International Journal of Sport Nutrition and Exercise Metabolism, 2015, 25, 603  -606

http://dx.doi.org/10.1123/ijsnem.2014-0241
© 2015 Human Kinetics, Inc. CASE STUDIES

Case Study: Symptomatic Exercise-Associated

Hyponatremia in an Endurance Runner Despite
Sodium Supplementation
Martin D. Hoffman and Thomas M. Myers

Symptomatic exercise-associated hyponatremia (EAH) is known to be a potential complication from over-

hydration 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.

Keywords: arginine vasopressin, hypertonic saline, sodium, syndrome of inappropriate ADH secretion, water–
electrolyte imbalance

Exercise-associated hyponatremia (EAH) is rec- Case Report

ognized as a potential complication during prolonged
competitive endurance sports (Ayus et al., 2000; Hoff-
man et al., 2015; Siegel et al., 2007) and hiking (Backer
et al., 1999; Basnyat et al., 2000; Coler et al., 2012; Noe
et al., 2013; Pearce et al., 2015; Rothwell & Rosengren,
2008; Spano et al., 2014; Zelingher et al., 1996). While
it is now recognized that avoiding overhydration is the
primary means of preventing EAH (Bennett et al., 2014;
Hew-Butler et al., 2008), it is commonly believed that
sodium supplementation is also important (Hoffman &
Stuempfle, 2014; Winger et al., 2013). The present case
demonstrates this misconception about sodium supple-
mentation as well as some important features related to
EAH treatment.
Hoffman is with Dept. of Physical Medicine and Rehabilita-
tion, Dept. of Veterans Affairs, Northern California Health Care
System, and University of California Davis Medical Center,
Sacramento, CA. Myers is with North Country HealthCare,
Flagstaff, AZ. Address author correspondence to Martin D.
Hoffman at mdhoffman@ucdavis.edu.
On April 11, 2014, a 52-year-old experienced endurance
runner ran and hiked at a moderate intensity the Grand
Canyon National Park 72-km “Rim-to-Rim-to-Rim,”
descending and then ascending approximately 1,500 m
in elevation twice over a 17-hr time period, along the
South Kaibab, North Kaibab, and Bright Angel Trails.
The participant had a medical history significant for
gallbladder removal, esophageal spasms, gastroesopha-
geal reflux disease, and a previous episode of EAH while
participating in an endurance event in 2010. He took no
medications other than an oral antifungal. His body mass
leading up to the run had been ~82 kg. His account of the
day, including details of his fluid and nutritional intake,
were obtained on April 16, 2014.
The day was clear and sunny with ambient tem-
peratures in the canyon reaching a high of 32.8 °C. He
began his run at 0400 hr and completed it at 2100 hr.
During the run, he attempted to maintain a hydration plan
recommended by a sports nutritionist he had consulted
that included water with energy drink (SPIZ Endurance
Energy Drink, Longevity Plus, Fallbrook, CA), sodium
supplements (1 capsule per hour of Succeed Buffer/
Electrolyte Caps, Succeed! Sportsdrink LLC, Fort

