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Updated Fluid Recommendation: Position Statement From the International Marathon Medical Directors Association (IMMDA)

Updated Fluid Recommendation: Position Statement
From the International Marathon Medical
Directors Association (IMMDA)
Tamara Hew-Butler, DPM,* Joseph G. Verbalis, MD,
and Timothy D. Noakes, MBChB, MD, DSc*
(Clin J Sport Med 2006;16:283–292)
Controversy exists regarding optimal fluid guidelines
for athletes engaging in different sports. Most
published recommendations emphasize the detrimental
consequences of dehydration,
while more recent
reports warn of the morbid consequences of hyperhydra-
Accordingly, individualized recommendations
emphasizing a balance between the two extremes have
These revised guidelines, however, continue
to promote static recommendations for what in reality are
very dynamic athletic situations.
Marathon running epitomizes a dynamic situation
that requires a constant adjustment to constantly chan-
ging homeostatic requirements. Real-time assessments of
fluid and sodium homeostasis are physiologically repre-
sented by changes in plasma osmolality (POsm). Pituitary
arginine vasopressin (AVP) secretion is stimulated when
POsm increases by only 1% to 2%, representing the
body’s attempt to prevent dehydration by decreasing
kidney water excretion. After maximal antidiuresis is
achieved, thirst is then stimulated to replace water losses
that are in excess of the ability of AVP-stimulated
antidiuresis to conserve body water. In general, the
osmotic threshold for thirst is 5 to 10 mOsm/g H
higher than that of AVP secretion. Thus, thirst is
stimulated with decreases in body water of approximately
1.7% to 3.5%.
Concomitant performance decrements
and cardiovascular strain are also documented when
baseline body fluid losses exceed approximately 2%.
The failure of athletes to replace 100% of body-
weight losses from ad libitum fluid intake has been
well-described as ‘‘involuntary’’
or ‘‘voluntary’’ dehy-
this phenomenon has resulted in the devalua-
tion of thirst as a ‘‘poor’’ indicator of body fluid needs.
The combination of laboratory with recent field data (see
Table 1 and subsequent discussion), however, suggests that
the body primarily defends POsm, and not blood or
extracellular fluid volume during prolonged endurance
exercise. Because it is well established that thirst is
stimulated in response to changes in tonicity in most land
it seems reasonable to conclude that
thirst would be the predominant physiologic and dynamic
regulator governing fluid balance during exercise.
This article will focus on the physiology of normal
fluid balance as the ultimate guide toward the evolution
of optimal fluid recommendations. Six physiologic con-
siderations of fluid and sodium balance will be detailed
followed by 6 practical recommendations. The neuro-
endocrine regulation of homeostasis will be emphasized in
defense of the behavioral drives for thirst and sodium
palatability during dynamic activities such as prolonged
endurance exercise. The behavioral drives to maintain
fluid and sodium balance are evolutionary stable,
essential for the safety and survival of the species, and
deeply rooted within the human genetic makeup.
1. Bodyweight is not an accurate surrogate for body
fluid volume during prolonged exercise: The field of
exercise science promotes fluid replacement at 100% of
bodyweight losses under the premise that sweat loss is
an accurate surrogate for changes in body fluid
This recommendation—to externally
defend bodyweight during exercise—remains entrenched
in the literature despite initial observations in 1932 stating
that voluntary water consumption replaced only 56% of
sweat lost during exercise.
Research on ad libitum fluid
intakes over the last 74 years have repeatedly verified that
Copyright r2006 by Lippincott Williams & Wilkins
Received for publication May 12, 2006; accepted May 26, 2006.
From the *Department of Human Biology, University of Cape Town,
Cape Town, South Africa; and wDivision of Endocrinology and
Metabolism, Georgetown University Medical Center, Washington,
This position statement was approved and endorsed by the IMMDA
Body on May 6, 2006 in Barcelona, Spain. The lay statement for
immediate release was editorially prepared by Lewis Maharam, MD,
FACSM (Chair), Arthur Siegel, MD, Marvin Adner, MD, W. Bruce
Adams, MD, Rudra Sabaratnam, MD, and Pedro Pujol, MD,
IMMDA address: Lewis G. Maharam, MD, IMMDA Board of
Governors at 24 West 57th Street, 6th floor, New York, NY 10019
Reprints: Tamara Hew-Butler, DPM, UCT/MRC Research Unit for
Exercise Science and Sports Medicine, Department of Human
Biology, University of Cape Town, P.O. Box 115, Newlands 7725,
South Africa (e-mail:
Clin J Sport Med Volume 16, Number 4, July 2006 283
humans, when given free access to fluids, replace no more
than 75% of net water losses during physical activ-
Abdominal distress, nausea and vomiting
have been reported in highly trained distance runners who
have tried to match fluid intakes to sweat rates.
ongoing discrepancy between thirst, satiation and the
inability to inherently maintain bodyweight during
prolonged endurance activity suggests that bodyweight
is only a marker of body fluid homeostasis and is not
regulated in itself. The remarkable capacity of the body to
maintain circulating plasma volume despite large deficits
in bodyweight due to ‘‘sweat losses’’ during prolonged
endurance exercise exemplifies the complex regulation of
body fluid volume and distribution
that are unrelated to
the maintenance of bodyweight.
2. Blanket fluid guidelines with fixed ranges will not
protect the diverse population currently participating in
athletic events: The American College of Sports Medi-
cine’s (ACSM) current guidelines promote a fluid intake
of 600 to 1200 mL/h; a range largely based on laboratory
studies performed on elite male athletes.
