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Statement of the Third International Exercise-Associated
Hyponatremia Consensus Development Conference,
Carlsbad, California, 2015
Tamara Hew-Butler, DPM, PhD,*Mitchell H. Rosner, MD,Sandra Fowkes-Godek, PhD, ATC,
Jonathan P. Dugas, PhD,§ Martin D. Hoffman, MD,¶ Douglas P. Lewis, MD,k
Ronald J. Maughan, PhD,** Kevin C. Miller, PhD, ATC,†† Scott J. Montain, PhD,‡‡
Nancy J. Rehrer, PhD,§§ William O. Roberts, MD, MSc,¶¶ Ian R. Rogers, MBBS,kk
Arthur J. Siegel, MD,*** Kristin J. Stuempe, PhD,††† James M. Winger, MD,‡‡‡
and Joseph G. Verbalis, MD§§§
Key Words: EAH, exercise-associated collapse, hydration
(Clin J Sport Med 2015;25:303320)
The third International Exercise-Associated Hyponatre-
mia (EAH) Consensus Development Conference convened in
Carlsbad, California in February 2015 with a panel of 17
international experts. The delegates represented 4 countries and
9 medical and scientic sub-specialties pertaining to athletic
training, exercise physiology, sports medicine, water/sodium
metabolism, and body uid homeostasis. The primary goal of
the panel was to review the existing data on EAH and update
the 2008 Consensus Statement.
This document serves to
replace the second International EAH Consensus Development
Conference Statement and launch an educational campaign
designed to address the morbidity and mortality associated
withapreventableandtreatableuid imbalance.
The following statement is a summary of the data
synthesized by the 2015 EAH Consensus Panel and represents
an evolution of the most current knowledge on EAH. This
document will summarize the most current information on the
prevalence, etiology, diagnosis, treatment and prevention of
EAH for medical personnel, athletes, athletic trainers, and the
greater public. The EAH Consensus Panel strove to clearly
articulate what we agreed upon, did not agree upon, and did not
know, including minority viewpoints that were supported by
clinical experience and experimental data. Further updates will
be necessary to both: (1) remain current with our understanding
and (2) critically assess the effectiveness of our present
recommendations. Suggestions for future research and educa-
tional strategies to reduce the incidence and prevalence of EAH
are provided at the end of the document as well as areas of
controversy that remain in this topic.
The third International Exercise-Associated Hyponatre-
mia Consensus Development Conference utilized National
Institutes of Health guidelines, amended for a more holistic
approach to t the needs of both the group and the topic.
Twenty-two individuals (17 accepted) were invited to partic-
ipate in the consensus conference who: (1) have made
scientic and/or clinical contributions to the topic of water
and sodium homeostasis and/or hyponatremia and (2) repre-
sented a specic group (eg, nephrology, endurance medicine,
etc.) or had unique topical expertise (eg, cystic brosis,
muscle cramps, uid balance, etc.). The present document is
intended to serve as the scientic record of the conference
with intent to widely disseminate this information to achieve
Submitted for publication April 30, 2015; accepted May 10, 2015.
From the *Exercise Science Program, Oakland University, Rochester, Mich-
igan; Division of Nephrology, University of Virginia Health System,
Charlottesville, Virginia; Department of Sports Medicine, West Chester
University, West Chester, Pennsylvania; §The Vitality Group, Chicago,
Illinois; ¶Department of Physical Medicine and Rehabilitation, VA
Northern California Health Care System and University of California
Davis, Sacramento, California; kFamily Medicine Residency Program,
Via Christi Hospitals Wichita, Inc, Wichita, Kansas; **Department of
Sport and Exercise Nutrition, Loughborough University, Leicestershire,
United Kingdom; ††Athletic Training Program, Central Michigan Uni-
versity, Mount Pleasant, Michigan; ‡‡Military Nutrition Division,
United States Army Research Institute of Environmental Medicine, Na-
tick, Massachusetts; §§School of Physical Education, Sport and Exercise
Science, University of Otago, Dunedin, New Zealand; ¶¶Department of
Family Medicine and Community Health, University of Minnesota, Min-
neapolis, Minnesota; kkDepartment of Emergency Medicine, St John of
God Murdoch Hospital and University of Notre Dame, Perth, Western
Australia; ***Department of Internal Medicine, Harvard Medical
School, Boston, Massachusetts; †††Health Sciences Department, Gettys-
burg College, Gettysburg, Pennsylvania; ‡‡‡Department of Family Med-
icine, Loyola University Chicago Stritch School of Medicine, Chicago,
Illinois; and §§§Department of Endocrinology and Metabolism, George-
town University Medical Center, Washington, District of Columbia.
R.J.M. has received research funding and consulting fees from the food and
beverage industry. He is currently Chair of the Science Advisory Board of
the European Hydration Institute. The remaining authors report no
conicts of interest.
Corresponding Author: Tamara Hew-Butler, DPM, PhD, School of Health
Science, Oakland University, Rochester, MI 48309-4482 (
Copyright © 2015 Hew-Butler T, Rosner MH, Fowkes-Godek S, Dugas JP,
Hoffman MD, Lewis DP, Maughan RJ, Miller KC, Rehrer NJ, Roberts WO,
Rogers IR, Siegel AJ, Stuempe KJ, Winger JM, Verbalis JG, All rights
Clin J Sport Med Volume 25, Number 4, July 2015 |303
maximum impact on both current health care practice and
future medical research.
The methodology governing the conduct of this con-
sensus development conference is summarized below:
1. A broad based expert panel was assembled. Panel members
included researchers and clinicians in endocrinology (J.G.V.),
nephrology (M.H.R.), emergency medicine (I.R.R.), family
medicine (W.O.R., J.M.W., D.P.L.), internal medicine
(A.J.S.), physical medicine and rehabilitation (M.D.H.),
sports medicine (W.O.R., J.M.W., D.P.L.), athletic train-
ing (S.F.-G., K.C.M.) and exercise physiology (J.P.D.,
S.F.-G., T.H.-B., M.D.H., R.J.M., S.J.M., N.J.R., K.J.S.).
2. These experts presented data on EAH in a day long public
session, followed by open question/answer and discussion
periods with the audience. The panel members met the
following day in a closed session to prepare the consensus
3. Workgroups were created 3 months prior to the February
2015 meeting to update the following EAH target areas:
epidemiology, etiology and pathophysiology, diagnosis,
treatment, and prevention. Each workgroup was asked to
present updated drafts for discussion during the closed
4. A systematic, comprehensive and updated literature review
was shared by the panel members prior to the February
2015 meeting, using a cloud storage service that was orga-
nized into workgroup categories (epidemiology, etiology
and pathophysiology, diagnosis, treatment and preven-
tion). All panel members had unlimited access to the cloud
storage service and could add digital versions of published
manuscripts to the EAH manuscript section at any time.
The panel chairperson (MHR) was responsible for
monitoring the progress of each work group, directing the
closed session and guiding the panels deliberations. Using
the previous 2 EAH consensus statements as a starting point,
each work-group was asked to: (1) incorporate new data into
each assigned section and (2) update any outdated informa-
tion. All recommendations were graded based on clinical
strength, using the grading scale described by the American
College of Chest Physicians (Table 1).
Particular emphasis
was placed on creating more generalized recommendations so
as to prevent and treat EAH across a wider variety of athletic
events, rather than the endurance sports focus of the 2 prior
EAH Consensus Statements.
The travel (except R.J.M. and I.R.R., who supported
their own travel), hotel and meal expenses for the participants
were funded by CrossFit, Inc (Solana Beach, CA). The open
conference was also sponsored by CrossFit, Inc. However, no
members from CrossFit, Inc participated in any of the closed
discussions or contributed to the development of the consen-
sus guidelines. Furthermore, no members from CrossFit, Inc
had access to the consensus document prior to publication.
EAH is used to describe hyponatremia occurring during
or up to 24 hours after physical activity. It is dened by
a serum, plasma or blood sodium concentration ([Na
]) below
the normal reference range of the laboratory performing the
test. For most laboratories, this is a [Na
] less than
135 mmol/L.
The main determinants of the serum [Na
the total content of exchangeable body sodium and potassium
relative to total body water and thus hyponatremia can result
TABLE 1. American College of Chest Physicians Classification Scheme for Grading Evidence and Recommendations Utilized in
This Statement
Grade Description Benets vs Risks and Burdens
Methodological Quality of
Supporting Evidence
1A Strong recommendation, high-quality
Benets clearly outweigh risks and
burdens or vice versa
RCTs without important limitations
or overwhelming evidence from
observational studies
1B Strong recommendation, moderate-
quality evidence
Benets clearly outweigh risks and
burdens or vice versa
RCTs with important limitations or
exceptionally strong evidence from
observational studies
1C Strong recommendation, low-quality
or very low quality evidence
Benets clearly outweigh risks and
burdens or vice versa
Observational studies or case series
2A Weak recommendation, high-quality
Benets closely balanced with risks
and burdens
RCTs without important limitations
or overwhelming evidence from
observational studies
2B Weak recommendation, moderate-
quality evidence
Benets closely balanced with risks
and burdens
RCTs with important limitations or
exceptionally strong evidence from
observational studies
2C Weak recommendation, low-quality
or very low quality evidence
Uncertainty in the estimates of
benets, risks and burden; benets,
risk and burden may be closely
Observational studies or case series
RCT, randomized controlled trial.
Hew-Butler et al Clin J Sport Med Volume 25, Number 4, July 2015
304 | Copyright © 2015 retained by authors Hew Butler T et al. All rights reserved.
from loss of solutes (sodium, potassium), a relative excess of
total body water or a combination of both.
However, in
most clinical scenarios, the driving force for the develop-
ment of hyponatremia is a relative excess of total body
The symptoms associated with EAH depend on
both the magnitude of the serum sodium decrease from base-
line level along with the rate at which this decrease occurs.
Symptomatic EAH can occur if the rate of fall approaches
7% to 10% within 24 hours.
Thus, more severe degrees of
hyponatremia (typically ,125 mmol/L) as well as more
modest serum sodium values (in the range of 125-130
mmol/L), that develop over a short period of time, can both
be associated with signs and symptoms.
The vast majority of recreationally active individuals
begin endurance races with a blood [Na
] above 135
mmol/L. Based on data pooled from 27 separate studies,
encompassing 2262 participants with a veriable pre-race
blood [Na
] measurement, only 0.8% (19/2262) presented
with hyponatremia prior to race start.