603
 604  Hoffman and Myers
Collins, CO, containing 341 mg of sodium per capsule),
and energy bars providing a total of ~700 mL water,
500–700 mg sodium, and ~250 kcal each hour. Based on
his reported intake, it is estimated he drank 9.2–10.6 L
of water and consumed >6,500 mg of sodium and 3,250
kcal. He recalled feeling thirsty during much of the run
and that he was urinating “more than usual,” a total of
four or five times throughout his run, with the urine
appearing clear in color.
The participant began experiencing “stomach upset”
and emesis about 5 km from completion of the run, as
well as abdominal pain, which gradually developed as
he completed the run, making it difficult to eat or drink
during the last 4 hr. Upon finishing the run, he recalled
being fatigued, indicating he felt “shaky and wobbly,” and
had an intermittent dull headache and severe abdominal
pain. Because of the increasing abdominal pain, Grand
Canyon National Park Service paramedics were requested
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at 2107 hr by his family members who had met him at
the end of his run.
First responders found him sitting, alert and oriented,
appearing anxious with slurred speech and a “thousand
yard stare” (a distant stare) and reporting a dull headache,
cramping abdominal pain, and transient “shooting” pain
in his right flank during his last urination. Light muscle
fasciculations were noted with gross motor movements;
however, the participant was able to ambulate with
minimal assistance. His initial Glasgow Coma Score
was 15, blood pressure was 130/79 mmHg, pulse was
55 beats/min, and respiratory rate was 30 breaths/min.
Pulse oximetry was 97% on room air, and finger-stick
glucose was 98 mg/dL. An electrocardiogram showed
sinus bradycardia without ectopy.
An intravenous (IV) line of normal saline was started
at a “to keep open” rate, and point-of-care testing revealed
a serum sodium concentration of 122 mEq/L, serum
potassium concentration of 4.8 mEq/L, and hemoglobin
and hematocrit of 14.6 g/dL and 43%, respectively. He
was treated with 4 mg of IV ondansetron for nausea and
50 mcg of IV fentanyl for abdominal pain. He was also
given an oral hypertonic solution of 800 mg sodium in
200 mL of water. An additional 4 mg of IV ondansetron
was given for persistent nausea and vomiting.
Upon arrival at the hospital emergency department
at 2400 hr, the participant had stable vital signs. He
remained oriented with no focal neurological deficits
observed but complained of returning abdominal cramp-
ing, epigastric pain, and nausea. Admission serum sodium
concentration was 127 mEq/L, blood urea nitrogen was
27 mg/dL, and serum creatinine was 1.3 mg/dL. Within
30 min of arrival, he produced a considerable amount of
urine with specific gravity of 1.005. He was diagnosed by
hospital physicians with dehydration despite the history
indicating overhydration and the submaximally concen-
trated urine, and he was treated with 2,000 mL of IV
lactated Ringer’s, 8 mg IV ondansetron, and an unknown
dose of IV morphine. His abdominal pain improved. After
tolerating food and drink, and his serum sodium concen-
IJSNEM Vol. 25, No. 6, 2015
tration increasing to 132 mEq/L, he was discharged at
0508. He recovered fully without complications.
Discussion
It is now known that the underlying pathophysiology of
EAH involves overhydration with fluid retention from
arginine vasopressin (AVP) secretion due to nonosmotic
stimuli such as nausea (Bennett et al., 2014; Hew-Butler
et al., 2008). However, the effectiveness of sodium
supplementation for prevention of EAH is more contro-
versial. Prior work suggests that serum sodium concentra-
tions are not affected by sodium supplementation during
exercise (Hew-Butler et al., 2006; Speedy et al., 2002;
Winger et al., 2013). It has also been demonstrated that
sodium supplementation is not necessary during exercise
up to 30 hr in hot conditions (Hoffman & Stuempfle,
2014, 2015). Nor does sodium supplementation prevent
EAH in cases where the individual is overhydrating
(Hoffman et al., 2015; Twerenbold et al., 2003), as was
evident in this case. This would be expected given that
EAH has been demonstrated to be associated with urinary
sodium loss related to elevations in brain natriuretic pep-
tide (Harris et al., 2012; Hoffman et al., 2015; Zelingher
et al., 1996). Nevertheless, sodium supplementation is
quite common among ultramarathon runners (Hoffman
& Stuempfle, 2014, 2015; Winger et al., 2013), at least
partially because of a rather universal belief that it will
prevent EAH.
Ironically, excessive sodium intake could even con-
tribute to overhydration and development of EAH, as we
have previously suggested (Hoffman et al., 2015). Gastro-
intestinal and/or hepatic-portal osmoreceptors are known
to provide an early stimulus of thirst without elevation
in blood osmolality in rats (Kraly et al., 1995; Stricker
et al., 2002; Stricker et al., 2003). If a similar mecha-
nism is present in humans, then this might help explain
a continued thirst drive despite overhydration when an
athlete is taking sodium supplements (Hoffman et al.,
2015). This could have been a factor in the present case
given that the participant reported being thirsty despite
his apparent overhydration based on reported urinary
frequency and urine color. Use of sodium supplements
and drinking beyond the dictates of thirst has been shown
to be unnecessary to maintain appropriate hydration
during prolonged exercise in hot conditions (Hoffman &
Stuempfle, 2014). Thus, it is appropriate that current EAH
prevention guidelines recommend avoidance of excessive
sodium supplementation in addition to drinking to thirst
during endurance activities (Bennett et al., 2014).
In the present case, the participant consumed
9.2–10.6 L of water over a 17-hr period of exercise with
some of that time in hot ambient conditions. This average
water intake of 541–624 ml/hr may not seem excessive
under such conditions, especially since he was not a
small individual and fluid intake rates of 400–800 ml/hr
have been suggested as a reasonable range for marathon
runners depending on body size, exercise intensity, and