The popularity
of marathon running increased markedly at the time these
guidelines were released, with charity running groups
enticing more recreational runners into the sport. Slower,
more inexperienced, female athletes heeded the upper
limit of the ACSM guidelines and developed exercise-
associated hyponatremia (EAH) by ingesting more fluid
than they could excrete over the course of a marathon
In 2001, the International Marathon Medical
Directors Association (IMMDA) approved guidelines
lowering the ‘‘acceptable’’ range to 400 to 800 mL/h to
adjust the upper limit and protect smaller athletes (mainly
female) from overdrinking.
Recently, mathematical models have proposed that
these ranges may not be ideal to cover the current
population of runners participating in marathon events.
Close inspection of a marathon field today illustrates the
variety of shapes, sizes and speeds that must be taken into
consideration when formulating fluid intake guidelines.
For example, the average weight of 7299 runners
registering for the 2005 Comrades Marathon was 73 kg.
The lightest competitor weighed 43 kg whereas the
heaviest runner weighed 119 kg. The fastest runner
averaged 16.4 km/h (winning time 5:27) whereas the
slowest runners ran at a 7.4 km/h pace (the official 12-h
cut-off pace). The 11,728 runners who completed the
89.2 km Comrades Marathon ran, on average, 49 minutes
slower during the second half of the race than they ran the
first half of the race with a minimum and maximum range
of 11 (negative split) and 180 minutes (positive split),
respectively. The wide variation between split times
exemplifies the late-race functional deterioration that
has been described elsewhere
and highlights the fact that
modern marathon running is a dynamic situation,
including participants with widely diverse physical
attributes and fitness levels. An even wider spread of
running speeds and bodyweights would be expected in a
standard 42.2 km marathon, as the Comrades Marathon
is more than double the distance, requires a qualifying
time for entry, has a defined cut-off and is held over a
grueling terrain; all of which precludes the participation
of unfit and novice runners. Conversely, relatively unfit
and untrained runners can often complete a standard
42 km marathon, amplifying the wide range of participant
The 3 main factors governing fluid loss during
exercise are mass (bodyweight), running speed (metabolic
rate), and ambient temperature.
Race day tempera-
tures in the New York City Marathon have varied
between 1 and 291C and have fluctuated as much as 171C
from start to finish.
Therefore, it would seem very
unlikely that ANY single ‘‘range’’ could successfully
encompass this wide spectrum of weather conditions,
bodyweights, and running speeds that characterize
modern day marathon running.
3. Drinking to thirst will preserve POsm within the
normal range and maintain intracellular volume and
homeostasis: Thirst is a subjective sensation characterized
by a deep-seated desire for water
and is generally
associated with oral sensations such as dryness, irritation,
and an ‘‘unpleasant taste’’ in the mouth.
Thirst has
been quantified using geometric and visual analog
and documented to increase when POsm
is 5 to 10 mOsm/kg above the threshold for AVP
secretion; well within the normal physiologic range of
B280 to 295 mOsm/kg H
POsm is maintained within this narrow range to
protect intracellular volume. Serum sodium concen-
trations [Na
] mirror POsm
because sodium is
the principal solute of extracellular fluid; thus [Na
and POsm are viewed as interchangeable in this discus-
sion, although the appropriate calculation is: POsm =
]+[BUN]+[glucose] (all in mmol/L).
The maintenance of intracellular volume is of vital
importance for cell function and survival. Hypertonicity
causes intracellular dehydration; a bodyweight loss of
5.5% during prolonged severe exercise elicits a reduction
in red cell volume by 3.2%.
A reduced intracellular volume can reduce the rates
of glycogen and protein synthesis
and hypertonicity
beyond serum sodium concentrations of 160 mmol/L can
cause encephalopathy and death.
Conversely, hypoto-
nicity causes intracellular expansion. Although high cell
volume can stimulate glycogen and protein synthesis,
excessive and acute cell swelling from serum sodium levels
below 125 mmol/L can lead to hyponatremic encephalo-
pathy, noncardiogenic pulmonary edema, and death.
Thirst and AVP secretion are intimately related:
synergistically lowering elevations in POsm by stimulat-
ing fluid intake and promoting antidiuresis. The threshold
for AVP release (B280 to 285 mOsm/kg H
O) is normally
set 5-10 mOsm/kg H
O below that for thirst (B290 to
295 mOsm/kg H
O), despite significant variation between
individual set points.
This evolutionary design liberates
individuals from constantly seeking water, as thirst is only
stimulated when antidiuresis is maximal and hypertoni-
city exceeds the capacity of the kidneys to cope with rising
tonicity. The strength of an intact thirst mechanism is
Hew-Butler et al Clin J Sport Med Volume 16, Number 4, July 2006
284 r2006 Lippincott Williams & Wilkins
exemplified in patients with the disorder of diabetes
insipidus, either due to inadequate AVP secretion or an
impaired kidney response to AVP, where a normal POsm
is maintained by stimulated thirst despite the excretion of
up to 20 L of fluid per day.
Oropharyngeal metering
and stomach fullness
provide inhibitory feedback
to terminate drinking more rapidly than the return of
POsm to normal levels, perhaps as a safety measure to
prevent overdrinking.
The strength and precision of the thirst mechanism
has been demonstrated both at rest and during exercise in
young adults. In one study involving seven men an
increase in POsm, in response to hypertonic saline
infusion, promoted a dipsogenesis proportional to the
increase in POsm; with 82% of the total volume of water
consumed within the first 5 minutes of rehydration with
the immediate cessation of intake due to ‘‘stomach
In a separate fluid deprivation study, 65%
of total water intake was consumed during the first 2.5
minutes of rehydration in 5 males.