These pooled data
represent blood [Na
] measurements collected in 7 countries
and between 5 minutes to 72 hours pre-competition. This
0.8% also includes 16 questionable below-normal [Na
ues possibly confounded by ngerstick hemolysis
outdated techniques.
Thus, baseline (pre-event) hyponatre-
mia in recreational exercisers appears to fall within the ex-
pected range for a normal population distribution (1%-2%),
and at a frequency well below what has been observed in
individuals presenting for non-hyponatremia related clinical
treatment situations
or in hospitalized patients.
thereby believe that EAH largely develops during or imme-
diately following exercise.
Exercise-associated hyponatremia can present in 2
forms: asymptomatic or symptomatic. Asymptomatic ath-
letes with [Na
],135 mmol/L have largely been detected
by blood samples taken post-exercise from athletes partici-
pating in research protocols or obtained for reasons other
than suspicion of EAH. Athletes with the symptomatic form
of EAH can present with mild, non-specicsymptoms
(eg, lightheadedness, nausea) but typically present with
headache, vomiting, and/or altered mental status (eg, confu-
sion, seizure) resulting from cerebral edema (termed
exercise-associated hyponatremic encephalopathy or EAHE)
that may
or may not
be associated with non-
cardiogenic pulmonary edema. EAHE is a life-threatening
condition that has been observed across a wide variety of
activities (Table 2). The incidence of asymptomatic and
symptomatic cases of EAH varies widely with regard to type
and duration of activity, location of the event, characteristics
of the participants (see risk factors) and heat or cold stress
during the event.
Epidemiology of Asymptomatic EAH
The reported incidence of asymptomatic EAH has
ranged from 0%
to 51%
immediately post-race. In
a study of an ultramarathon, 67% of the participants were
hyponatremic (asymptomatic) at some point during the race,
but only 27% nished the with serum [Na
],135 mmol/L
(40% self-corrected prior to nishing the event).
The high-
est reported incidence of asymptomatic hyponatremia post-
race has been consistently noted in 161-km ultramarathons,
in which the reported incidence of EAH has ranged between
5% and 51%.
The incidence of asymptomatic EAH in
Ironman triathlons in different environments has been re-
ported to range from negligible
to as high as 18%
In studies on endurance cyclists the incidence of
asymptomatic EAH has ranged from 0% in a 720-km race
to 12% in a 109-km race.
In a 26.4-km swim, 17% of
swimmers developed asymptomatic hyponatremia.
The re-
ported incidences at the standard marathon distance run
(42.2 km) have ranged from 0%
to 12% to 13% of race
Additionally, asymptomatic hyponatremia was
observed in 33% of premier league UK rugby players fol-
lowing an 80 minutes rugby competition
and 70% of elite
rowers during a 28-day training camp.
Epidemiology of Symptomatic EAH
Symptomatic EAH is rare and occurs with considerably
less frequency than asymptomatic EAH, but complications
associated with EAH have led to at least 14 athlete related
deaths since 1981.
Symptomatic EAH generally
occurs as an isolated case or in small clusters during or fol-
lowing endurance events with participants reporting to the
race medical facilities or to hospital emergency departments
within 24 hours after participation. In general, participants
seek treatment for a constellation of symptoms ranging from
feeling unwell to convulsions. Clusters of cases have occurred
in military training exercises, marathons, Ironman triathlons
and ultramarathons. The incidence of symptomatic EAH has
been reported to be as high as 23%
and 38%
of athletes
seeking medical care in an Ironman Triathlon and an ultra-
marathon, respectively, but most endurance events report no
cases of symptomatic EAH, especially at the marathon dis-
tance and below.
Two studies have examined large compilations of data
to help dene the incidence of symptomatic and asymptom-
atic EAH.
In the rst study of 2135 athletes from 8 endur-
ance events ranging in length from 42.2 to 161 km,
incidence of symptomatic EAH was 1% (compared to 6%
with asymptomatic EAH) among study participants. In the
TABLE 2. Activities in Which Symptomatic EAH Has Been
Reported. Those Activities in Which Known Deaths Have
Occurred Are Noted With an Asterik (*)
Documentation of Symptomatic EAH
Endurance competitions (marathon*, canoe race*, ultramarathon, triathlon,
Military exercises*
Police training*
American rules football*
Fraternity hazing*
Bikram yoga
Lawn bowling
Clin J Sport Med Volume 25, Number 4, July 2015 Third EAH Consensus Statement
Copyright © 2015 retained by authors Hew Butler T et al. All rights reserved. |305
second study of 669 161-km ultramarathon runners,
one case (0.1% among study participants) of symptomatic
EAH presented during the 5-year sampling period (compared
to 13% with asymptomatic EAH), but considering the total
number of race participants over this time period, the actual
incidence of symptomatic EAH was approximately 0.06%.
Symptomatic EAH has also been reported in hikers
and military personnel.
Symptomatic EAH accounted for
16% of Grand Canyon hikers seeking medical care for
exercise-associated collapse or exhaustion from May 31,
1993 through September 31, 1993 providing an estimated
incidence rate between 2 and 4 per 100,000 persons.
thermore, suspected hyponatremia was found to account for
19% of non-fatal suspected heat-related incidents in the
Grand Canyon National Park from April through September
during 2004 through 2009 hiking seasons.
In the US active
duty military, the annual incidence rate of hyponatremia from
1999 through 2012 has ranged from ;4 to 13 cases per
100,000 person-years (averaged 6.7 cases per 100 000
However, this incidence is probably inated
as the data were derived from a medical coded database that
does not have a specic designation for EAH and likely in-
cludes hyponatremia from both exercise and non-exercise
related conditions.
Alarmingly, symptomatic EAH is now being reported
in a more diverse set of sporting activities. For instance,
symptomatic EAH has been reported in shorter distance
endurance competitions, such as a half marathon
with slower
nishers completing the distance in 2 to 3 hours and a sprint
triathlon with slower nishers taking approximately 2 hours to
In addition, EAH has been reported in US pro-
fessional and college American rules football players
has led to the deaths of 3 US high school football players
between 2008 and 2014.
Symptomatic hyponatremia
has also been reported in a 48 year old lawn bowler who
was heterozygous for the Delta F508 cystic brosis (CF) muta-
tion, although it is unclear if complete genetic analysis for all
possible CF mutations was performed,
a 34 year old woman
following a Bikram Yoga session
and in a 39 year old woman
following a 2 hour workout including tennis and weightlift-
Cases of symptomatic EAH have also been induced in 2
separate laboratory studies involving low intensity exercise
conducted in high ambient temperatures.
Deaths from
symptomatic EAH have occurred in a 25 year old male police
ofcer participating in a 19-km bicycle training ride
and at
least partially contributed to a case of fraternity hazing
involving a male pledge performing calisthenics.
It is likely
that other cases of symptomatic hyponatremia have either not
been recognized or reported.
Risk Factors
The major risk factors for developing EAH are listed
in Table 3. The single most important risk factor is sus-
tained, excessive uid (water, sports drinks or other hypo-
tonic uids) intake in volumes greater than loss through
sweat, respiratory and renal water excretion so that a positive
uid balance accrues over time.
Almost all cases of
symptomatic EAH have occurred in individuals who have
gained or maintained weight during activities in which some
weight loss would represent uid balance and euhydra-
Body weight losses of ,0.75 kg after a standard
and ,1% after an 80 minutes rugby match
have been associated with asymptomatic EAH. All sports
beverages are hypotonic to plasma (typical sodium content
in sports drinks are approximately 10-38 mmol/L
); thus the
magnitude of excessive uid volume ingestion will over-
whelm any protective effect of the beveragessodium con-
tent on maintaining serum [Na
From a practical standpoint, it is the smaller individ-
uals and those who participate at a slower pace and drink
more than sweat losses that are more likely to develop
EAH. Although the incidence of women experiencing EAH
is greater than that of men,
adjusted for BMI and
racing time, the apparent sex difference is not statistically
Nonsteroidal anti-inammatory drugs (NSAIDs) have
been implicated as a risk factor in the development of
presumably by potentiating the water retention
effects of arginine vasopressin (AVP) at the level of the kid-
ney collecting duct.
However, data are conicting,
and further investigation is necessary to determine whether
NSAID usagewith respect to both classication and
dosageis a risk factor for the development of EAH. The
possible pathophysiological contributions of intrinsic renal
and low solute diets
on water retention, high
sweat sodium concentrations
in extreme environments,
and the potentiation of thirst by non-osmotic stimuli during
warrant further investigation as secondary
risk factors for EAH. Whether common medications that
are associated with hyponatremia and the syndrome of inap-
propriate anti-diuretic hormone secretion (SIADH) in the gen-
eral population, such as selective serotonin reuptake
inhibitors, can potentiate the development of EAH is not
known and warrants further investigation.
There is a paucity of evidence suggesting that those
developing symptomatic EAH have either been a salty
or a heterozygous carrier of the cystic brosis
Athletes with homozygous CF, however, are at
risk for developing hyponatremia as demonstrated by
numerous instances when an individual is diagnosed with
CF after the development of hyponatremia during prolonged
physical exertion
or prolonged exposure to high ambi-
ent temperatures.
As individuals with CF experience
a longer lifespan (median predicted survival age in 2012 was
41.1 years
) and are encouraged to consider exercise as
TABLE 3. Risk Factors for the Development of Asymptomatic
and Symptomatic EAH
Risk Factors for EAH
Overdrinking water, sports drinks, and other hypotonic beverages
Weight gain during exercise
Exercise duration .4h
Event inexperience or inadequate training
Slow running or performance pace
High or low body mass index (BMI)
Readily available uids
Hew-Butler et al Clin J Sport Med Volume 25, Number 4, July 2015
306 | Copyright © 2015 retained by authors Hew Butler T et al. All rights reserved.
one of their therapies,
this population may be at increased
risk for EAH due to the combination of high sweat uid and
sweat [Na
Etiology and Pathophysiology of EAH
The predominant pathophysiology of EAH, and of most
serious medical concern, is dilutional hyponatremia caused by
sustained overdrinking and AVP induced impaired water
clearance, which overwhelms the ability of the kidney to
excrete the excess water load. Dilutional hyponatremia is the
primary pathophysiological variant of clinically symptomatic
EAH and largely (if not exclusively) associated with all
reported cases of morbidity and mortality that are listed in
Table 2. Dilutional EAH is an acute onset form of hypona-
tremia, which is now occurring in non-endurance sports, with
3 deaths, recently reported amongst the approximately 7.5
million American high school football player-years from
2008 through the 2014 seasons.
