Effect of age on long-term facilitation and chemosensitivity during NREM sleep
Effect of age on long-term facilitation and chemosensitivity during NREM sleep
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DOI：
10.1152/japplphysiol.00030.2015
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发表时间：
2015-11-15
影响因子：
3.3
通讯作者：
Badr, M. Safwan
中科院分区：
文献类型：
--
作者：
Chowdhuri, Susmita;Pranathiageswaran, Sukanya;Badr, M. Safwan
老年人中以中枢性呼吸暂停为主的睡眠呼吸障碍增多的原因尚不清楚。我们推测通气控制不稳定可能在衰老和睡眠期间呼吸不稳定之间存在联系。我们试图研究健康老年人睡眠期间潜在的潜在机制。我们假设，老年人在非快速眼动 (NREM) 睡眠期间，1) 呼吸可塑性或通气长期促进 (LTF) 下降，和/或 2) 通气化疗敏感性增加。 14 名老年人经历了 15 次 1 分钟的等二氧化碳缺氧 (EH) 事件，最低 O-2 饱和度：87.0 +/- 0.8%。分别在控制、缺氧和 EH 协议后 20 分钟恢复期间获得每分钟通气量 (VI)、计时和吸气上呼吸道阻力 (R-UA) 的测量值。结果如下。 1) 与基线相比，EH 期间 VI 显着增加（158 +/- 11%，P < 0.05），但这并不伴随连续缺氧试验期间 VI 的增加，也不伴随恢复期 VI 的增加（94.4 +/- 3.5%，P = 不显着），表明不存在 LTF。试验期间吸气 RUA 没有变化。这与我们之前关于年轻人睡眠期间呼吸可塑性的发现形成鲜明对比。假手术研究没有显示任何测量参数的变化。 2) 我们观察到，在 NREM 睡眠期间，老年人与年轻人相比，化疗敏感性随着等二氧化碳低氧通气反应的增加和 VI 高氧抑制而增加。因此，不受呼吸可塑性限制的化学敏感性增加可能解释了老年人在 NREM 睡眠期间周期性呼吸和中枢性呼吸暂停的增加。
The reason for increased sleep-disordered breathing with a predominance of central apneas in the elderly is unknown. We speculate that ventilatory control instability may provide a link between aging and the onset of unstable breathing during sleep. We sought to investigate potential underlying mechanisms in healthy, elderly adults during sleep. We hypothesized that there is 1) a decline in respiratory plasticity or long-term facilitation (LTF) of ventilation and/or 2) increased ventilatory chemosensitivity in older adults during non-, this should be hyphenated, non-rapid rapid eye movement (NREM) sleep. Fourteen elderly adults underwent 15, 1-min episodes of isocapnic hypoxia (EH), nadir O-2 saturation: 87.0 +/- 0.8%. Measurements were obtained during control, hypoxia, and up to 20 min of recovery following the EH protocol, respectively, for minute ventilation (VI), timing, and inspiratory upper-airway resistances (R-UA). The results showed the following. 1) Compared with baseline, there was a significant increase in VI (158 +/- 11%, P < 0.05) during EH, but this was not accompanied by augmentation of VI during the successive hypoxia trials nor in VI during the recovery period (94.4 +/- 3.5%, P = not significant), indicating an absence of LTF. There was no change in inspiratory RUA during the trials. This is in contrast to our previous findings of respiratory plasticity in young adults during sleep. Sham studies did not show a change in any of the measured parameters. 2) We observed increased chemosensitivity with increased isocapnic hypoxic ventilatory response and hyperoxic suppression of VI in older vs. young adults during NREM sleep. Thus increased chemosensitivity, unconstrained by respiratory plasticity, may explain increased periodic breathing and central apneas in elderly adults during NREM sleep.