Subjective ratings of
dry mouth and plasma protein concentrations returned to
baseline levels in 2.5 minutes, plasma volume returned to
baseline levels within 5 minutes and serum sodium
concentrations began to decrease within 5 minutes;
returning to baseline values within 12.5 minutes. This
initial drinking bout was also interrupted by sensations of
‘‘stomach fullness’’. During prolonged endurance exer-
cise, 8 female and 10 male athletes responded to graded
levels of hypohydration with ad libitum fluid intakes
sufficient enough to restore POsm, replace sweat losses,
and attenuate thermal and circulatory strain.
Thus, humans respond to increases in serum [Na
with AVP secretion, thirst and water intake that occur
when POsm is still well within normal ranges. The
precision and magnitude of the thirst drive is related to
ancestral areas of the brain that are associated with
vegetative functions such as the hunger for air and food,
micturition and pain.
To assume that the thirst drive
would be an ‘‘inaccurate index’’ of fluid balance during
exercise (the dynamic homeostatic imbalance alterna-
tively described as the ‘‘flight or fight’’ response) would
seem contradictory to the evolution of our species.
Although there is concern that thirst due to
intracellular dehydration or extracellular volume deple-
tion may be confused with the sensations of a dry mouth
(xerostomia) during exercise, thirst due to xerostomia has
not been shown to lead to severe polydipsia.
sensation of a dry mouth can promote more frequent
drinking episodes, but total fluid intake is similar, or
counter regulated by increased urinary output, in tested
clinical and experimental settings.
Recent studies on
xerostomia, thirst, and interdialytic weight gain have not
factored in osmolality and therefore do not provide
convincing evidence that a dry mouth without changes in
POsm can contribute to excessive fluid intakes or to
hyponatremia from fluid overload without inappropriate
AVP secretion.
4. The body defends POsm and volume over
bodyweight. ‘‘Involuntary dehydration’’ is a homeostatic
mechanism designed to protect POsm and cellular volume
in response to hypotonic sweat losses: The reluctance of
man to voluntarily replace fluids at amounts equivalent to
bodyweight losses during exercise was recognized in 1933,
when Dill
hypothesized that humans only drunk as
much fluid to maintain constant osmolarity of the
extracellular fluid. This ‘‘failure’’ of man to replace
100% of body fluid losses, generally using bodyweight
as a surrogate marker of body fluid volume, has been
subsequently recognized as ‘‘voluntary’’ or ‘‘involuntary’’
dehydration; this has had the effect of minimizing the
importance of thirst as an adequate indicator of body
fluid needs.
Actual field study data from multiple endurance
studies indicates that the maintenance of bodyweight will
actually lead to reductions in serum sodium concentra-
tions from prerace to postrace (Table 1). Most athletes
who lose less than 2% of bodyweight experience a
decrease in serum [Na
Athletes who gain weight
progress from normonatremia to hyponatremia.
contrast, POsm is maintained within normal ranges
(± 3 mmol/L) when percent bodyweight losses are be-
tween 2% and 4%.
Whereas most athletes who lose
more than 4% of bodyweight demonstrate increases in
serum [Na
] above normal ranges.
Thus, the
cumulative data in Table 1 suggest that the body defends
POsm over body fluid volume, as reflected by changes in
bodyweight, during prolonged endurance activity lasting
between 2.7 and 38.2 hours, and can maintain POsm and
therefore intracellular volume, best between 2% and 4%
cumulative bodyweight losses. Acute bodyweight changes
below 2% or above 4% cannot be compensated for
internally, and may lead to dysregulation of serum [Na
with resultant clinical symptomatology.
Concordant with these field data, 3 laboratory
studies replacing fluids to 100% of bodyweight losses
confirm a reduction in serum sodium concentrations
during prolonged endurance exercise lasting between 2
and 6 hours.
Although these decreases in serum
sodium concentrations were generally within normal
physiologic ranges, fluid replacement at or above 100%
does not seem to offer any performance benefits.
Advocates of replacing 100% of bodyweight losses
argue that cardiovascular drift—the downward drift in
central venous pressure and stroke volume with con-
comitant rise in heart rate—commences with a 1%
decrease in bodyweight losses.
Subsequent studies
normalizing blood volume while inducing hypohydration
have confirmed, however, that cardiac drift during
exercise can and often does result from factors other
than hypovolemia.
The corresponding increase in
heart rate with progressive dehydration is accompanied
by a proportional decrease in stroke volume which
serves to maintain cardiac output.
These reductions in
stroke volume are more related to elevations in core
temperature, circulating catecholamine concentrations
and heart rate than due to the redistribution of blood
flow or circulating blood volume.
Only at degrees of
dehydration beyond B3% is cardiac output significantly
Clin J Sport Med Volume 16, Number 4, July 2006 Updated Fluid Recommendation
r2006 Lippincott Williams & Wilkins 285
diminished as a result of a reduction in circulating blood
This bodyweight loss exceeds the threshold
level at which AVP secretion and thirst are generally
Equations predicting ad libitum fluid intake from
multiple regression analyses identify POsm as the primary
factor driving voluntary fluid intake during exercise or
under stressful environmental conditions; with plasma
volume and subjective symptoms of secondary impor-
Thus, under acute situations involving sweat
sodium losses, the body will defend osmolality and
intracellular volume through fluid shifts from the extra-
cellular (primarily interstitial) fluid compartments
until B4% bodyweight losses through sweating accrue;
after which intracellular fluid volume is compromised and
an external fluid supply is necessary.
