title: Long-term facilitation in obstructive sleep apnea patients during NREM sleep.
abstract: Repetitive hypoxia followed by persistently increased ventilatory motor output is referred to as long-term facilitation (LTF). LTF is activated during sleep after repetitive hypoxia in snorers. We hypothesized that LTF is activated in obstructive sleep apnea (OSA) patients. Eleven subjects with OSA (apnea/hypopnea index = 43.6 +/- 18.7/h) were included. Every subject had a baseline polysomnographic study on the appropriate continuous positive airway pressure (CPAP). CPAP was retitrated to eliminate apnea/hypopnea but to maintain inspiratory flow limitation (sham night). Each subject was studied on 2 separate nights. These two studies are separated by 1 mo of optimal nasal CPAP treatment for a minimum of 4-6 h/night. The device was capable of covert pressure monitoring. During night 1 (N1), study subjects used nasal CPAP at suboptimal pressure to have significant air flow limitation (>60% breaths) without apneas/hypopneas. After stable sleep was reached, we induced brief isocapnic hypoxia [inspired O(2) fraction (FI(O(2))) = 8%] (3 min) followed by 5 min of room air. This sequence was repeated 10 times. Measurements were obtained during control, hypoxia, and at 5, 20, and 40 min of recovery for ventilation, timing (n = 11), and supraglottic pressure (n = 6). Upper airway resistance (Rua) was calculated at peak inspiratory flow. During the recovery period, there was no change in minute ventilation (99 +/- 8% of control), despite decreased Rua to 58 +/- 24% of control (P < 0.05). There was a reduction in the ratio of inspiratory time to total time for a breath (duty cycle) (0.5 to 0.45, P < 0.05) but no effect on inspiratory time. During night 2 (N2), the protocol of N1 was repeated. N2 revealed no changes compared with N1 during the recovery period. In conclusion, 1) reduced Rua in the recovery period indicates LTF of upper airway dilators; 2) lack of hyperpnea in the recovery period suggests that thoracic pump muscles do not demonstrate LTF; 3) we speculate that LTF may temporarily stabilize respiration in OSA patients after repeated apneas/hypopneas; and 4) nasal CPAP did not alter the ability of OSA patients to elicit LTF at the thoracic pump muscle.
authors.affiliation: Medical Service, John D. Dingell Veterans Affairs Medical Center, Wayne State University School of Medicine, Detroit, MI 48201, USA. salahmd@home.com
authors.forename: S E
authors.initials: SE
authors.lastname: Aboubakr
authors.forename: A
authors.initials: A
authors.lastname: Taylor
authors.forename: R
authors.initials: R
authors.lastname: Ford
authors.forename: S
authors.initials: S
authors.lastname: Siddiqi
authors.forename: M S
authors.initials: MS
authors.lastname: Badr
mesh_terms: D000328:Adult; D000368:Aged; D000403:Airway Resistance; D005260:Female; D006801:Humans; D000860:Hypoxia / Q000503:physiopathology; D017774:Long-Term Potentiation; D008297:Male; D008875:Middle Aged; D009296:Nasal Cavity; D011175:Positive-Pressure Respiration; D012123:Pulmonary Ventilation; D012016:Reference Values; D012119:Respiration; D012891:Sleep Apnea Syndromes / Q000503:physiopathology* / Q000628:therapy; D012894:Sleep Stages / Q000502:physiology*