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Acute mountain sickness, chemosensitivity, and cardiorespiratory responses in humans exposed to hypobaric and normobaric hypoxia

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We examined the control of breathing, cardiorespiratory effects, and the incidence of acute mountain sickness (AMS) in humans exposed to hypobaric hypoxia (HH) and normobaric hypoxia (NH), and under two control conditions [hypobaric normoxia (HN) and normobaric normoxia (NN)]. Exposures were 6 h in duration, and separated by 2 wk between hypoxic exposures and 1 wk between normoxic exposures. Before and after exposures, subjects ( n = 11) underwent hyperoxic and hypoxic Duffin CO2rebreathing tests and a hypoxic ventilatory response test (HVR). Inside the environmental chamber, minute ventilation (V̇e), tidal volume (Vt), frequency of breathing ( fB), blood oxygenation, heart rate, and blood pressure were measured at 5 and 30 min and hourly until exit. Symptoms of AMS were evaluated using the Lake Louise score (LLS). Both the hyperoxic and hypoxic CO2thresholds were lower after HH and NH, whereas CO2sensitivity was increased after HH and NH in the hypoxic test and after NH in the hyperoxic test. Values for HVR were similar across the four exposures. No major differences were observed for V̇e or any other cardiorespiratory variables between NH and HH. The LLS was greater in AMS-susceptible than in AMS-resistant subjects; however, LLS was alike between HH and NH. In AMS-susceptible subjects, fBcorrelated positively and Vt negatively with the LLS. We conclude that 6 h of hypoxic exposure is sufficient to lower the peripheral and central CO2threshold but does not induce differences in cardiorespiratory variables or AMS incidence between HH and NH.
Title: Acute mountain sickness, chemosensitivity, and cardiorespiratory responses in humans exposed to hypobaric and normobaric hypoxia
Description:
We examined the control of breathing, cardiorespiratory effects, and the incidence of acute mountain sickness (AMS) in humans exposed to hypobaric hypoxia (HH) and normobaric hypoxia (NH), and under two control conditions [hypobaric normoxia (HN) and normobaric normoxia (NN)].
Exposures were 6 h in duration, and separated by 2 wk between hypoxic exposures and 1 wk between normoxic exposures.
Before and after exposures, subjects ( n = 11) underwent hyperoxic and hypoxic Duffin CO2rebreathing tests and a hypoxic ventilatory response test (HVR).
Inside the environmental chamber, minute ventilation (V̇e), tidal volume (Vt), frequency of breathing ( fB), blood oxygenation, heart rate, and blood pressure were measured at 5 and 30 min and hourly until exit.
Symptoms of AMS were evaluated using the Lake Louise score (LLS).
Both the hyperoxic and hypoxic CO2thresholds were lower after HH and NH, whereas CO2sensitivity was increased after HH and NH in the hypoxic test and after NH in the hyperoxic test.
Values for HVR were similar across the four exposures.
No major differences were observed for V̇e or any other cardiorespiratory variables between NH and HH.
The LLS was greater in AMS-susceptible than in AMS-resistant subjects; however, LLS was alike between HH and NH.
In AMS-susceptible subjects, fBcorrelated positively and Vt negatively with the LLS.
We conclude that 6 h of hypoxic exposure is sufficient to lower the peripheral and central CO2threshold but does not induce differences in cardiorespiratory variables or AMS incidence between HH and NH.

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