4.5 Article

Sensorimotor function of the upper-airway muscles and respiratory sensory processing in untreated obstructive sleep apnea

期刊

JOURNAL OF APPLIED PHYSIOLOGY
卷 111, 期 6, 页码 1644-1653

出版社

AMER PHYSIOLOGICAL SOC
DOI: 10.1152/japplphysiol.00653.2011

关键词

sleep-disordered breathing; genioglossus; tensor palatini; respiratory-related evoked potential; lung

资金

  1. National Institutes of Health [HL-73146, R01-HL-085188-01A2, R01-HL-090897-01A2, K24-HL-093218-01A1, 1P01-HL-095491-01A1]
  2. National Health and Medical Research Council of Australia Biomedical [510392]
  3. American Heart Association [10SDG3510018]
  4. [UL1-RR-025758-01]

向作者/读者索取更多资源

Eckert DJ, Lo YL, Saboisky JP, Jordan AS, White DP, Malhotra A. Sensorimotor function of the upper-airway muscles and respiratory sensory processing in untreated obstructive sleep apnea. J Appl Physiol 111: 1644-1653, 2011. First published September 1, 2011; doi:10.1152/japplphysiol.00653.2011.-Numerous studies have demonstrated upper-airway neuromuscular abnormalities during wakefulness in snorers and obstructive sleep apnea (OSA) patients. However, the functional role of sensorimotor impairment in OSA pathogenesis/disease progression and its potential effects on protective upperairway reflexes, measures of respiratory sensory processing, and force characteristics remain unclear. This study aimed to gain physiological insight into the potential role of sensorimotor impairment in OSA pathogenesis/disease progression by comparing sensory processing properties (respiratory-related evoked potentials; RREP), functionally important protective reflexes (genioglossus and tensor palatini) across a range of negative pressures (brief pulses and entrained iron lung ventilation), and tongue force and time to task failure characteristics between 12 untreated OSA patients and 13 controls. We hypothesized that abnormalities in these measures would be present in OSA patients. Upper-airway reflexes (e. g., genioglossus onset latency, 20 +/- 1 vs. 19 +/- 2 ms, P = 0.82), early RREP components (e. g., P1 latency 25 +/- 2 vs. 25 +/- 1 ms, P = 0.78), and the slope of epiglottic pressure vs. genioglossus activity during iron lung ventilation (-0.68 +/- 1.0 vs. -0.80 +/- 2.0 cmH(2)O/%max, P = 0.59) were not different between patients and controls. Maximal tongue protrusion force was greater in OSA patients vs. controls (35 +/- 2 vs. 27 +/- 2 N, P < 0.01), but task failure occurred more rapidly (149 +/- 24 vs. 254 +/- 23 s, P < 0.01). Upper-airway protective reflexes across a range of negative pressures as measured by electromyography and the early P1 component of the RREP are preserved in OSA patients during wakefulness. Consistent with an adaptive training effect, tongue protrusion force is increased, not decreased, in untreated OSA patients. However, OSA patients may be vulnerable to fatigue of upper-airway dilator muscles, which could contribute to disease progression.

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