Alteration in upper airway dilator muscle co-activation during sleep: comparison of patients with OSA and healthy subjects.

In patients with OSA, substantial increases in genioglossus (GG) activity during hypopneas/apneas usually fail to restore normal airflow. We have previously suggested that sleep-induced alteration in tongue muscle coordination may explain this finding, as retractor muscles co-activation was reduced during sleep, as compared to wakefulness. The present study was undertaken to evaluate if these alterations in dilator muscle activation during sleep play a role in the pathogenesis of OSA, and whether co-activation of additional peri-pharyngeal muscles (non-GG muscles: styloglossus, geniohyoid, sternohyoid and sterno-cleido-mastoid) is also impaired during sleep. We compared GG and non-GG muscles EMG activity in 8 OSA patients and 12 healthy subjects during wakefulness, while breathing through inspiratory resistors, to the activity observed during sleep, towards the end of flow limitation, before arousal, at equivalent esophageal pressures. During wakefulness, resistive breathing triggered increases in both GG and non-GG muscles activity. During sleep, flow limitation was associated with increases in GG EMG that reached, on the average, more than two-fold the level observed while awake. In contrast, EMGs of the non-GG muscles, recorded simultaneously, reached on the average only about 2/3 the wakefulness level. We conclude that during sleep GG activity may increase to levels that exceed substantially those sufficient to prevent pharyngeal collapse during wakefulness, whereas other peri-pharyngeal muscles do not co-activate during sleep in both OSA and healthy subjects. We speculate that upper airway muscle dyssynchrony during sleep may explain why GG EMG activation fails to alleviate flow limitation and stabilize airway patency during sleep.

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