Brigham and Women's Hospital, Div. of Sleep Medicine, Sleep Disorders Program, Boston, MA 02115, USA.
J Appl Physiol (1985). 2011 Dec;111(6):1644-53. doi: 10.1152/japplphysiol.00653.2011. Epub 2011 Sep 1.
Numerous studies have demonstrated upper-airway neuromuscular abnormalities during wakefulness in snorers and obstructive sleep apnea (OSA) patients. However, the functional role of sensorimotor impairment in OSA pathogenesis/disease progression and its potential effects on protective upper-airway reflexes, measures of respiratory sensory processing, and force characteristics remain unclear. This study aimed to gain physiological insight into the potential role of sensorimotor impairment in OSA pathogenesis/disease progression by comparing sensory processing properties (respiratory-related evoked potentials; RREP), functionally important protective reflexes (genioglossus and tensor palatini) across a range of negative pressures (brief pulses and entrained iron lung ventilation), and tongue force and time to task failure characteristics between 12 untreated OSA patients and 13 controls. We hypothesized that abnormalities in these measures would be present in OSA patients. Upper-airway reflexes (e.g., genioglossus onset latency, 20 ± 1 vs. 19 ± 2 ms, P = 0.82), early RREP components (e.g., P1 latency 25 ± 2 vs. 25 ± 1 ms, P = 0.78), and the slope of epiglottic pressure vs. genioglossus activity during iron lung ventilation (-0.68 ± 1.0 vs. -0.80 ± 2.0 cmH(2)O/%max, P = 0.59) were not different between patients and controls. Maximal tongue protrusion force was greater in OSA patients vs. controls (35 ± 2 vs. 27 ± 2 N, P < 0.01), but task failure occurred more rapidly (149 ± 24 vs. 254 ± 23 s, P < 0.01). Upper-airway protective reflexes across a range of negative pressures as measured by electromyography and the early P1 component of the RREP are preserved in OSA patients during wakefulness. Consistent with an adaptive training effect, tongue protrusion force is increased, not decreased, in untreated OSA patients. However, OSA patients may be vulnerable to fatigue of upper-airway dilator muscles, which could contribute to disease progression.
许多研究已经证明,在打鼾者和阻塞性睡眠呼吸暂停(OSA)患者清醒时,上气道神经肌肉存在异常。然而,感觉运动障碍在 OSA 发病机制/疾病进展中的功能作用及其对上气道保护反射、呼吸感觉处理措施和力特征的潜在影响仍不清楚。本研究旨在通过比较一系列负压力(短暂脉冲和诱导铁肺通气)下的感觉处理特性(呼吸相关诱发电位;RREP)、功能上重要的保护反射(颏舌肌和腭帆张肌)以及舌力和任务失败时间特征,来深入了解感觉运动障碍在上气道的潜在作用在 OSA 发病机制/疾病进展中的作用,从而获得生理洞察力。我们假设这些措施在 OSA 患者中会存在异常。上气道反射(例如,颏舌肌起始潜伏期,20±1 对 19±2 ms,P=0.82)、早期 RREP 成分(例如,P1 潜伏期 25±2 对 25±1 ms,P=0.78)以及铁肺通气期间会厌压与颏舌肌活动的斜率(-0.68±1.0 对-0.80±2.0 cmH2O/%max,P=0.59)在患者和对照组之间没有差异。OSA 患者的最大舌伸出力大于对照组(35±2 对 27±2 N,P<0.01),但任务失败发生得更快(149±24 对 254±23 s,P<0.01)。在清醒状态下,通过肌电图和 RREP 的早期 P1 成分测量,OSA 患者在上气道保护反射范围内的负压力下保持不变。与适应性训练效应一致,未经治疗的 OSA 患者的舌伸出力增加,而不是减少。然而,OSA 患者可能对上气道扩张肌疲劳敏感,这可能导致疾病进展。