期刊
EXPERIMENTAL NEUROLOGY
卷 342, 期 -, 页码 -出版社
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.expneurol.2021.113735
关键词
Acute intermittent hypoxia; Respiratory function; Spinal cord injury; Rehabilitation; Respiratory plasticity; Human
资金
- Brooks-PHHP Research Collaboration
- University of Florida Breathing Research and Therapeutics Center
- McKnight Brain Institute
- NIH K12 Rehabilitation Research Career Development Program [NIH/NICHD K12 HD055929]
- Department of Defense CDMRP [W81XWH1810718]
- [1R01HL139708-01A1]
- U.S. Department of Defense (DOD) [W81XWH1810718] Funding Source: U.S. Department of Defense (DOD)
The study found that a single session of acute intermittent hypoxia (AIH) can increase maximal inspiratory pressure generation in adults with chronic spinal cord injury (SCI), but does not affect other breathing functions. Further investigation into the potential therapeutic effects is warranted.
After spinal cord injury (SCI) respiratory complications are a leading cause of morbidity and mortality. Acute intermittent hypoxia (AIH) triggers spinal respiratory motor plasticity in rodent models, and repetitive AIH may have the potential to restore breathing capacity in those with SCI. As an initial approach to provide proof of principle for such effects, we tested single-session AIH effects on breathing function in adults with chronic SCI. 17 adults (13 males; 34.1 +/- 14.5 years old; 13 motor complete SCI; >6 months post injury) completed two randomly ordered sessions, AIH versus sham. AIH consisted of 15, 1-min episodes (hypoxia: 10.3% O2; sham: 21% O2) interspersed with room air breathing (1.5 min, 21% oxygen); no attempt was made to regulate arterial CO2 levels. Blood oxygen saturation (SpO2), maximal inspiratory and expiratory pressures (MIP; MEP), forced vital capacity (FVC), and mouth occlusion pressure within 0.1 s (P0.1) were assessed. Outcomes were compared using nonparametric Wilcoxon's tests, or a 2 x 2 ANOVA. Baseline SpO2 was 97.2 +/- 1.3% and was unchanged during sham experiments. During hypoxic episodes, SpO2 decreased to 84.7 +/- 0.9%, and returned to baseline levels during normoxic intervals. Outcomes were unchanged from baseline post-sham. Greater increases in MIP were evident post AIH vs. sham (median values; +10.8 cmH2O vs. -2.6 cmH2O respectively, 95% confidence interval (-18.7) - (-4.3), p = .006) with a moderate Cohen's effect size (0.68). P0.1, MEP and FVC did not change postAIH. A single AIH session increased maximal inspiratory pressure generation, but not other breathing functions in adults with SCI. Reasons may include greater spared innervation to inspiratory versus expiratory muscles or differences in the capacity for AIH-induced plasticity in inspiratory motor neuron pools. Based on our findings, the therapeutic potential of AIH on breathing capacity in people with SCI warrants further investigation.
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