Heat acclimatization blunts copeptin responses to hypertonicity from dehydrating exercise in humans

Abstract

Acclimatization favors greater extracellular tonicity from lower sweat sodium, yet hyperosmolality may impair thermoregulation during heat stress. Enhanced secretion or action of vasopressin could mitigate this through increased free water retention. Aims were to determine responses of the vasopressin surrogate copeptin to dehydrating exercise and investigate its relationships with tonicity during short and long‐term acclimatization. Twenty‐three participants completed a structured exercise programme following arrival from a temperate to a hot climate. A Heat Tolerance Test (HTT) was conducted on Day‐2, 6, 9 and 23, consisting of 60‐min block‐stepping at 50% VO 2peak, with no fluid intake. Resting sweat [Na+] was measured by iontophoresis. Changes in body mass (sweat loss), core temperature, heart rate, osmolality (serum and urine) and copeptin and aldosterone (plasma) were measured with each Test. From Day 2 to Day 23, sweat [Na+] decreased significantly (adjusted P < 0.05) and core temperature and heart rate fell. Over the same interval, HTT‐associated excursions were increased for serum osmolality (5 [−1, 9] vs. 9 [5, 12] mosm·kg−1), did not differ for copeptin (9.6 [6.0, 15.0] vs. 7.9 [4.3, 14.7] pmol·L−1) and were reduced for aldosterone (602 [415, 946] vs. 347 [263, 537] pmol·L−1). Urine osmolality was unchanging and related consistently to copeptin at end‐exercise, whereas the association between copeptin and serum osmolality was right‐shifted (P = 0.0109) with acclimatization. Unchanging urine:serum osmolality argued against increased renal action of vasopressin. In conclusion, where exercise in the heat is performed without fluid replacement, heat acclimatization does not appear to enhance AVP‐mediated free water retention in humans.

Exercise upregulates copeptin levels which is not regulated by interleukin-1

“…[23] Another study investigating medium intensity exercise in a warm environment showed 2.6-fold copeptin increases (peak 14.3 pmol/l). [25] Lippi et al reported a 6.4-fold increase in copeptin in healthy males participating in an ultramarathon (peak levels were 40 pmol/l). [21] Consistent with these findings, Aakre et al reported a 3.5-fold elevation of copeptin in middle aged males after a bike endurance race (peak 12.8 pmol/l).…”

“…These studies have been performed either in an elderly population with comorbidities, in young volunteers in a hot environment, or under extreme conditions like an ultramarathon. [19–25] Moreover, all of these studies have measured copeptin levels only twice, before and after exercise. Although increasing osmolality and plasma volume loss seem to be potent drivers of AVP/copeptin production in exercising participants, this does not explain the whole effect: Three studies reported increased AVP and copeptin levels after an ultramarathon in spite of decreased sodium values and osmolality.…”

Variation in renal responses to exercise in the heat with progressive acclimatisation

“…With the exception of IL-6 assays and the determination of AKI status, the methods used in this study and a range of parallel findings compatible with declining strain from HA have been reported previously. 22,26 A cohort of male United Kingdom (UK) military personnel were recruited, of whom 20 provided complete measures relevant to the analysis. Volunteers first attended the UK Institute of Naval Medicine to undergo baseline anthropometric measures, peak oxygen uptake (VO2peak) assessment and Heat Tolerance Test (HTT).…”

Impact of passive heat acclimation on markers of kidney function during heat stress

“…Studies in animal models suggest that chronic production of vasopressin, as observed during heat stress (Finberg & Berlyne, 1977; Melin et al., 1997), might blunt its action to protect the kidneys from frequent vasopressin‐mediated hyperfiltration (Bouby & Fernandes, 2003; García‐Arroyo et al., 2017). Evidence from exercise‐based heat acclimation protocols suggests that vasopressin release is reduced (Greenleaf, Brock, Keil, & Morse, 1983) or unchanged (Stacey et al., 2018) during exercise in the heat performed after heat acclimation. To our knowledge, no studies have examined this question during acute passive heat stress enforced before and after passive heat acclimation to isolate the effect of heat exposure from that of exercise.…”