Differential Clamping of Hypoxia Induces Distinct Changes in Intracortical and Spinal Neural Networks: Proceedings of International Hypoxia Symposium, 2023

The purpose of this study was to examine how two common methods of continuous hypoxia impact the activity of intracortical circuits responsible for inhibition and facilitation of motor output, and spinal excitability. Ten participants were exposed to 2 hr of hypoxia at 0.13 fraction of inspired oxygen (FIO2 clamped protocol) and 80% of peripheral capillary oxygen saturation (SpO2 clamped protocol) using a simulating high altitude device on two visits separated by a week. Using transcranial magnetic and peripheral nerve stimulation, unconditioned motor evoked potential (MEP) area, short intracortical inhibition (SICI) and facilitation (ICF), and F-wave persistence and area, were assessed in the first dorsal interosseous muscle before titration, 1 and 2 hr of hypoxic exposure, and at reoxygenation. The clamped protocols resulted in differing reductions in SpO2 by 2 hr (FIO2 clamped protocol: 90.6 ± 2.5%, SpO2 clamped protocol: 81.9 ± 1.3%). Although unconditioned MEP area did not differ between the protocols, SICI was significantly lower at 2 hr (P < 0.001) and ICF was higher throughout (P = 0.005) the FIO2 clamped protocol compared to the SpO2 clamped protocol. Furthermore, a negative correlation between SICI and SpO2 (r = 0.31) and a positive correlation between ICF and SpO2 (r = 0.30) were determined, where greater reductions in SpO2 resulted in less inhibition and less facilitation of MEP responses. Although F-wave area progressively increased similarly throughout the protocols (P = 0.036), persistence of responses was reduced at 2 hr and reoxygenation (Ps < 0.01) during the SpO2 clamped protocol compared to the FIO2 clamped protocol. This study demonstrates that activity in intracortical networks responsible for facilitating and inhibiting motor output from the motor cortex, and activity of spinal motoneurones, are dependent on the degree of hypoxia, where greater severities of exposure lead to reduced excitability of these networks.