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Articles in PresS, published online ahead of print September 6, 2002
J Appl Physiol, 10.1152/jap.00476.2002
Submitted on May 31, 2002
Accepted on September 3, 2002
1 Division of Pulmonary/Critical Care and Sleep Medicine, Department of Medicine, Wayne State University School of Medicine, Detroit, MI, USA; Sleep Research Laboratory, Medical Service, John D. Dingell Veterans Affairs Medical Center, 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 episodic peripheral chemoreceptor stimulation. We have previously shown that LTF is activated during sleep following repetitive hypoxia in snorers. The purpose of this study was: 1) to ascertain the relative contribution of inspiratory flow limitation to the development of LTF and 2) to determine the effect of eliminating inspiratory flow limitation by nasal CPAP on LTF. We studied 25 normal subjects during stable NREM sleep. We induced ten episodes of brief repetitive isocapnic hypoxia (FIO2=8%) (3min.) followed by 5 min. of room air. Measurements were obtained during control, and after 20 min. of recovery (R-20). During the episodic hypoxia study, VI increased from 6.7±1.9 L/min during the control period to 8.2±2.7 L/min at R-20, 122% of control) (P<0.05). Linear regression analysis confirmed that inspiratory flow limitation during control was the only independent determinant of the presence of LTF (P=0.005). Eleven subjects underwent a sham study with no hypoxia; VI at R-20 was unchanged compared to room air control. Six subjects were re-studied using nCPAP to ascertain the effect of eliminating inspiratory flow limitation on LTF. VI during the recovery period was 97±10% (P>0.05). Conclusions: 1) Repetitive hypoxia in sleeping humans is followed by increased VI in the recovery period indicative of development of LTF. 2) Inspiratory flow limitation is the only independent determinant of post-hypoxic LTF in sleeping human. 3) Elimination of inspiratory flow limitation abolished the ventilatory manifestations of LTF. 4) We propose that increased VI in the recovery period was due to preferential recruitment of upper airway dilators by repetitive hypoxia.
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