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Statement of the Third International Exercise-Associated Hyponatremia Consensus Development Conference, Carlsbad, California, 2015

July 2015
Clinical journal of sport medicine: official journal of the Canadian Academy of Sport Medicine 25(4):303-320

DOI:10.1097/JSM.0000000000000221

Source
PubMed

Authors:

Tamara D Hew-Butler

Wayne State University

Mitchell Rosner

University of Virginia

Sandra Fowkes Godek

West Chester University

Jonathan Dugas

University of Cape Town

Show all 16 authorsHide

. American College of Chest Physicians Classification Scheme for Grading Evidence and Recommendations Utilized in This Statement 2

…

. 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, 123 Speedy et al, 140 and Speedy et al 141 ) Versus Suspected Hypovolemic Hyponatremia (Owen et al 139 )

…

. 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

…

. Four Case Reports Reporting Symptomatic EAH While Drinking Either ad libitum (First 2 Cases) or in Response to Thirst (Second 2 Cases)

…

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CONSENSUS STATEMENT

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. Stuempﬂe, PhD,††† James M. Winger, MD,‡‡‡

and Joseph G. Verbalis, MD§§§

Key Words: EAH, exercise-associated collapse, hydration

(Clin J Sport Med 2015;25:303–320)

INTRODUCTION

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 scientiﬁc sub-specialties pertaining to athletic

training, exercise physiology, sports medicine, water/sodium

metabolism, and body ﬂuid 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

withapreventableandtreatableﬂuid 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.

CONSENSUS METHODOLOGY

The third International Exercise-Associated Hyponatre-

mia Consensus Development Conference utilized National

Institutes of Health guidelines, amended for a more holistic

approach to ﬁt 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

scientiﬁc and/or clinical contributions to the topic of water

and sodium homeostasis and/or hyponatremia and (2) repre-

sented a speciﬁc group (eg, nephrology, endurance medicine,

etc.) or had unique topical expertise (eg, cystic ﬁbrosis,

muscle cramps, ﬂuid balance, etc.). The present document is

intended to serve as the scientiﬁc 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

conﬂicts of interest.

Corresponding Author: Tamara Hew-Butler, DPM, PhD, School of Health

Science, Oakland University, Rochester, MI 48309-4482 (hew@oakland.edu).

Hoffman MD, Lewis DP, Maughan RJ, Miller KC, Rehrer NJ, Roberts WO,

Rogers IR, Siegel AJ, Stuempﬂe KJ, Winger JM, Verbalis JG, All rights

reserved.

Clin J Sport Med Volume 25, Number 4, July 2015 www.cjsportmed.com |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

statement.

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

session.

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 panel’s 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.

Sponsorship

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.

RESULTS AND DISCUSSION

Deﬁnition

EAH is used to describe hyponatremia occurring during

or up to 24 hours after physical activity. It is deﬁned 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

]are

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 Beneﬁts vs Risks and Burdens

Methodological Quality of

Supporting Evidence

1A Strong recommendation, high-quality

evidence

Beneﬁts clearly outweigh risks and

burdens or vice versa

RCTs without important limitations

or overwhelming evidence from

observational studies

1B Strong recommendation, moderate-

quality evidence

Beneﬁts 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

Beneﬁts clearly outweigh risks and

burdens or vice versa

Observational studies or case series

2A Weak recommendation, high-quality

evidence

Beneﬁts closely balanced with risks

and burdens

RCTs without important limitations

or overwhelming evidence from

observational studies

2B Weak recommendation, moderate-

quality evidence

Beneﬁts 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

beneﬁts, risks and burden; beneﬁts,

risk and burden may be closely

balanced

Observational studies or case series

RCT, randomized controlled trial.

Hew-Butler et al Clin J Sport Med Volume 25, Number 4, July 2015

from loss of solutes (sodium, potassium), a relative excess of

total body water or a combination of both.