Athletes rehydrating with either water or an
electrolyte-containing beverage restore 68% and 82% of
fluid losses, respectively, after an exercise-induced dehy-
dration of 2.3%.
Changes in free water clearance
followed changes in POsm and rehydration with only
water restored POsm to control (isotonic) levels. Con-
versely, extracellular fluid space was fully restored
only through consumption of the electrolyte-containing
beverage. Ad libitum fluid intake did not match 100%
bodyweight losses during 3 hours of rehydration
with either beverage (hence the ‘‘involuntary’’ dehydra-
tion), illustrating the immediate defense of the body to
preserve POsm first and only secondarily intravascular
Metabolic water formation, from the combustion of
fat and carbohydrate combined with the liberation of
glycogen-bound water, may contribute an internal water
source to offset sweat losses and sustain internal fluid
balance during prolonged or intense physical activity.
The activation or inactivation of internal sodium stores
has also been hypothesized as a mechanism aiding in the
defense of POsm during prolonged endurance exer-
Data from 2135 weighed competitive athletic
performances demonstrate that athletes who overhydrate,
underhydrate, or euhydrate during prolonged endurance
races generally maintain serum sodium concentrations
within normal ranges (Fig. 1 reprinted with permission).
Despite this wide variation in bodyweight changes, 80%
of the athletes in this large and diverse pool maintained
POsm and intracellular volume during prolonged
continuous athletic activity.
Thus, the combination of laboratory work with field
data requires a re-examination of the phrase ‘‘voluntary
dehydration’’ to more accurately reflect the preservation
of POsm (and therefore intracellular volume) over
extracellular fluid (ECF) and plasma volume, secondary
to sweat NaCl losses during endurance exercise. The body
does not defend ECF and plasma volume over POsm
during an acute exercise bout, and the immediate
replacement of body fluids at 100% of bodyweight losses
is not beneficial to performance. AVP secretion and thirst
are stimulated when POsm increases 1% to 4%; well
within the physiologic ranges of homeostatic compensa-
tion. Performance and cardiovascular decrements are
clearly documented when bodyweight losses exceed 4%;
however, this range is well beyond the protective capacity
of the synergistic AVP and thirst mechanisms, whose
primary physiologic interaction is to preserve osmolality
within relatively narrow physiologic ranges. Only after
POsm is stabilized will the body then activate mechanisms
to gradually restore plasma volume by increasing
sodium consumption and fluid intake over the next 24
5. Plasma volume contraction, resulting from the
preservation of POsm during exercise,will be restored over
a period of 24 hours by hormonal mechanisms which will
increase the palatability for sodium-containing foods and
beverages. When sodium is ingested,plasma volume will
gradually return to baseline levels: The primary rationale
for the inclusion of sodium into rehydration beverages is
TABLE 1. Field Study Data: Serum Sodium and Bodyweight Change
Race Distance
] Prerace
] Postrace
] Change
(Prepost Race)
Loss (%)
Time (h)
Twerenbold et al
(N = 13) B41 run 137 ± 1 133 ± 2 4 2 ± 1 weight gain 4
Glace et al
(N = 13) 160 run 144 140 4126
Gerth et al
(N = 51) 100 run 137 ± 5 131 ± 2 6114
Hew-Butler (unpublished) (N = 33) 109 cycle 139 ± 3 138 ± 3 12±15±1
Stuempfle et al
(N = 20) 161 snow race 141 ± 1 138 ± 2 3238±7
Nelson et al
(N = 45) 42 run 139 ± 0 142 ± 0 3 3 4
Refsum et al
(N = 41) 90 ski 142 141 138
Cohen and Zimmerman
42 run 139 ± 2 142 ± 2 3 3 3
Noakes and Carter
(N = 13) 160 run 144 ± 1 140 ± 3 4316±6
Kavanagh and Shephard
(N = 9) 42 run 146 ± 2 148 ± 2 2 3 4± 1
Hew-Butler (unpublished) (N = 82) 56 run 139 ± 3 138 ± 3 14±16±1
Hew-Butler et al
(N = 413) 226 triathlon 141 ± 2 141 ± 3 0 4 ± 2 12 ± 2
Maron et al
(N = 6) 42 run 141 ± 1 141 ± 1 0 4 ± 1 3 ± 0
Gastmann et al
(N = 9) 453 triathlon 138 ± 4 133 ± 4 5526
Rocker et al
42 run 144 149 5 5 3
Beckner and Winsor
42 run 141 156 7 5 No time
Riley et al
32–42 run 143 ± 1 148 ± 1 5 5 4
Astrand and Saltin
(N = 6) 85 ski 144 152 8 6 9
Hew-Butler et al Clin J Sport Med Volume 16, Number 4, July 2006
286 r2006 Lippincott Williams & Wilkins
to aid in the restoration of plasma volume
rather than
prevent the development of EAH.
The presence of a
sodium appetite is equivocal in humans,
but studies
on sodium palatability and preference have revealed
significant associations with sodium loss and defi-
A peculiar theme echoing throughout
these studies is the delayed expression of the attractive-
ness of sodium-containing items after cumulative sodium
losses, particularly in studies involving sweat sodium
losses after exercise.
