Imparied insulin sensitivity in the early hours following either active or passive ascent to 3600m is associated with acute mountain sickness susceptibility
Authors: Reitnauer Kyle , Beidleman Beth , Landspurg Steven , Buller Mark , Femling Jon , Williams Jason , Mayschak Trevor 
Published: May 2024

Reduced insulin sensitivity (a higher glucose level for the same insulin concentration) at baseline residence (BLR) has been associated with increased susceptibility to acute mountain sickness. (AMS) at high altitude (HA). The objective of this study was to determine whether fasting blood glucose (GLU), lactate (LAC) and insulin (INS) were impacted during an active versus passive ascent to 3600m in AMS-susceptible and AMS-resistant individuals. We hypothesized that insulin sensitivity would be reduced at BLR in the AMS-susceptible cohort based on previous research. To test this hypothesis, 78 active-duty Soldiers were tested at baseline residence (BLR), transported to Taos, New Mexico (2,845m), then hiked (n=39) or were driven (n=39) to 3600m, and stayed for four days. AMS-C was assessed using the Environmental Symptoms Questionnaire (ESQ) at HA twice on day 1, five times on days 2 and 3 and once on day 4. If AMS-C was ≥0.7 at any timepoint, individuals were categorized as AMS-susceptible (AMS+, n=33); others categorized as resistant (AMS−, n=45). Fasting rested blood GLU and LAC responses collected at 06:00 were measured using a blood gas analyzer and serum INS responses were measured using an ELISA assay at BLR, HA2 (14-h post-ascent), HA3 (38-h post ascent), and HA4 (62-h post ascent). An additional sample for blood GLU and LAC was collected on HA1 at 18:00 (2-h post ascent). As expected, the active compared to passive ascent group demonstrated an increase (p<0.05) in GLU (113.6±14.3 vs. 101.9±15.1) and LAC (2.56±0.93 vs. 1.73±0.78) on HA1 most likely due to sympathetic stimulation following active ascent. However, differences in fasting GLU and LAC between ascent groups did not persist on HA2 through HA4. There were also no ascent group differences INS in any of the conditions. Fasting GLU levels on HA2 were higher in the AMS+ vs. AMS− cohorts (99.8±9.8 vs 95.3±7.9 mg/dl; p<0.05) but fasting INS levels on HA2 did not differ between cohorts (9.8±5.4 vs.7.1±3.4 mIU/ml; p>0.05) indicating impaired insulin sensitivity in those susceptible to AMS early in the HA exposure. There were no differences, however, in GLU and INS levels between AMS+ vs. AMS− cohorts on BLR, HA3 or HA4. Fasting LAC also demonstrated no differences in any of the conditions in the active vs. passive ascent groups or AMS+ vs. AMS− cohorts. In conclusion, the increase in blood GLU and LAC at HA1 following active compared to passive ascent was expected. Contrary to our hypothesis, however, a reduction in insulin sensitivity was not found in AMS-susceptible individuals at BLR but was found at 14-h post ascent to 3600m and quickly resolved thereafter. The inability to effectively utilize glucose as an O2-effcient fuel in the early hours of HA exposure may contribute to AMS symptoms. 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.