3,4

However, in

most clinical scenarios, the driving force for the develop-

ment of hyponatremia is a relative excess of total body

water.

5,6

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.

Epidemiology

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 veriﬁable pre-race

blood [Na

] measurement, only 0.8% (19/2262) presented

with hyponatremia prior to race start.

9–35

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

]val-

ues possibly confounded by ﬁngerstick hemolysis

and/or

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-speciﬁcsymptoms

(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

38–48

or may not

49–52

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%

30,53

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% ﬁnished the with serum [Na

],135 mmol/L

(40% self-corrected prior to ﬁnishing 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%.

18,54–56

The incidence of asymptomatic EAH in

Ironman triathlons in different environments has been re-

ported to range from negligible

to as high as 18%

and

25%.

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

ﬁnishers.

28,58

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.

28,38,47,50,61–69

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 deﬁne the incidence of symptomatic and asymptom-

atic EAH.

55,71

In the ﬁrst study of 2135 athletes from 8 endur-

ance events ranging in length from 42.2 to 161 km,

the

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,

swimming)

Hiking*

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

second study of 669 161-km ultramarathon runners,

55,72

only

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

73–75

and military personnel.

75–77

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.

73,78

Fur-

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

person-years).

However, this incidence is probably inﬂated

as the data were derived from a medical coded database that

does not have a speciﬁc 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

ﬁnishers completing the distance in 2 to 3 hours and a sprint

triathlon with slower ﬁnishers taking approximately 2 hours to

complete.

In addition, EAH has been reported in US pro-

fessional and college American rules football players

40,41

and

has led to the deaths of 3 US high school football players

between 2008 and 2014.

63,64,69

Symptomatic hyponatremia

has also been reported in a 48 year old lawn bowler who

was heterozygous for the Delta F508 cystic ﬁbrosis (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-

ing.

Cases of symptomatic EAH have also been induced in 2

separate laboratory studies involving low intensity exercise

conducted in high ambient temperatures.

84,85

Deaths from

symptomatic EAH have occurred in a 25 year old male police

ofﬁcer 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 ﬂuid (water, sports drinks or other hypo-

tonic ﬂuids) intake in volumes greater than loss through

sweat, respiratory and renal water excretion so that a positive

ﬂuid balance accrues over time.

86,87

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 ﬂuid balance and euhydra-

tion.

71,72

Body weight losses of ,0.75 kg after a standard

marathon

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 ﬂuid volume ingestion will over-

whelm any protective effect of the beverages’sodium con-

tent on maintaining serum [Na

89,90

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,

38,58,61

adjusted for BMI and

racing time, the apparent sex difference is not statistically

signiﬁcant.

Nonsteroidal anti-inﬂammatory drugs (NSAIDs) have

been implicated as a risk factor in the development of

EAH

38,91,92

presumably by potentiating the water retention

effects of arginine vasopressin (AVP) at the level of the kid-

ney collecting duct.

93,94

However, data are conﬂicting,

26,58,61

and further investigation is necessary to determine whether

NSAID usage—with respect to both classiﬁcation and

dosage—is a risk factor for the development of EAH. The

possible pathophysiological contributions of intrinsic renal

disease

and low solute diets

96–98

on water retention, high

sweat sodium concentrations

in extreme environments,

and the potentiation of thirst by non-osmotic stimuli during

exercise

72,100–103

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.

104

There is a paucity of evidence suggesting that those

developing symptomatic EAH have either been a “salty

sweater”

99,105

or a heterozygous carrier of the cystic ﬁbrosis

genotype.

106

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

105,107

or prolonged exposure to high ambi-

ent temperatures.

108–110

As individuals with CF experience

a longer lifespan (median predicted survival age in 2012 was

41.1 years

111

) 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 ﬂuids

Hew-Butler et al Clin J Sport Med Volume 25, Number 4, July 2015

one of their therapies,

112

this population may be at increased

risk for EAH due to the combination of high sweat ﬂuid and

sweat [Na

]loss.

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.

