Copeptin reflects physiological strain during thermal stress

To prevent heat-related illnesses, guidelines recommend limiting core body temperature (T (c)) ae<currency> 38 A degrees C during thermal stress. Copeptin, a surrogate for arginine vasopressin secretion, could provide useful information about fluid balance, thermal strain and health risks. It was hypothesised that plasma copeptin would rise with dehydration from occupational heat stress, concurrent with sympathoadrenal activation and reduced glomerular filtration, and that these changes would reflect T (c) responses. Volunteers (n = 15) were recruited from a British Army unit deployed to East Africa. During a simulated combat assault (3.5 h, final ambient temperature 27 A degrees C), T (c) was recorded by radiotelemetry to differentiate volunteers with maximum T (c) > 38 A degrees C versus ae<currency> 38 A degrees C. Blood was sampled beforehand and afterwards, for measurement of copeptin, cortisol, free normetanephrine, osmolality and creatinine. There was a significant (P < 0.05) rise in copeptin from pre- to post-assault (10.0 +/- 6.3 vs. 16.7 +/- 9.6 pmol L-1, P < 0.001). Although osmolality did not increase, copeptin correlated strongly with osmolality after the exposure (r = 0.70, P = 0.004). In volunteers with maximum T (c) > 38 A degrees C (n = 8) vs ae<currency> 38 A degrees C (n = 7) there were significantly greater elevations in copeptin (10.4 vs. 2.4 pmol L-1) and creatinine (10 vs. 2 mu mol L-1), but no differences in cortisol, free normetanephrine or osmolality. Changes in copeptin reflected T (c) response more closely than sympathoadrenal markers or osmolality. Dynamic relationships with tonicity and kidney function may help to explain this finding. As a surrogate for integrated physiological strain during work in a field environment, copeptin assay could inform future measures to prevent heat-related illnesses.