These football players
were encouraged to ingest copious volumes of hypotonic
uids and sports drinks to prevent or relieve exercise-
associated muscle cramps (EAMC),
in the belief that
EAMC was caused by dehydration and electrolyte imbal-
However, experimental
and observational
studies speculate that EAMC may reect neurological
changes due to fatigue rather than uncompensated water
and sodium losses incurred during exercise in some cases.
Muscle cramping and tremor have also been associated with
overdrinking and hyponatremia in athletes,
and animals.
Symptoms associated with EAH are due to osmotically-
induced shifts of water into the intracellular compartment. In
the conned space of the cranium these shifts of water into the
central nervous system (CNS) tissues lead to cellular edema
and pathological increases in intracranial pressure. Acutely,
this may manifest in symptoms previously described and in
the extreme may lead to brain stem herniation and death.
Etiology of Euvolemic/Hypervolemic EAH
Total body water expansion relative to the
amount of total body exchangeable sodium is the main
pathogenic cause of asymptomatic and symptomatic
Dilutional EAH
can be euvolemic (total body water expansion without changes
in total exchangeable sodium) or hypervolemic (total body
water expansion above concomitant increases in total
exchangeable sodium). The primary etiologic factor in dilu-
tional hyponatremia is consumption of uids (water, sports
drinks or other hypotonic uids) in excess of total body uid
losses, which includes the sum of insensible (cutaneous, respi-
ratory, and gastrointestinal),
sweat and renal (urine) uid
Hyponatremia caused solely by the overconsumption of
uids, above known maximal urine excretory rates of 800 to
1000 mL/,
has been demonstrated at rest in athletes with
and without a history of EAH.
Although some cases of
EAH may be due to pure water intoxication from overcon-
sumption of uids, non-osmotic AVP secretion is a key con-
tributing factor in most athlete-related symptomatic cases.
Known stimuli to AVP secretion that are commonly
associated with exercise include: nausea/vomiting
interleukin-6 release
; plasma volume contraction
; hypo-
; elevated body temperature
; and/or other hor-
monal mediators.
Even small increases in circulating AVP
levels can markedly reduce renal water excretion well below
maximal levels,
resulting in retained body water not only
when drinking rates do not exceed those necessary to prevent
excessive dehydration, but also when drinking rates are well
in excess of uid replacement need.
The primary etiology and pathophysiological mecha-
nism underlying EAHand all known fatalitiesis the over-
consumption of hypotonic uids relative to exchangeable
sodium in likely combination with non-osmotic AVP secre-
tion (Grade 1A).
Etiology of Hypovolemic EAH
There is persisting debate as to the relative contribution
of under-replaced sodium losses to the lowered sodium
concentrations observed in EAH. While in clinical medicine,
electrolyte depletion without expansion of total body water
or hypovolemic hyponatremia is well described,
EAH this variant has been more difcult to dene and is
much less likely to be encountered except in extreme events
usually over prolonged periods (such as ultra-marathons)
or hot Ironman distance triathlons.
The data regarding
sodium losses during exercise (as measured during recovery)
and their potential contribution to the development of symp-
tomatic hyponatremia in longer and hotter races
have been
consolidated in Table 4 against data collected from relatively
shorter and cooler races
where uid overload hypo-
natremia has been veried. From the standpoint of the clin-
ical literature, hypovolemic hyponatremia reects a loss of
total body exchangeable sodium that manifests as volume
Hypovolemic EAH would be predicted
to occur in athletes exercising for longer periods of time (such
as 161 km ultramarathons; .20 hours),
and/or in
environments and/or with higher sweat
sodium losses.
Clinical conrmation of the hypovolemic
form of hyponatremia is supported by a spot urine sodium
concentration (U[Na
]) below 30 mmol/L
in conjunc-
tion with a serum or plasma [Na
] below 135 mmol/L. A spot
],30 mmol/L is 100% specic and 80% sensitive for
predicting a sustained increase (.5 mmol/L) in serum [Na
following isotonic saline administration
in clinical patients.
Elevated blood urea nitrogen levels (.20 mg/dL)
weight loss
may also suggest volume depletion as
a pathogenic contributor to EAH. However, these biochem-
ical tests are not always available at the point of care and
thus clinical assessment (vital signs, weight change, and
physical examination) may be the only indication of volume
Under-replaced sodium losses contribute to serum
] independent of distance (Grade 1A). However, there
Clin J Sport Med Volume 25, Number 4, July 2015 Third EAH Consensus Statement
Copyright © 2015 retained by authors Hew Butler T et al. All rights reserved. |307
is paucity of data supporting sodium loss as the primary
mechanism of symptomatic EAH even in those who exercise
for prolonged periods of time and in warm weather (Grade
2C). In these cases, relative over-drinking of hypotonic uids
with sustained non-osmotic AVP secretion is likely involved
in the development of symptomatic EAH.
The Role of Thirst
Since drinking uid volume above sweat and urinary
losses during and after activity is the main pathophysiolog-
ical mechanism underlying asymptomatic, symptomatic and
fatal cases of EAH, prevention is dependent on drinking
less. Thirst should provide adequate stimulus for preventing
excess dehydration and markedly reduce the risk of devel-
oping EAH in all sports. Physiologically-driven thirst has
been dened as a generalized, deep seated feeling of desire
for water
and is an evolutionarily conserved, nely
tuned, regulatory mechanism serving to protect both plasma
osmolality and circulating plasma volume.
located within the circumventricular organs of the brain
(highly vascularized structures located around the third
and fourth ventricles and characterized by the lack of
a bloodbrain barrier that are points of communication
between the blood, the brain parenchyma, and the cerebral
spinal uid) and baroreceptors located within the aortic arch,
carotid sinus and great veins provide real-timeneural
input to higher centers of the brain which continuously
and simultaneously coordinate the regulation of both thirst
and AVP secretion. Thus, there are physiological sensing
mechanisms in place to prompt when to drink and therefore
guard against excessive dehydration. Earlier published rec-
ommendations to begin drinking before thirst was largely
meant for situations where sweating rates were high, above
maximal rates of gastric emptying, and dehydration would
rapidly accrue over time. Unfortunately, this advice has fos-
tered the misconception that thirst is a poor guide to uid
replacement and has facilitated inadvertent overdrinking and
pathological dilutional EAH.
Clinical Classification and Diagnosis of EAH
The diagnosis of EAH is made when the blood, serum
or plasma [Na
] is below the normal reference range of the
laboratory performing the test (typically ,135 mmol/L) and
is associated with typical clinical constellation of symptoms
and signs. In our collective experience, EAH is best classied
by clinical severity (symptoms) and not the absolute numer-
ical [Na
] value to best guide treatment strategies.
Characteristics of Asymptomatic EAH
Asymptomatic EAH represents a biochemical nding,
diagnosed by blood electrolyte testing for research or
unrelated metabolic screening purposes.
This group of subjects presents without any discernable
symptoms or may have mild, generalized and transient
complaints commonly experienced by other participants
who do not typically seek medical care following exercise.
In normally distributed populations, up to 5% of all athletes
tested would fall outside of the normal range for [Na
with half of those (2.5%) falling in the range of asymptom-
atic EAH values.
Characteristics of Mild EAH
Mildly symptomatic EAH typically presents with non-
specic signs and symptoms without clear signs of encepha-
lopathy (Table 5). Athletes with mild EAH may have normal
vital signs, may not have any orthostatic hypotension, and the
symptoms do not resolve after placing athletes in the Trende-
lenburg position
as would be expected with exercise
TABLE 4. Comparisons of Sodium and fluid Balance Measured During the Recovery Period After Exercise Demonstrating Race
Characteristics and Biochemical Differences Between Fluid Overload Hyponatremia (Irving et al,
Speedy et al,
and Speedy
et al
) Versus Suspected Hypovolemic Hyponatremia (Owen et al
Variable Irving et al
Speedy et al
Speedy et al (2 cases)
Owen et al
EAH subjects (classication)* 8 (symptomatic) 7 (symptomatic) 2 (asymptomatic) 26 (asymptomatic)
Peak race temperature (8C) NR 21 21 33
Mean exercise duration (h) ,11 (mean NR) 12 13/12 (case 1/case 2) 22
Monitored recovery time (h) 16 11.6 11.7/13 1
Presenting U[Na
] (mmol/L) NR 17(41 controls)* NR 15 pre-trial (22.3 post-trial)
Presenting BUN (mg/dL) 15.5 pre-trial (9.8 post-trial) NR NR 31 (pre and post-trial)
Body sodium retained
(mean value)
48% 284 mmol (0 mmol controls)* 34%/0% 96%
Excess uid excreted (mL)§ +2953 +1670 (2441 controls)* +1500/+2500 +20
Presenting serum [Na
(mean 6SD) (mmol/L)
122 62 127 64 131/130 131 63
Body weight change (post-race 2
pre-race) (%)
NR NR +0.9/+2.5 22.4 63.1
*EAH data compared with control group of normonatremic triathletes partaking in the same event.
All but one of these 7 athletes with EAH was released from the hospital with hyponatremia.
This represents the total amount of sodium retained by the body and expressed as a percentage of the total amount of sodium that was administered during the monitored recovery
period (sodium decit/sodium given). In Speedy et al 2000,
this was expressed as a positive or negative amount (mmol) of sodium administered so that a negative value reected the
amount of sodium retained by the body (UNa
output minus Na
§This represents the amount of uid excreted (urine volume) during the recovery period compared with the amount of uid that was administered during the recovery period.
NR, not reported in the manuscript.
Hew-Butler et al Clin J Sport Med Volume 25, Number 4, July 2015
308 | Copyright © 2015 retained by authors Hew Butler T et al. All rights reserved.
associated postural hypotension.
The clinical symptoms of
mild symptomatic EAH are not specic or sensitive, but
should raise the index of suspicion for EAH and necessitate
a low threshold for [Na
] measurement, as athletes can rap-
idly progress from mild symptoms to severe and life-
threatening EAHE (Table 5).
