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Articles in PresS, published online ahead of print March 1, 2002
J Appl Physiol, 10.1152/jap.00938.2001
Submitted on September 11, 2001
Accepted on February 25, 2002
1 Department of Medicine, John D. Dingell Veterans Affairs Medical Center, Detroit, MI, USA
2 Division of Pulmonary/Critical Care and Sleep Medicine, Department of Medicine, Wayne State University School of Medicine, Detroit, MI, USA
* To whom correspondence should be addressed. E-mail: sbadr{at}intmed.wayne.edu.
Long-term facilitation (LTF) is a prolonged increase in ventilatory motor output following peripheral chemoreceptor stimulation. We have previously shown that LTF is activated during sleep following repetitive hypoxia in snorers. We hypothesized that ventilatory LTF is due to decreased upper airway resistance. We studied 11 normal subjects during stable NREM sleep. We induced brief isocapnic hypoxia (FIO2=8%) (3min.) 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 (R-20) for ventilation, timing and upper airway resistance (RUA). To ensure that changes in the recovery period were not due to time dependent effects, 9 subjects were studied in a sham study with no hypoxic exposure. Measurements were obtained at control and after 100 minutes, corresponding with R-20. During the episodic hypoxia study, VI increased from 7.1±1.8 L/min during the control period to 8.3±1.8 L/min at R-20, 119% of control) (P<0.05). Conversely, there was no change in EMGdia. between control (16.1±6.9 au) and R-20 (15.3±4.9 au) (95% of control; P>0.05). In contrast, increased VI was associated with decreased RUA from 10.7±7.5 cmH2O/L/sec during control to 8.2±4.4 cmH2O/L/sec at R-20 (77% of control) (P<0.05). The findings of the sham study differed from the episodic hypoxia study with no change in VI, RUA or EMGdia. during the recovery period relative to control. Conclusions: 1) Repetitive hypoxia in sleeping humans is followed by increased VI in the recovery period indicative of development of LTF. 2) The lack of increased EMGdia. suggests lack of LTF to the diaphragm. 3) Reduced RUA suggests LTF of upper airway dilators. 4) We propose that increased VI in the recovery period is due to "unloading" of the upper airway by LTF of upper airway dilators.
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