Immune system remains affected by acute high-altitude exposure one month following return to sea level

High altitude presents a difficult environment for the body to adapt to, with reduced atmospheric pressure, reduced oxygen tension, reduced temperature, and increased ultraviolet radiation. Previous studies have demonstrated that the immune system exhibits an inflammatory shift during high-altitude acclimatization, even in the absence of active infection. What specific factors present at altitude are responsible for the shift observed or the duration of these effects after return to sea-level are not well understood. We investigated these questions using acetazolamide in a randomized, double-blind, placebo controlled clinical trial, incorporating two post-return visits. Participants (N=18) were taken to Barcroft Station in the White Mountain Research Center (3800m elev.) and had fasting blood draws taken at sea level on the day of ascent (SL), each morning for 3 days at high-altitude (HA1, HA2, HA3), and both seven days and thirty days after returning to sea-level (SL7 & SL30). Cells were stained for flow cytometry on site. Neutrophils were found to be decreased over the course of acclimatization when compared to baseline (HA2 p = 0.170, HA3 p < 0.0001) and did not completely recover upon return to sea-level (SL7 p = 0.151, SL30 p = 0.0075). Conversely, B cells increased on all days of acclimatization compared to baseline (p = 0.0234; p = 0.0209; and p = 0.0009, respectively) and remained elevated upon return (SL7 p = 0.0338, SL30 p = 0.0045). Our results demonstrate a lasting impact on the immune system that persists for at least a month following return to sea level. This abstract was presented at the American Physiology Summit 2026 and is only available in HTML format. There is no downloadable file or PDF version. The Physiology editorial board was not involved in the peer review process.