Effect of acute exposure to 3,660 m altitude on orthostatic responses and tolerance

• Published in: Journal of applied physiology (1985) Vol. 95; no. 2; pp. 591 - 601
• Main Authors: Blaber, A. P, Hartley, T, Pretorius, P. J
• Format: Journal Article
• Language: English
• Published: Bethesda, MD Am Physiological Soc 01.08.2003; American Physiological Society
• Subjects: Altitude; Applied physiology; Biological and medical sciences; Circulatory system; Human physiology applied to population studies and life conditions. Human ecophysiology; Medical sciences; Nervous system; Reflexes; Respiratory system; Transports. Aerospace. Diving. Altitude; Human; Heart rate; High altitude; Baroreflex; Hypocapnia; Variability; Environmental factor; Orthostatic tolerance
• ISSN: 8750-7587; 1522-1601
• DOI: 10.1152/japplphysiol.00749.2002

Aerospace Physiology Laboratory, School of Kinesiology, Simon Fraser University, Burnaby, British Columbia, Canada V5A 1S6 Submitted 13 August 2002 ; accepted in final form 18 April 2003 Orthostatic reflexes were examined at 375 m and after 60 min of exposure in a hypobaric chamber at 3,660 m using a 20-min 70° head-up tilt (HUT) test. Mean arterial blood pressure, R wave-R wave interval (RRI), and mean cerebral blood flow velocity (MFV) were examined with coarse-graining spectral analysis. Of 14 subjects, 7 at 375 m and 12 at 3,660 m were presyncopal. Immediately on arrival to high altitude, breathing frequency and MFV increased, and endtidal P CO2 , RRI, RRI complexity, and the parasympathetic nervous system indicator decreased. MFV was similar in HUT at both altitudes. The sympathetic nervous system indicator increased with tilt at 3,660 m, whereas parasympathetic nervous system indicator decreased with tilt at both altitudes. Multiple regression analysis of supine variables from either 375 or 3,660 m and the time to presyncope at 3,660 m indicated that, after 1 h of exposure, increased presyncope at altitude was the result of 1 ) ineffective peripheral vasoconstriction, despite increased cardiac sympathetic nervous system activity with HUT, and 2 ) insufficient cerebral perfusion owing to cerebral vasoconstriction as the result of hypoxic hyperventilation-induced hypocapnia. head-up tilt; heart rate variability; transcranial Doppler; spontaneous baroreflex sensitivity; cerebrovascular reactivity Address for reprint requests and other correspondence: A. P. Blaber, Aerospace Physiology Laboratory, School of Kinesiology, Simon Fraser Univ., 8888 Univ. Drive, Burnaby, BC V5A 1S6, Canada (E-mail: ablaber{at}sfu.ca ).