Alteration in upper airway dilator muscle coactivation during sleep: comparison of patients with obstructive sleep apnea and healthy subjects.
Alteration in upper airway dilator muscle coactivation during sleep: comparison of patients with obstructive sleep apnea and healthy subjects.
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DOI：
10.1152/japplphysiol.01067.2016
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发表时间：
2018-02
影响因子：
3.3
通讯作者：
Ron Oliven;G. Cohen;Y. Dotan;M. Somri;A. Schwartz;A. Oliven
中科院分区：
文献类型：
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作者：
Ron Oliven;G. Cohen;Y. Dotan;M. Somri;A. Schwartz;A. Oliven
在阻塞性睡眠呼吸暂停（OSA）患者中，在呼吸不足/呼吸暂停期间颏舌肌（GG）活动的显著增加通常无法恢复正常气流。我们以前曾提出，睡眠引起的舌肌协调性改变可能解释了这一发现，因为与清醒相比，睡眠期间牵开肌共激活减少。本研究旨在评估睡眠期间扩张肌激活的这些变化是否在OSA的发病机制中发挥作用，以及其他咽周肌（非GG肌肉：茎突舌肌，颏舌骨肌，胸骨舌骨肌和胸锁乳突肌）的共激活是否在睡眠期间也受损。我们比较了8例OSA患者和12例健康受试者在清醒状态下通过吸气电阻呼吸时的GG和非GG肌肉肌电图（EMG）活动与在睡眠期间观察到的活动，在觉醒前，在相等的食管压力下，在流量限制结束时。在清醒期间，阻力性呼吸触发了GG和非GG肌肉活动的增加。在睡眠期间，血流受限与GG-EMG的增加相关，平均达到清醒时观察到的水平的2倍以上。相比之下，同时记录的非GG肌肉的EMG平均仅达到清醒水平的2/3。我们的结论是，在睡眠期间GG活动可能会增加到水平，大大超过那些足以防止咽部塌陷在清醒状态下，而其他咽周肌不共激活睡眠期间在OSA患者和健康受试者。我们推测，睡眠期间上气道肌肉的不同步性可能解释了为什么GG-EMG激活不能缓解流量限制和稳定睡眠期间气道通畅。新&值得注意的是，睡眠期间的咽阻塞可能会触发颏舌肌活动水平大大超过清醒时观察到的水平，而不会改善流量限制。相比之下，阻塞性睡眠呼吸暂停患者和健康受试者的其他咽周肌在睡眠期间表现出低得多的活动。协调的肌肉协同作用使咽部稳定，尽管清醒时活动相对较低，但当睡眠期间其他扩张肌的同时活动不足时，甚至更高的颏舌活动允许咽部阻塞。
In patients with obstructive sleep apnea (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 muscle coactivation was reduced during sleep compared with wakefulness. The present study was undertaken to evaluate whether these alterations in dilator muscle activation during sleep play a role in the pathogenesis of OSA and whether coactivation of additional peripharyngeal muscles (non-GG muscles: styloglossus, geniohyoid, sternohyoid, and sternocleidomastoid) is also impaired during sleep. We compared GG and non-GG muscle electromyographic (EMG) activity in 8 patients with OSA and 12 healthy subjects during wakefulness while breathing through inspiratory resistors with the activity observed during sleep toward the end of flow limitation, before arousal, at equivalent esophageal pressures. During wakefulness, resistive breathing triggered increases in both GG and non-GG muscle activity. During sleep, flow limitation was associated with increases in GG-EMG that reached, on average, >2-fold the level observed while awake. In contrast, EMGs of the non-GG muscles, recorded simultaneously, reached, on average, only ~2/3 the wakefulness level. We conclude that during sleep GG activity may increase to levels that substantially exceed those sufficient to prevent pharyngeal collapse during wakefulness, whereas other peripharyngeal muscles do not coactivate during sleep in both patients with 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. NEW & NOTEWORTHY Pharyngeal obstruction during sleep may trigger genioglossus activity to levels substantially exceeding those observed during wakefulness, without ameliorating flow limitation. In contrast, other peripharyngeal muscles exhibit a much lower activity during sleep in both patients with obstructive sleep apnea and healthy subjects. Coordinated muscular synergy stabilizes the pharynx despite relatively low activity while awake, yet even higher genioglossal activity allows the pharynx to obstruct when simultaneous activity of other dilator muscles is inadequate during sleep.