleep. The critical pressure was partitioned between its passive mechanical properties (passive critical pressure) and active dynamic responses to upper airway obstruction (active critical pressure). Compared with normal subjects, sleep apnea patients demonstrated elevated mechanical loads as demonstrated by higher passive critical pressures [0.05 (SD 2.4) vs. 4.5 cmH 2 O (SD 3.0), P = 0.0003]. Dynamic responses were depressed in sleep apnea patients, as suggested by failure to lower their active critical pressures [1.6 (SD 3.5) vs. 11.1 cmH 2 O (SD 5.3), P < 0.0001] in response to upper airway obstruction. Moreover, elevated mechanical loads placed some normal individuals at risk for sleep apnea. In this subset, dynamic responses to upper airway obstruction compensated for mechanical loads and maintained airway patency by lowering the active critical pressure. The present study suggests that increased mechanical loads and blunted neuromuscular responses are both required for the development of obstructive sleep apnea.
obstructive sleep apnea; critical pressure; mechanical properties; neuromuscular control
Address for reprint requests and other correspondence: S. P. Patil, Johns Hopkins Sleep Disorders Center, Asthma and Allergy Bldg., 5501 Hopkins Bayview Circle, Rm. 4B30A, Baltimore, MD 21224 (e-mail: spatil{at}jhmi.edu )</description><identifier>ISSN: 8750-7587</identifier><identifier>EISSN: 1522-1601</identifier><identifier>DOI: 10.1152/japplphysiol.00282.2006</identifier><identifier>PMID: 17008440</identifier><identifier>CODEN: JAPHEV</identifier><language>eng</language><publisher>Bethesda, MD: Am Physiological Soc</publisher><subject>Adult ; Biological and medical sciences ; Biomechanical Phenomena ; Case-Control Studies ; Continuous Positive Airway Pressure ; Electromyography ; Female ; Fundamental and applied biological sciences. Psychology ; Humans ; Male ; Middle Aged ; Neurology ; Neuromuscular Junction - physiology ; Neurons ; Neurotransmitters ; Pharynx - physiopathology ; Polysomnography ; Respiratory Mechanics - physiology ; Respiratory Muscles - innervation ; Respiratory Muscles - physiopathology ; Respiratory System - innervation ; Respiratory System - physiopathology ; Risk Factors ; Sleep - physiology ; Sleep Apnea, Obstructive - etiology ; Sleep Apnea, Obstructive - physiopathology ; Sleep disorders</subject><ispartof>Journal of applied physiology (1985), 2007-02, Vol.102 (2), p.547-556</ispartof><rights>2007 INIST-CNRS</rights><rights>Copyright American Physiological Society Feb 2007</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c592t-53c9287a23fd7c0aa9f3c7788e1086acfafe46dd8d07dab7bd7fe942731d0ae13</citedby><cites>FETCH-LOGICAL-c592t-53c9287a23fd7c0aa9f3c7788e1086acfafe46dd8d07dab7bd7fe942731d0ae13</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,3026,27901,27902</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=18534226$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/17008440$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Patil, Susheel P</creatorcontrib><creatorcontrib>Schneider, Hartmut</creatorcontrib><creatorcontrib>Marx, Jason J</creatorcontrib><creatorcontrib>Gladmon, Elizabeth</creatorcontrib><creatorcontrib>Schwartz, Alan R</creatorcontrib><creatorcontrib>Smith, Philip L</creatorcontrib><title>Neuromechanical control of upper airway patency during sleep</title><title>Journal of applied physiology (1985)</title><addtitle>J Appl Physiol (1985)</addtitle><description>Department of Medicine, Division of Pulmonary and Critical Care Medicine, Johns Hopkins University, Baltimore, Maryland
Submitted 6 March 2006
; accepted in final form 26 September 2006
Obstructive sleep apnea is caused by pharyngeal occlusion due to alterations in upper airway mechanical properties and/or disturbances in neuromuscular control. The objective of the study was to determine the relative contribution of mechanical loads and dynamic neuromuscular responses to pharyngeal collapse during sleep. Sixteen obstructive sleep apnea patients and sixteen normal subjects were matched on age, sex, and body mass index. Pharyngeal collapsibility, defined by the critical pressure, was measured during sleep. The critical pressure was partitioned between its passive mechanical properties (passive critical pressure) and active dynamic responses to upper airway obstruction (active critical pressure). Compared with normal subjects, sleep apnea patients demonstrated elevated mechanical loads as demonstrated by higher passive critical pressures [0.05 (SD 2.4) vs. 4.5 cmH 2 O (SD 3.0), P = 0.0003]. Dynamic responses were depressed in sleep apnea patients, as suggested by failure to lower their active critical pressures [1.6 (SD 3.5) vs. 11.1 cmH 2 O (SD 5.3), P < 0.0001] in response to upper airway obstruction. Moreover, elevated mechanical loads placed some normal individuals at risk for sleep apnea. In this subset, dynamic responses to upper airway obstruction compensated for mechanical loads and maintained airway patency by lowering the active critical pressure. The present study suggests that increased mechanical loads and blunted neuromuscular responses are both required for the development of obstructive sleep apnea.
