Neural Control of Movement Laboratory, Menzies Health Institute Queensland, Griffith University, Gold Coast, Queensland, Australia.
Department of Psychology, Faculty of Society and Design, Bond University, Gold Coast, Queensland, Australia.
Exp Physiol. 2023 Sep;108(9):1203-1214. doi: 10.1113/EP091224. Epub 2023 Aug 7.
The purpose of this study was to examine how two common methods of continuous hypoxaemia impact the activity of intracortical circuits responsible for inhibition and facilitation of motor output, and spinal excitability. Ten participants were exposed to 2 h of hypoxaemia at 0.13 fraction of inspired oxygen ( clamping protocol) and 80% of peripheral capillary oxygen saturation ( clamping protocol) using a simulating altitude device on two visits separated by a week. Using transcranial magnetic and peripheral nerve stimulation, unconditioned motor evoked potential (MEP) area, short-interval intracortical inhibition (SICI) and intracortical facilitation (ICF), and F-wave persistence and area were assessed in the first dorsal interosseous (FDI) muscle before titration, after 1 and 2 h of hypoxic exposure, and at reoxygenation. The clamping protocols resulted in differing reductions in by 2 h ( clamping protocol: 81.9 ± 1.3%, clamping protocol: 90.6 ± 2.5%). Although unconditioned MEP peak to peak amplitude and area did not differ between the protocols, SICI during clamping was significantly lower at 2 h compared to clamping (P = 0.011) and baseline (P < 0.001), whereas ICF was higher throughout the clamping compared to clamping (P = 0.005). Furthermore, a negative correlation between SICI and (r = -0.56, P = 0.002) and a positive correlation between ICF and (r = 0.69, P = 0.001) were determined, where greater reductions in correlated with less inhibition and less facilitation of MEP responses. Although F-wave area progressively increased similarly throughout the protocols (P = 0.037), persistence of responses was reduced at 2 h and reoxygenation (P < 0.01) during the clamping protocol compared to the clamping protocol. After 2 h of hypoxic exposure, there is a reduction in the activity of intracortical circuits responsible for inhibiting motor output, as well as excitability of spinal motoneurones. However, these effects can be influenced by other physiological responses to hypoxia (i.e., hyperventilation and hypocapnia). NEW FINDINGS: What is the central question of this study? How do two common methods of acute hypoxic exposure influence the excitability of intracortical networks and spinal circuits responsible for motor output? What is the main finding and its importance? The excitability of spinal circuits and intracortical networks responsible for inhibition of motor output was reduced during severe acute exposure to hypoxia at 2 h, but this was not seen during less severe exposure. This provides insight into the potential cause of variance seen in motor evoked potential responses to transcranial magnetic stimulation (corticospinal excitability measures) when exposed to hypoxia.
这项研究的目的是检验两种常见的持续低氧血症方法如何影响负责抑制和促进运动输出以及脊髓兴奋性的皮质内回路的活动。10 名参与者在两次访问中使用模拟海拔设备暴露于 0.13 分比吸入氧（ 钳位方案）和 80%外周毛细血管血氧饱和度（ 钳位方案）下 2 小时。使用经颅磁刺激和外周神经刺激，在滴定前、缺氧暴露 1 小时和 2 小时以及再氧化时评估第一背间骨（FDI）肌肉中的未条件运动诱发电位（MEP）面积、短程皮质内抑制（SICI）和皮质内易化（ICF）以及 F 波持续时间和面积。钳位方案导致 2 小时内 降低不同（ 钳位方案：81.9 ± 1.3%， 钳位方案：90.6 ± 2.5%）。尽管两个方案之间的未条件 MEP 峰峰值幅度和面积没有差异，但与 钳位相比，在 2 小时时 SICI 显著降低（P = 0.011）和基线（P < 0.001），而 ICF 在整个 钳位期间均高于 钳位（P = 0.005）。此外，还确定了 SICI 与 （r = -0.56，P = 0.002）之间的负相关关系，以及 ICF 与 （r = 0.69，P = 0.001）之间的正相关关系，其中 降低与 MEP 反应的抑制和易化减少相关。尽管 F 波面积在整个方案中相似地逐渐增加（P = 0.037），但与 钳位方案相比，在 2 小时和再氧化时（P < 0.01）响应的持久性降低。在 2 小时的缺氧暴露后，负责抑制运动输出的皮质内回路以及脊髓运动神经元的兴奋性降低。然而，这些影响可能会受到其他对缺氧的生理反应（即过度通气和低碳酸血症）的影响。新发现：这项研究的核心问题是什么？两种常见的急性低氧暴露方法如何影响负责运动输出的皮质内网络和脊髓回路的兴奋性？主要发现及其重要性是什么？在 2 小时的严重急性缺氧暴露期间，负责抑制运动输出的脊髓回路和皮质内网络的兴奋性降低，但在较不严重的暴露期间并未观察到这种情况。这提供了对在暴露于缺氧时经颅磁刺激（皮质脊髓兴奋性测量）引起的运动诱发电位反应中观察到的变异性的潜在原因的深入了解。
