title: Cardiovascular regulation response to hypoxia during stepwise decreases from 21% to 15% inhaled oxygen.
abstract: BACKGROUND
  The classical view states that hypoxia beyond an oxygen concentration of about 17% induces tachycardia. However, few studies have investigated the dose-dependent effects of acute normobaric hypoxia on autonomic nervous regulation of the cardiovascular system. Therefore, we evaluated the effects of stepwise hypoxia on cardiovascular neural regulation and postulated that acute normobaric hypoxia causes vagal withdrawal and sympathetic activation from 17% 02.
  
  
  METHODS
  There were 18 healthy men who were exposed to acute stepwise normobaric hypoxia (21%, 19%, 17%, 15% 02). Spectral analysis of the RR interval and BP variability were used.
  
  
  RESULTS
  BP was not altered. Heart rate significantly increased at 15% (21%, 59 +/- 2; 15%, 62 +/- 2 bpm). The low-frequency power of systolic BP variability (an index of vasomotor sympathetic nerve activity) significantly increased at 15% (21%, 6.1 +/- 1.3; 15%, 9.9 +/- 1.3 mmHg2). The low-frequency power of the RR interval variability significantly increased from 17% (21%, 1036 +/- 233; 17%, 1892 +/- 409; 15%, 1966 +/- 362 ms2), However, the high-frequency power of RR interval variability (an index of cardiac parasympathetic nerve activity) did not change. Associated with these changes, the ratio of low- to high-frequency power of RR interval variability as an index of relative cardiac autonomic balance significantly shifted toward sympathetic dominance (21%, 1.5 +/- 0.3; 15%, 2.2 +/- 0.3). All indices of cardiac baroreflex function (transfer function and sequence gains) were unchanged.
  
  
  CONCLUSIONS
  These results suggest that acute exposure to normobaric mild hypoxia (O2 > or = 15%) induces increases in sympathetic vasomotor activity and cardiac sympathetic dominance resulting in an increased heart rate. However, 15% O2 hypoxia might not induce changes in static BP, vagal activity, or spontaneous arterial-cardiac baroreflex function.
authors.affiliation: Department of Hygiene and Space Medicine, Nihon University School of Medicine, Tokyo, Japan. kiwasaki@med.nihon-u.ac.jp
authors.forename: Ken-ichi
authors.initials: K
authors.lastname: Iwasaki
authors.forename: Yojiro
authors.initials: Y
authors.lastname: Ogawa
authors.forename: Ken
authors.initials: K
authors.lastname: Aoki
authors.forename: Takashi
authors.initials: T
authors.lastname: Saitoh
authors.forename: Akira
authors.initials: A
authors.lastname: Otsubo
authors.forename: Shigeki
authors.initials: S
authors.lastname: Shibata
mesh_terms: D001794:Blood Pressure; D002319:Cardiovascular System / Q000503:physiopathology*; D006801:Humans; D000860:Hypoxia / Q000503:physiopathology*; D008297:Male; D010102:Oxygen Inhalation Therapy