EAH must be differentiated from other causes of
collapse that may present with similar signs and symptoms
including exertional heat illness,
acute mountain sickness,
and exercise associated postural hypo-
It is important for medical staff to perform a rapid
history and physical examination to help determine the eti-
ology of these nonspecic symptoms. However, any clini-
cal suspicion of EAH should lead to prompt measurement
of [Na
], if possible. It is common for athletes with EAH to
maintain or gain weight during exercise.
EAH in the presence of weight loss has been documented
in ultra-endurance races in the heat.
Thus, the
presence of weight loss does not necessarily exclude
EAH. Weight gain or weight maintenance associated with
any symptoms listed in Table 5 is an indication to measure
the athletes[Na
]inordertoconrm or exclude the
diagnosis of EAH or to consider empiric treatment if
on-site [Na
] cannot be measured, such as in remote
Characteristics of Severe EAH (EAHE)
Severe symptomatic EAH is characterized by neuro-
logical signs and symptoms due to cerebral edema that
occur when water ows along the osmotic gradient from the
extracellular uid into the intracellular compartment
(Table 3).
Severe symptomatic EAH may
may not
be accompanied by the respiratory distress of
CNS-triggered non-cardiogenic pulmonary edema (Table 5).
EAHE is a life threatening condition that requires urgent
intervention and should be evaluated with an immediate
] measurement if available.
EAH can present with a wide range of symptoms
ranging from nonspecic mild complaints to severe en-
cephalopathy. The severity of symptoms and not the
absolute value of the [Na
] should guide the choice of
therapy (Grade 1A). Rapid determination of [Na
] is criti-
cal in conrming clinical suspicion but may not always be
Treatment of EAH
Any athlete exhibiting signs or symptoms consistent
with acute hyponatremia (Table 5) should be screened for
EAH. The capacity for onsite [Na
management of EAH and is recommended for any large-
scale endurance event. However, this capability is not
always practical or possible (eg, small or remote
Treatment should be based on the degree of
neurological impairment, not simply the [Na
] level
brain edema is dependent upon both the magnitude and rate
of fall of [Na
] not just the lowest level reached, as stated
previously. The following treatment protocols are recom-
mended for EAH and EAHE based on either [Na
] measure-
ment and clinic assessment or clinical assessment alone if
] measurement is not available.
Onsite Treatment of Asymptomatic EAH Found Via
] Measurement
Asymptomatic hyponatremia is not normally detected
unless an athlete has blood electrolyte concentrations tested
for some other reason.
In athletes with
this incidental biochemical diagnosis, oral or intravenous
hypotonic uid intake should be restricted until the onset
of urination (which suggest that AVP levels have fallen and
that the urine is likely dilute) to reduce the risk of further
decreasing [Na
] with continued AVP-mediated water
Furthermore, isotonic intravenous uids
should be administered with great caution or withheld until
urination as, in the setting of elevated AVP levels and a con-
centrated urine, these uids may lower the [Na
or delay
Although there is no compelling reason to actively treat
asymptomatic EAH, it is clinically appropriate to administer
oral hypertonic saline solutions (HTS), to reduce the risk of
progression to symptomatic hyponatremia
; this is par-
ticularly relevant for those with a [Na
],130 mmol/L. Upon
departure from the event site, athletes with asymptomatic
EAH should be advised to seek urgent medical attention if
any neurologic signs or symptoms of EAH develop within 24
hours after event nish, since delayed-onset symptomatic
EAH may frequently occur.
an athlete with asymptomatic EAH should have a companion
upon discharge from the medical area to observe the affected
athlete for signs and symptoms of evolving EAH, since the
neurological impairments associated with EAH may limit the
athletes ability to accurately self-assess his or her status.
TABLE 5. Signs and Symptoms of Mild and Severe (Life-
threatening) EAH. Signs and Symptoms Related to Other
Conditions Associated With Exercise-Associated Collapse
Noted With an Asterisk (*)
Symptoms and Signs Associated With Mild EAH
Body weight gain from baseline
Symptoms and Signs Associated With Severe EAH and EAHE
Altered mental status* (confusion, disorientation, agitation, delirium, feelings
of impending doom,obtundation)
Phantom running
Signs of impending brain herniation (decorticate posturing, mydriasis)
Dyspnea (non-cardiogenic pulmonary edema)
Frothy sputum (non-cardiogenic pulmonary edema)
Clin J Sport Med Volume 25, Number 4, July 2015 Third EAH Consensus Statement
Copyright © 2015 retained by authors Hew Butler T et al. All rights reserved. |309
The major clinical relevance of asymptomatic EAH lies
in its potential for asymptomatic athletes to quickly transition
and progress into symptomatic stages if hypotonic uids are
given intravenously or ingested (Grade 1C). Thus, in patients
identied with EAH, hypotonic or isotonic uids should be
withheld until urination is documented (Grade 1C).
Onsite Treatment of Symptomatic EAH Found
Via [Na
] Measurement
Severe EAH (EAHE)
Acute severely symptomatic hyponatremia is a rapidly
progressing, life threatening emergency that requires imme-
diate administration of IV hypertonic saline (HTS) (such as
3% sodium chloride).
Because EAH is an
acute rather than chronic process, athletes presenting with
symptomatic hyponatremia can and should be treated with
HTS as there is no risk of osmotic demyelination after
exposure to HTS, but there is grave risk of brain herniation
and non-cardiogenic pulmonary edema if HTS is not
Any athlete with EAH associated with signs or
symptoms of encephalopathy should be immediately treated
with an IV bolus or infusion of HTS to acutely reduce brain
edema, with additional IV boluses administered until there is
clinical improvement
(Table 6). The dose and route of
HTS administration should be based upon the severity of
clinical symptoms and the available HTS formulations, as
discussed in Table 6. Numerous case reports and case series
have validated the efcacy and safety use of IV HTS admin-
istration in symptomatic EAH
one runner receiving 950 mL of 3% over a 7-hour period
without complications
and another swimmer receiving 40
mL of 20% HTS
without complication.
In the event that an athlete presents with symptoms of
severe, life-threatening encephalopathy (eg, seizures, coma,
or signs of impending brain herniation) it is acceptable and
highly recommended to administer the rst bolus of HTS
before [Na
] is measured. Conrmed symptomatic dilutional
(euvolemic or hypervolemic) EAH is a contraindication to the
administration of IV hypotonic uids, lactated Ringers, or
isotonic (normal) saline, all of which can worsen the degree
of hyponatremia
or delay recovery.
The efcacy of IV HTS as the denitive treatment of
acute hyponatremic encephalopathy has been validated
extensively in both hospital and eld settings since it was
rst utilized successfully in 1938.
This treatment is based
on the capacity of an IV HTS bolus to increase the serum
] 2 to 5 mmol/L, resulting in a concomitant decrease of
intracranial pressure and improvement in symptoms.
approach does not pose any substantial danger to the patient,
because osmotic demyelination syndrome has not been asso-
ciated with either the rapid correction of acute hyponatremia
(ie, ,48 hours duration) in clinical
or exercise set-
or with the limited increase
in [Na
] produced by a single bolus of HT.
Also, of
note, if the athlete was wrongly assumed to have EAHE,
the administration of HTS in small boluses is not associated
with any negative consequences and serves as an excellent
volume expander.
The goal of this therapy is to stabilize the athlete for
transfer to an advanced medical care facility for further
evaluation, monitoring and treatment. Ideally, the athlete
should be transported with knowledgeable event medical
personnel able to maintain the same level of care en route
and to ensure that the treatment is not interrupted for
evaluation such as computerized tomography (CT) imaging
of the brain or treatments that may worsen hyponatremia,
such as administration of hypotonic uids, lactated Ring-
ers, or isotonic (normal) saline. The diagnosis of EAH or
EAHE must be communicated to the receiving physician
upon transfer of care.
For those athletes presenting with signs and symptoms
consistent with EAHE, emergent intravenous treatment
therapy with hypertonic saline is indicated and should not
be delayed pending laboratory measurement or other diag-
nostic testing (Grade 1B).
Mild EAH
Any athlete with mild EAH symptoms (Table 6) may
be treated with an IV bolus of HTS as described above.
Alternatively, a mildly symptomatic athlete may be treated
with oral hypertonic solutions when tolerated
(Table 6) or observation until urination, as seen in clinical
Oral sodium tablets may not be as efcacious as
hypertonic solutions, as suggested in a single case report
and requires further investigation. The efcacy and tolerance
of oral HTS has been supported by limited eld
TABLE 6. Recommended Treatment for Both Mild and Severe
(Life-threatening) Symptomatic EAH in Field or in the Hospital
Treatment of Mild EAH
Observation (restrict hypotonic and isotonic uids until urinating freely)
Administration of intravenous HTS (see below for severe symptomatology)
Administration of oral HTS:
Concentrated bouillon (4 bouillon cubes in 125 mL, ½ cup, of water)
3% NaCl (100 mL), preferably with the addition of a avoring (eg, Crystal
Light, Kool Aid)
Equivalent volumes of other solutions of high sodium concentration
(eg, 3%-9%)
Treatment of Severe EAH
Administration of intravenous HTS:
100 mL bolus of 3% NaCl, repeated twice if there is no clinical
improvement (10 min intervals have been recommended, but this should
be determined by the clinical judgment of the treating physician)
Comparable amounts of more concentrated Na
-containing solutions
(eg, 10 mL of 20% NaCl; 50 mL of 8.4% NaHCO
) may be used as an
alternative to 3% NaCl
In some situations (ie, more severe encephalopathic symptomatology such
as seizures, coma or signs of impending brain herniation) it may be
appropriate to administer larger HTS boluses initially rather than waiting
to assess clinical improvement after repeated smaller boluses
HTS, hypertonic saline.
Hew-Butler et al Clin J Sport Med Volume 25, Number 4, July 2015
310 | Copyright © 2015 retained by authors Hew Butler T et al. All rights reserved.
and may offer practical advantages in some
settings (eg, IV HTS or IV access is not available). In con-
trast to athletes with severe EAH, those with mild symptoms
may be discharged from onsite medical care once symptoms
have resolved and spontaneous urination has occurred.
Repeat measurement of [Na
] is generally not required
unless the patient has persistent symptoms after the initial
treatment. As is recommended for asymptomatic EAH, upon
departure from the event site athletes should be advised to
seek urgent medical attention if any signs or symptoms of
EAH develop after discharge and ideally should have a com-
panion capable of monitoring for signs and symptoms of
which the athlete may not be aware.
