Literature DB >> 20378702

A secondary reflex suppression phase is present in genioglossus but not tensor palatini in response to negative upper airway pressure.

Danny J Eckert1, Julian P Saboisky, Amy S Jordan, David P White, Atul Malhotra.   

Abstract

On the basis of recent reports, the genioglossus (GG) negative-pressure reflex consists initially of excitation followed by a secondary state-dependent suppression phase. The mechanistic origin and functional role of GG suppression is unknown but has been hypothesized to arise from transient inhibition of respiratory active neurons as a protective reflex to prevent aspiration, as observed in other respiratory muscles (e.g., diaphragm) during airway occlusion. Unlike GG, tensor palatini (TP) is a tonic muscle with minimal respiratory phasic activation during relaxed breathing, although both muscles are important in preserving pharyngeal patency. This study aimed to compare GG vs. TP reflex responses to the same negative-pressure stimulus. We hypothesized that reflex suppression would be present in GG, but not TP. Intramuscular GG and TP EMGs were recorded in 12 awake, healthy subjects (6 female). Reflex responses were generated via 250-ms pulses of negative upper airway pressure (approximately -16 cmH2O mask pressure) delivered in early inspiration. GG and TP demonstrated reflex activation in response to negative pressure (peak latency 31+/-4 vs. 31+/-6 ms and peak amplitude 318+/-55 vs. 314+/-26% baseline, respectively). A secondary suppression phase was present in 8 of 12 subjects for GG (nadir latency 54+/-7 ms, nadir amplitude 64+/-6% baseline), but not in any subject for TP. These data provide further support for the presence of excitatory and inhibitory components of GG (phasic muscle) in response to brief upper airway negative-pressure pulses. Conversely, no reflex suppression below baseline was present in TP (tonic muscle) in response to the same stimuli. These differential responses support the hypothesis that GG reflex suppression may be mediated via inhibition of respiratory-related premotor input.

Mesh:

Year:  2010        PMID: 20378702      PMCID: PMC2886693          DOI: 10.1152/japplphysiol.01437.2009

Source DB:  PubMed          Journal:  J Appl Physiol (1985)        ISSN: 0161-7567


  43 in total

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