Brief exposure to systemic hypoxia enhances plasticity of the central nervous system in spinal cord injured animals and man.

Abstract

We have known for many decades that animals that sustain injuries to the neuraxis, which result in respiratory impairment, are able to develop rapid neural compensation for these injuries. This compensation, which is linked to the systemic hypoxia resulting from damage to the respiratory apparatus, is a potent manifestation of neural plasticity. Hypoxia-induced plasticity is also applicable to somatic neural systems that regulate motor activity in extremity muscles. We report on recent developments in our understanding of the mechanisms underlying this seemingly beneficial action of acute intermittent hypoxia (AIH). AIH improves breathing in animal models of spinal cord injury, and increases strength and endurance in individuals with incomplete spinal injuries. The role of AIH as a therapeutic intervention remains to be confirmed but it has proved to be well tolerated for use in humans with no adverse effects reported to date. The effects of AIH emerge rapidly and persist for several hours raising the possibility that the intervention may serve as a priming mechanism for facilitating rehabilitation and promoting recovery after neurologic injury in man. AIH is emerging as a potent and relatively inexpensive modality for inducing neuroplasticity, so it may prove feasible to use AIH in a clinical setting.