Intermittent hypoxia is usually studied as a complication contributing to other medical problems, including sleep-disordered breathing (SDB). However, it has been measured in a few research studies as a training protocol to improve somatic motor function and increase growth factor expression in the central nervous system (Dale et al. 2014). Complication rates, cost, and QOL are among the many important factors to consider in all forms of assisted ventilation training.
The study of Tester et al. (2014) compared intermittent hypoxia for 10 days (5 days/week) to a sham procedure in 8 patients with incomplete SCI. They showed evidence that acute exposure to intermittent hypoxia provides a significant increase in VE for 30 min after the exposure, but not after a sham exposure. However, the magnitude of ventilatory long-term facilitation was not enhanced over 10 days of exposure.
The study of Sankari et al. (2015) analyzed 8 patients with cervical SCI, 8 patients with thoracic SCI and 8 non-SCI participants who underwent acute intermittent hypoxia (15 episodes of 1 minute) or sham protocol. Patients with chronic SCI experienced a significant increase in VE (only patients with cervical SCI) and VT (most prominent in patients with cervical SCI, less prominent in those with thoracic SCI, and absent in non-SCI participants), compared with prehypoxia baseline levels, during the recovery phase after acute intermittent hypoxia.
However, Welch et al. (2021) found that acute intermittent hypoxia did not increase diaphragm PEmax amplitude or diaphragm compound muscle action potentials, and there was no evidence of diaphragm long-term facilitation. More research is needed before acute intermittent hypoxia could be recommended.
There is level 4 evidence (from one pre-post study: Tester et al. 2014) that the exposure to intermittent hypoxia during 10 days (5 days/week) provided short-term improvements in ventilation.
There is level 2 evidence (from one cohort study: Sankari et al. 2015) that the exposure to acute intermittent hypoxia increases the VE (only in patients with cervical SCI) and VT (significant increase in patients with cervical SCI), compared to prehypoxia baseline levels during the recovery phase after the exposure.