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Abstract

Although millions of people travelling to or living at high altitude experience hypoxia (low oxygen), there is inconclusive research on how hypoxia alters postural control, as well as the underlying mechanisms (e.g., neural excitability). Further, in normoxia, it is unknown whether the documented increase of corticospinal excitability when standing compared to sitting is representative of alterations at the cortical and/or motoneuronal levels. Therefore, the purpose of this thesis was to determine if normobaric hypoxia altered cortical, motoneuronal and/or peripheral excitability during sitting and standing. When seated, 15 participants (7 female) completed isometric maximal voluntary contractions (MVCs) of the plantar flexors with assessment of voluntary activation. Afterwards, in both the seated and standing postures, they received a stimulation sequence in the following order: 1) electrical thoracic spine stimulation (TSS) eliciting a thoracic motor evoked potential (TMEP), 2) transcranial magnetic stimulation (TMS) to the motor cortex eliciting a motor evoked potential (MEP), and 3) peripheral electrical stimulation (PNS) to the tibial nerve eliciting a compound muscle action potential (Mmax). Participants received TSS, TMS, and PNS while their right limb maintained soleus muscle activity that was equivalent to the level recorded when performing a seated isometric contraction at 20% MVC torque Three blocks of testing were completed: one before entering the normobaric hypoxia chamber (baseline; fraction of inspired oxygen [F₁O₂]=0.21), then after both 1h and 2h in the chamber (F₁O₂≈0.11). Ratios of the areas of the evoked potentials were used to evaluate cortical (MEP/TMEP) and motoneuronal (TMEP/Mmax) excitability, whereas Mmax area was used to evaluate peripheral excitability. Compared to sitting, the standing posture had greater cortical excitability (p=0.001), no difference in motoneuronal excitability (p=0.101) and decreased peripheral excitability (p=0.001). Thus, the previously reported increase of corticospinal excitability when standing compared to sitting is likely explained by greater cortical excitability. Compared to baseline, cortical excitability was unaltered (p=0.929), motoneuronal excitability increased (p=0.001), and peripheral excitability decreased (p=0.008) following 2h of hypoxia. Therefore, the main hypoxia-related findings indicate that greater motoneuronal excitability may contribute to the reported motor control alterations (e.g., increased postural sway) at high altitude.