Ad libitum water consumption prevents exercise-associated hyponatremia and protects against dehydration in soldiers performing a 40-km route-march

Heinrich W Nolte,Tamara Hew-Butler,Kim Nolte

doi:10.1186/s40779-019-0192-y

Abstract

BackgroundIt remains unclear if ad libitum water drinking, as a hydration strategy, prevents exercise-associated hyponatremia (EAH) during prolonged exercise. The aim of this study was to determine the incidence of EAH within the broader context of fluid regulation among soldiers performing a 40-km route-march ingesting water ad libitum.MethodsTwenty-eight healthy male soldiers participated in this observational trial. Pre- and post-exercise body mass, blood and urine samples were collected. Blood samples were assessed for serum sodium ([Na+]), glucose, creatinine, urea nitrogen (BUN), plasma osmolality, creatine kinase (CK), and plasma arginine vasopressin (AVP) concentrations. Plasma volume (PV) was calculated using hematocrit and hemoglobin. Urine samples were analyzed for osmolality and [Na+]. Water intake was assessed by weighing bottles before, during and after the march. The mean relative humidity was 55.7% (21.9–94.3%) and the mean dry bulb temperature was 27.1 °C (19.5 °C - 37.0 °C) during the exercise.ResultsTwenty-five soldiers (72 ± 10 kg) (Mean ± SD) completed the march in 09:11 ± 00:43 (hr:min). Participants consumed 736 ± 259 ml/h of water and lost 2.8 ± 0.9 kg (4.0% ± 1.4%, P < 0.05) of body mass. Significant (pre-march vs. post-march; P < 0.05) decreases in serum [Na+] (141 mmol/L vs. 136 mmol/L), plasma osmolality (303 mOsmol/kg H2O vs. 298 mOsmol/kg H2O), and serum creatinine (111 μmol/L vs. 101 μmol/L) and urine [Na+] (168 mmol/L vs. 142 mmol/L), as well as significant increases in plasma AVP (2 pg/ml vs. 11 pg/ml), plasma CK (1423 U/L vs. 3894 U/L) and urine osmolality (1035 mOsmol/kg H2O vs. 1097 mOsmol/kg H2O) were found. The soldier (72 kg) with the lowest post-exercise sodium level completed the march in 08:38. He drank 800 ml/h, lost 2% body mass, and demonstrated (pre-post) increases in plasma osmolality (294–314 mOsmol/kg H2O), BUN (20–30 mg/dl), AVP (2–16 pg/ml) and PV (41%). His urine osmolality decreased from 1114 mOsmol/kg H2O to 1110 mOsmol/kg H2O. No participants finished the route-march with a serum [Na+] indicating hypernatremia (range, 134–143 mmol/L).ConclusionsAd libitum drinking resulted in 4% body mass loss with a 2 mmol/L serum [Na+] reduction in conjunction with high urine osmolality (> 1000 mOsmol/kg H2O) and plasma AVP. No single hydration strategy likely prevents EAH, but hypernatremia (cellular dehydration) was not seen despite > 2% body mass losses and high urine osmolality.

Highlights

It remains unclear if ad libitum water drinking, as a hydration strategy, prevents exercise-associated hyponatremia (EAH) during prolonged exercise
While all three mechanisms are plausible in the development of low serum sodium concentrations ([Na+]), evidence suggests that total body water expansion relative to the amount of total body exchangeable sodium (Na+) is the main pathogenic cause of both asymptomatic and symptomatic EAH [2]
This soldier lost the second least amount of body mass (1.42 kg) during the march. He demonstrated the largest decrease in serum [Na+] during the march (6 mmol/L) and had the lowest pre- and post-march urine [Na+] compared with the rest of the normonatremic cohort. This hyponatremic soldier demonstrated a pre- to post-march increase in plasma volume (41% vs. -14%) and plasma osmolality (20 mOsmol/kg H2O vs. -5 mOsmol/kg H2O) when compared with the normonatremic cohort

Summary

Introduction

It remains unclear if ad libitum water drinking, as a hydration strategy, prevents exercise-associated hyponatremia (EAH) during prolonged exercise. Exercise-associated hyponatremia (EAH) is a potentially fatal sodium imbalance (serum sodium concentration < 135 mmol/L) resulting from a loss of solutes (sodium and potassium), relative excess of total body water, or likely a combination of both [1]. Drinking according to thirst is widely advocated as the most appropriate individualized hydration strategy to prevent both hyponatremia and hypernatremia (serum [Na+] > 145 mmol/L; or cellular dehydration) [5, 6]. Most hydration strategies advocated by sports medicine specialists aim to minimize the deleterious health and performance effects of dehydration [10]. Most of the current hydration guidelines advocate that athletes drink above thirst to limit body mass losses to < 2% and/or maintain a dilute urine output (urine osmolality < 700 mOsmol/kg H2O), with sodium ingestion as the main strategy to prevent EAH during exercise [10]

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