Ascent to high altitudes arouses the sympathetic nervous system in non-acclimatized healthy humans. Such activation is provoked by hypobaric hypoxia combined with other stressors. While this is an adaptive response, it also contributes to the general physical deterioration consequent to prolonged exposure to high altitudes, and is even implied in specific syndromes: acute mountain sickness, high altitude pulmonary edema (HAPE), and high altitude cerebral edema. Muscular sympathetic nervous activity increases at simulated high altitudes (hypoxic mixture or hypobaric chamber), and HAPE-susceptible subjects show an exaggerated response. Increases in plasma and urinary catecholamines take several days to appear: they are observed rarely at simulated altitudes but frequently on the field. Heart rate variability decreases at high altitudes, particularly in subjects suffering from acute mountain sickness. The low frequency component has been described in healthy subjects as increased or decreased, but is reduced in symptomatic subjects; increases in the low frequency/high frequency ratio are reported in all studies. Few and discordant data are available regarding baroreflex sensitivity at high altitudes. Some (past and present) authors regard parasympathetic fitness as a defense against illness at high altitudes. Current guidelines advise against high altitude exposure for cardiac patients in whom sympathetic arousal would be too risky.
|Translated title of the contribution||High altitude and autonomic nervous system|
|Number of pages||5|
|Journal||Italian Heart Journal Supplement|
|Publication status||Published - 2001|
ASJC Scopus subject areas
- Cardiology and Cardiovascular Medicine