Athletes presenting with mild symptoms associated with
EAH can be treated with an IV bolus of HTS (Grade 1B), oral
hypertonic saline uids or observation until the onset of
urination as dictated by clinical symptoms (Grade 2B).
Onsite Treatment of EAH Suspected Clinically
but Unable to Confirm Via [Na
The situation may arise where EAH is strongly
suspected based on the clinical evaluation of the athlete
(ie, history and physical examination showing neurological
symptoms or signs of EAH; Table 3) but [Na
such as in a remote setting.
In this
situation empiric treatment is justied using the same treat-
ment recommendations described above for EAH docu-
mented with a [Na
] (Table 6). This empiric approach
can be lifesaving and is unlikely to do harm, since: (1)
the additional small increase in serum osmolality from
a single bolus of HTS will not signicantly worsen the
neurological status and (2) a bolus of HTS will expand
the intravascular volume by increasing the serum [Na
partially reducing any hypovolemic component of the
In Hospital Treatment of Symptomatic EAH
Athletes presenting to a hospital or medical facility,
whether primarily or as a transfer from the event site, with
signs or symptoms of hyponatremia will require immediate
measurement of electrolytes and should be treated as
described above without delay once EAH is conrmed
(Table 6). If symptomatic EAH persists or worsens follow-
ing the initial intervention with IV HTS, current treatment
guidelines for acute symptomatic hyponatremia should be
instituted and the patient managed in an intensive or critical
care setting with care provided or guided by a specialist
familiar with this life threatening condition.
Athletes presenting to a medical facility with EAH
should be treated as per other settings (Grade 1C). However,
diagnostic testing in these scenarios should not delay
potentially life-saving therapy with HTS (Grade 1C).
Athletes and support crews need to carefully consider
uid and electrolyte supplementation during and after
exercise and the rationale behind those decisions. Excessive
uid replacement beyond thirst (whether water, sports drinks
or other hypotonic uids) is not a panacea for all instances of
fatigue, collapse, muscle cramping, or exertional heat stroke
(Table 7). The drinking of uid volumes sufciently above
sweat and urinary losses before, during and after activity and
the accrual a positive water balance, is the primary underly-
ing pathophysiological mechanism of symptomatic and fatal
EAH cases.
34,41,45,52,57,58,61,71,73,75,76,84 ,119,122126,162,163
fore, prevention strategies must target drinking behavior.
Fluid intake recommendations suggesting that athletes begin
to drink uids before the onset of the sensation of thirst were
targeting those exercising in situations where high sweat
rates were present and dehydration could evolve rapidly
with known medical and performance outcomes. Unfortu-
nately, this advice fostered the misconception that thirst is
a poor guide to uid replacement in lower sweat rate situa-
tions. We believe that this has facilitated individuals choos-
ing to inadvertently adopt overdrinking and develop
pathologic dilutional EAH, as demonstrated in 41 cases
Modest to moderate levels of dehydration are tolerable
and pose little risk to life in otherwise healthy individuals.
Laboratory and eld studies indicate that uid decits less
than and up to a volume approximately equal to 3% of normal
body mass (or ;5% total body water) can be tolerated with-
out a reduction in endurance performance or muscular power
when in cool to temperate (2108C-208C) temperatures.
Therefore, aggressive drinking to prevent dehydration is
unnecessary and carries with it greater risk of developing
symptomatic EAH.
Body weight is a reasonable surrogate measure of
hydration state when measured day to day after sleep
can be used to relatively accurately assess changes in
hydration state accompanying upwards to 1 to 2 hours of
activity. However, it is a very imprecise measure during the
athletic events where EAH is most likely to develop, that is,
multiple hours of sustained activity. This is in large part
due to body mass changes accompanying energy
and unknown amounts of food consumed,
bathroom stops, etc. Moreover, consolidation of 4 studies
(786 athletes) comparing body weight changes taken at
registration (1-3 days prior) and again within 60 minutes
of race start demonstrate an average 1% increase in body
from registration to race start. However,
this average value conceals that fact that large gains in
occur in some
individuals while substantial weight losses occur in others
over that last day or 2 before competition. This weight
increase further confounds the accuracy of bodyweight as
a proxy measure of body water in eld events. With
that said, a body mass measured after several hours of
activity that is equal to or above the individuals normal
body mass is a positive indicator for the presence of uid
Clin J Sport Med Volume 25, Number 4, July 2015 Third EAH Consensus Statement
Copyright © 2015 retained by authors Hew Butler T et al. All rights reserved. |311
The safest individualized hydration strategy before,
during and immediately following exercise is to drink
palatable uids when thirsty (Figure). Marathon runners
with hypernatremia report thirstinessas a physiologically
expected symptom
while a weak but statistically signif-
icant relationship has been demonstrated between thirst rat-
ings and plasma [Na
] immediately following a 161 km
Studies verify that participants allowed free access
TABLE 7. Thirteen Studies Representing 41 Cases of Symptomatic EAH Which Provided Comment on Drinking Plan or Motivation
for Chosen Drinking Behaviors [*Case Reports Involving Multiple Subjects: Total Number Subjects (Number of Female/Male
Subjects Age (yo), Sex (♂♀),
Serum [Na
] mmol/L
(Initial or Range)
Symptomatic EAH With Drinking Above Thirst
(Comments From Report)
Frizzell et al
24, /45, , Ultra-runners 123/118 Runners as a group are taught to push uids
Athletes are instructed to drink more than their thirst
Armstrong et al
21, , Lab subject 122 .voluntarily consumed this large volume of uid
because he believed that drinking water copiously
would decrease his risk of heat illness
Herfel et al
22, , Football player 121 He was diagnosed with muscle cramps secondary to
dehydration. Therefore, ve liters (L) of 0.45%
normal saline in 5% dextrose was administered
intravenously along with 3L of liquids by mouth over
ave hour period
Reynolds et al
*6 (4/2), Soldiers 118-134 .consuming large volumes of water as protection
against becoming a heat casualtypredisposed these
troops to the physical impairment that they intended to
Backer et al
*7 (6/1), Hikers 109-127 Most patients diagnosed as having hyponatremia have
a distinct history of high uid intake.
.unlike heat exhaustion patients, few of our
hyponatremic patients were thirsty when evaluated,
perhaps because they drank more uids and were
Garigan and Ristedt
18, , Soldier 121 .complained of thirst, drank 3 quarts then
vomited.told to drink 1 quart every 30 minutes.
With encouragement by unit members, he consumed
10 quarts of water during the next 90 minutes
.with encouragement by unit members
Hew et al
*21 (9/8), Marathon runners 117-134 Advice given to runners was drink until your urine is
clearand do not wait until you are thirsty to drink
27, , Football player 116 .complained of feeling ill.encouraged to consume
sports drinks
.Admits to drinking 2-3 gallons water every day
because he had been taught that water is the best
replacement uidand because that is what he was
advised to do growing up in Texas
Hew-Butler et al
41, , Ironman triathlete 132 (nadir) Subject reports he was never thirsty, but drank to stay
ahead of thirst
Draper et al 2009
37, , Marathon runner 117 .she followed a strategy (as advised by fellow
experienced marathon runners) to begin the race
well-hydrated(drinking greater volumes than her
thirst dictated)
.warnings were issued over the public address system
at the race start relating to ensuring a high intake of
uids was maintained
Rothwell and Rosengren
43, , Hiker 107 .complained of abdominal pains and leg cramps for 24
hours leading up to collapse
.on the evening before and day of collapse, fellow
trekkers and guides encouraged him to drink large
amounts of water
Coler et al
85, , Hiker 120 Subject was encouraged to.Push uidsabove thirst
Rogers et al 2015
46, , Swimmer 118 Her intended uid regimen.was 200mL of uid every
20 minutes
She reported no sensation of thirst throughout the race
.although she did not feel thirsty, she was encouraged
to drink by the support staff
Hew-Butler et al Clin J Sport Med Volume 25, Number 4, July 2015
312 | Copyright © 2015 retained by authors Hew Butler T et al. All rights reserved.
to uids during treadmill walking in the heat
or running
30 km under different ambient conditions
plasma osmolality by drinking to thirst. Moreover, the cues
to drink provided by osmolality and blood volume persist in
both hot
and cold
environments. Thus, drinking to
thirst will, in most cases, prevent both dilutional EAH and
performance decrements due to excessive dehydration.
Potential exceptions to this uid replacement strategy
are thirst stimulated by confounding oral variables such
as dry mouth (xerostomia),
genetic inuences,
FIGURE. Primary recommended
fluid intake strategy to prevent
symptomatic EAH.
TABLE 8. Four Case Reports Reporting Symptomatic EAH While Drinking Either ad libitum (First 2 Cases) or in Response to Thirst
(Second 2 Cases)
Subjects Age (yo), Sex (♂♀),
Plasma [Na
] mmol/L
Symptomatic EAH With ad libitum Drinking (Comments
From Report)
Baker et al
65, , Lab trial 126 46kgdrank 2.8L water and gained 2.4 kg in 2.5 hr
intermittent cycling trial 308C
Subjects were not encouraged to drink but told that more uid
was readily available if needed
28, , cyclist 114 Subject followed her normal practice of ingesting a GU packet
with 200mL of water every
45 minutes with Coke and water ad libitum for an estimated
uid consumption rate of ;550ml/hr
Subjects Age (yo), Sex (♂♀),
Plasma [Na
] mmol/L
Symptomatic EAH With Drinking in Response to Thirst
(Comments From Report)
Khodaee et al 2013
44, , Mountain biker 116 84kgdrank 29L water and 5.3 g sodium during plus after race
(;14 hrs total)
History of muscle cramping after 5-6hr cycling. Felt very
thirstyafter the race
Initial labwork in hospital: urine[Na
] = 31 mmol/L and BUN =
19 mg/dl
Labwork 2 months after hospitalization: plasma [Na
] = 133
mmol/L, BUN = 10 mg/dl
Hoffman et al 2015
53, , Ultra-runner 122 Subject began using regular sodium supplementationand
very thirstyat 100km
2.2% weight gain noted at 126km and dropped out of race at
145km (28 hrs)
Initial labwork in hospital: BUN = 22 mg/dl
17 hrs later in hospital (.10.4L 0.9% saline), plasma [Na
136 mmol/L and BUN = 10 mg/dl
Subject received 20L of IV uids in hospital and discharged
with positive uid balance of 6.6L
Clin J Sport Med Volume 25, Number 4, July 2015 Third EAH Consensus Statement
Copyright © 2015 retained by authors Hew Butler T et al. All rights reserved. |313
known discrepancies between drinking ad libitumversus
drinking according to the dictates of thirst,
sodium intake and/or other non-osmotic or hypovolemic
factors that are yet to be determined and require further
investigation (Table 8).
