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Medical Service, John D. Dingell Veterans Affairs Medical Center, and Division of Pulmonary/Critical Care and Sleep Medicine, Department of Medicine, Wayne State University School of Medicine, Detroit, Michigan 48201
We hypothesized that long-term
facilitation (LTF) is due to decreased upper airway resistance (Rua).
We studied 11 normal subjects during stable non-rapid eye movement
sleep. We induced brief isocapnic hypoxia (inspired O2
fraction = 8%) (3 min) followed by 5 min of room air. This
sequence was repeated 10 times. Measurements were obtained during
control, hypoxia, and at 20 min of recovery (R20) for
ventilation, timing, and Rua. In addition, nine subjects were studied
in a sham study with no hypoxic exposure. During the episodic hypoxia
study, inspiratory minute ventilation (
I) increased
from 7.1 ± 1.8 l/min during the control period to 8.3 ± 1.8 l/min at R20 (117% of control; P < 0.05). Conversely, there was no change in diaphragmatic
electromyogram (EMGdia) between control (16.1 ± 6.9 arbitrary units) and R20 (15.3 ± 4.9 arbitrary units)
(95% of control; P > 0.05). In contrast, increased
I was associated with decreased Rua from 10.7 ± 7.5 cmH2O · l
1 · s during
control to 8.2 ± 4.4 cmH2O · l
1 · s at
R20 (77% of control; P < 0.05). No change
was noted in
I, Rua, or EMGdia during
the recovery period relative to control during the sham study. We
conclude the following: 1) increased
I in
the recovery period is indicative of LTF, 2) the lack of increased EMGdia suggests lack of LTF to the diaphragm,
3) reduced Rua suggests LTF of upper airway dilators, and
4) increased
I in the recovery period is
due to "unloading" of the upper airway by LTF of upper airway dilators.
peripheral chemoreceptors; unloading; upper airway; non-rapid eye movement sleep
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