A significant reduction in cold-induced vasodilation (CIVD) is observed at high altitudes. No agreement is found in the literature about acclimatization effects on CIVD. Two studies were performed to investigate the effect of altitude acclimatization on CIVD. In the first study 13 male subjects immersed the distal phalanx of the left middle finger in water of 0 degrees C for 30 min to evoke CIVD. Five subjects were exposed to altitudes of 5,100 to 7,000 m for 45 days (A). Eight subjects were exposed to an altitude of 5,100 m for <3 days (NA). The groups did not differ in age, weight, and stature. No significant differences were observed between A and NA. However, the maximum finger skin temperature of group A tended to return to sea level values (6.9 +/- 3.2 degrees C at sea level vs. 6.0 +/- 0.7 degrees C at altitude), while a strong reduction was observed for the NA group (7.7 +/- 4.3 degrees C vs. 3.7 +/- 3.1 degrees C). This indicates that the CIVD response at altitude tended to be stronger for the acclimatized subjects. In a second study, nine males were followed in a longitudinal study. CIVD was measured before, during and after 7 days of exposure to 4,350 m. Maximum finger skin temperature before and after exposure did not differ (8.5 +/- 2.6 degrees C vs. 7.8 +/- 1.6 degrees C), and was reduced at altitude. There was no difference in maximum finger skin temperature between the 7 days at altitude (e.g., 5.3 +/- 2.7 degrees C at day 2 and 4.7 +/- 1.1 degrees C at Day 7). It can be concluded that no acclimatization effects of CIVD occur during the first 7 days of altitude exposure, but that differences may occur after altitude exposure of several weeks.

This study examines the potential for a ventilatory drive, independent of mean PCO2, but depending instead on changes in PCO2 that occur during the respiratory cycle. This responsiveness is referred to here as "dynamic ventilatory sensitivity." The normal, spontaneous, respiratory oscillations in alveolar PCO2 have been modified with inspiratory pulses approximating alveolar PCO2 concentrations, both at sea level and at high altitude (5,000 m, 16,400 ft.). All tests were conducted with subjects exercising on a cycle ergometer at 60 W. The pulses last about half the inspiratory duration and are timed to arrive in the alveoli during early or late inspiration. Differences in ventilation, which then occur in the face of similar end-tidal PCO2 values, are taken to result from dynamic ventilatory sensitivity. Highly significant ventilatory responses (early pulse response greater than late) occurred in hypoxia and normoxia at sea level and after more than 4 days at 5,000 m. The response at high altitude was eliminated by normalizing PO2 and was reduced or eliminated with acetazolamide. No response was present soon after arrival (<4 days) at base camp, 5,000 m, on either of two high-altitude expeditions (BMEME, 1994, and Kanchenjunga, 1998). The largest responses at 5,000 m were obtained in subjects returning from very high altitude (7,100-8,848 m). The present study confirms and extends previous investigations that suggest that alveolar PCO2 oscillations provide a feedback signal for respiratory control, independent of changes in mean PCO2, suggesting that natural PCO2 oscillations drive breathing in exercise.