63,64,69

These football players

were encouraged to ingest copious volumes of hypotonic

ﬂuids and sports drinks to prevent or relieve exercise-

associated muscle cramps (EAMC),

63,64,69

in the belief that

EAMC was caused by dehydration and electrolyte imbal-

ance.

113

However, experimental

114,115

and observational

116,117

studies speculate that EAMC may reﬂect 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,

82,100,118,119

clinical

populations,

120

and animals.

121

Symptoms associated with EAH are due to osmotically-

induced shifts of water into the intracellular compartment. In

the conﬁned 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

EAH.

34,41,45,52,57,58,61,71,73,75,76,84,119,122–126

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 ﬂuids (water, sports

drinks or other hypotonic ﬂuids) in excess of total body ﬂuid

losses, which includes the sum of insensible (cutaneous, respi-

ratory, and gastrointestinal),

127,128

sweat and renal (urine) ﬂuid

losses.

34,45,52,57,58,61,73,75,76,84,119,122–125

Hyponatremia caused solely by the overconsumption of

ﬂuids, above known maximal urine excretory rates of 800 to

1000 mL/,

129

has been demonstrated at rest in athletes with

and without a history of EAH.

34,86,87

Although some cases of

EAH may be due to pure water intoxication from overcon-

sumption of ﬂuids, non-osmotic AVP secretion is a key con-

tributing factor in most athlete-related symptomatic cases.

5,19

Known stimuli to AVP secretion that are commonly

associated with exercise include: nausea/vomiting

130

;

interleukin-6 release

; plasma volume contraction

; hypo-

glycemia

131

; elevated body temperature

132

; and/or other hor-

monal mediators.

Even small increases in circulating AVP

levels can markedly reduce renal water excretion well below

maximal levels,

133

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 ﬂuid replacement need.

49,134

SUMMARY STATEMENT

The primary etiology and pathophysiological mecha-

nism underlying EAH—and all known fatalities—is the over-

consumption of hypotonic ﬂuids 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,

5,6,135–138

EAH this variant has been more difﬁcult to deﬁne and is

much less likely to be encountered except in extreme events

usually over prolonged periods (such as ultra-marathons)

139

or hot Ironman distance triathlons.

19,20

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

139

have been

consolidated in Table 4 against data collected from relatively

shorter and cooler races

123,140,141

where ﬂuid overload hypo-

natremia has been veriﬁed. From the standpoint of the clin-

ical literature, hypovolemic hyponatremia reﬂects a loss of

total body exchangeable sodium that manifests as volume

depletion.

5,6,135,142,143

Hypovolemic EAH would be predicted

to occur in athletes exercising for longer periods of time (such

as 161 km ultramarathons; .20 hours),

11,54–56

and/or in

hotter

11,19,20,55,108,109

environments and/or with higher sweat

sodium losses.

99,101

Clinical conﬁrmation of the hypovolemic

form of hyponatremia is supported by a spot urine sodium

concentration (U[Na

]) below 30 mmol/L

136,137,144

in conjunc-

tion with a serum or plasma [Na

] below 135 mmol/L. A spot

U[Na

],30 mmol/L is 100% speciﬁc and 80% sensitive for

predicting a sustained increase (.5 mmol/L) in serum [Na

]

following isotonic saline administration

136

in clinical patients.

Elevated blood urea nitrogen levels (.20 mg/dL)

136,139

and

weight loss

19,20,55

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

depletion.

SUMMARY STATEMENT

Under-replaced sodium losses contribute to serum

[Na

] independent of distance (Grade 1A). However, there

Clin J Sport Med Volume 25, Number 4, July 2015 Third EAH Consensus Statement

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 ﬂuids

with sustained non-osmotic AVP secretion is likely involved

in the development of symptomatic EAH.

The Role of Thirst

Since drinking ﬂuid 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 deﬁned as a “generalized, deep seated feeling of desire

for water”

145

and is an evolutionarily conserved, ﬁnely

tuned, regulatory mechanism serving to protect both plasma

osmolality and circulating plasma volume.