Given that excessive uid consumption is a primary
etiologic factor in EAH, using the innate thirst mechanism to
guide uid consumption is a strategy that should limit drinking
in excess and developing hyponatremia while providing
sufcient uid to prevent excessive dehydration (Grade 1C).
Additional Strategies to Prevent EAH
Sodium Supplementation
When uid intake matches or even slightly exceeds
sweat losses, the ingestion of sodium-containing sports drinks
can attenuate the rate of fall of [Na
] over the course of 2
hours of continuous
or intermittent
cycling and ;4 hours
of running.
However, it is critical to emphasize that
sodium containing sports drinks, which are hypotonic, will
not prevent EAH in athletes who overdrink during exercise,
as all sports drinks have a signicantly lower [Na
] (10-38
mmol/L) than serum (;140 mmol/L). The dilutional effect of
volume excess overwhelms any positive effect of sodium and
electrolytes in sports drinks.
Therefore, while modest salt
replacement is likely not harmful and has been associated
with signicant increases
or no change
in serum
] during competitive eld events it will be of modest to
no benet in situations where excess uids are being con-
sumed. The potential detrimental effects of excessive sodium
supplementation are not clear.
Sodium supplementation is a strategy for attenuating
sodium concentration reductions that can develop when uid
intakes approximate sweat losses during prolonged exercise
but cannot prevent EAH in the setting of a persistent excessive
uid intake that produces uid overload (Grade 1C).
Education and Event Management Efforts
Athlete and support team educational strategies should
be instituted to improve knowledge of safe hydration
practices and reduce the overemphasis on high uid intakes.
For example, an education program for an Ironman triathlon
advising athletes of the risks incurred by overdrinking
coupledwithdecreasingthenumberofuid stations
to limit the uid availability reduced the incidence of
Dissemination of appropriate drinking advice
alone has also been shown to reduce the incidence of
EAH in a 90 km footrace.
Past studies have demonstrated that cycling uid
stations placed 20 km apart in an Ironman triathlon and
running uid stations placed 5 km apart in a standard
marathon have reduced or prevented EAH.
this proposed strategy and its effect on the incidence of
EAH needs further study to determine the optimal number
and spacing of uid stations in different terrains and ambient
temperatures. Furthermore, alternative strategies will be
needed in settings where EAH has been noted but either aid
stations are not provided or in situations where drinks are
freely available and/or athletes transport their own uids.
Athletes who seek more quantitative guidance are
encouraged to weigh themselves before and after training to
assess their sweating rates and uid replacement needs. Some
weight loss associated with activity will be unrelated to uid
status as non-water mass is lost as energy is expended
(;0.23-0.24 g/kcal)
and is increased with increasing
duration and intensity of exercise.
The presence of weight
gain is positive indicator that uid intake has been in excess
of uid losses and water overload is present.
Educational efforts regarding the risks of overhydra-
tion should be encouraged and disseminated widely to
athletes, coaches, and event management personnel (Grade
1C). These efforts should include all sporting events where
EAH has been encountered. Event management strategies
such as limiting access to uids may be of benet, but
require broader study.
Dissemination of Advice for Prevention and
Treatment of EAH
Athletes, Coaches, Parents
Educational strategies and programs are needed that
effectively communicate to coaches, athletes, and parents
rational uid replacement, avoidance of overconsuming uids
(water, sports drinks or other hypotonic uids), to recognize
the signs and symptoms of EAH, and to understand the
critical need for immediate medical attention for suspected
casualties. Athletes, coaches and parents must be alert to the
risks of excessive uid consumption and understand that high
uid intakes will not necessarily prevent exercise-associated
maladies such as muscle cramps or exertional heat stroke.
On-site Medical Professionals (Medics, Paramedics,
Emergency Medical Technicians, Athletic Trainers,
Physiotherapists, and Others)
The educational strategies for on-site medical person-
nel must address the circumstances (during or following
events or practices during acclimatization), identication,
evaluation and management of EAH and EAHE, and
emphasize that the life-threatening nature of these rare
conditions require immediate intervention. The pathophys-
iology of EAH and the drinking behaviours involved in the
evolution of EAH must be clearly recognized. It should be
stressed that: (1) EAH is caused primarily by the consump-
tion of hypotonic uid in excess of sweat and urinary losses
and (2) excessive uid intake (water, sports drinks or other
hypotonic beverages) may not prevent muscle cramps or
exertional heatstroke and in rare cases may even be
On-site personnel must under-
stand that oral uid intake and IV uid infusion of hypotonic
and isotonic uids is contraindicated in all suspected cases
Hew-Butler et al Clin J Sport Med Volume 25, Number 4, July 2015
314 | Copyright © 2015 retained by authors Hew Butler T et al. All rights reserved.
of EAH and rapid transfer to a hospital is necessary. The
potential life-saving role of HTS requires wide-spread edu-
cation and should be considered the equivalent of automatic
external debrillators and ice/cold water immersion in the
rst aidof sudden cardiac arrest and exertional heat
stroke, respectively.
Team Physicians and Medical Directors of
Athletic Events
Team physicians and medical directors of athletic
events should be involved in all decisions regarding medical
management including overseeing medical protocols, med-
ical supplies/equipment, strategies for uid replacement that
optimize safe hydration practices, placement of uid sta-
tions, and the use of intravenous rehydration. Important
athletic event decisions include spacing and placement of
uid stations, distribution of uid replacement advice to
athletes, and training of the aid station personnel and
spectators. Drinking advice distributed to participants by
sponsors should be reviewed by and approved by the event
medical team to avoid conict with the ofcial race
educational information.
Team physicians and event medical directors should
ideally have onsite point of care [Na
] analysis available and
hypertonic saline on hand for management of EAH and
EAHE. The event organizer/medical director should be in
contact with the local emergency medical services to ensure
that transportation to an advanced care medical facility is
available during events with high risk for EAH (Table 2).
A record of EAH cases should be kept, including follow
up and outcome, to aid in planning for future events and to
establish both incidence and prevalence for different events.
Emergency Medical Services and Hospitals
Prior to the race or athletic event, the medical team
should establish a relationship with the local emergency
response and transport teams, medical facilities and emer-
gency department physicians. This may include specic
collaborative education programs aimed at all of these groups
and pre-event checklists to ensure that the appropriate course
of action is taken and the needed supplies are available in the
emergency room when an athlete arrives in extremis.
Prevention of EAH requires broad educational pro-
grams with consistent messages that stress the importance of
appropriate hydration practices, recognition of EAH and
proper therapy (Grade 1C).
Controversies in EAH
Hypovolemic Hyponatremia
It is unclear whether the hypovolemic variant of EAH
has medical consequences. At present, we have apparent
evidence of hypovolemic hyponatremia developing over the
course of ultra-endurance event, but we lack data regarding: (1)
the relative contribution of solute decits versus uid status
and (2) whether or not the hypovolemic component is
somehow compromising the aficted individual. Most of the
contributions of sweat and urinary sodium losses are negligible
to the overall pathogenesis of EAH with the possible exception
of volume depleted athletes with low serum sodium levels.
Thermoregulatory sweat is hypotonic, with sweat sodium
concentrations ranging between 10 and 70 mmol/L,
are well below the normal (isotonic) range of values for serum
] (135-145 mmol/L). While there will always be some
contribution of sodium loss to the pathogenesis of EAH
which will vary signicantly in magnitude depending on: exer-
cise intensity, exercise duration, body size, and relative
ambient temperature
it is not clear whether or not sweat
sodium losses alone can account for the changes in hypovole-
mic hyponatremia in athletes. The potential role of urinary
sodium losses from exercise-induced brain natriuretic peptide
secretion contributing to EAH is also unclear.
There are 3 distinct groups of athletes that demonstrate
extreme sodium conservation which may increase the sus-
ceptibility towards the development of hypovolemic hypona-
tremia: (1) runners participating in 161 km races under hot
; (2) Ironman triathletes participating in hot and
humid Ironman triathlons
and (3) football players during
the rst week of training camp.
These 3 groups would
hypothetically be at greater risk for developing the hypovo-
lemic variant of EAH from more vigorous and sustained
sweating (and associated sweat sodium and potassium losses)
coupled with an inability to eat sufcient foods to offset the
sodium and potassium losses. Football players may also lack
adequate adaptations to heat stress, at the onset of pre-season
training, which would prevent excessive sweat sodium losses
with repeated exposure.
Treatment of Hypovolemic Hyponatremia
Participants with suspected hypovolemic EAH and
developing signs of encephalopathy would be best treated
initially with an IV HTS bolus to reverse intracerebral edema
and expand the intravascular volume. The initial bolus of
HTS can be followed by IV 0.9% saline, if neurological
symptoms improve. At least one panel member has success-
fully treated athletes who were clinically volume depleted,
with measures of [Na
] as low as 124 mmol/L, with IV nor-
mal saline infusion. As in all cases of EAH, it would be
harmful to treat with hypotonic IV solutions.
Clinical Importance of Asymptomatic EAH
The clinical relevance of the asymptomatic form of
EAH continues to be disputed. We agree that the main clinical
relevance of asymptomatic EAH lays in the potential for
asymptomatic athletes to transition to symptomatic EAH with
the continued ingestion of hypotonic uids.
symptomatic EAH can rapidly progress to life-threatening
symptomatic hyponatremia if large volumes of hypotonic
uids are ingested after identication of asymptomatic EAH
is present
or are administered intravenously
during recov-
ery from exercise.
Prospective and controlled clinical trials should be
performed both in the laboratory and in the eld to best
Clin J Sport Med Volume 25, Number 4, July 2015 Third EAH Consensus Statement
Copyright © 2015 retained by authors Hew Butler T et al. All rights reserved. |315
determine optimal preventative and therapeutic strategies.
Some of the remaining issues for study include:
Examining nutritional requirements and/or role of diet on
the risk for EAH.
