Background: To assess the prevalence of exercise-associated hyponatremia (EAH) in two 24-hour mountain bike (MTB) (R1,R2), one 24-hour running (R3) and one multi-stage MTB (R4) races held in the Czech Republic in a cluster of four cross-sectional studies.
Methods: In 27 ultra-mountain bikers (ultra-MTBers), 12 ultra-runners, and 14 multi-stage MTBers, fluid intake, changes (Δ) in body mass, hematocrit, plasma volume, plasma [Na+], plasma [K+], plasma osmolality, urine [Na+], urine [K+], urine specific gravity, urine osmolality, K+/Na+ ratio in urine, transtubular potassium gradient and glomerular filtration rate were measured and calculated. The use of non-steroidal anti-inflammatory drugs and symptoms of EAH were recorded using post-race questionnaires.
Results: Of the 53 finishers, three (5.7%) developed post-race EAH, thereof one (3.7%) ultra-MTBer, one (8.3%) ultra-runner and one (7.1%) multi-stage MTBer. Plasma [Na+] decreased significantly (p < 0.001) only in R4. Urine osmolality (R1, R3, R4 p < 0.001; R2 p < 0.05) and glomerular filtration rate (p < 0.001) increased, and body mass decreased in all races (p < 0.05). Δ body mass was inversely related to the number of kilometers achieved (p < 0.001) in R2 where better ultra-MTBers tended to lose more weight. Δ body mass (p < 0.001) and %Δ body mass (p = 0.05) were positively related to lower post-race plasma [Na+] in R3 that was associated with increased loss in body mass. Fluid intake was positively related to race performance in R1 and R2 (R1: p = 0.04; R2: p = 0.01) where ultra-MTBers in R1 and R2 who drank more finished ahead of those who drank less. Post-race plasma [Na+] was negatively associated with race performance in ultra-MTBers in R2 (p < 0.05), similarly ultra-runners in R3 (p < 0.05) where finishers with more kilometres had lower post-race plasma [Na+].
Conclusions: The prevalence of EAH in the Czech Republic was no higher compared to existing reports on ultra-endurance athletes in other countries. Lower plasma [Na+] and development of EAH may be attributed to overdrinking, a pituitary secretion of vasopressin, an impaired mobilization of osmotically inactive sodium stores, and/or an inappropriate inactivation of osmotically active sodium.