146

Osmoreceptors

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 blood–brain barrier that are points of communication

between the blood, the brain parenchyma, and the cerebral

spinal ﬂuid) and baroreceptors located within the aortic arch,

carotid sinus and great veins provide “real-time”neural

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 ﬂuid

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 classiﬁed

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 ﬁnding,

diagnosed by blood electrolyte testing for research or

unrelated metabolic screening purposes.

10,15,18,19,28,30,32,53–59

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-

speciﬁc 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

147

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,

123

Speedy et al,

140

and Speedy

et al

141

) Versus Suspected Hypovolemic Hyponatremia (Owen et al

139

)

Variable Irving et al

123

Speedy et al

140

Speedy et al (2 cases)

141

Owen et al

139

EAH subjects (classiﬁcation)* 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 ﬂuid 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 deﬁcit/sodium given). In Speedy et al 2000,

140

this was expressed as a positive or negative amount (mmol) of sodium administered so that a negative value reﬂected the

amount of sodium retained by the body (UNa

output minus Na

input).

§This represents the amount of ﬂuid excreted (urine volume) during the recovery period compared with the amount of ﬂuid 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

associated postural hypotension.

148

The clinical symptoms of

mild symptomatic EAH are not speciﬁc 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,

hypernatremia,

149,150

and exercise associated postural hypo-

tension.

148

It is important for medical staff to perform a rapid

history and physical examination to help determine the eti-

ology of these nonspeciﬁc 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.

58,71,72

However,

EAH in the presence of weight loss has been documented

in ultra-endurance races in the heat.

19,20,55,59

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 athlete’s[Na

]inordertoconﬁrm or exclude the

diagnosis of EAH or to consider empiric treatment if

on-site [Na

] cannot be measured, such as in remote

settings.

72,118,151

Characteristics of Severe EAH (EAHE)

Severe symptomatic EAH is characterized by neuro-

logical signs and symptoms due to cerebral edema that

occur when water ﬂows along the osmotic gradient from the

extracellular ﬂuid into the intracellular compartment

(Table 3).

38–52,152

Severe symptomatic EAH may

38–48

may not

49–52

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

[Na

] measurement if available.

SUMMARY STATEMENT

EAH can present with a wide range of symptoms

ranging from nonspeciﬁc 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 conﬁrming clinical suspicion but may not always be

available.

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

]analysisisoptimalfor

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

events).

118,151

Treatment should be based on the degree of

neurological impairment, not simply the [Na

] level

5,6

;as

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

[Na

] measurement is not available.

Onsite Treatment of Asymptomatic EAH Found Via

[Na

] Measurement

Asymptomatic hyponatremia is not normally detected

unless an athlete has blood electrolyte concentrations tested

for some other reason.

10,15,18,19,28,30,32,53–59

In athletes with

this incidental biochemical diagnosis, oral or intravenous

hypotonic ﬂuid 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

retention.

5,6,120

Furthermore, isotonic intravenous ﬂuids

should be administered with great caution or withheld until

urination as, in the setting of elevated AVP levels and a con-

centrated urine, these ﬂuids may lower the [Na

]

153

or delay

recovery.

91,151,154

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

139,155

; 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 ﬁnish, since delayed-onset symptomatic

EAH may frequently occur.

40,42,46,52,72,80,82,91,100,122,156

Ideally,

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

athlete’s 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

Lightheadedness*

Dizziness*

Nausea*

Pufﬁness

Body weight gain from baseline

Symptoms and Signs Associated With Severe EAH and EAHE

Vomiting*

Headache*

Altered mental status* (confusion, disorientation, agitation, delirium, feelings

of “impending doom,”obtundation)

Phantom running

Seizure*

Coma*

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

SUMMARY STATEMENT

The major clinical relevance of asymptomatic EAH lies

in its potential for asymptomatic athletes to quickly transition

and progress into symptomatic stages if hypotonic ﬂuids are

given intravenously or ingested (Grade 1C). Thus, in patients

identiﬁed with EAH, hypotonic or isotonic ﬂuids 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).

