Elevated sympathoadrenal response following active ascent to 3,600m is not associated with acute mountain sickness

Abstract

Previous reports have suggested an increase in plasma epinephrine (EPI) and either an increase, no change or decrease in norepinephrine (NE) following acute (< 4 h) exposure to high altitude (HA). In addition, previous research has demonstrated an exercise-induced increase in EPI and NE during exercise initiated following arrival at HA. Last, some but not others have reported an association between increased sympathoadrenal activity and acute mountain sickness (AMS). We hypothesized that elevated sympathoadrenal activity induced from active ascent on foot to 3,600m may contribute to the development of AMS. Thirty-seven Soldiers (mean ± SD; 6 women; age=25.5±4.9 years) were tested at their baseline residence (BLR; Fort Bliss, TX, 1,190m), transported to Taos, NM (2,845m), then hiked (n=18) or were driven (n=19) to the HA data collection site where they resided for four days (68hrs). AMS Cerebral Factor Score (AMS-C) was determined using the Environmental Symptoms Questionnaire (ESQ-III) recorded twice at HA on day 1 (HA1), five times on days 2 (HA2) and 3 (HA3) and once on day 4 (HA4). If AMS-C was ≥0.7 on any measurement occasion, individuals were categorized as AMS-susceptible (AMS+, n=11) others were AMS-resistant (AMS─, n=26). Plasma EPI (pg/ml) and NE (pg/ml) were measured from venous blood draws at 06:00 at BLR, a non-fasted blood draw at 18:00 following ascent on HA1, and subsequent fasted blood samples at 06:00 on each morning at HA (HA2, HA3, HA4). AMS-susceptibility was not associated with the EPI or NE response in any condition so both cohorts were combined. The EPI response to active vs. passive ascent was similar with an increase (p<0.05) from BLR (28.0±26.8) to HA1 (47.5±40.3) followed by a subsequent decrease (p<0.05) from HA1 to HA2 (28.0±18.6) through HA4 (25.4±16.9). NE, however, increased (p<0.05) only in the active ascent group from BLR (413±216) to HA1 (729±281) and remained stable from HA1 through HA4 (644±192). The passive ascent group demonstrated no change in NE from BLR (327±126) to HA1 (413±181) through HA4 (466±144). NE levels were similar (p>0.05) in the active vs passive ascent group at BLR but higher (p<0.05) in the active ascenders on HA1 through HA4. In conclusion, contrary to our hypothesis, the sympathoadrenal response to HA was not impacted by AMS susceptibility but active ascent induced a greater NE response following ascent and throughout the duration of the HA stay. USAMRDC. Authors’ views not offcial U.S. Army or DoD policy. This is the full abstract presented at the American Physiology Summit 2024 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.