obstructive sleep apnea; critical pressure; mechanical properties; neuromuscular control
Address for reprint requests and other correspondence: S. P. Patil, Johns Hopkins Sleep Disorders Center, Asthma and Allergy Bldg., 5501 Hopkins Bayview Circle, Rm. 4B30A, Baltimore, MD 21224 (e-mail: spatil{at}jhmi.edu )</description><subject>Adult</subject><subject>Biological and medical sciences</subject><subject>Biomechanical Phenomena</subject><subject>Case-Control Studies</subject><subject>Continuous Positive Airway Pressure</subject><subject>Electromyography</subject><subject>Female</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Humans</subject><subject>Male</subject><subject>Middle Aged</subject><subject>Neurology</subject><subject>Neuromuscular Junction - physiology</subject><subject>Neurons</subject><subject>Neurotransmitters</subject><subject>Pharynx - physiopathology</subject><subject>Polysomnography</subject><subject>Respiratory Mechanics - physiology</subject><subject>Respiratory Muscles - innervation</subject><subject>Respiratory Muscles - physiopathology</subject><subject>Respiratory System - innervation</subject><subject>Respiratory System - physiopathology</subject><subject>Risk Factors</subject><subject>Sleep - physiology</subject><subject>Sleep Apnea, Obstructive - etiology</subject><subject>Sleep Apnea, Obstructive - physiopathology</subject><subject>Sleep disorders</subject><issn>8750-7587</issn><issn>1522-1601</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2007</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkV-L1DAUxYMo7rj6FbQIii8db9K0ScEXWVwVFn1Zn0Mmf2YyZJqYtKz99qZOcUUQ85KH_M45N_cg9ALDFuOWvD3KGH08zNkFvwUgnGwJQPcAbcorqXEH-CHacNZCzVrOLtCTnI8AmNIWP0YXmAFwSmGD3n0xUwonow5ycEr6SoVhTMFXwVZTjCZV0qU7OVdRjmZQc6Wn5IZ9lb0x8Sl6ZKXP5tl6X6Jv1x9urz7VN18_fr56f1Ortidj3TaqJ5xJ0ljNFEjZ20YxxrnBwDuprLSGdlpzDUzLHdtpZk1PCWuwBmlwc4len31jCt8nk0dxclkZ7-VgwpRFx3vek47_F8R92_UUdwV8-Rd4DFMayicEKQcopaRA7AypFHJOxoqY3EmmWWAQSw3izxrErxrEUkNRPl_tp93J6HvduvcCvFoBmcvWbZKDcvme421DCVmM3py5g9sf7lwyYk0L-3lJL5OUSNFSVlD6b_R68v7W_BgXzW-JiNo2PwHj3LWZ</recordid><startdate>20070201</startdate><enddate>20070201</enddate><creator>Patil, Susheel P</creator><creator>Schneider, Hartmut</creator><creator>Marx, Jason J</creator><creator>Gladmon, Elizabeth</creator><creator>Schwartz, Alan R</creator><creator>Smith, Philip L</creator><general>Am Physiological Soc</general><general>American Physiological Society</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QP</scope><scope>7QR</scope><scope>7TK</scope><scope>7TS</scope><scope>7U7</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>P64</scope><scope>7X8</scope></search><sort><creationdate>20070201</creationdate><title>Neuromechanical control of upper airway patency during sleep</title><author>Patil, Susheel P ; Schneider, Hartmut ; Marx, Jason J ; Gladmon, Elizabeth ; Schwartz, Alan R ; Smith, Philip L</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c592t-53c9287a23fd7c0aa9f3c7788e1086acfafe46dd8d07dab7bd7fe942731d0ae13</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2007</creationdate><topic>Adult</topic><topic>Biological and medical sciences</topic><topic>Biomechanical Phenomena</topic><topic>Case-Control Studies</topic><topic>Continuous Positive Airway Pressure</topic><topic>Electromyography</topic><topic>Female</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Humans</topic><topic>Male</topic><topic>Middle Aged</topic><topic>Neurology</topic><topic>Neuromuscular Junction - physiology</topic><topic>Neurons</topic><topic>Neurotransmitters</topic><topic>Pharynx - physiopathology</topic><topic>Polysomnography</topic><topic>Respiratory Mechanics - physiology</topic><topic>Respiratory Muscles - innervation</topic><topic>Respiratory Muscles - physiopathology</topic><topic>Respiratory System - innervation</topic><topic>Respiratory System - physiopathology</topic><topic>Risk Factors</topic><topic>Sleep - physiology</topic><topic>Sleep Apnea, Obstructive - etiology</topic><topic>Sleep Apnea, Obstructive - physiopathology</topic><topic>Sleep disorders</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Patil, Susheel P</creatorcontrib><creatorcontrib>Schneider, Hartmut</creatorcontrib><creatorcontrib>Marx, Jason