The effects of exposure to moderate altitude on cardiovascular autonomic function in normal subjects

Cardiovascular responses to altitude have been studied on well-trained youn g subjects, generally at high altitudes (>4000 m). Less known are the effec ts of exposure to lower altitudes, easily reached by the general population . The aim of the study was to evaluate the effects of exposure to a moderat e altitude (2950 m) on heart rate (HR), blood pressure (BP) profile, and ca rdiovascular autonomic function, and their correlation with hemoglobin oxyg en saturation (HbO2S), in untrained subjects of a aide age range. Twenty-se ven healthy normotensive subjects (age range 6-83; 8 children, 9 adults, an d 10 elderly subjects) underwent a battery of noninvasive cardiovascular re fer tests and 24-h ambulatory BP monitoring. Corrected QT interval was also calculated. HbO(2)S was measured with a transcutaneous oxy-meter. All meas urements were performed at about 200 m (s.l.) and repeated at 2950 m. 24-h HR and systolic/diastolic BP mean values increased at 2950 m in children (% change respectively: 6.4 +/- 6.4, p<0.05; 6.5 +/- 4.0/13.5 +/- 6.9, p < 0. 05), adults (4.9 +/- 8.1, NS; 6.0 +/- 5.1/8.1 +/- 5.8, p < 0.05), and elder ly subjects (7.2 +/- 4.8, p < 0.05; 5.1 +/- 2.3/2.8 +/- 4.1, p < 0.05 for s ystolic BP only). Standard deviation of BP mean values increased during nig ht-time in the adult group (p < 0.05). All subjects scored normal cardiovas cular test results and no differences were observed after exposure to 2950m , at both 1 hour and 24 hours from arrival, After exposure to altitude, HbO (2)S decreased significantly in the three groups, both on arrival and after 24 hours. No correlation was found between changes in HbO(2)S and BP/HR re sponses, and cardiovascular test results. In conclusion, exposure to modera te altitudes, easily and often reached by the general population, causes a small but significant increase in BP and HR in healthy untrained subjects o f a wide age range (6-83 years). Some physiological factors (eg, lower envi ronmental temperature and lifestyle modification) together with hypoxia, po ssibly more than altered cardiovascular reactivity, seem responsible for th is cardiovascular change. In terms of end-organ damage, the clinical releva nce of this increase in BP and BP variability for repeated exposure is not known.