38,42,49,51,62,72,82,91

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

administered.

5,6,38,47,50,62

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

42,51,72

(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 efﬁcacy and safety use of IV HTS admin-

istration in symptomatic EAH

8,38,48,49,52,62,72,82,91,100,122,154

with

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 ﬁrst bolus of HTS

before [Na

] is measured. Conﬁrmed symptomatic dilutional

(euvolemic or hypervolemic) EAH is a contraindication to the

administration of IV hypotonic ﬂuids, lactated Ringer’s, or

isotonic (normal) saline, all of which can worsen the degree

of hyponatremia

41,47,50,134

or delay recovery.

91,118,122,151,154,157

The efﬁcacy of IV HTS as the deﬁnitive treatment of

acute hyponatremic encephalopathy has been validated

extensively in both hospital and ﬁeld settings since it was

ﬁrst utilized successfully in 1938.

158

This treatment is based

on the capacity of an IV HTS bolus to increase the serum

[Na

] 2 to 5 mmol/L, resulting in a concomitant decrease of

intracranial pressure and improvement in symptoms.

5,6

This

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

159

or exercise set-

tings

8,38,48,49,52,62,72,82,91,100,122,154

or with the limited increase

in [Na

] produced by a single bolus of HT.

139,160

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.

139

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 ﬂuids, lactated Ring-

er’s, or isotonic (normal) saline. The diagnosis of EAH or

EAHE must be communicated to the receiving physician

upon transfer of care.

SUMMARY STATEMENT

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

139,155,160

(Table 6) or observation until urination, as seen in clinical

settings.

6,120

Oral sodium tablets may not be as efﬁcacious as

hypertonic solutions, as suggested in a single case report

124

and requires further investigation. The efﬁcacy and tolerance

of oral HTS has been supported by limited ﬁeld

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 ﬂuids 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 ﬂavoring (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

studies,

139,155

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.

SUMMARY STATEMENT

Athletes presenting with mild symptoms associated with

EAH can be treated with an IV bolus of HTS (Grade 1B), oral

hypertonic saline ﬂuids 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

]

Measurement

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

]cannotbe

determined,

such as in a remote setting.

39,118,151

In this

situation empiric treatment is justiﬁed 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 signiﬁcantly 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

hyponatremia.

139

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 conﬁrmed

(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.

5,6

SUMMARY STATEMENT

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

Athletes and support crews need to carefully consider

ﬂuid and electrolyte supplementation during and after

exercise and the rationale behind those decisions. Excessive

ﬂuid replacement beyond thirst (whether water, sports drinks

or other hypotonic ﬂuids) is not a panacea for all instances of

fatigue, collapse, muscle cramping, or exertional heat stroke

(Table 7). The drinking of ﬂuid volumes sufﬁciently 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 ,119,122–126,162,163

There-

fore, prevention strategies must target drinking behavior.

Fluid intake recommendations suggesting that athletes begin

to drink ﬂuids 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 ﬂuid 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

evaluatedinTable7.

Modest to moderate levels of dehydration are tolerable

and pose little risk to life in otherwise healthy individuals.

Laboratory and ﬁeld studies indicate that ﬂuid deﬁcits 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.

164

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

165

and

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

combustion

128

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

weight

9,10,12,166

from registration to race start. However,

this average value conceals that fact that large gains in

weight(uptoatleast4%ofbodymass)

166,167

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 ﬁeld 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 ﬂuid

overload.

Clin J Sport Med Volume 25, Number 4, July 2015 Third EAH Consensus Statement

The safest individualized hydration strategy before,

during and immediately following exercise is to drink

palatable ﬂuids when thirsty (Figure). Marathon runners

with hypernatremia report “thirstiness”as a physiologically

expected symptom

149

while a weak but statistically signif-

icant relationship has been demonstrated between thirst rat-

ings and plasma [Na

] immediately following a 161 km

race.