A study by Takamata et al
confirms that the body
protects osmolality over extracellular volume after 7
hours of intermittent exercise at 351C. Elevated serum
sodium concentrations after exercise increased the palat-
ability for water and decreased the pleasantness of
concentrated sodium beverages during the first hour of
rehydration. POsm returned to baseline levels 3 hours
after rehydration had begun, at which time the palat-
ability rating for sodium-containing beverages signifi-
cantly increased over baseline levels. The palatability of
highly concentrated sodium beverages continued to
increase at 6, 17, and 23 hours after the cessation of
exercise which correlated with significant increases in
aldosterone secretion, but not AVP or POsm. The
authors concluded that ‘‘increased H
O palatability is
only associated with osmotically induced thirst and thus
contributes to body fluid osmoregulation. In contrast,
ECF thirst accompanied by an increased Na
appears after a delay of many hours after osmoregulatory
responses occur and may contribute to ECF volume
Thus, the palatability for sodium is delayed after
exercise until POsm is restored to normal levels from the
ingestion of, and preference for, plain water. Only after
POsm returns to baseline levels—through the ingestion of
plain water to dilute elevated serum sodium concentra-
tions—will the body seek sodium (by a palatability
increase) to return plasma volume to baseline levels in
the succeeding hours after the exercise bout. This is
presumably facilitated by the natriorexogenic and dipso-
genic actions of aldosterone and angiotensin II, which are
known to stimulate these actions.
This phenomenon has
also been supported by studies of exercising students,
with low sweat rates, who expressed a decreased avidity
for sodium when given high doses of salt before
and has also been clearly demonstrated in rats
made hypovolemic by polyethylene glycol injection.
Figure 2 illustrates that hypovolemic rats, on a normal
sodium diet, will respond to isotonic hypovolemia by first
ingesting only water until the decline in POsm inhibits
water intake. Thereafter, the rats will drink saline until
POsm increases, which will again stimulate water intake.
The rat will then alternate between saline and water
consumption until plasma volume is returned to baseline
levels; maintaining a stable POsm throughout the gradual
return to euvolemia. Thus, it has been shown in both
animals and humans that sodium ingestion is necessary to
restore plasma volume once osmolality has been
stabilized. This restoration normally progresses over
the course of 24 hours after the hypovolemic insult.
Because sodium is clearly necessary to restore and
maintain plasma volume after sweat sodium losses from
FIGURE 1. Distributions of postrace [Na
] in 2135 overhydrated, euhydrated, and dehydrated athletes. Reprinted with
permission from T. D. Noakes.
Clin J Sport Med Volume 16, Number 4, July 2006 Updated Fluid Recommendation
r2006 Lippincott Williams & Wilkins 287
exercise, the beneficial effect of sodium ingestion during
exercise is a topic of substantial debate. Studies
have shown that consumption of hypotonic sodium-
containing beverages do not prevent the development of
hyponatremia in athletes replacing 100% fluid loses or
or in polydipsic psychiatric patients,
because most of the sodium ingested is rapidly lost
through the urine.
In conditions of fluid overload,
however, a mild blunting of serum sodium decline occurs
with consumption of sodium-containing beverages. This
blunting does not eliminate the development of hypona-
tremia in athletes who continue to overdrink, however.
There are no studies documenting that sodium
ingestion during exercise provides a clinical, physiological
or performance benefit.
On the contrary, there
are several studies linking sodium ingestion with negative
physiologic and performance effects.
et al
supplemented normal dietary intakes with 10.2 g
(173 mmol) of sodium 3 days before a 2-hour exercise
bout (60% VO2 Max on a cycle ergometer) with fluid
intake matching sweat rate. The authors concluded that
the ‘‘salt loading’’ did not have a beneficial effect on
temperature and fluid balance and in fact, elicited
undesirable effects including significant increases in
bodyweight, heart rate, and rectal temperature.
Furthermore, the extra sodium was rapidly excreted in
the urine, suggesting that the body had no need for the
extra NaCl. Similarly, Pitts and Consolazio
tered 9 g of NaCl to 11 subjects just before a 10-mile
march. Water was replaced at equal volumes to sweat loss
every 2 miles. The supplemental sodium ingestion also led
to elevated heart rates and rectal temperatures, along with
complaints of ‘‘gastrointestinal uneasiness.’’
mance in a VO2 Max test was impaired after rapid
infusion of 30 mL/kg of isotonic saline 30 minutes
before the exercise bout.
There was a consistent
increase in ventilation after every exercise work level
after rapid saline infusion, as well as significant reductions
in forced vital capacity and forced expiratory volume. All
of these subjects felt more fatigued at maximal effort and
reported sensations of ‘‘increased leg tightness’’ These
authors hypothesized that the symptoms were due to
increased intramuscular tissue pressure and resultant
edema from the saline infusion.
Thus, sodium supplementation has no documented
advantages when consumed during exercise, with over-
replacement exhibiting detrimental cardiorespiratory and
thermoregulatory effects during exercise. Because sodium
is necessary for plasma volume restoration in the 24 hours
after exercise, once POsm has been normalized,
electrolyte-containing food and beverages should be
freely available after exercise and ingested according to
palatability and tolerability.
6. Conditions where changes in plasma volume alter
the set-point between thirst and tonicity: advanced age,the
syndrome of inappropriate antidiuretic hormone secretion
(SIADH) and exercise in extreme heat or cold: It is well
documented that individuals over the age of 65 years
demonstrate a reduced thirst drive—with corresponding
decreases in fluid intake—in response to rising tonicity,
when compared with younger adults.
suggests that this ‘‘reduced thirst drive’’ alternatively
represents an upward shift in the operating set point ra-
ther than an age-related defect in osmoregulation.
Studies confirm that healthy older men demonstrate
appropriate, although delayed, reflex adjustments
serving to maintain osmotic homeostasis during condi-
tions of hypertonic hypovolemia
and hypervolemia,
when the rehydration period is sufficiently long (3 h).
