Proof of concept: hypovolemic hyponatremia may precede and augment creatine kinase elevations during an ultramarathon.

Abstract

It is not known if exercise-associated hyponatremia (EAH) is a cause or consequence of exertional rhabdomyolysis (ER).We hypothesized that osmotic stress (EAH) coupled with mechanical stress (running) potentiated muscle cell breakdown (ER). This concept would be supported if a nadir in serum sodium concentration ([Na(+)]) temporally preceded peak creatine kinase levels (CK) during an ultramarathon run. Fifteen participants ran ≥104 km and had blood drawn: prior to start; 53; 104 km; and 24-h post run. Serum [Na(+)], CK, urea, creatinine and estimated glomerular filtration rate (eGFR) were measured from serial blood samples. Two-way repeated-measures ANOVA was used to examine differences regarding both race distance and natremia status. Ten of 15 participants demonstrated EAH (serum [Na(+)] <135 mmol/L) at least once during serial testing. Participants were categorized post hoc into one of three natremia groups based on lowest recorded [Na(+)]: (1) <129 mmol/L (n = 3; moderate EAH); (2) between 129 and 134 mmol/L (n = 7; mild EAH); and (3) >134 mmol/L (n = 5; normonatremia). Participants with lowest [Na(+)] demonstrated highest CK values at subsequent checkpoints. Significant natremia group differences noted at the 53 km point (p = 0.0002) for [Na(+)] while significant natremia group effect noted for CK seen at the 24-h post-finish testing point (p = 0.02). Significant natremia group effects noted for renal biomarkers, with the moderate EAH group documenting the lowest eGFR (p = 0.005), and highest serum urea (p = 0.0006) and creatinine (p < 0.0001) levels. Hyponatremic runners had lower post-race urine [Na(+)] than normonatremic runners (26 ± 15 vs. 89 ± 79 mmol/L; p = 0.03). Preliminary data support the possibility that transient hypovolemic EAH may precede and augment CK during an ultramarathon.