Exposure to high altitude has been shown to enhance both glucose and lipid utilization depending on experimental protocol. In addition, high and low blood glucose levels have been reported at high altitude. We hypothesized that gradual ascent to high altitude results in changes in glucose levels in healthy young adults.

Twenty-five adult volunteers, split into two teams, took part in the British Services Dhaulagiri Medical Research Expedition completing 14 d of trekking around the Dhaulagiri circuit in Nepal reaching a peak altitude of 5300 m on day 11 of the trek. Participants wore blinded continuous glucose monitors (CGM) throughout. Blood samples for C-peptide, proinsulin, and triacylglycerides were taken at sea level (United Kingdom) and in acclimatization camps at 3600, 4650, and 5120 m. Energy intake was determined from food diaries.

There was no difference in time spent in hypoglycemia stratified by altitude. Nocturnal CGM readings (2200–0600 h) were chosen to reduce the short-term effect of physical activity and food intake and showed a significant (P < 0.0001) increase at 3600 m (5.53 ± 0.22 mmol·L−1), 4650 m (4.77 ± 0.30 mmol·L−1), and 5120 m (4.78 ± 0.24 mmol·L−1) compared with baseline altitude 1100 m (vs 4.61 ± 0.25 mmol·L−1). Energy intake did not differ by altitude. Insulin resistance and beta-cell function, calculated by homeostatic model assessment, were reduced at 3600 m compared with sea level.

We observed a significant increase in nocturnal CGM glucose at 3600 m and greater despite gradual ascent from 1100 m. Taken with the changes in insulin resistance and beta-cell function, it is possible that the stress response to high altitude dominates exercise-enhanced insulin sensitivity, resulting in relative hyperglycemia.