168

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)]

Study

Subjects Age (yo), Sex (♂♀),

Activity

Serum [Na

] mmol/L

(Initial or Range)

Symptomatic EAH With Drinking Above Thirst

(Comments From Report)

Frizzell et al

122

24, ♂/45, ♂, Ultra-runners 123/118 Runners as a group are taught to “push ﬂuids”

Athletes are instructed to drink more than their thirst

dictates

Armstrong et al

21, ♂, Lab subject 122 .voluntarily consumed this large volume of ﬂuid

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, ﬁve liters (L) of 0.45%

normal saline in 5% dextrose was administered

intravenously along with 3L of liquids by mouth over

aﬁve hour period

Reynolds et al

161

*6 (4♀/2♂), Soldiers 118-134 .consuming large volumes of water as “protection

against becoming a heat casualty”predisposed these

troops to the physical impairment that they intended to

avoid

Backer et al

*7 (6♀/1♂), Hikers 109-127 Most patients diagnosed as having hyponatremia have

a distinct history of high ﬂuid intake.

.unlike heat exhaustion patients, few of our

hyponatremic patients were thirsty when evaluated,

perhaps because they drank more ﬂuids and were

hyperhydrated

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

clear”and “do not wait until you are thirsty to drink”

Dimeff

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 ﬂuid”and 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

ﬂuids was maintained

Rothwell and Rosengren

118

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

151

85, ♂, Hiker 120 Subject was encouraged to.“Push ﬂuids”above thirst

Rogers et al 2015

46, ♀, Swimmer 118 Her intended ﬂuid regimen.was 200mL of ﬂuid 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

to ﬂuids during treadmill walking in the heat

169

or running

30 km under different ambient conditions

170

maintain

plasma osmolality by drinking to thirst. Moreover, the cues

to drink provided by osmolality and blood volume persist in

both hot

101

and cold

171

environments. Thus, drinking to

thirst will, in most cases, prevent both dilutional EAH and

performance decrements due to excessive dehydration.

Potential exceptions to this ﬂuid replacement strategy

are thirst stimulated by confounding oral variables such

as dry mouth (xerostomia),

102,172

genetic inﬂuences,

103

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)

Study

Subjects Age (yo), Sex (♂♀),

Activity

Plasma [Na

] mmol/L

(Initial)

Symptomatic EAH With ad libitum Drinking (Comments

From Report)

Baker et al

65, ♀, Lab trial 126 46kg♀drank 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 ﬂuid

was readily available if needed

Hew-Butler

2012

134

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

ﬂuid consumption rate of ;550ml/hr

Study

Subjects Age (yo), Sex (♂♀),

Activity

Plasma [Na

] mmol/L

(Initial)

Symptomatic EAH With Drinking in Response to Thirst

(Comments From Report)

Khodaee et al 2013

100

44, ♂, Mountain biker 116 84kg♂drank 29L water and 5.3 g sodium during plus after race

(;14 hrs total)

History of muscle cramping after 5-6hr cycling. Felt “very

thirsty”after 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 supplementation”and

“very thirsty”at 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 ﬂuids in hospital and discharged

with positive ﬂuid balance of 6.6L

Clin J Sport Med Volume 25, Number 4, July 2015 Third EAH Consensus Statement

known discrepancies between drinking “ad libitum”versus

drinking according to the dictates of thirst,

173

excessive

sodium intake and/or other non-osmotic or hypovolemic

factors that are yet to be determined and require further

investigation (Table 8).

72,100

SUMMARY STATEMENT

Given that excessive ﬂuid consumption is a primary

etiologic factor in EAH, using the innate thirst mechanism to

guide ﬂuid consumption is a strategy that should limit drinking

in excess and developing hyponatremia while providing

sufﬁcient ﬂuid to prevent excessive dehydration (Grade 1C).

