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tivity of the laryngeal abductor muscle, the posterior cricoarytenoid, was recorded and compared to the activity of the diaphragm. Electrical stimulation of the reticular activating system caused an increase in the duration of abductor activity, an increase in the discharge frequency of abductor motor units, and a recruitment of larger abductor motor units. These effects were observed at stimulation intensities below those necessary to obtain changes in the intensity of diaphragmatic activity. It was the differential sensitivity of the upper-airway muscles and of the diaphragm that seemed significant for understanding obstructive sleep apnea. It implied that the muscles of the upper airway would be affected more than the diaphragm by the loss of wakefulness and that this could lead to occlusive collapse during sleep. Subsequent studies indicated that the neural systems driving upper-airway motoneurons are more sensitive than those of phrenic motoneurons to the depressive effects of ethanol, diazepam, pentobarbital, halothane, hypocapnia, and chemical and thermal depression of the ventral medullary surface. 3-8 Similarly, the systems controlling the upper-airway muscles are more sensitive than those of the diaphragm to the excitatory effects of protriptyline, strychnine, cyanide, and doxapram. 4,6 These studies led St. John 7 to test the hypothesis that reticular

Tonic Activity in the Respiratory System in Wakefulness, NREM and REM Sleep