TY - JOUR
T1 - Correlation between genioglossal and diaphragmatic responses to hypercapnia during sleep
AU - Parisi, R. A.
AU - Neubauer, J. A.
AU - Frank, M. M.
AU - Edelman, N. H.
AU - Santiago, T. V.
PY - 1987
Y1 - 1987
N2 - Oropharyngeal patency during sleep is dependent on the dilating force of the genioglossus, the main tongue protrusor muscle. We measured the ventilatory (V̇I), diaphragmatic (EMGdi), and genioglossal (EMGgg) electromyographic responses to CO2 in awake and sleeping goats; ΔV̇I/ΔPET(CO2) decreased from awake (0.85 ± 0.087 L/min/mm Hg) to NREM sleep (0.69 ± 0.069) to REM sleep (0.57 ± 0.078, p < 0.005 versus awake). There were minimal decreases in ΔEMGdi/ΔPET(CO2) and EMGdi at a PET(CO2) of 55 mm Hg from awake to NREM, but significant decrease in EMGdi at a PET(CO2) of 55 mm Hg during REM sleep (p < 0.025 versus NREM). Inspiratory EMGgg was only present above a PCO2 threshold, which was similar for each state (49.3 ± 2.3 mm Hg PET(CO2) awake, 48.8 ± 2.4 during NREM, 49.5 ± 2.5 during REM), and ΔEMGgg/ΔPET(CO2) tended to be less during both sleep states compared with that while awake (p = 0.10). At any PCO2, inspiratory EMGgg was markedly inhibited during REM sleep when rapid eye movements were present (phasic REM). We conclude that there is disproportionate inhibition of the genioglossus relative to the diaphragm at low CO2 tensions and at any PCO2 during phasic REM sleep. This imbalance may predispose the upper airway to inspiratory occlusion during sleep.
AB - Oropharyngeal patency during sleep is dependent on the dilating force of the genioglossus, the main tongue protrusor muscle. We measured the ventilatory (V̇I), diaphragmatic (EMGdi), and genioglossal (EMGgg) electromyographic responses to CO2 in awake and sleeping goats; ΔV̇I/ΔPET(CO2) decreased from awake (0.85 ± 0.087 L/min/mm Hg) to NREM sleep (0.69 ± 0.069) to REM sleep (0.57 ± 0.078, p < 0.005 versus awake). There were minimal decreases in ΔEMGdi/ΔPET(CO2) and EMGdi at a PET(CO2) of 55 mm Hg from awake to NREM, but significant decrease in EMGdi at a PET(CO2) of 55 mm Hg during REM sleep (p < 0.025 versus NREM). Inspiratory EMGgg was only present above a PCO2 threshold, which was similar for each state (49.3 ± 2.3 mm Hg PET(CO2) awake, 48.8 ± 2.4 during NREM, 49.5 ± 2.5 during REM), and ΔEMGgg/ΔPET(CO2) tended to be less during both sleep states compared with that while awake (p = 0.10). At any PCO2, inspiratory EMGgg was markedly inhibited during REM sleep when rapid eye movements were present (phasic REM). We conclude that there is disproportionate inhibition of the genioglossus relative to the diaphragm at low CO2 tensions and at any PCO2 during phasic REM sleep. This imbalance may predispose the upper airway to inspiratory occlusion during sleep.
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M3 - Article
C2 - 3813200
AN - SCOPUS:0023147635
SN - 0003-0805
VL - 135
SP - 378
EP - 382
JO - American Review of Respiratory Disease
JF - American Review of Respiratory Disease
IS - 2
ER -