Exposure to acute intermittent hypoxia augments somatic motor function in humans with incomplete spinal cord injury

Neural plasticity may contribute to motor recovery following spinal cord injury (SCI). In rat models of SCI with respiratory impairment, acute intermittent hypoxia (AIH) strengthens synaptic inputs to phrenic motor neurons, thereby improving respiratory function by a mechanism known as respiratory long-term facilitation. Similar intermittent hypoxia-induced facilitation may be feasible in somatic motor pathways in humans.

Using a randomized crossover design, the authors tested the hypothesis that AIH increases ankle strength in people with incomplete SCI.

Ankle strength was measured in 13 individuals with chronic, incomplete SCI before and after AIH. Voluntary ankle strength was estimated using changes in maximum isometric ankle plantar flexion torque generation and plantar flexor electromyogram activity following 15 low oxygen exposures (Fio(2) = 0.09, 1-minute intervals). Results were compared with trials where subjects received sham exposure to room air.

AIH increased plantar flexion torque by 82 ± 33% (P < .003) immediately following AIH and was sustained above baseline for more than 90 minutes (P < .007). Increased ankle plantar flexor electromyogram activity (P = .01) correlated with increased torque (r(2) = .5; P < .001). No differences in plantar flexion strength or electromyogram activity were observed in sham experiments.

AIH elicits sustained increases in volitional somatic motor output in persons with chronic SCI. Thus, AIH has promise as a therapeutic tool to induce plasticity and enhance motor function in SCI patients.