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J Appl Physiol (April 25, 2003). doi:10.1152/japplphysiol.00749.2002
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Submitted on August 13, 2002
Accepted on April 18, 2003

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

Andrew P Blaber1*, Tim Hartley1, and Peter J Pretorius1

1 School of Kinesiology, Aerospace Physiology Laboratory, Simon Fraser University, Burnaby, British Columbia, Canada

* To whom correspondence should be addressed. E-mail: ablaber{at}sfu.ca.

Orthostatic reflexes were examined at 375 m and, after 60 minutes of exposure in a hypobaric chamber at 3,660 m using a 20-minute seventy-degree head-up tilt (HUT) test. Mean arterial blood pressure, RR-interval (RRI), and mean cerebral blood flow velocity (MFV) were examined with coarse-graining spectral analysis. Of 14 subjects, seven at 375 m and 12 at 3,660 m were presyncopal. Immediately upon arrival to high altitude, breathing frequency and MFV increased and end-tidal PCO2 (PETCO2), RRI, RRI complexity and the parasympathetic nervous system (PNS) indicator decreased. MFV was similar in HUT at both altitudes. The sympathetic nervous system (SNS) indicator increased with tilt at 3,660 m while PNS indicator decreased with tilt at both altitudes. Multiple regression analysis of supine variables from either 375 m or 3,660 m and the time to presyncope at 3,660 m indicated that, after one hour of exposure, increased presyncope at altitude was the result of: 1) ineffective peripheral vasoconstriction, despite increased cardiac SNS activity with HUT; and, 2) insufficient cerebral perfusion due to cerebral vasoconstriction as the result of hypoxic hyperventilation-induced hypocapnia.




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J Appl Physiol, March 1, 2005; 98(3): 1050 - 1056.
[Abstract] [Full Text] [PDF]




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