title: Ventilatory responses to hypercapnia during wakefulness and sleep in obese adolescents with and without obstructive sleep apnea syndrome.
abstract: OBJECTIVE
  Abnormal ventilatory drive may contribute to the pathophysiology of the childhood obstructive sleep apnea syndrome (OSAS). Concomitant with the obesity epidemic, more adolescents are developing OSAS. However, few studies have specifically evaluated the obese adolescent group. The authors hypothesized that obese adolescents with OSAS would have a blunted hypercapnic ventilatory response (HCVR) while awake and blunted ventilatory responses to carbon dioxide (CO(2)) during sleep compared with obese and lean adolescents without OSAS.
  
  
  METHODS
  CVR was measured during wakefulness. During nonrapid eye movement (NREM) and rapid eye movement (REM) sleep, respiratory parameters and genioglossal electromyogram were measured during CO(2) administration in comparison with room air in obese adolescents with OSAS, obese control study participants, and lean control study participants.
  
  
  METHODS
  Sleep laboratory.
  
  
  METHODS
  Twenty-eight obese patients with OSAS, 21 obese control study participants, and 37 lean control study participants.
  
  
  RESULTS
  The obese OSAS and obese control groups had a higher HCVR compared with the lean control group during wakefulness. During both sleep states, all 3 groups had a response to CO(2); however, the obese OSAS group had lower percentage changes in minute ventilation, inspiratory flow, inspiratory time, and tidal volume compared with the 2 control groups. There were no significance differences in genioglossal activity between groups.
  
  
  CONCLUSIONS
  HCVR during wakefulness is increased in obese adolescents. Obese adolescents with OSAS have blunted ventilatory responses to CO(2) during sleep and do not have a compensatory prolongation of inspiratory time, despite having normal CO(2) responsivity during wakefulness. Central drive may play a greater role than upper airway neuromotor tone in adapting to hypercapnia.
authors.affiliation: Division of Respiratory Diseases, First Hospital of Jilin University, Changchun, Jilin, China.
authors.forename: Haibo
authors.initials: H
authors.lastname: Yuan
authors.forename: Swaroop J
authors.initials: SJ
authors.lastname: Pinto
authors.forename: Jingtao
authors.initials: J
authors.lastname: Huang
authors.forename: Joseph M
authors.initials: JM
authors.lastname: McDonough
authors.forename: Michelle B
authors.initials: MB
authors.lastname: Ward
authors.forename: Yin N
authors.initials: YN
authors.lastname: Lee
authors.forename: Ruth M
authors.initials: RM
authors.lastname: Bradford
authors.forename: Paul R
authors.initials: PR
authors.lastname: Gallagher
authors.forename: Justine
authors.initials: J
authors.lastname: Shults
authors.forename: Sophia
authors.initials: S
authors.lastname: Konstantinopoulou
authors.forename: John M
authors.initials: JM
authors.lastname: Samuel
authors.forename: Eliot S
authors.initials: ES
authors.lastname: Katz
authors.forename: Shucheng
authors.initials: S
authors.lastname: Hua
authors.forename: Ignacio E
authors.initials: IE
authors.lastname: Tapia
authors.forename: Carole L
authors.initials: CL
authors.lastname: Marcus
mesh_terms: D000293:Adolescent; D000704:Analysis of Variance; D002245:Carbon Dioxide / Q000008:administration & dosage / Q000378:metabolism; D002648:Child; D005260:Female; D006801:Humans; D006935:Hypercapnia / Q000209:etiology* / Q000378:metabolism / Q000503:physiopathology*; D008297:Male; D008991:Monitoring, Physiologic / Q000379:methods; D009765:Obesity / Q000150:complications* / Q000378:metabolism / Q000503:physiopathology; D017286:Polysomnography / Q000379:methods; D012129:Respiratory Function Tests; D012890:Sleep; D020181:Sleep Apnea, Obstructive / Q000150:complications* / Q000378:metabolism / Q000503:physiopathology*; D012895:Sleep, REM; D014851:Wakefulness
chemical_list: D002245:Carbon Dioxide