Department of Physiology, Wayne State University School of Medicine, Wayne State University, Detroit, Michigan, USA.
J Appl Physiol (1985). 2012 Feb;112(3):367-77. doi: 10.1152/japplphysiol.00702.2011. Epub 2011 Nov 3.
We examined whether exposure to intermittent hypoxia (IH) during wakefulness impacted on the apnea/hypopnea index (AHI) during sleep in individuals with sleep apnea. Participants were exposed to twelve 4-min episodes of hypoxia in the presence of sustained mild hypercapnia each day for 10 days. A control group was exposed to sustained mild hypercapnia for a similar duration. The intermittent hypoxia protocol was completed in the evening on day 1 and 10 and was followed by a sleep study. During all sleep studies, the change in esophageal pressure (ΔPes) from the beginning to the end of an apnea and the tidal volume immediately following apneic events were used to measure respiratory drive. Following exposure to IH on day 1 and 10, the AHI increased above baseline measures (day 1: 1.95 ± 0.42 fraction of baseline, P ≤ 0.01, vs. day 10: 1.53 ± 0.24 fraction of baseline, P < 0.06). The indexes were correlated to the hypoxic ventilatory response (HVR) measured during the IH protocol but were not correlated to the magnitude of ventilatory long-term facilitation (vLTF). Likewise, ΔPes and tidal volume measures were greater on day 1 and 10 compared with baseline (ΔPes: -8.37 ± 0.84 vs. -5.90 ± 1.30 cmH(2)0, P ≤ 0.04; tidal volume: 1,193.36 ± 101.85 vs. 1,015.14 ± 119.83 ml, P ≤ 0.01). This was not the case in the control group. Interestingly, the AHI on day 10 (0.78 ± 0.13 fraction of baseline, P ≤ 0.01) was significantly less than measures obtained during baseline and day 1 in the mild hypercapnia control group. We conclude that enhancement of the HVR initiated by exposure to IH may lead to increases in the AHI during sleep and that initiation of vLTF did not appear to impact on breathing stability. Lastly, our results suggest that repeated daily exposure to mild sustained hypercapnia may lead to a decrease in breathing events.
我们研究了清醒时间歇性低氧（IH）暴露是否会影响睡眠呼吸暂停/低通气指数（AHI）。参与者每天接受 12 次 4 分钟的低氧暴露，同时伴有持续的轻度高碳酸血症，共 10 天。对照组暴露于持续的轻度高碳酸血症相似的时间。间歇性低氧方案在第 1 天和第 10 天晚上完成，随后进行睡眠研究。在所有睡眠研究中，使用食管压力（ΔPes）从呼吸暂停开始到结束的变化以及紧随呼吸暂停事件之后的潮气量来测量呼吸驱动。在第 1 天和第 10 天暴露于 IH 后，AHI 高于基线测量值（第 1 天：1.95±0.42 为基线的分数，P≤0.01，第 10 天：1.53±0.24 为基线的分数，P<0.06）。这些指标与 IH 方案期间测量的低氧通气反应（HVR）相关，但与通气长期易化（vLTF）的幅度无关。同样，与基线相比，第 1 天和第 10 天的 ΔPes 和潮气量测量值更大（ΔPes：-8.37±0.84 对-5.90±1.30 cmH20，P≤0.04；潮气量：1193.36±101.85 对 1015.14±119.83 ml，P≤0.01）。在对照组中并非如此。有趣的是，第 10 天的 AHI（0.78±0.13 为基线的分数，P≤0.01）明显低于轻度高碳酸血症对照组在基础和第 1 天获得的测量值。我们得出结论，IH 暴露引发的 HVR 增强可能导致睡眠期间 AHI 增加，而 vLTF 的启动似乎不会影响呼吸稳定性。最后，我们的结果表明，重复每日暴露于轻度持续高碳酸血症可能导致呼吸事件减少。