Additional Strategies to Prevent EAH

Sodium Supplementation

When ﬂuid 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

174

or intermittent

cycling and ;4 hours

of running.

89,175

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 signiﬁcantly 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 signiﬁcant increases

176

or no change

14,177

in serum

[Na

] during competitive ﬁeld events it will be of modest to

no beneﬁt in situations where excess ﬂuids are being con-

sumed. The potential detrimental effects of excessive sodium

supplementation are not clear.

72,178

SUMMARY STATEMENT

Sodium supplementation is a strategy for attenuating

sodium concentration reductions that can develop when ﬂuid

intakes approximate sweat losses during prolonged exercise

but cannot prevent EAH in the setting of a persistent excessive

ﬂuid intake that produces ﬂuid 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 ﬂuid intakes.

For example, an education program for an Ironman triathlon

advising athletes of the risks incurred by overdrinking

coupledwithdecreasingthenumberofﬂuid stations

to limit the ﬂuid availability reduced the incidence of

EAH.

179–181

Dissemination of appropriate drinking advice

alone has also been shown to reduce the incidence of

EAH in a 90 km footrace.

150,182

Past studies have demonstrated that cycling ﬂuid

stations placed 20 km apart in an Ironman triathlon and

running ﬂuid stations placed 5 km apart in a standard

marathon have reduced or prevented EAH.

53,180

However,

this proposed strategy and its effect on the incidence of

EAH needs further study to determine the optimal number

and spacing of ﬂuid 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 ﬂuids.

Athletes who seek more quantitative guidance are

encouraged to weigh themselves before and after training to

assess their sweating rates and ﬂuid replacement needs. Some

weight loss associated with activity will be unrelated to ﬂuid

status as non-water mass is lost as energy is expended

(;0.23-0.24 g/kcal)

128,183

and is increased with increasing

duration and intensity of exercise.

128

The presence of weight

gain is positive indicator that ﬂuid intake has been in excess

of ﬂuid losses and water overload is present.

SUMMARY STATEMENT

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 ﬂuids may be of beneﬁt, 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 ﬂuid replacement, avoidance of overconsuming ﬂuids

(water, sports drinks or other hypotonic ﬂuids), 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 ﬂuid consumption and understand that high

ﬂuid 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), identiﬁcation,

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 ﬂuid in excess of sweat and urinary losses

and (2) excessive ﬂuid intake (water, sports drinks or other

hypotonic beverages) may not prevent muscle cramps or

exertional heatstroke and in rare cases may even be

associative.

82,100,118–120,184

On-site personnel must under-

stand that oral ﬂuid intake and IV ﬂuid infusion of hypotonic

and isotonic ﬂuids is contraindicated in all suspected cases

Hew-Butler et al Clin J Sport Med Volume 25, Number 4, July 2015

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 deﬁbrillators and ice/cold water immersion in the

“ﬁrst aid”of 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 ﬂuid replacement that

optimize safe hydration practices, placement of ﬂuid sta-

tions, and the use of intravenous rehydration. Important

athletic event decisions include spacing and placement of

ﬂuid stations, distribution of ﬂuid 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 conﬂict with the ofﬁcial 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 speciﬁc

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.

SUMMARY STATEMENT

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 deﬁcits versus ﬂuid status

and (2) whether or not the hypovolemic component is

somehow compromising the afﬂicted 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,

164

which

are well below the normal (isotonic) range of values for serum

[Na

] (135-145 mmol/L). While there will always be some

contribution of sodium loss to the pathogenesis of EAH—

which will vary signiﬁcantly in magnitude depending on: exer-

cise intensity, exercise duration, body size, and relative

ambient temperature

185–187

—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.

16,188

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

conditions

139

; (2) Ironman triathletes participating in hot and

humid Ironman triathlons

19,20

and (3) football players during

the ﬁrst week of training camp.

189

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 sufﬁcient 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 ﬂuids.