Osmotic stimulation of AVP has been shown to elicit
a 3-fold greater increase per unit rise in POsm
in older men
but follows the same pattern as
that of younger men when exposed to similar
osmotic stimuli.
Thus, evidence suggests that it
is not a reduction in the osmotic drive that is primarily
responsible for the attenuation of thirst during aging, but
rather a reduction in the sensitivity of cardiopulmonary
baroreceptors to plasma volume expansion that may
contribute to an upward shift in the operating set
The diminished inhibitory effect of central
volume expansion on thirst may result from an age-
related impairment of plasma volume maintenance and
expansion; perhaps from the inability to mobilize or
maintain proteins in the vascular space.
impairment in older males to expand or maintain plasma
volume has been demonstrated in situations of hypertonic
saline infusion,
thermal dehydration,
and during
repeated exercise/heat stress.
The inability of most
elderly people to expand plasma volume may necessitate
elevation of the osmotic thirst threshold because age-
related declines in renal function could concomitantly
facilitate the development of fluid overload hyponatremia
if lower, more ‘‘physiologic,’’ osmotic thresholds con-
tinued to exist.
Exercise in cold conditions may also elevate the
osmotic threshold for which thirst and AVP secretion are
FIGURE 2. Changes in [Na
] and cumulative fluid intake in
hypovolemic rats (after subcutaneous injection of 30%
polyethylene glycol solution) with free access to water and
concentrated saline solutions over a 24-hour period. Redrawn
from American Scientist. 1988;76:261–267 with permission
from J. G. Verbalis.
Hew-Butler et al Clin J Sport Med Volume 16, Number 4, July 2006
288 r2006 Lippincott Williams & Wilkins
stimulated. Subjects hypohydrated by B3% to 4%
experience a decline in both AVP secretion and perceived
thirst sensations when entering a cold (41C) chamber,
despite resting plasma osmolalities above 295 mosmol/kg
These subjects relate significantly lower thirst
ratings at 40 and 60 minutes of treadmill exercise—when
euhydrated and hypohydrated—in cold compared with
temperate environments (271C), despite similar plasma
osmolalities. Thus, the authors of this study hypothesize
that thirst and AVP secretion are ‘‘attenuated’’ from
central volume expansion, secondary to peripheral
vasoconstriction in the cold. These findings suggest that
the osmotic operating set point in cold conditions could
be elevated due to increased central blood volume.
Conversely, nonosmotic pituitary AVP secretion,
leading to dilutional hyponatremia and SIADH, may
cause a downward resetting of the osmotic threshold
for thirst.
The presence of thirst at low osmolalities
has been hypothesized to pathologically contribute to the
development of hyponatremia,
as patients with chronic
SIADH relate the sensation of thirst and report daily fluid
intakes similar to healthy individuals. The study by Smith
et al
demonstrates, however, that SIADH patients with
chronic dilutional hyponatremia (average serum sodium
concentration: 125.8 ± 2.7 mmol/L) respond appropri-
ately to osmotic challenge by hypertonic saline infusion.
Baseline plasma osmolalities and the osmotic thresholds
for both thirst and AVP release were 20 mosmol/kg H
lower in the SIADH group when compared with a group
of healthy matched controls. Thirst ratings, elevations in
AVP, urine osmolalities, and fluid intakes were similar
between the 2 groups with parallel elevations in POsm.
Perceived ratings of thirst returned to baseline levels in
both groups after 30 minutes of drinking and fluid
consumption led to an immediate fall in thirst ratings
within 5 minutes in both cohorts. Thus, the suppression
of thirst in the SIADH group was similar to that of the
control group, suggesting that the neural inhibition of
thirst and drinking is preserved in patients with SIADH.
These laboratory-based conclusions have been verified in
the field setting, where marathon runners diagnosed with
EAH reportedly consumed fluids in excess of excretion
rates not because they were thirsty, but because they were
fearful of becoming dehydrated.
The sensation of thirst
should not be confused with the act of drinking. The act
of drinking occurs from regulated (drinking to physiolo-
gic thirst) and unregulated (social, habitual, palatability)
fluid intake which may be governed by factors (market-
ing, commercialism) unrelated to the osmotic set point.
Work performance at the initial stages of acclima-
tization during exercise in extreme heat may improve with
‘‘forced’’ fluid intakes—beyond thirst—at volumes
equivalent to sweat loss.
The environmental
temperatures in these trials were extreme, ranging from
to 461C
and involved a limited number of
subjects. Subjects in the Bean and Eichna trial
water equivalent to weight lost (1200 mL) and were able
to complete 5 work cycles ‘‘without great difficulty’’ on
the first day of exercise compared with subjects receiving
only enough fluid to quench thirst (600 mL). On the
fourth day of exercise, however, the degree of acclima-
tization—as measured by heart rate, rectal temperature
and blood pressure—was similar between the two groups.
The one subject in the Pitts et al
trial also reported less
fatigue and had lower rectal temperatures when ‘‘forced’’
to drink water equal to sweat losses. The fact that the
rectal temperatures between ad libitum fluid replacement
and ‘‘full’’ replacement varied greatly between trials
(B0.3 to 11C) suggests that initial acclimatization
requires fluid intakes beyond thirst to accommodate
plasma volume expansion. After plasma volume is
appropriately expanded, the need to ingest fluid beyond
ad libitum intakes is not necessary to maintain similar
rectal temperatures, heart rates and blood pressures.
Alternatively, Moroff and Bass
administered a water
preload of 2000 mL to nonacclimatized subjects and
reported that when these subjects were water loaded, they
had lower rectal temperatures and pulse rates compared
with when not preloaded. Acclimatized subjects given the
same preload, however, displayed lower heart rates with
similar rectal temperatures for reasons that are unclear.