Examining tolerance versus risk for various forms (tablets
vs solution) and amounts of sodium supplementation on
health, performance and natremia status.
Gathering evidence with regards to the success of the
drink to thirststrategy on prevention and/or reduction
of the incidence of EAH in athletic events.
Determining if the development of EAH increases the risk
for recurrence and/or long-term health problems.
Identifying genetic markers which may predispose individ-
uals to developing EAH.
Additional research is necessary to understand whether in-
dividuals consuming NSAIDS are at heightened risk of
developing EAH.
Investigating the efcacy of alternative treatments for non-
life threatening EAH, including oral hypertonic sodium sol-
utions, sodium tablets and vasopressin receptor antagonists.
Clarifying the etiology behind the apparent hypovolemic
variant of EAH and the potential for pathophysiological
Evaluating the variability in [Na
] in the days leading up to
the event, at event start and during the event.
Evaluating the variability in body weight in the days lead-
ing up to the event and at event start.
Etiology of EAH
1. The primary etiology and pathophysiological mechanism
underlying EAHand all known fatalitiesis the over-
consumption of hypotonic uids relative to exchangeable
sodium in likely combination with non-osmotic AVP
secretion (Grade 1A).
2. Under-replaced sodium losses contribute to serum [Na
independent of distance (Grade 1A). However, there is
paucity of data supporting sodium loss as the primary
mechanism of symptomatic EAH even in those who exer-
cise for prolonged periods of time and in warm weather
(Grade 2C). In these cases, relative over-drinking of hypo-
tonic uids with sustained non-osmotic AVP secretion is
likely involved in the development of symptomatic EAH.
Clinical Classication and Diagnosis of EAH
1. EAH can present with a wide range of symptoms ranging
from nonspecic mild complaints to severe encephalopa-
thy. The severity of symptoms and not the absolute value
of the [Na
] should guide the choice of therapy (Grade
1A). Rapid determination of [Na
] is critical in conrming
clinical suspicion but may not always be available.
Treatment of EAH
1. The major clinical relevance of asymptomatic EAH lies in is
its potential for asymptomatic athletes to quickly transition
progression into symptomatic stages if hypotonic uids are
given intravenously or ingested (Grade 1C). Thus, in patients
identied with EAH, hypotonic or isotonic uids should be
withheld until urination is documented (Grade 1C).
2. For those athletes presenting with signs and symptoms
consistent with EAHE, emergent intravenous treatment
therapy with hypertonic saline is indicated and should
not be delayed pending laboratory measurement or other
diagnostic testing (Grade 1B).
3. Athletes presenting with mild symptoms associated with
EAH can be treated with an IV bolus of HTS (Grade 1B),
oral hypertonic saline uids or observation until the onset
of urination as dictated by clinical symptoms (Grade 2B).
4. Athletes presenting to a medical facility with EAH should
be treated as per other settings (Grade 1C). However,
diagnostic testing in these scenarios should not delay
potentially life-saving therapy with HTS (Grade 1C).
Prevention of EAH
1. Given that excessive uid consumption is a primary etio-
logic factor in EAH, using the innate thirst mechanism to
guide uid consumption is a strategy that should limit
drinking in excess and developing hyponatremia while
providing sufcient uid to prevent excessive dehydration
(Grade 1C).
2. Prevention of EAH requires broad educational programs
with consistent messages that stress the importance of
appropriate hydration practices, recognition of EAH and
proper therapy (Grade 1C).
Dr. Dale Benjamin Speedy presented at the conference
and had input into the initial drafts, but withdrew authorship
before the nal version. We thank CrossFit, Inc for support of
this consensus conference.
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... Exercise-associated hyponatremia refers to a clinically relevant reduction in blood sodium concentrations during or up to 24 hours after physical activity. This can be a result of solute (primarily sodium) loss and/or excess fluid load [275]. Women are at greater risk for exercise-associated hyponatremia, and this risk has been primarily attributed to their lower body weight and size, excess water ingestion, and longer racing times relative to men [276]. ...
... Some participants consumed more fluid than fluid lost Exercise-associated hyponatremia (EAH) is a potentially fatal condition that is characterized by serum sodium levels < 130 mmol/L (Backer et al., 1993). The primary risk factor for EAH is excessive fluid intakeintake of fluid volumes greater than the volume of fluid losses through sweat, respiratory and renal losses (Hew-Butler et al., 2015). Researchers examined cases of EAH in hikers in the Grand Canyon. ...
Background: Education may improve hiker safety on trails. Aim: To investigate the impact of an educational video on hiker fluid selection and fluid consumption in a hot environment. Methods: Quasi-experimental field study at hiking trails in which the intervention group (INT) viewed a three-minute hydration education video, whereas the control group (CON) did not. Before the hike, all hikers were asked if they wanted to select extra fluid, which was provided by the research team. Results: A total of n = 97 hikers participated in the study, with n = 56 in INT (32 male) and n = 41 in CON (25 male). Despite absolute differences in environmental conditions, the differences fell within the same WBGT category. The total amount of fluid brought to the trails by participants was different between INT: 904 (503-1758) mL and CON: 1509 (880-2176) mL (P = 0.006), but participants in the INT group selected extra fluid (41%; n = 23) significantly more often when compared with participants in the CON group (7%; n = 3; P < 0.001). As a result, there was no difference in the amount of fluid brought on the trail between INT: 1047 (611-1936) mL and CON: 1509 (932-2176) mL (P = 0.069), nor for fluid consumption between INT: 433 (289-615) mL/h and CON: 489 (374-719) mL/h (P = 0.18). Conclusions and Implications: A 3-min educational video may encourage hikers to select additional fluid before the start of their hike but does not appear to increase fluid intake.
... AVP can be stimulated by pain, emotion, exercise, nausea, heat stress, hypoglycaemia, medications (NSAIDs) [107,116,117], and elevated inflammatory cytokines all of which have been found in ultra-athletes [118]. Over-drinking beyond the feelings of thirst in conjunction with non-osmotic AVP secretion induced by protracted endurance exercise results in fluid retention and EAH [119]. ...
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Increasingly popular, ultra-endurance participation exposes athletes to extremely high levels of functional and structural damage. Ultra-endurance athletes commonly develop acute kidney injury (AKI) and other pathologies harmful to kidney health. There is strong evidence that non-steroidal anti-inflammatory drugs, common amongst ultra-athletes, is linked to increased risk and severity of AKI and potentially ischaemic renal injury, i.e., acute tubular necrosis. Ultra-endurance participation also increases the risk of exertional rhabdomyolysis, exercise-associated hyponatremia, and gastrointestinal symptoms, interlinked pathologies all with potential to increase the risk of AKI. Hydration and fuelling both also play a role with the development of multiple pathologies and ultimately AKI, highlighting the need for individualised nutritional and hydration plans to promote athlete health. Faster athletes, supplementing nitrates, and being female also increase the risk of developing AKI in this setting. Serum creatinine criteria do not provide the best indicator for AKI for ultra-athletes therefore further investigations are needed to assess the practicality and accuracy of new renal biomarkers such as neutrophil gelatinase-associated lipocalin (NGAL). The potential of recurring episodes of AKI provide need for further research to assess the longitudinal renal health impact of ultra-participation to provide appropriate advice to athletes, coaches, medical staff, and event organisers.
... In addition, the amount of fluid consumed and its composition should be carefully considered. Indeed, the excessive consumption of liquids without the necessary composition can induce a state of hyponatremia [8] and rehydration with an electrolyte-enriched drink may reduce susceptibility to sudden painful involuntary contractions [9]. Therefore, both the volume of the rehydration fluid and its composition are critical for maintaining whole body fluid homeostasis. ...
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In different endurance events, athletes have limited access to fluid intake, such as ultra-endurance running. For this reason, it is necessary to establish an adequate hydration strategy for this type of long-duration sporting event. Indeed, it seems that the intake of seawater is a suitable hydration alternative to improve post-exercise recovery in this type of endurance event. This seawater is characterized by being a deep natural mineral water of moderate mineralization, which is usually extracted from a depth of about 700 m. Therefore, the aim of this systematic review is to evaluate the efficacy of seawater consumption in both performance and post-exercise recovery in long-duration sport events. A systematic and comprehensive literature search was performed in PubMed, Scopus, and Web of Science in September 2022. Initially, 8 out of 558 articles met the inclusion criteria. Among these eight studies, six were randomized clinical trials, and two were observational studies (one cross-sectional and one prospective study in well-conditioned student athletes). The results showed that deep sea water consumption accelerated the recovery of aerobic capacity and leg muscle capacity on running performance. In addition, the lactate production after the running exercise in seawater was significantly lower than in pure water. In conclusion, the present review demonstrates that seawater consumption could significantly improve the capacity of recovery after exercise.
... Bongers et al., 2015). Furthermore, studies by Hue et al., 2014, concluded that a shorter distance with higher exercise intensity leads to high risk of getting hyperthermia compared to low intensity with longer running distance (Hew-Butler et al., 2015). Poor acclimatisation should be considered the main risk factor for heat-related illness. ...
... In addition, the amount of fluid consumed should be carefully considered. Indeed, excessive water consumption may induce a state of hyponatremia [4] and rehydration with an electrolyte-enriched drink may reduce susceptibility to muscle cramps [5]. Therefore, both the volume of the rehydration fluid and its composition are critical for maintaining whole-body fluid homeostasis. ...
Full-text available
A triathlon is an endurance event in which athletes need an efficient hydration strategy since hydration is restricted at different stages. However, it seems that seawater intake can be a suitable hydration alternative for this type of endurance event. Therefore, the aim of this study was to evaluate the efficacy of seawater hydration during a triathlon on cytokine production. Fifteen trained male triathletes (age = 38.8 ± 5.62 years old; BMI = 22.58 ± 2.51 kg/m2) randomly performed three triathlons, one of them consuming seawater (Totum SPORT, Laboratories Quinton International, S.L., Valencia, Spain), the other one consuming tap water ad libitum, and the last a physiologic saline solution as placebo. The triathlon consisted of an 800 m swim, a 90 km bike ride, and a 10 km run. Blood samples were taken at rest and after training, where markers of inflammation, hemoglobin, and hematocrit concentration were assessed. While the seawater was not ergogenic, it significantly increased the release of IL-6 and apelin post-exercise. However, no differences were found between the fractalkine, IL-15, EPO, osteonectin, myostatin, oncostatin, irisin, FSTL1, osteocrin, BDNF, and FGF-21 values over those of the placebo group. The present study demonstrates that hydration with seawater stimulates myokine production, which could lead to improved performance recovery after exercise.
