Abstract
Acute intermittent hypoxia (AIH) enhances voluntary motor output in humans with central nervous system damage. The neural mechanisms contributing to these beneficial effects are unknown. We examined corticospinal function by evaluating motor evoked potentials (MEPs) elicited by cortical and subcortical stimulation of corticospinal axons and the activity in intracortical circuits in a finger muscle before and after 30 min of AIH or sham AIH. We found thatthe amplitude of cortically and subcortically elicited MEPs increased for 75 min after AIH but not sham AIH while intracortical activity remained unchanged. To examine further these subcortical effects, we assessed spike-timingdependent plasticity (STDP) targeting spinal synapses and the excitability of spinal motoneurons. Notably, AIH increased STDP outcomes while spinal motoneuron excitability remained unchanged. Our results provide the first evidence that AIH changes corticospinal function in humans, likely by altering corticospinal-motoneuronal synaptic transmission. AIH may represent a novel noninvasive approach for inducing spinal plasticity in humans.
Highlights
Brief exposures to hypoxic air interspersed with periods of breathing ambient room air, known as acute intermittent hypoxia (AIH), impacts the respiratory, cardiovascular, immune, metabolic, bone and nervous systems (Dale et al, 2014; Gonzalez-Rothi et al, 2015)
Tukey Post hoc tests showed that motor evoked potentials (MEPs) amplitude increased after 15 (29.4 ± 26.2%; p
We followed up the effects of AIH in one individual and found out that the MEP amplitude returned to baseline ~120 min after AIH
Summary
Brief exposures to hypoxic air interspersed with periods of breathing ambient room air, known as acute intermittent hypoxia (AIH), impacts the respiratory, cardiovascular, immune, metabolic, bone and nervous systems (Dale et al, 2014; Gonzalez-Rothi et al, 2015). An increasing number of studies support the view that AIH affects the damaged central nervous system, triggering recovery of motor function in humans with partial paralysis due to spinal cord injury (Trumbower et al, 2012; Lynch et al, 2017; Navarrete-Opazo et al, 2017a, b). The neural mechanisms contributing to the beneficial effects of AIH in the human motor system remain unknown. Studies in animal models have demonstrated that single and multiple exposures to AIH cause phrenic motor facilitation (Baker and Mitchell, 2000; Golder and Mitchell, 2005) and increase expression of brain-derived neurotrophic factor (BDNF) in respiratory motor neurons (Baker-Herman et al, 2004; Satriotomo et al, 2012). Other studies showed that AIH elicits plasticity in neural systems not directly linked to the respiratory system. A critical question is if AIH can modulate activity in descending motor pathways in intact humans and its mechanisms of action
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