Respiratory impairment is a leading cause of morbidity and mortality after spinal cord injury (SCI), highlighting the need for interventions that improve breathing function. In people with SCI, acute intermittent hypoxia (AIH) elicits respiratory motor plasticity and improves inspiratory function. However, in uninjured people, facilitation of corticospinal diaphragm motor-evoked potential (MEP) amplitude occurs only when AIH is combined with mild hypercapnia (acute intermittent hypercapnic hypoxia; AIHH). It remains unclear whether AIHH similarly enhances diaphragm corticospinal excitability after SCI. We tested the hypothesis that AIHH increases diaphragm MEP amplitude and reduces MEP onset latency in individuals with chronic SCI, whereas AIH and sham have little effect. Ten individuals with chronic cervical or high thoracic SCI (6 cervical injuries; 6 classified as motor complete) completed a randomized, double-blind, crossover study with ≥1-week washout between interventions. Each intervention consisted of 15, 1-minute episodes of AIH (9% inspired O 2 ), AIHH (9% O 2 + 5% CO 2 ), and sham (21% O 2 ), separated by 1.5- minute normoxic intervals. Bayesian hierarchical modeling demonstrated a 99% probability that both AIH and AIHH increased diaphragm MEP amplitude, with no change following sham. AIHH showed consistent evidence of reduced diaphragm MEP latency, consistent with enhanced corticospinal transmission, whereas AIH demonstrated a similar but more uncertain reduction. These findings demonstrate that AIH increases diaphragm corticospinal excitability after chronic SCI, and that the addition of mild hypercapnia may further enhances plasticity. Thus, both AIH and AIHH represent feasible, noninvasive strategies to enhance respiratory motor plasticity and potentially improve breathing function after SCI.
Bogard et al. (Thu,) studied this question.