Thesis Defence: The Effect of Normobaric Hypoxia and Postural Demand on Cortical and Motoneuronal Excitability
June 17 at 10:00 am - 2:00 pm
Eric Bennett, supervised by Dr. Brian Dalton, will defend their thesis titled “The Effect of Normobaric Hypoxia and Postural Demand on Cortical and Motoneuronal Excitability” in partial fulfillment of the requirements for the degree of Master of Science in Health and Exercise Sciences.
An abstract for Eric Bennett’s thesis is included below.
Defences are open to all members of the campus community as well as the general public. Registration is not required for in-person defences.
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, it is unknown whether the documented increase in 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. Fifteen participants (7 female) completed maximal voluntary isometric contractions (MVCs) of the plantar flexors with assessment of voluntary activation. Afterwards, they received 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 maintaining soleus muscle activity equivalent to 20% MVC torque (determined in the sitting posture) during a sustained, unilateral isometric plantar flexion as well as standing task. Three blocks of testing were completed: one before entering the normobaric hypoxia chamber (baseline; fraction of inspired oxygen [FIO2]=0.21), then after both 1h and 2h in the chamber (FIO2≈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), unchanged motoneuronal excitability (p=0.101) and decreased peripheral excitability (p=0.001). Thus, the previously reported increase in corticospinal excitability when standing compared to sitting is likely explain by greater cortical excitability while standing. Further, compared to baseline, 2h of hypoxia had no effect on cortical excitability (p=0.929), while motoneuronal excitability increased (p=0.001) and peripheral excitability decreased (p=0.008). Therefore, the main hypoxia-related findings indicate that greater motoneuronal excitability may contribute to the reported alterations in motor control (e.g., standing balance) at high altitude.