environmental conditions (American College of Sports
Medicine et al., 2007). This points to the potential for
overhydration in some individuals even with fluid intake
that may seem modest.
While sodium supplementation may not prevent
EAH when occurring in conjunction with overhydration,
mildly symptomatic cases of EAH may be treated suc-
cessfully with an oral hypertonic saline bolus in combina-
tion with fluid restriction (Owen et al., 2014; Rogers et al.,
2011; Siegel et al., 2009) as demonstrated in the present
case. The goal of this treatment is to acutely increase
serum sodium concentration adequately to reduce cere-
bral edema. More severely symptomatic cases of EAH
should be treated with bolused IV hypertonic saline, and
this can be done so without concern of osmotic demyelin-
ation or central pontine myelinolysis (Bennett et al., 2014;
Hew-Butler et al., 2008). Furthermore, the literature is
clear about the potential adverse effects of isotonic or
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hypotonic saline in EAH (Bennett et al., 2013; Hoffman
et al., 2015; Hoffman & Weiss, 2014). Fortunately, the
participant in the present report suffered no consequences
despite hospital treatment with isotonic IV fluids, likely
because he received appropriate initial management and
was able to produce an aquaresis from suppression of
AVP secretion after his nausea was controlled.
This case demonstrates the apparent paradox of EAH
wherein sodium supplementation does not necessarily
prevent EAH in the presence of overhydration, but field
management with an oral bolus of hypertonic saline in
combination with fluid restriction can be effective at
treating mildly symptomatic EAH. First responders and
emergency department providers should recognize that
current management guidelines for EAH involve use of
hypertonic saline.
Acknowledgments
This material is the result of work supported with resources
and the use of facilities at the VA Northern California Health
Care System. The contents reported here do not represent the
views of the Department of Veterans Affairs or the United
States Government.
Both authors participated in conceptualization, information
collection and interpretation, and manuscript preparation. Both
authors approved the final version of the paper.
The authors report no conflict of interest.
References
American College of Sports Medicine, Sawka, M.N., Burke,
L.M., Eichner, E.R., Maughan, R.J., Montain, S.J., &
Stachenfeld, N.S. (2007). American College of Sports
Medicine position stand: Exercise and fluid replacement.
Medicine and Science in Sports and Exercise, 39, 377–390.
PubMed
Ayus, J.C., Varon, J., & Arieff, A.I. (2000). Hyponatremia,
cerebral edema, and noncardiogenic pulmonary edema
in marathon runners. Annals of Internal Medicine, 132,
IJSNEM Vol. 25, No. 6, 2015
EAH in a Runner Despite Sodium Supplementation  605
711–714. PubMed doi:10.7326/0003-4819-132-9-
200005020-00005
Backer, H.D., Shopes, E., Collins, S.L., & Barkan, H. (1999).
Exertional heat illness and hyponatremia in hikers. The
American Journal of Emergency Medicine, 17, 532–539.
PubMed doi:10.1016/S0735-6757(99)90191-2
Basnyat, B., Sleggs, J., & Spinger, M. (2000). Seizures
and delirium in a trekker: The consequences of exces-
sive water drinking? Wilderness & Environmental
