The Effect of Hypoxia on the Neural Control of Muscle Contraction

Abstract

The availability of oxygen (O2) is vital for maintaining neurological function during exercise. This is clear when performing exercise in low oxygen environments, such as high altitude, where reductions in O2 availability result in limitations in motor performance. However, the ongoing contribution of central and peripheral mechanisms to hypoxia-related limitations in motor performance is yet to be fully understood. A wide variety of experimental designs have been used to test motor pathways during hypoxic exposure. Indeed, there is little consistency in the literature with regards to 1) the severity of hypoxic exposure, 2) the duration of hypoxic exposure, 3) the fatigue-state of the motor system, and 4) the intensity of exercise. This Thesis presents a series of controlled laboratory experiments which assess the effects of acute hypoxia (2 hr at 80% SpO2) on central and peripheral motor mechanisms. The experiments used high-density electromyography, electrical stimulation of the motor nerve (MNS), and transcranial magnetic stimulation (TMS) of the motor cortex, to clarify how motor activity is affected with hypoxia. The first experiment assessed how the firing characteristics of biceps brachii motor units (MU) were modulated by acute hypoxia when performing sustained isometric elbow flexions. Maximal voluntary contraction (MVC) toque remained unaffected during hypoxia, however, individuals exhibited specific changes in MU firing. Bidirectional changes in MU discharge were strongly correlated to the rate of desaturation and sensitivity to O2 availability during the titration phase. Differences in intrinsic properties of neurons, afferent input to motoneurones, neuromodulation, and sympathetic nerve activity may explain these differences. The second experiment assessed how corticospinal excitability, voluntary activation using motor nerve stimulation (VAMNS) and perception of fatigue (RPF) during brief and sustained MVCs were modulated by acute hypoxia. RPF and corticospinal excitability increased, while VAMNS decreased across the hypoxia protocol. Changes in the motor evoked potential (MEP) area and VAMNS were only seen during the brief MVCs and not the sustained MVCs. This may be due to redirection of blood flow to active areas of the motor system during prolonged contraction. The third experiment assessed how acute hypoxia altered neural mechanisms of muscle activation during, and following recovery from, a sustained submaximal (20% MVC) fatiguing contraction. MVC torque, root mean square EMG (EMGRMS), VAMNS and voluntary activation using TMS (VATMS), RPF, MEP area, and silent period duration (SP) were measured to characterise muscle activation. Hypoxia effects were only seen during the recovery phase, where VAMNS and VATMS, as well as MEP area, was reduced during acute hypoxia. This was likely due to hypoxia-related mechanisms involving supraspinal motor circuits that were impaired during the recovery phase. The fourth experiment assessed how acute hypoxia altered the neural mechanisms of muscle activation across a full range of force output once fatigued. MVC torque, EMGRMS, VAMNS and VATMS, MEP area, and SP were assessed following the sustained MVC. VATMS was reduced during hypoxia, which was not reflected in VAMNS. This indicates that acute hypoxia significantly impaired the ability of the motor cortex to voluntarily activate the fatigued muscle. This was partly due to suboptimal output from the motor cortex. Collectively, the findings of the four experiments in this Thesis provide novel evidence that a moderate acute hypoxic stimulus 1) reduces VA of a muscle during maximal and submaximal contraction due to suboptimal output from the motor cortex, 2) modulates the excitability of the corticospinal pathway, and 3) enhances perceptions of muscle fatigue during maximal, but not submaximal, fatiguing contractions. For these findings to occur, the elbow flexor muscle group needed to be sufficiently fatigued during at least 2 hr of prolonged exposure to a moderate hypoxic stimulus.