Neuroscience Research Australia, Sydney, New South Wales, Australia.
University of New South Wales, Sydney, New South Wales, Australia.
Exp Physiol. 2022 Jun;107(6):615-630. doi: 10.1113/EP090099. Epub 2022 Apr 19.
What is the central question of this study? Does a single session of repeated bouts of acute intermittent hypoxic breathing enhance the motoneuronal output of the limb muscles of healthy able-bodied participants? What is the main finding and its importance? Compared to breathing room air, there were some increases in motoneuronal output following acute intermittent hypoxia, but the increases were variable across participants and in time after the intervention and depended on which neurophysiological measure was checked.
Acute intermittent hypoxia (AIH) induces persistent increases in output from rat phrenic motoneurones. Studies in people with spinal cord injury (SCI) suggest that AIH improves limb performance, perhaps via postsynaptic changes at cortico-motoneuronal synapses. We assessed whether limb motoneurone output in response to reflex and descending synaptic activation is facilitated after one session of AIH in healthy able-bodied volunteers. Fourteen participants completed two experimental days, with either AIH or a sham intervention (randomised crossover design). We measured H-reflex recruitment curves and homosynaptic post-activation depression (HPAD) of the H-reflex in soleus, and motor evoked potentials (MEPs) evoked by transcranial magnetic stimulation (TMS) and their recruitment curves in first dorsal interosseous. All measurements were performed at rest and occurred at baseline, 0, 20, 40 and 60 min post-intervention. The intervention was 30 min of either normoxia (sham, ≈ 0.21) or AIH (alternate 1-min hypoxia [ ≈ 0.09], 1-min normoxia). After AIH, the H-reflex recruitment curve shifted leftward. Lower stimulation intensities were needed to evoke 5%, 50% and 99% of the maximal H-reflex at 40 and 60 min after AIH (P < 0.04). The maximal H-reflex, recruitment slope and HPAD were unchanged after AIH. MEPs evoked by constant intensity TMS were larger 40 min after AIH (P = 0.027). There was no change in MEP recruitment or the maximal MEP. In conclusion, some measures of the evoked responses from limb motoneurones increased after a single AIH session, but only at discrete time points. It is unclear to what extent these changes alter functional performance.
本研究的核心问题是什么？单次重复急性间歇性低氧呼吸是否会增强健康健全参与者肢体肌肉的运动神经元输出？主要发现及其重要性是什么？与呼吸空气相比，急性间歇性低氧后运动神经元输出有一些增加，但增加在参与者之间和干预后时间上是可变的，并且取决于所检查的神经生理学测量。
急性间歇性低氧（AIH）会引起大鼠膈神经运动神经元持续增加输出。在脊髓损伤（SCI）患者中的研究表明，AIH 通过皮质运动神经元突触的突触后变化改善肢体功能，我们评估了在健康健全志愿者中单次 AIH 后，对反射和下行突触激活的肢体运动神经元输出是否得到促进。14 名参与者完成了两天的实验，接受 AIH 或假干预（随机交叉设计）。我们测量了比目鱼肌的 H 反射募集曲线和 H 反射的同突触后激活抑制（HPAD），以及经颅磁刺激（TMS）诱发的运动诱发电位（MEP）及其在第一背侧骨间肌中的募集曲线。所有测量均在休息时进行，并且在基线、0、20、40 和 60 分钟时进行。干预措施是 30 分钟的常氧（假，约 0.21）或 AIH（交替 1 分钟低氧[约 0.09]，1 分钟常氧）。AIH 后，H 反射募集曲线向左移动。在 AIH 后 40 和 60 分钟时，需要更低的刺激强度来诱发 5%、50%和 99%的最大 H 反射（P < 0.04）。H 反射的最大幅度、募集斜率和 HPAD 在 AIH 后不变。在 AIH 后 40 分钟时，由恒定强度 TMS 诱发的 MEP 更大（P = 0.027）。MEP 募集或最大 MEP 没有变化。总之，单次 AIH 后，一些肢体运动神经元诱发反应的测量值增加，但仅在离散时间点增加。尚不清楚这些变化在多大程度上改变了功能表现。