Medicine, 11, 69–70. PubMed doi:10.1580/1080-
6032(2000)011[0069:LTTE]2.3.CO;2
Bennett, B.L., Hew-Butler, T., Hoffman, M.D., Rogers, I.R., &
Rosner, M.H. (2013). In reply to clinical practice guide-
lines for treatment of exercise-associated hyponatremia.
Wilderness & Environmental Medicine, 24, 468–471.
PubMed doi:10.1016/j.wem.2013.06.004
Bennett, B.L., Hew-Butler, T., Hoffman, M.D., Rogers, I.R.,
& Rosner, M.H. (2014). Wilderness Medical Society
practice guidelines for treatment of exercise-associated
hyponatremia: 2014 update. Wilderness & Environmental
Medicine, 25(4, Suppl.) S30–S42. PubMed doi:10.1016/j.
wem.2014.08.009
Coler, C., Hoffman, M.D., Towle, G., & Hew-Butler, T. (2012).
Hyponatremia in an 85-year-old hiker: When depletion
plus dilution produces delirium. Wilderness & Environ-
mental Medicine, 23, 153–157. PubMed doi:10.1016/j.
wem.2012.02.013
Harris, G., Reid, S., Sikaris, K., & McCrory, P. (2012). Hypo-
natremia is associated with higher NT-proBNP than
normonatremia after prolonged exercise. Clinical Journal
of Sport Medicine, 22, 488–494. PubMed doi:10.1097/
JSM.0b013e3182580ce8
Hew-Butler, T., Rosner, M.H., Fowkes-Godek, S., Dugas,
J.P., Hoffman, M.D., Lewis, D.P., . . . Verbalis, J.G.
(2015). Statement of the Third International Exercise-
Associated Hyponatremia Consensus Development
Conference, Carlsbad, California, 2015. Clinical Journal
of Sport Medicine, 25, 303–320. PubMed doi:10.1097/
JSM.0000000000000221
Hew-Butler, T.D., Sharwood, K., Collins, M., Speedy, D., &
Noakes, T. (2006). Sodium supplementation is not required
to maintain serum sodium concentrations during an Iron-
man triathlon. British Journal of Sports Medicine, 40,
255–259. PubMed doi:10.1136/bjsm.2005.022418
Hoffman, M.D., & Stuempfle, K.J. (2014). Hydration strategies,
weight change and performance in a 161 km ultramara-
thon. Research in Sports Medicine, 22, 213–225. PubMed
doi:10.1080/15438627.2014.915838
Hoffman, M.D., & Stuempfle, K.J. (2015). Sodium supple-
mentation and exercise-associated hyponatremia during
prolonged exercise. Medicine and Science in Sports and
Exercise, 47, 1781–1787. PubMed
Hoffman, M.D., Stuempfle, K.J., Sullivan, K., & Weiss, R.H.
(2015). Exercise-associated hyponatremia with exertional
rhabdomyolysis: Importance of proper treatment. Clinical
Nephrology, 83, 235–242. PubMed
Hoffman, M.D., & Weiss, R.H. (2014). Symptomatic hypo-
tonic hyponatremia presenting at high altitude. Wilder-
 606  Hoffman and Myers
ness & Environmental Medicine, 25, 362–363. PubMed
doi:10.1016/j.wem.2014.01.008
Kraly, F.S., Kim, Y.M., Dunham, L.M., & Tribuzio, R.A. (1995).
Drinking after intragastric NaCl without increase in sys-
temic plasma osmolality in rats. The American Journal of
Physiology, 269(5 Pt 2), R1085–R1092. PubMed
Noe, R.S., Choudhary, E., Cheng-Dobson, J., Wolkin, A., &
Newman, S. (2013). Exertional heat-related illnesses at
the Grand Canyon National Park, 2004–2009. Wilder-
ness & Environmental Medicine, 24, 422–428. PubMed
doi:10.1016/j.wem.2013.06.008
Owen, B.E., Rogers, I.R., Hoffman, M.D., Stuempfle, K.J.,
Lewis, D., Fogard, K., . . . Hew-Butler, T. (2014). Efficacy
of oral versus intravenous hypertonic saline in runners with
hyponatremia. Journal of Science and Medicine in Sport,
17, 457–462. PubMed doi:10.1016/j.jsams.2013.09.001
Pearce, E.A., Myers, T.M., & Hoffman, M.D. (2015).Three
