Endocrine Abstracts

Background: Work in a hot environment can cause elevated core body temperature (Tc), circulatory insufficiency and death from Exertional Heat Illness (EHI). Failure to undergo successful heat acclimatisation (HA) is seen in ~5% of otherwise healthy volunteers and may lead to significant EHI, but pathways to severe illness remain poorly understood. Copeptin, a glycopeptide co-secreted with the pituitary hormone arginine vasopressin, reflects osmotic and cardiovascular stress and could inform assessment of EHI susceptibility.

Case report: Changes in body mass, Tc, heart rate and plasma copeptin were investigated in UK military volunteers performing structured exercise, both during and after heat acclimatisation (HA). Volunteer B had served in several hot countries, but reported difficulty acclimatising and poor performance in high humidity. In a field trial during early HA in Kenya (n=15), Volunteer B demonstrated marked loss of body mass from sweating vs the rest of the group, in association with elevated copeptin (35.1 vs 15.3±8.4 pmol.l⁻¹) and failure to dissipate body heat.

In more controlled laboratory exposures during early HA in Cyprus (n=25), high loss of body mass in Volunteer B vs the group (4.3±0.5 vs 2.0±0.5%.h⁻¹) was accompanied by greater Tc (38.9 vs 38.2±0.3 °C) and heart rate (176 vs 154±19 b.min⁻¹) and exaggerated copeptin response (52.9 vs 15.6±20.9 pmol.L⁻¹). With repeated exposures, heart rate and copeptin fell by 22 and 49%, respectively, though relative exuberance of sweating rate and Tc response persisted.

Discussion: Fluid depletion from maladaptive thermal sweating explained failure of initial HA in Volunteer B. This was reflected by plasma copeptin concentration, which did not fall until greater cardiovascular stability had been established with more advanced HA. Copeptin may have applicability in defining EHI mechanisms and could contribute to risk stratification during and after HA.