title: Reduced autonomic activity during stepwise exposure to high altitude.
abstract: Several studies have shown increased sympathetic activity during acute exposure to hypobaric hypoxia. In a recent field study we found reduced plasma catecholamines during the first days after a stepwise ascent to high altitude. In the present study 14 subjects were exposed to a simulated ascent in a hypobaric chamber to test the hypothesis of a temporary reduction in autonomic activity. The altitude was increased stepwise to 4500 m over 3 days. Heart rate variability (HRV) was assessed continuously in seven subjects. Baroreceptor reflex sensitivity (BRS) was determined in eight subjects with the 'Transfer Function' method at baseline, at 4500 m and after returning to baseline. Resting plasma catecholamines and cardiovascular- and plasma catecholamine- responses to cold pressor- (CPT) and mental stress-test (MST) were assessed daily in all and 12 subjects, respectively. Data are mean +/- SEM. Compared with baseline at 4500 m there were lower total power (TP) (35 457 +/- 26 302 vs. 15 001 +/- 11 176 ms2), low frequency (LF) power (3112 +/- 809 vs. 1741 +/- 604 ms2), high frequency (HF) power (1466 +/- 520 vs. 459 +/- 189 ms2) and HF normalized units (46 +/- 0.007 vs. 44 +/- 0.006%), P < or = 0.001. Baroreceptor reflex sensitivity decreased (15.6 +/- 2.1 vs. 9.5 +/- 2.6 ms mmHg(-1), P = 0.015). Resting noradrenaline (NA) decreased (522 +/- 98 vs. 357 +/- 60 pmol L(-1), P = 0.027). The increase in systolic blood pressure (SBP) and NA during mental stress was less pronounced (21 +/- 4 vs. 10 +/- 2% and 25 +/- 9 vs. -2 +/- 8%, respectively, P < 0.05). The increase in SBP during cold pressor test decreased (16 +/- 3 vs. 1 +/- 6%, P = 0.03). Diastolic blood pressure, HR and adrenaline displayed similar tendencies. We conclude that a transient reduction in parasympathetic and sympathetic activity was demonstrated during stepwise exposure to high altitude.
authors.affiliation: Department of Cardiology, Ullevål University Hospital, Oslo, Norway.
authors.forename: K
authors.initials: K
authors.lastname: Sevre
authors.forename: B
authors.initials: B
authors.lastname: Bendz
authors.forename: E
authors.initials: E
authors.lastname: Hankø
authors.forename: A R
authors.initials: AR
authors.lastname: Nakstad
authors.forename: A
authors.initials: A
authors.lastname: Hauge
authors.forename: J I
authors.initials: JI
authors.lastname: Kåsin
authors.forename: J D
authors.initials: JD
authors.lastname: Lefrandt
authors.forename: A J
authors.initials: AJ
authors.lastname: Smit
authors.forename: I
authors.initials: I
authors.lastname: Eide
authors.forename: M
authors.initials: M
authors.lastname: Rostrup
mesh_terms: D000328:Adult; D000531:Altitude; D000532:Altitude Sickness / Q000503:physiopathology*; D001127:Arginine Vasopressin / Q000097:blood; D001273:Atmosphere Exposure Chambers; D001341:Autonomic Nervous System / Q000503:physiopathology*; D017704:Baroreflex / Q000502:physiology; D001794:Blood Pressure / Q000502:physiology; D002245:Carbon Dioxide / Q000097:blood; D003080:Cold Temperature; D004837:Epinephrine / Q000097:blood*; D005260:Female; D006339:Heart Rate / Q000502:physiology; D006801:Humans; D006863:Hydrogen-Ion Concentration; D000860:Hypoxia / Q000503:physiopathology; D008297:Male; D009638:Norepinephrine / Q000097:blood*; D010100:Oxygen / Q000097:blood; D012119:Respiration; D013312:Stress, Physiological / Q000503:physiopathology
chemical_list: D001127:Arginine Vasopressin; D002245:Carbon Dioxide; D010100:Oxygen; D009638:Norepinephrine; D004837:Epinephrine