36,120

Moreover,

symptomatic EAH can rapidly progress to life-threatening

symptomatic hyponatremia if large volumes of hypotonic

ﬂuids are ingested after identiﬁcation of asymptomatic EAH

is present

or are administered intravenously

134

during recov-

ery from exercise.

SUGGESTIONS FOR FUTURE RESEARCH

Prospective and controlled clinical trials should be

performed both in the laboratory and in the ﬁeld to best

Clin J Sport Med Volume 25, Number 4, July 2015 Third EAH Consensus Statement

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 thirst”strategy 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 efﬁcacy 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

consequences.

•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.

SUMMARY OF RECOMMENDATIONS

Etiology of EAH

1. The primary etiology and pathophysiological mechanism

underlying EAH—and all known fatalities—is the over-

consumption of hypotonic ﬂuids 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 ﬂuids with sustained non-osmotic AVP secretion is

likely involved in the development of symptomatic EAH.

Clinical Classiﬁcation and Diagnosis of EAH

1. EAH can present with a wide range of symptoms ranging

from nonspeciﬁc 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 conﬁrming

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 ﬂuids are

given intravenously or ingested (Grade 1C). Thus, in patients

identiﬁed with EAH, hypotonic or isotonic ﬂuids 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 ﬂuids 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 ﬂuid consumption is a primary etio-

logic factor in EAH, using the innate thirst mechanism to

guide ﬂuid consumption is a strategy that should limit

drinking in excess and developing hyponatremia while

providing sufﬁcient ﬂuid 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).

ACKNOWLEDGMENTS

Dr. Dale Benjamin Speedy presented at the conference

and had input into the initial drafts, but withdrew authorship

before the ﬁnal version. We thank CrossFit, Inc for support of

this consensus conference.

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International society of sports nutrition position stand: nutritional concerns of the female athlete

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Aug 2022
Int J Environ Res Publ Health

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.

Clinical presentation of exercise‐associated hyponatremia in male and female IRONMAN® triathletes over three decades

Article

Full-text available

May 2023
SCAND J MED SCI SPOR

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.

Physiology of the Wildland Firefighter: Managing Extreme Energy Demands in Hostile, Smoky, Mountainous Environments

Article

Full-text available

Mar 2023

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.

Skin-Interfaced Wearable Sweat Sensors for Precision Medicine

Article

Mar 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.

Relationship of BMI with Proteinuria and Hematuria after One Session of Intense Continuous and Interval Exercise in Girls

Article

Full-text available

Jul 2022

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.

The ‘Phantom Runner’

Article

Dec 2004

Sodium-free fluid ingestion decreases plasma sodium during exercise in the heat

Article

Jun 1999

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.

Seizure disorder in a professional American football player

Article

Mar 2014

Robert J. Dimeff

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.

Hyponatraemia guideline development group. Clinical practice guideline on diagnosis and treatment of hyponatraemia

Article

Jan 2014
NEPHROL DIAL TRANSPL

Update: exertional hyponatremia, active component, U.S. Armed Forces, 1999-2010.

Article

Mar 2011

Armed Forces Health Surveillance Center (AFHSC

Oral salt supplementation during ultradistance exercise

Article

Sep 2002
CLIN J SPORT MED

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.

Hyponatremia in a Marathoner

Article

Oct 1988

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.

Grading strength of recommendations and quality of evidence in clinical guidelines: report from an American Collof Chest Physicians Task Force

Article

Jan 2006
CHEST

Hormones and behavior: The biology of thirst and sodium appetite

Article

Jan 1988

Hyponatremia and Ultramarathon Running

Article

Feb 1986

R. Tyler Frizzell

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)

Statement of the Third International Exercise-Associated Hyponatremia Consensus Development Conference, Carlsbad, California, 2015

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Henke's California Law Guide- Chapter 8 Administrative Law- Updated August 2017

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TRANSFER STATION RECYCLES 100 TONS PER DAY.