Abstract

Objective To evaluate the osmotic and non-osmotic regulation of arginine vasopressin (AVP) during endurance cycling.

Design Observational study.

Setting 109 km cycle race.

Participants 33 Cyclists.

Interventions None.

Main outcome measurements Plasma sodium concentration ([Na⁺]), plasma volume (PV) and plasma arginine vasopressin (AVP) concentration ([AVP]_p).

Results A fourfold increase in [AVP]_p occurred despite a 2-mmol l⁻¹ decrease in plasma [Na⁺] combined with only modest (5%) PV contraction. A significant inverse correlation was noted between [AVP]_p Δ and urine osmolality Δ (r = −0.41, p<0.05), whereas non-significant inverse correlations were noted between [AVP]_p and both plasma [Na⁺] Δ and % PV Δ. Four cyclists finished the race with asymptomatic hyponatraemia. The only significant difference between the entire cohort with this subset of athletes was postrace plasma [Na⁺] (137.7 vs 133.5 mmol l⁻¹, p<0.001) and plasma [Na⁺] Δ (−1.9 vs −5.1 mmol l⁻¹, p<0.05). The mean prerace [AVP]_p of these four cyclists was just below the minimum detectable limit (0.3 pg ml⁻¹) and increased marginally (0.4 pg ml⁻¹) despite the decline in plasma [Na⁺].

Conclusions The osmotic regulation of [AVP]_p during competitive cycling was overshadowed by non-osmotic AVP secretion. The modest decrease in PV was not the primary non-osmotic stimulus to AVP. Partial suppression of AVP occurred in four (12%) cyclists who developed hyponatraemia during 5 h of riding. Therefore, these results confirm that non-osmotic AVP secretion and exercise-associated hyponatraemia does, in fact, occur in cyclists participating in a 109 km cycle race. However, the stimuli to AVP is likely different between cycling and running.