cases of severe hyponatremia during a river run in
Downloaded by York Univ Libraries on 09/17/16, Volume 25, Article Number 6
Grand Canyon National Park. Wilderness & Environ-
mental Medicine, 26, 189–195. PubMed doi:10.1016/j.
wem.2014.08.007
Rogers, I.R., Hook, G., Stuempfle, K.J., Hoffman, M.D., &
Hew-Butler, T. (2011). An intervention study of oral
versus intravenous hypertonic saline administration in
ultramarathon runners with exercise-associated hypona-
tremia: A preliminary randomized trial. Clinical Journal
of Sport Medicine, 21, 200–203. PubMed doi:10.1097/
JSM.0b013e31821a6450
Rothwell, S.P., & Rosengren, D. (2008). Severe exercise-
associated hyponatremia on the Kokoda Trail, Papua New
Guinea. Wilderness & Environmental Medicine, 19, 42–44.
PubMed doi:10.1580/07-WEME-CR-116.1
Siegel, A.J., d’Hemecourt, P., Adner, M.M., Shirey, T., Brown,
J.L., & Lewandrowski, K.B. (2009). Exertional dysna-
tremia in collapsed marathon runners: A critical role for
point-of-care testing to guide appropriate therapy. Ameri-
can Journal of Clinical Pathology, 132, 336–340. PubMed
doi:10.1309/AJCP30OGLSLWLEIY
Siegel, A.J., Verbalis, J.G., Clement, S., Mendelson, J.H.,
Mello, N.K., Adner, M., . . . Lewandrowski, K.B. (2007).
IJSNEM Vol. 25, No. 6, 2015
Hyponatremia in marathon runners due to inappropriate
arginine vasopressin secretion. The American Journal of
Medicine, 120, 461.e11–461.e17. PubMed doi:10.1016/j.
amjmed.2006.10.027
Spano, S.J., Reagle, Z., & Evans, T. (2014). Symptomatic
hypotonic hyponatremia presenting at high altitude. Wil-
derness & Environmental Medicine, 25, 69–74. PubMed
doi:10.1016/j.wem.2013.09.014
Speedy, D.B., Thompson, J.M., Rodgers, I., Collins, M., Shar-
wood, K., & Noakes, T.D. (2002). Oral salt supplementa-
tion during ultradistance exercise. Clinical Journal of Sport
Medicine, 12, 279–284. PubMed doi:10.1097/00042752-
200209000-00004
Stricker, E.M., Callahan, J.B., Huang, W., & Sved, A.F. (2002).
Early osmoregulatory stimulation of neurohypophyseal
hormone secretion and thirst after gastric NaCl loads.
American Journal of Physiology. Regulatory, Integra-
tive and Comparative Physiology, 282, R1710–R1717.
PubMed doi:10.1152/ajpregu.00548.2001
Stricker, E.M., Hoffmann, M.L., Riccardi, C.J., & Smith, J.C.
(2003). Increased water intake by rats maintained on high
NaCl diet: Analysis of ingestive behavior. Physiology
& Behavior, 79, 621–631. PubMed doi:10.1016/S0031-
9384(03)00172-0
Twerenbold, R., Knechtle, B., Kakebeeke, T.H., Eser, P., Müller,
G., von Arx, P., & Knecht, H. (2003). Effects of different
sodium concentrations in replacement fluids during pro-
longed exercise in women. British Journal of Sports Medi-
cine, 37, 300–303. PubMed doi:10.1136/bjsm.37.4.300
Winger, J.M., Hoffman, M.D., Hew-Butler, T., Stuempfle, K.J.,
Dugas, J.P., Fogard, K., & Dugas, L.R. (2013). The effect
of physiology and hydration beliefs on race behavior and
postrace sodium in 161-km ultramarathon finishers. Inter-
national Journal of Sports Physiology and Performance,
8, 536–541. PubMed
Zelingher, J., Putterman, C., Ilan, Y., Dann, E.J., Zveibil, F.,
Shvil, Y., & Galun, E. (1996). Case series: Hyponatre-
mia associated with moderate exercise. The American
Journal of the Medical Sciences, 311, 86–91. PubMed
doi:10.1097/00000441-199602000-00007