Thus, initial exercise in extreme heat may require transient
fluid intakes beyond thirst to facilitate the expansion of
plasma volume—and heat acclimatization—irrespective
of the current operating osmotic set point.
1. Drinking to thirst is the body’s dynamic physiologic
fluid calculator and in most cases will protect athletes
from the hazards of both over and underdrinking by
providing real-time feedback on tonicity.
2. A static fluid calculator can provide an estimate of
body fluid losses thereby providing a numeric range as
ageneralized strategy for fluid replacement during
racing and training.
3. Athletes are advised to understand their individualized
fluid needs through use of a static fluid calculator but
ALWAYS defer to physiologic cues to increase fluid
intake (thirst) or decrease fluid consumption (increased
urination, bloating, weight gain) while running.
4. Water, sodium and glucose (in foods and or beverages)
should be freely available at fluid replacement stations,
spaced 1.6 km (minimum) to 5 km (maximum) apart.
The quantity and amount of food and fluid consumed
should be guided by individual palatability and
tolerance for such items.
5. Calibrated scales along a marathon course should be at
the discretion of the medical team; a weight loss of
>4% or any weight gain constitutes justification for
medical consultation.
6. Exercise in extreme heat (>381C) may require
hydration beyond thirst during the initial days of
heat acclimatization whereas advanced age (>65 y)
and cooler environmental temperatures ( < 51C) may
elevate the operating set point for the stimulation
of thirst.
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r2006 Lippincott Williams & Wilkins 289
Marathon running is a serious endeavor that
requires a personal commitment to sustained physical
training. The hazards of marathon running have been
highlighted by the recent deaths of 4 novice female
runners from EAH. Understanding individual fluid
requirements before tackling a 42.2-km race is pivotal
toward ensuring the successful and safe completion of
such an event.
Although our society revolves around rules and
algorithms to guide us through different situations,
individuals should not be confined to these rules in a
dynamic setting. There are no shortcuts toward great
achievement, and marathon running is no exception.
Clinicians and scientists must resist handing out unrea-
listic ‘‘blanket advice’’ to individuals seeking simple
answers, but rather should encourage athletes to explore,
understand and be flexible toward their own needs. By
providing guidelines and advice on how to appropriately
understand individual fluid replacement needs, we can
eliminate future fluid balance problems by avoiding the
temptation to generalize one rule for every situation and
every athlete.
1. Convertino VA, Armstrong LE, Coyle EF, et al. American College
of Sports Medicine position stand. Exercise and fluid replacement.
Med Sci Sports Exerc 1996;28:i–vii.
2. Coris EE, Ramirez AM, Van Durme DJ. Heat illness in athletes:
the dangerous combination of heat, humidity and exercise. Sports
Med. 2004;34:9–16.
3. Cheuvront SN, Carter R III, Sawka MN. Fluid balance and
endurance exercise performance. Curr Sports Med Rep. 2003;
4. Coyle EF. Fluid and fuel intake during exercise. J Sports Sci.
5. Hew-Butler TD, Almond CS, Ayus JC, et al. Consensus Statement
of the 1st International Exercise-Associated Hyponatremia
Consensus Development Conference, Cape Town, South Africa,
2005. Clin J Sport Med. 2005;15:208–213.
6. Noakes TD. Overconsumption of fluids by athletes. BMJ. 2003;
7. Noakes TD. Fluid replacement during marathon running. Clin
J Sport Med. 2003;13:309–318.
8. Casa, DJ. USATF Self-Testing Program for optimal hydration.
Available at:
USATFSelfTestingforOptimalHydration.pdf. 2003.
9. GSSI. Gatorade Sports Science Institute Fluid Calculator. Avail-
able at:
calculator.htm. 2005.
10. PowerBar. PowerBar event nutrition calculator. Available at: http:/
/ 2005.
11. Robertson GL. Abnormalities of thirst regulation. Kidney Int.
12. McKinley MJ, Johnson AK. The physiological regulation of thirst
and fluid intake. News Physiol Sci. 2004;19:1–6.
13. Verbalis JG. Disorders of body water homeostasis. Best Pract Res
Clin Endocrinol Metab. 2003;17:471–503.
14. Nose H, Mack GW, Shi XR, et al. Role of osmolality and plasma
volume during rehydration in humans. J Appl Physiol. 1988;
15. Greenleaf JE. Problem: thirst, drinking behavior, and involuntary
dehydration. Med Sci Sports Exerc. 1992;24:645–656.
16. Greenleaf JE, Sargent F. Voluntary dehydration in man. J Appl
Physiol. 1965;20:719–724.
17. Cheuvront SN, Haymes EM. Ad libitum fluid intakes and
thermoregulatory responses of female distance runners in three
environments. J Sports Sci. 2001;19:845–854.
18. Hubbard RW, Sandick BL, Matthew WT, et al. Voluntary
dehydration and alliesthesia for water. J Appl Physiol. 1984;
19. McKinley MJ, Cairns MJ, Denton DA, et al. Physiological and
pathophysiological influences on thirst. Physiol Behav. 2004;
20. Stricker EM, Verbalis JG. Hormones and behavior. Am Scientist.
21. Rolls BJ, Wood RJ, Rolls ET, et al. Thirst following water
deprivation in humans. Am J Physiol. 1980;239:R476–R482.
22. Phillips PA, Rolls BJ, Ledingham JG, et al. Osmotic thirst and
vasopressin release in humans: a double-blind crossover study.
