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An Intervention Study of Oral Versus Intravenous Hypertonic Saline Administration in Ultramarathon Runners With Exercise-Associated Hyponatremia: A Preliminary Randomized Trial

Rogers, Ian R MBBS*†; Hook, Ginger RN; Stuempfle, Kristin J PhD§; Hoffman, Martin D MD; Hew-Butler, Tamara DPM, PhD

Clinical Journal of Sport Medicine: May 2011 - Volume 21 - Issue 3 - p 200-203
doi: 10.1097/JSM.0b013e31821a6450
Original Research

Objective: To determine whether asymptomatic exercise-associated hyponatremia (EAH) in ultramarathon runners can be corrected with either oral or intravenous (IV) 3% hypertonic saline (HTS).

Design: Prospective with randomization into 1 of 2 intervention arms.

Setting: Western States (161 km) Endurance Run, California.

Participants: Forty-seven finishers in the event consented to be screened to identify those with EAH, defined as plasma sodium ([Na+]p) <135 mmol/L at race end.

Interventions: Participants with EAH but without symptoms were randomized to receive a single 100 mL dose of either oral or IV 3% HTS. Blood was drawn before intervention and at 60 minutes postintervention to measure [Na+]p, and concentrations of plasma potassium, proteins, and arginine vasopressin (AVP). Body mass, percent total body water, and percent body fat were measured prerace and postrace using impedance scales.

Main Outcome Measures: Change in [Na+]p.

Results: Fourteen of 47 consenting finishers (30%) had EAH. Eight agreed to be randomized into the intervention protocol. Only in the IV group did [Na+]p change significantly (from 130.8 to 134.6 mmol/L) over the 60 minutes post-HTS administration. Elevated AVP concentrations were seen at race finish in both the groups and remained so after HTS treatment.

Conclusions: In this preliminary trial, prompt administration of a 100 mL bolus of IV 3% HTS was associated with normalization of [Na+]p in asymptomatic EAH, but a similar effect was not demonstrated for the same dose orally. Elevated AVP levels were observed and may play a part in the development of EAH but were not suppressed significantly by either intervention.

From the *Discipline of Emergency Medicine, University of Western Australia, Western Australia, Australia; †Department of Medicine, Sir Charles Gairdner Hospital, Perth, Western Australia, Australia; ‡Department of Kinesiology, Arizona State University, Tempe, Arizona; §Department of Health Sciences, Gettysburg College, Gettysburg, Pennsylvania; ¶Physical Medicine and Rehabilitation Service, Department of Veterans Affairs, Northern California Health Care System, Mather, California and Department of Physical Medicine and Rehabilitation, University of California Davis Medical Center, Sacramento, California; and ∥Department of Exercise Science, School of Health Science, Oakland University, Rochester, Michigan.

Submitted for publication August 18, 2010; accepted February 23, 2011.

Supported by the Western States Endurance Run Foundation.

Presented in part at the 57th Annual Meeting of the American College of Sports Medicine; June 2, 2010; Baltimore, Maryland.

Authors' Contribution: I. R. Rogers, K. J. Stuempfle, M. D. Hoffman, and T. Hew-Butler conceived the study and designed the trial; M. D. Hoffman, and T. Hew-Butler obtained research funding; all authors supervised the trial, enrolled participants, and collected data; T. Hew-Butler provided statistical advice and analyzed the data; T. Hew-Butler and I. R. Rogers drafted the manuscript; I. R. Rogers takes responsibility for the paper as a whole.

The authors report no conflict of interest.

Corresponding Author: Ian R. Rogers, MBBS, FACEM, Department of Post Graduate Medical Education, 1st Floor E Block, Sir Charles Gairdner Hospital, Hospital Ave, Nedlands, Western Australia 6009, Australia (ian.rogers@health.wa.gov.au).

© 2011 Lippincott Williams & Wilkins, Inc.