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1 Department of Physical Therapy, University of Florida, Gainesville, Florida, USA
* To whom correspondence should be addressed. E-mail: dfuller{at}phhp.ufl.edu.
Hypoxic episodes can evoke a prolonged augmentation of inspiratory motor output called long-term facilitation (LTF). Hypoglossal (XII) LTF has been assumed to represent
increased tongue protrudor muscle activation and pharyngeal airway dilation. However, recent studies indicate that tongue protrudor and retractor muscles are co-activated during inspiration, a behavior that promotes upper airway patency by reducing airway compliance. These experiments tested the hypothesis that XII LTF is manifest as increased inspiratory drive to both tongue protrudor and retractor muscles. Neurograms were recorded in the medial XII nerve branch (XIIMED, contains tongue protrudor motor axons), the lateral XII nerve branch (XIILAT, contains tongue retractor motor axons), and the phrenic nerve in anesthetized, vagotomized, paralyzed, ventilated male rats. Strict isocapnia was maintained for 60 min following 5, 3-min hypoxic episodes (PaO2 = 35 ± 2 mmHg) or sham treatment. Peak inspiratory burst amplitude showed a persistent increase in XIIMED, XIILAT, and phrenic nerves during the hour following episodic hypoxia (p<0.05 vs. sham). This effect was present regardless of the quantification method (e.g.
% baseline vs. % maximum), however, comparisons of the relative magnitude of LTF between neurograms (e.g. XIIMED vs. XIILAT) varied with the normalization procedure.
There was no persistent effect of episodic hypoxia on inspiratory burst frequency (p>0.05 vs. sham). These data demonstrate that episodic hypoxia induces LTF of inspiratory drive to both tongue protrudor and retractor muscles and underscore the potential contribution
of tongue muscle co-activation to regulation of upper airway patency.
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