Symptomatic exercise-associated hyponatremia (EAH) is known to be a potential complication from overhydration during exercise, but there remains a general belief that sodium supplementation will prevent EAH. We present a case in which a runner with a prior history of EAH consulted a sports nutritionist who advised him to consume considerable supplemental sodium, which did not prevent him from developing symptomatic EAH during a subsequent long run. Emergency medical services were requested for this runner shortly after he finished a 17-hr, 72-km run and hike in Grand Canyon National Park during which he reported having consumed 9.2–10.6 L of water and >6,500 mg of sodium. First responders determined his serum sodium concentration with point-of-care testing was 122 mEq/L. His hyponatremia was documented to have improved from field treatment with an oral hypertonic solution of 800 mg of sodium in 200 ml of water, and it improved further after significant aquaresis despite in-hospital treatment with isotonic fluids (lactated Ringer’s). He was discharged about 5 hr after admission in good condition. This case demonstrates that while oral sodium supplementation does not necessarily prevent symptomatic EAH associated with overhydration, early recognition and field management with oral hypertonic saline in combination with fluid restriction can be effective treatment for mild EAH. There continues to be a lack of universal understanding of the underlying pathophysiology and appropriate hospital management of EAH.
Martin D. Hoffman and Thomas M. Myers
J. Luke Pryor, Evan C. Johnson, Jeffery Del Favero, Andrew Monteleone, Lawrence E. Armstrong, and Nancy R. Rodriguez
Postexercise protein and sodium supplementation may aid recovery and rehydration. Preserved beef provides protein and contains high quantities of sodium that may alter performance related variables in runners. The purpose of this study was to determine the effects of consuming a commercial beef product postexercise on sodium and water balance. A secondary objective was to characterize effects of the supplementation protocols on hydration, blood pressure, body mass, and running economy. Eight trained males (age = 22 ± 3 y, V̇O2max = 66.4 ± 4.2 ml·kg-1·min-1) completed three identical weeks of run training (6 run·wk-1, 45 ± 6 min·run-1, 74 ± 5% HRR). After exercise, subjects consumed either, a beef nutritional supplement (beef jerky; [B]), a standard recovery drink (SRD), or SRD+B in a randomized counterbalanced design. Hydration status was assessed via urinary biomarkers and body mass. No main effects of treatment were observed for 24 hr urine volume (SRD, 1.7 ± 0.5; B, 1.8 ± 0.6; SRD+B, 1.4 ± 0.4 L·d-1), urine specific gravity (1.016 ± 0.005, 1.018 ± 0.006, 1.017 ± 0.006) or body mass (68.4 ± 8.2, 68.3 ± 7.7, 68.2 ± 8.1 kg). No main effect of treatment existed for sodium intake—loss (-713 ± 1486; -973 ± 1123; -980 ± 1220 mg·d-1). Mean arterial pressure (81.0 ± 4.6, 81.1 ± 7.3, 83.8 ± 5.4 mm Hg) and average exercise running economy (V̇O2: SRD, 47.9 ± 3.2; B, 47.2 ± 2.6; SRD+B, 46.2 ± 3.4 ml·kg-1·min-1) was not affected. Urinary sodium excretion accounted for the daily sodium intake due to the beef nutritional supplement. Findings suggest the commercial beef snack is a viable recovery supplement following endurance exercise without concern for hydration status, performance decrements, or cardiovascular consequences.
J.D. Adams, Miranda Badolato, Ethan Pierce, Abbie Cantrell, Zac Parker, and Donya Farzam
Assessment of urine concentrations of sodium (Na + ), potassium (K + ), and chloride (Cl − ) is a widely available, rapid, and low cost option for observing fluid and electrolyte balance in health and sport. Specifically, urine excretion of electrolytes can be used for observing changes in renal
Jason C. Siegler, Amelia J. Carr, William T. Jardine, Lilia Convit, Rebecca Cross, Dale Chapman, Louise M. Burke, and Megan Ross
one buffer (sodium bicarbonate [BIC]; Maughan et al., 2018 ), and a number of reviews have highlighted potential mechanisms of action, effective ingestion strategies, and potential side effects of these buffering mediums ( Carr, Hopkins, et al., 2011 ; Lancha Junior et al., 2015 ; McNaughton et
Kevin C. Miller, Brendon P. McDermott, and Susan W. Yeargin
). Many studies associate EAMCs with fluid, sodium (Na + ), potassium (K + ), or chloride (Cl − ) losses because of their importance in fluid balance, muscle contraction, and nerve conduction. Sweat losses, whether matched or unmatched by fluid or dietary intake, may result in hypohydration, acute or
Alan J. McCubbin, Gregory R. Cox, and Ricardo J.S. Costa
During endurance exercise, muscular contractions produce heat, resulting in sweating to support thermoregulation ( Sawka et al., 2007 ). Considering sodium is the most abundant electrolyte present in sweat, prolonged heavy sweating can cause significant sodium losses ( Baker, 2017 ). While this is
Charles S. Urwin, Rodney J. Snow, Dominique Condo, Rhiannon M.J. Snipe, Glenn D. Wadley, Lilia Convit, and Amelia J. Carr
such as 4,000 m cycling, 1,500 m running, and 2,000 m rowing can aim to minimize the inhibitory effect of acidosis by inducing blood alkalosis (increased blood pH and [HCO 3 − ]) prior to their event ( Maughan et al., 2018 ). Blood alkalosis can be induced by sodium citrate (SC) or sodium bicarbonate
Michael F. Bergeron
A 17-year-old, nationally ranked, male tennis player (AH) had been experiencing heat cramps during tennis match play. His medical history and previous physical exams were unremarkable, and his in-office blood chemistry profiles were normal. On-court evaluation and an analysis of a 3-day dietary record revealed that AH's sweat rate was extensive (2.5 L · hr−1) and that his potential daily on-court sweat sodium losses (89.8 mmol · hr of play') could readily exceed his average daily intake of sodium (87.0-174.0 mmol · day−1). The combined effects of excessive and repeated fluid and sodium losses likely predisposed AH to heat cramps during play. AH was ultimately able to eliminate heat cramps during competition and training by increasing his daily dietary intake of sodium.
Nathan Philip Hilton, Nicholas Keith Leach, Melissa May Craig, S. Andy Sparks, and Lars Robert McNaughton
Gastrointestinal (GI) disturbances are widely reported following sodium bicarbonate (NaHCO 3 ) supplementation ( Burke & Pyne, 2007 ; Cameron et al., 2010 ; Kahle et al., 2013 ), and although the etiology of GI disturbances involves multiple mechanisms, the neutralization of gastric acid is
Ronald J. Maughan, Phillip Watson, Philip A.A. Cordery, Neil P. Walsh, Samuel J. Oliver, Alberto Dolci, Nidia Rodriguez-Sanchez, and Stuart D.R. Galloway
) promote longer term retention of the ingested volume ( Maughan et al., 2016 ). These differences in fluid retention are likely due to mechanisms involving both fluid delivery to the circulation ( Calbet & Holst, 2004 ; Mahe et al., 1992 ) and the effect of electrolytes (particularly sodium) on expansion