UNLABELLED: Episodic hypoxia (EH) is followed by increased ventilatory motor output in the recovery period indicative of long-term facilitation (LTF). We hypothesized that episodic hypoxia evokes LTF of genioglossus (GG) muscle activity in humans during non-rapid eye movement sleep (NREM) sleep. We studied 12 normal non-flow limited humans during stable NREM sleep. We induced 10 brief (3 min) episodes of isocapnic hypoxia followed by 5 min of room air. Measurements were obtained during control, hypoxia, and at 5, 10, 20, 30 and 40 min of recovery, respectively, for minute ventilation (V(I)), supraglottic pressure (P(SG)), upper airway resistance (R(UA)) and phasic GG electromyogram (EMG(GG)). In addition, sham studies were conducted on room air. During hypoxia there was a significant increase in phasic EMG(GG) (202.7+/-24.1% of control, p<0.01) and in V (I) (123.0+/-3.3% of control, p<0.05); however, only phasic EMG(GG) demonstrated a significant persistent increase throughout the recovery. (198.9+/-30.9%, 203.6+/-29.9% and 205.4+/-26.4% of control, at 5, 10, and 20 min of recovery, respectively, p<0.01). In multivariate regression analysis, age and phasic EMG(GG) activity during hypoxia were significant predictors of EMG(GG) at recovery 20 min. No significant changes in any of the measured parameters were noted during sham studies. CONCLUSION: (1) EH elicits LTF of GG in normal non-flow limited humans during NREM sleep, without concomitant ventilatory or mechanical LTF. (2) GG activity during the recovery period correlates with the magnitude of GG activation during hypoxia, and inversely with age.
UNLABELLED: Episodic hypoxia (EH) is followed by increased ventilatory motor output in the recovery period indicative of long-term facilitation (LTF). We hypothesized that episodic hypoxia evokes LTF of genioglossus (GG) muscle activity in humans during non-rapid eye movement sleep (NREM) sleep. We studied 12 normal non-flow limited humans during stable NREM sleep. We induced 10 brief (3 min) episodes of isocapnic hypoxia followed by 5 min of room air. Measurements were obtained during control, hypoxia, and at 5, 10, 20, 30 and 40 min of recovery, respectively, for minute ventilation (V(I)), supraglottic pressure (P(SG)), upper airway resistance (R(UA)) and phasic GG electromyogram (EMG(GG)). In addition, sham studies were conducted on room air. During hypoxia there was a significant increase in phasic EMG(GG) (202.7+/-24.1% of control, p<0.01) and in V (I) (123.0+/-3.3% of control, p<0.05); however, only phasic EMG(GG) demonstrated a significant persistent increase throughout the recovery. (198.9+/-30.9%, 203.6+/-29.9% and 205.4+/-26.4% of control, at 5, 10, and 20 min of recovery, respectively, p<0.01). In multivariate regression analysis, age and phasic EMG(GG) activity during hypoxia were significant predictors of EMG(GG) at recovery 20 min. No significant changes in any of the measured parameters were noted during sham studies. CONCLUSION: (1) EH elicits LTF of GG in normal non-flow limited humans during NREM sleep, without concomitant ventilatory or mechanical LTF. (2) GG activity during the recovery period correlates with the magnitude of GG activation during hypoxia, and inversely with age.
Authors: Sanar S Yokhana; David G Gerst; Dorothy S Lee; M Safwan Badr; Tabarak Qureshi; Jason H Mateika Journal: J Appl Physiol (1985) Date: 2011-11-03
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Authors: Michelle McGuire; Jaime L Tartar; Ying Cao; Robert W McCarley; David P White; Robert E Strecker; Liming Ling Journal: J Physiol Date: 2008-09-11 Impact factor: 5.182