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Purpose Exercise‐associated hyponatremia (EAH) is common in ultra‐endurance events and severe cases are more common in females. The purpose of this paper is to compare the clinical presentation of EAH between male and female triathletes in ultra‐endurance competitions. Methods Medical records with sodium concentrations (n = 3138) from the IRONMAN® World Championships over the timeframe of 1989–2019 were reviewed for both male (n = 2253) and female (n = 885) competitors. Logistic regression was used to explore the relationships between sex, sodium concentration, and various clinical presentations. Results When comparing male and female triathletes, clinical variables found to have a different relationship with sodium concentration include altered mental status (inversely related in males and not related in females), abdominal pain, muscle cramps, hypotension, and tachycardia (directly related in males and not related in females), and vomiting and hypokalemia (not related in males and inversely related in females). Overall, males lost significantly more weight than females, and notably, approximately half of all athletes were dehydrated and lost weight. Conclusions Altered mental status, vomiting, abdominal pain, muscle cramps, hypotension, tachycardia, and hyperkalemia appear to present differently between sexes when comparing hyponatremic to eunatremic athletes. Although overhydration is the most common etiology of hypervolemic hyponatremia, hypovolemic hyponatremia comprises a significant amount of hyponatremic triathletes. Further understanding of how EAH presents helps athletes and medical professionals identify it early and prevent life‐threatening complications.
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Wildland firefighters (WLFFs) are inserted as the front-line defense to minimize loss of natural resources, property, and human life when fires erupt in forested regions of the world. The WLFF occupation is physically demanding as exemplified by total daily energy expenditures that can exceed 25 MJ/day (6000 calories). WLFFs must also cope with complex physical and environmental situations (i.e., heat, altitude, smoke, compromised sleep, elevated stress) which challenge thermoregulatory responses, impair recovery, and increase short- and long-term injury/health risks while presenting logistical obstacles to nutrient and fluid replenishment. The occupation also imposes emotional strain on both the firefighter and their families. The long-term implications of wildfire management and suppression on the physical and mental health of WLFFs are significant, as the frequency and intensity of wildland fire outbreaks as well as the duration of the fire season is lengthening and expected to continue to expand over the next three decades. This article details the physical demands and emerging health concerns facing WLFFs, in addition to the challenges that the U.S. Forest Service and other international agencies must address to protect the health and performance of WLFFs and their ability to endure the strain of an increasingly dangerous work environment. © 2023 American Physiological Society. Compr Physiol 13:4587-4615, 2023.
Wearable sensors hold great potential in empowering personalized health monitoring, predictive analytics, and timely intervention toward personalized healthcare. Advances in flexible electronics, materials science, and electrochemistry have spurred the development of wearable sweat sensors that enable the continuous and noninvasive screening of analytes indicative of health status. Existing major challenges in wearable sensors include: improving the sweat extraction and sweat sensing capabilities, improving the form factor of the wearable device for minimal discomfort and reliable measurements when worn, and understanding the clinical value of sweat analytes toward biomarker discovery. This review provides a comprehensive review of wearable sweat sensors and outlines state-of-the-art technologies and research that strive to bridge these gaps. The physiology of sweat, materials, biosensing mechanisms and advances, and approaches for sweat induction and sampling are introduced. Additionally, design considerations for the system-level development of wearable sweat sensing devices, spanning from strategies for prolonged sweat extraction to efficient powering of wearables, are discussed. Furthermore, the applications, data analytics, commercialization efforts, challenges, and prospects of wearable sweat sensors for precision medicine are discussed.
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Introduction: Obesity effects on kidney function. Urinary disorders after exercise are also common, and probably due to transient hemodynamic problems in the glomerular and tubular renal function. The purpose of this research is to investigate the relationship of BMI with proteinuria and hematuria after one session of intense continuous and interval exercise in girls. Methods: In this quasi-experimental research, 45 hostelry high school girl students with a mean age of 15.18 ± 0.39 years were randomly selected and in three groups of 15, they ran 1600 meters in a continuous and interval manner. Urine test collected before, one and 24 hours after activity. The results were analyzed by SPSS version 16 software and one way ANOVA and Pearson correlation coefficient. Results: Increased proteinuria was significant one hour (P = 0.002) and 24 hours after activity (P = 0.001) in the continuous group. In the continuous group, the relationship between fat percentage (P=0.017) and body mass index (P=0.001) with protein excretion 24 hours after activity was positive and significant. One hour after activity, protein excretion with fat percentage and Body mass index (BMI) had no significant relationship. Hematuria was also not significant after activity. Conclusion: Body mass index (BMI) and fat percentage were effective on protein excretion after one session of intense physical activity and had no significant effect on hematuria. Therefore, overweight people were advised to participate in interval exercise to lose weight.
This study assessed whether replacing sweat losses with sodium-free fluid can lower the plasma sodium concentration and thereby precipitate the development of hyponatremia. Ten male endurance athletes participated in one 1-h exercise pretrial to estimate fluid needs and two 3-h experimental trials on a cycle ergometer at 55% of maximum O 2 consumption at 34°C and 65% relative humidity. In the experimental trials, fluid loss was replaced by distilled water (W) or a sodium-containing (18 mmol/l) sports drink, Gatorade (G). Six subjects did not complete 3 h in trial W, and four did not complete 3 h in trial G. The rate of change in plasma sodium concentration in all subjects, regardless of exercise time completed, was greater with W than with G (−2.48 ± 2.25 vs. −0.86 ± 1.61 mmol ⋅ l ⁻¹ ⋅ h ⁻¹ , P = 0.0198). One subject developed hyponatremia (plasma sodium 128 mmol/l) at exhaustion (2.5 h) in the W trial. A decrease in sodium concentration was correlated with decreased exercise time ( R = 0.674; P = 0.022). A lower rate of urine production correlated with a greater rate of sodium decrease ( R = −0.478; P = 0.0447). Sweat production was not significantly correlated with plasma sodium reduction. The results show that decreased plasma sodium concentration can result from replacement of sweat losses with plain W, when sweat losses are large, and can precipitate the development of hyponatremia, particularly in individuals who have a decreased urine production during exercise. Exercise performance is also reduced with a decrease in plasma sodium concentration. We, therefore, recommend consumption of a sodium-containing beverage to compensate for large sweat losses incurred during exercise.
This 27-year-old previously healthy professional football player developed a tonic-clonic seizure and delirium due to acute hyponatremia. This appears to be the first case of hyponatremia in an American football player. Hyponatremia was due to acute water intoxication; sodium losses through sweat and emesis may have partially contributed. There may have also been some contribution from renal dysfunction and diuresis due to his supplement use. Proper education regarding appropriate type and volume of fluid consumption, additional dietary salt intake, general nutrition, and close monitoring of body weight should prevent this disorder. The CT scan and chest radiograph findings appear to have been artifacts, but complicated the treatment of this patient. Because of these radiographic findings and the history of chronic excessive water consumption, the patient was treated as having chronic hyponatremia. In retrospect, he should have been treated as having acute hyponatremia with water restriction, and possibly diuretics or IV 3% saline.
Objective: The objective of this study was to determine whether sodium supplementation 1) influences changes in body weight, serum sodium [Na], and plasma volume (PV), and 2) prevents hyponatremia in Ironman triathletes. Setting: The study was carried out at the South African Ironman triathlon. Participants: Thirty-eight athletes competing in the triathlon were given salt tablets to ingest during the race. Data collected from these athletes [salt intake group (SI)] were compared with data from athletes not given salt [no salt group (NS)]. Interventions: Salt tablets were given to the SI group to provide approximately 700 mg/h of sodium. Main Outcome Measurements: Serum sodium, hemoglobin, and hematocrit were measured at race registration and after the race. Weights were measured before and after the race. Members of SI were retrospectively matched to subjects in NS for 1) weight change and 2) pre-race [Na]. Results: The SI group developed a 3.3-kg weight loss (p < 0.0001) and significantly increased their [Na] (A[Na] 1.52 mmol/L; p = 0.005). When matched for weight change during the race, SI increased their [Na] compared with NS (mean 1.52 versus 0.04 mmol/L), but this did not reach statistical significance (p = 0.08). When matched for pre-race [Na], SI had a significantly smaller percent body weight loss than NS (-4.3% versus -5.1%; p = 0.04). There was no significant difference in the increase of [Na] in both groups (1.57 versus 0.84 mmol/L). PV increased. equally in both groups. None of the subjects finished the race with [Na] < 135 mmol/L. Conclusions: Sodium ingestion was associated with a decrease in the extent of weight loss during the race. There was no evidence that sodium ingestion significantly influenced changes in [Na] or PV more than fluid replacement alone in the Ironman triathletes in this study. Sodium supplementation Was not necessary to prevent the development of hyponatremia in these athletes who lost weight, indicating that they had only partially replaced their fluid and other losses during the Ironman triathlon.
This is the first reported case of hyponatremia associated with increased intracranial pressure, altered mental status, and neurogenic pulmonary edema resulting after a marathon-distance run; the syndrome has been documented previously to occur at distances greater than a marathon. The cause is most likely a combination of salt loss through sweat and retention of high volumes of hypotonic fluids. Preventive measures for the athlete to take include (1) estimating the potential fluid and electrolyte losses before a race and (2) planning a replacement scheme that includes a combination of water and glucose electrolyte solutions. Treatment of the hyponatremia syndrome is primarily supportive and includes infusion of normal saline.
Two ultramarathon runners were hospitalized with hyponatremic encephalopathy after completing 80 and 100 km (50 and 62 miles), respectively, of the 1983 American Medical Joggers Association ultramarathon race in Chicago. The two runners consumed such large quantities of free water during the race that apparent water intoxication developed. Both recovered satisfactorily after treatment with intravenous saline. The hyponatremia was caused primarily by increased intake and retention of dilute fluids and contributed to by excessive sweat sodium loss. A possible explanation for the postrace onset of symptoms might be the sudden absorption of fluid in the gastrointestinal tract after exercise ceased, with subsequent further dilution of the plasma sodium. Hyponatremia, which has not been commonly associated with exercise, should be considered as a possible consequence of ultraendurance events. (JAMA 1986;255:772-774)