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1 Internal Medicine, Wayne State University, Detroit, MI, USA; Research and Development, John D. Dingell Veterans Administration Medical Center, Detroit, MI, USA; Physiology, Wayne State University, Detroit, MI, USA
2 Internal Medicine, Wayne State University, Detroit, MI, USA
3 Internal Medicine, Wayne State University, Detroit, MI, USA; Research and Development, John D. Dingell Veterans Administration Medical Center, Detroit, MI, USA; Biomedical Engineering, Wayne State University, Detroit, MI, USA
* To whom correspondence should be addressed. E-mail: jmateika{at}med.wayne.edu.
Exposure to acute episodic hypoxia (e.g. 30 minutes) in animals leads to increases in ventilation that persist when normoxia is restored. This phenomenon, known as long-term facilitation, has not been observed in awake humans. The purpose of the present study was to determine whether the acute ventilatory response to hypoxia is enhanced after exposure to episodic hypoxia in awake humans despite the lack of expression of long-term facilitation. Eleven healthy subjects completed a series of rebreathing trials before and after exposure to eight 4 - minute episodes of hypoxia (8 %) separated by 5 minutes of breathing atmospheric air. During the rebreathing trials subjects initially hyperventilated to reduce the partial pressure of carbon dioxide (PETCO2)below 25 mmHg. Subjects were then switched into a rebreathing bag containing a normocapnic (42 mmHg) low oxygen {partial pressure of end tidal oxygen(PETO2) = 50 mmHg} or high oxygen (PETO2 = 140 mmHg) gas mixture. During the trial PETCO2 increased while PETO2 was maintained at a constant level. The point at which ventilation began to rise in a linear fashion as PETCO2 increased was considered to be the ventilatory recruitment threshold. The slope of the ventilatory response above the recruitment threshold (i.e. chemoreflex responsiveness) was determined. Two trials for a given oxygen level were completed before and after exposure to episodic hypoxia. During episodic hypoxia ventilation did not increase during the normoxic periods that separated the hypoxic episodes. Additionally, ventilation did not persist above baseline values after exposure to episodic hypoxia; however PETCO2 levels were reduced compared to baseline. In contrast, compared to baseline, the ventilatory response to progressive increases in carbon dioxide during rebreathing trials in the presence of low but not high oxygen levels was increased after exposure to episodic hypoxia. This increase occurred when carbon dioxide levels were above but not below the ventilatory recruitment threshold. We conclude that long-term facilitation is not expressed in awake humans after exposure to acute episodic hypoxia in the presence of hypocapnia. Despite this lack of expression the acute ventilatory response to hypoxia in the presence of hypercapnia is increased after exposure to episodic hypoxia.
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