Long-Term Facilitation of Ventilation in Humans with Chronic Spinal Cord Injury

Abstract

Ventilatory long-term facilitation can be evoked by brief periods of hypoxia in humans with chronic spinal cord injury. Thus, intermittent hypoxia may represent a strategy for inducing respiratory neuroplasticity after declines in respiratory function that are related to neurological impairment. Clinical trial registered with www.clinicaltrials.gov (NCT01272011).

Hypoxia triggers short term potentiation of phrenic motoneuron discharge after chronic cervical spinal cord injury

“…This response, termed phrenic long-term facilitation (LTF), can be evoked following chronic C2Hx in rats, and the response is more robust in the ipsilateral compared to contralateral motor output (Doperalski and Fuller, 2006). A recent report confirms that LTF of ventilation occurs following intermittent hypoxia in humans with SCI (Tester et al, 2014). …”

“…The relative strength of the CPP, however, can be considerably enhanced with neurorehabilitation strategies (Alilain et al, 2011; Doperalski and Fuller, 2006; Gransee et al, 2013; Lovett-Barr et al, 2012). Controlled exposure to hypoxia holds promise in this regard since appropriate paradigms can trigger robust spinal neuroplasticity (Baker-Herman et al, 2004) and both somatic (Hayes et al, 2014; Trumbower et al, 2012) and respiratory (Tester et al, 2014) motor recovery after SCI in humans. To date, studies involving short-term exposure to hypoxia in SCI models have focused on the persistent increase in phrenic activity that is triggered by repeated exposures.…”

Humans In Hypoxia: A Conspiracy Of Maladaptation?!

“…Most notably, this noncyclical pattern, short duration, and mild severity type of IH induces respiratory motoneuron plasticity characterized by a progressive increase in phrenic and hypoglossal nerve outputs following IH application, with enhancement of ventilation in rodents and even in humans with spinal cord injury (3,24,37,67,117). Apparently, these forms of short-term, low-frequency moderate IH alter the expression of hypoxic-sensitive growth and trophic factors within respiratory motoneurons (3,24,37).…”

Fitness and therapeutic potential of intermittent hypoxia training: a matter of dose

“…None of the articles that use such concentrations describe adverse effects. There are few papers which documented adverse effects, but starting with 8-9% FiO 2 [40][41][42][43][44][45][46][47]. All study results cited in the A rightward shift in the oxyhemoglobin equilibrium response, attenuated tachycardiac response to hypoxia while significantly enhancing normoxic R-R interval variability in low-frequency and highfrequency spectra without changes in arterial blood pressure at rest or during hypoxia, i.e.…”