J</creatorcontrib><creatorcontrib>Gladmon, Elizabeth</creatorcontrib><creatorcontrib>Schwartz, Alan R</creatorcontrib><creatorcontrib>Smith, Philip L</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Physical Education Index</collection><collection>Toxicology Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of applied physiology (1985)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Patil, Susheel P</au><au>Schneider, Hartmut</au><au>Marx, Jason J</au><au>Gladmon, Elizabeth</au><au>Schwartz, Alan R</au><au>Smith, Philip L</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Neuromechanical control of upper airway patency during sleep</atitle><jtitle>Journal of applied physiology (1985)</jtitle><addtitle>J Appl Physiol (1985)</addtitle><date>2007-02-01</date><risdate>2007</risdate><volume>102</volume><issue>2</issue><spage>547</spage><epage>556</epage><pages>547-556</pages><issn>8750-7587</issn><eissn>1522-1601</eissn><coden>JAPHEV</coden><abstract>Department of Medicine, Division of Pulmonary and Critical Care Medicine, Johns Hopkins University, Baltimore, Maryland
Submitted 6 March 2006
; accepted in final form 26 September 2006
Obstructive sleep apnea is caused by pharyngeal occlusion due to alterations in upper airway mechanical properties and/or disturbances in neuromuscular control. The objective of the study was to determine the relative contribution of mechanical loads and dynamic neuromuscular responses to pharyngeal collapse during sleep. Sixteen obstructive sleep apnea patients and sixteen normal subjects were matched on age, sex, and body mass index. Pharyngeal collapsibility, defined by the critical pressure, was measured during sleep. The critical pressure was partitioned between its passive mechanical properties (passive critical pressure) and active dynamic responses to upper airway obstruction (active critical pressure). Compared with normal subjects, sleep apnea patients demonstrated elevated mechanical loads as demonstrated by higher passive critical pressures [0.05 (SD 2.4) vs. 4.5 cmH 2 O (SD 3.0), P = 0.0003]. Dynamic responses were depressed in sleep apnea patients, as suggested by failure to lower their active critical pressures [1.6 (SD 3.5) vs. 11.1 cmH 2 O (SD 5.3), P < 0.0001] in response to upper airway obstruction. Moreover, elevated mechanical loads placed some normal individuals at risk for sleep apnea. In this subset, dynamic responses to upper airway obstruction compensated for mechanical loads and maintained airway patency by lowering the active critical pressure. The present study suggests that increased mechanical loads and blunted neuromuscular responses are both required for the development of obstructive sleep apnea.
obstructive sleep apnea; critical pressure; mechanical properties; neuromuscular control
Address for reprint requests and other correspondence: S. P. Patil, Johns Hopkins Sleep Disorders Center, Asthma and Allergy Bldg., 5501 Hopkins Bayview Circle, Rm. 4B30A, Baltimore, MD 21224 (e-mail: spatil{at}jhmi.edu )</abstract><cop>Bethesda, MD</cop><pub>Am Physiological Soc</pub><pmid>17008440</pmid><doi>10.1152/japplphysiol.00282.2006</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record> |
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source | MEDLINE; American Physiological Society; EZB-FREE-00999 freely available EZB journals; Alma/SFX Local Collection |
subjects | Adult Biological and medical sciences Biomechanical Phenomena Case-Control Studies Continuous Positive Airway Pressure Electromyography Female Fundamental and applied biological sciences. Psychology Humans Male Middle Aged Neurology Neuromuscular Junction - physiology Neurons Neurotransmitters Pharynx - physiopathology Polysomnography Respiratory Mechanics - physiology Respiratory Muscles - innervation Respiratory Muscles - physiopathology Respiratory System - innervation Respiratory System - physiopathology Risk Factors Sleep - physiology Sleep Apnea, Obstructive - etiology Sleep Apnea, Obstructive - physiopathology Sleep disorders |
title | Neuromechanical control of upper airway patency during sleep |
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