Effect of gender on the development of hypocapnic apnea/hypopnea during NREM sleep.
ABSTRACT We hypothesized that a decreased susceptibility to the development of hypocapnic central apnea during non-rapid eye movement (NREM) sleep in women compared with men could be an explanation for the gender difference in the sleep apnea/hypopnea syndrome. We studied eight men (age 25-35 yr) and eight women in the midluteal phase of the menstrual cycle (age 21-43 yr); we repeated studies in six women during the midfollicular phase. Hypocapnia was induced via nasal mechanical ventilation for 3 min, with respiratory frequency matched to eupneic frequency. Tidal volume (VT) was increased between 110 and 200% of eupneic control. Cessation of mechanical ventilation resulted in hypocapnic central apnea or hypopnea, depending on the magnitude of hypocapnia. Nadir minute ventilation in the recovery period was plotted against the change in end-tidal PCO(2) (PET(CO(2))) per trial; minute ventilation was given a value of 0 during central apnea. The apneic threshold was defined as the x-intercept of the linear regression line. In women, induction of a central apnea required an increase in VT to 155 +/- 29% (mean +/- SD) and a reduction of PET(CO(2)) by -4.72 +/- 0.57 Torr. In men, induction of a central apnea required an increase in VT to 142 +/- 13% and a reduction of PET(CO(2)) by -3.54 +/- 0.31 Torr (P = 0.002). There was no difference in the apneic threshold between the follicular and the luteal phase in women. Premenopausal women are less susceptible to hypocapnic disfacilitation during NREM sleep than men. This effect was not explained by progesterone. Preservation of ventilatory motor output during hypocapnia may explain the gender difference in sleep apnea.
SourceAvailable from: Rita A Perri[Show abstract] [Hide abstract]
ABSTRACT: Obstructive sleep apnea (OSA) is more common in men than women. Body size is greater in males (sexual dimorphism), but large body habitus is associated with OSA for both genders. We speculated that male–female phenotypical convergence (reduced sexual dimorphism via identical phenotype acquisition) occurs with OSA and tested hypotheses: (1) phenotypical features pathogenic for OSA differ between OSA and healthy subjects irrespective of gender; and (2) such characteristics exhibit phenotypical convergence. Utilizing an existing database, we calculated male–female (group average) ratios for eight anthropometric and 33 surface cephalometric variables from 104 Caucasian OSA patients [72 males; apnea–hypopnea index (events h−1): males: 42.3 ± 24.7 versus females: 42.6 ± 26.1 (P > 0.9)] and 85 Caucasian, healthy, non-OSA, community volunteers (36 males). Log-transformed data were analysed using a general linear model with post-hoc unpaired t-tests and significance at P < 0.0012 (Bonferroni multiple-comparison correction). OSA patients were older (56.9 ± 14.4 versus 38.0 ± 13.8 years), but there were no within-group gender-based age differences. All anthropometric variables (except height), plus cranial base width, mandibular breadth and retromandibular width diagonal were larger in gender-matched OSA versus healthy comparisons; thus satisfying hypothesis (1). Male–female ratios were mostly >1.0 across groups, but with no significant group × gender interactions no variable satisfied hypothesis (2). Thus, in this exploratory study, OSA patients had gender-common phenotypical differences to healthy subjects, but sexual dimorphism was preserved. Lack of complete phenotypical convergence may indicate gender-based critical phenotype-level attainment for OSA and/or gender-based OSA prevalence arises from factors other than those in this study.Journal of Sleep Research 08/2014; 24(1). DOI:10.1111/jsr.12205 · 2.95 Impact Factor
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ABSTRACT: Spinal cord injury (SCI) is associated with 2-5 times greater prevalence of sleep disordered breathing (SDB) than the general population. The contribution of SCI on sleep and breathing at different levels of injury using two scoring methods has not been assessed. The objectives of this study were to characterize the sleep disturbances in the SCI population and the associated physiological abnormalities using quantitative polysomnography and to determine the contribution of SCI level on the SDB mechanism. We studied 26 consecutive patients with SCI (8 females; age 42.5 ± 15.5 years; BMI 25.9 ± 4.9 kg/m(2); 15 cervical and 11 thoracic levels) by spirometry, a battery of questionnaires and by attended polysomnography with flow and pharyngeal pressure measurements. Inclusion criteria for SCI: chronic SCI (> 6 months post injury), level T6 and above and not on mechanical ventilation. Ventilation, end-tidal CO2 (PETCO2), variability in minute ventilation (VI-CV) and upper airway resistance (RUA) were monitored during wakefulness and NREM sleep in all subjects. Each subject completed brief history and exam, Epworth Sleepiness Scale (ESS), Pittsburgh Sleep Quality Index (PSQI), Berlin questionnaire (BQ) and fatigue severity scale (FSS). Sleep studies were scored twice, first using standard 2007 American Academy of Sleep Medicine (AASM) criteria and second using new 2012 recommended AASM criteria. Mean PSQI was increased to 10.3 ± 3.7 in SCI patients and 92% had poor sleep quality. Mean ESS was increased 10.4 ± 4.4 in SCI patients and excessive daytime sleepiness (ESS ≥ 10) was present in 59% of the patients. Daytime fatigue (FSS > 20) was reported in 96% of SCI, while only 46% had high-risk score of SDB on BQ. Forced vital capacity (FVC) in SCI was reduced to 70.5% predicted in supine compared to 78.5% predicted in upright positions (p < 0.05). Likewise forced expiratory volume in first second (FEV1) was 64.9% predicted in supine compared to 74.7% predicted in upright positions (p < 0.05). Mean AHI in SCI patients was 29.3 ± 25.0 vs. 20.0 ± 22.8 events/h using the new and conventional AASM scoring criteria, respectively (p < 0.001). SCI patients had SDB (AHI > 5 events/h) in 77% of the cases using the new AASM scoring criteria compared to 65% using standard conventional criteria (p < 0.05). In cervical SCI, VI decreased from 7.2 ± 1.6 to 5.5 ± 1.3 L/min, whereas PETCO2 and VI-CV, increased during sleep compared to thoracic SCI. The majority of SCI survivors have symptomatic SDB and poor sleep that may be missed if not carefully assessed. Decreased VI and increased PETCO2 during sleep in patients with cervical SCI relative to thoracic SCI suggests that sleep related hypoventilation may contribute to the pathogenesis SDB in patients with chronic cervical SCI. Sankari A; Bascom A; Oomman S; Badr MS. Sleep disordered breathing in chronic spinal cord injury. J Clin Sleep Med 2014;10(1):65-72.Journal of clinical sleep medicine: JCSM: official publication of the American Academy of Sleep Medicine 01/2014; 10(1):65-72. DOI:10.5664/jcsm.3362 · 2.83 Impact Factor
Chapter: OSA in Women and pregnancyObstructive Sleep Apnoea, Edited by Ferrán Barbé and Jean Louis Pepin, 03/2015: chapter European Respiratory Monograph: pages 66-89; European Respirtaory Society., ISBN: 978-1-84984-059-0