Am J Physiol. 1985;248:R645–R650.
23. Fitzsimons JT. Angiotensin, thirst, and sodium appetite. Physiol
Rev. 1998;78:583–686.
24. Barr SI. Effects of dehydration on exercise performance.
Can J Appl Physiol. 1999;24:164–172.
25. Broad EM, Burke LM, Cox GR, et al. Body weight changes and
voluntary fluid intakes during training and competition sessions in
team sports. Int J Sport Nutr. 1996;6:307–320.
26. Cheuvront SN, Haymes EM, Sawka MN. Comparison of sweat
loss estimates for women during prolonged high-intensity running.
Med Sci Sports Exerc. 2002;34:1344–1350.
27. Barr SI, Costill DL. Water: can the endurance athlete get too much
of a good thing? J Am Diet Assoc. 1989;89:1629–1632, 1635.
28. Galloway SD. Dehydration, rehydration, and exercise in the heat:
rehydration strategies for athletic competition. Can J Appl Physiol.
29. Vernon HM, Warner CG. The influence of the humidity of the
air on capacity for work at high temperatures. J Hyg. 1932;
30. Maresh CM, Gabaree-Boulant CL, Armstrong LE, et al. Effect of
hydration status on thirst, drinking, and related hormonal
responses during low-intensity exercise in the heat. J Appl Physiol.
31. Armstrong LE, Maresh CM, Gabaree CV, et al. Thermal and
circulatory responses during exercise: effects of hypohydration,
dehydration, and water intake. J Appl Physiol. 1997;82:2028–2035.
32. Dill DB, Bock AV, Edwards HT. Mechanisms for dissipating heat
in man and dog. Am J Physiol. 1933;104:36–43.
33. Costill DL, Kammer WF, Fisher A. Fluid ingestion during
distance running. Arch Environ Health. 1970;21:520–525.
34. Senay LC Jr, Pivarnik JM. Fluid shifts during exercise. Exerc Sport
Sci Rev. 1985;13:335–387.
35. Hew TD, Chorley JN, Cianca JC, et al. The incidence, risk factors,
and clinical manifestations of hyponatremia in marathon runners.
Clin J Sport Med. 2003;13:41–47.
36. Almond CS, Shin AY, Fortescue EB, et al. Hyponatremia among
runners in the Boston Marathon. N Engl J Med. 2005;
37. Montain SJ, Cheuvront SN, Sawka MN. Exercise associated
hyponatraemia: quantitative analysis to understand the aetiology.
Br J Sport Med. 2006;40:98–105.
38. Cade R, Packer D, Zauner C, et al. Marathon running:
physiological and chemical changes accompanying late-race
functional deterioration. Eur J Appl Physiol Occup Physiol.
39. Cheuvront SN, Haymes EM. Thermoregulation and marathon
running: biological and environmental influences. Sports Med.
40. Engell DB, Maller O, Sawka MN, et al. Thirst and fluid intake
following graded hypohydration levels in humans. Physiol Behav.
41. Wright M, Woodrow G, O’Brien S, et al. Polydipsia: a feature of
peritoneal dialysis. Nephrol Dial Transplant. 2004;19:1581–1586.
42. Valtin H. ‘‘Drink at least eight glasses of water a day.’’ Really? Is
there scientific evidence for ‘‘8 8’’? Am J Physiol Regul Integr
Comp Physiol. 2002;283:R993–R1004.
Hew-Butler et al Clin J Sport Med Volume 16, Number 4, July 2006
290 r2006 Lippincott Williams & Wilkins
43. Kratz A, Siegel AJ, Verbalis JG, et al. Sodium status of collapsed
marathon runners. Arch Pathol Lab Med. 2005;129:227–230.
44. Astrand PO, Saltin B. Plasma and cell volume alterations after
prolonged severe exercise. J Appl Physiol. 1964;19:829–832.
45. Shirreffs SM, Maughan RJ. Rehydration and recovery of fluid
balance after exercise. Exerc Sport Sci Rev. 2000;28:27–32.
46. Riggs JE. Neurologic manifestations of electrolyte disturbances.
Neurol Clin. 2002;20:227–239, vii.
47. Ayus JC, Varon J, Arieff AI. Hyponatremia, cerebral edema, and
noncardiogenic pulmonary edema in marathon runners. Ann Intern
Med. 2000;132:711–714.
48. Figaro MK, Mack GW. Regulation of fluid intake in dehydrated
humans: role of oropharyngeal stimulation. Am J Physiol. 1997;
49. Salata RA, Verbalis JG, Robinson AG. Cold water stimulation of
oropharyngeal receptors in man inhibits release of vasopressin.
J Clin Endocrinol Metab. 1987;65:561–567.
50. Seckl JR, Williams TD, Lightman SL. Oral hypertonic saline
causes transient fall of vasopressin in humans. Am J Physiol. 1986;
51. Egan G, Silk T, Zamarripa F, et al. Neural correlates of the
emergence of consciousness of thirst. Proc Natl Acad Sci USA.
52. Steggerda FR. Observations on the water intake in an adult man
with dysfunctioning salivary glands. Am J Physiol. 1941;132:
53. Brunstrom JM. Effects of mouth dryness on drinking behavior and
beverage acceptability. Physiol Behav. 2002;76:423–429.
54. Brunstrom JM, Tribbeck PM, MacRae AW. The role of mouth
state in the termination of drinking behavior in humans. Physiol
Behav. 2000;68:579–583.
55. Bots CP, Brand HS, Veerman EC, et al. Chewing gum and a saliva
substitute alleviate thirst and xerostomia in patients on haemodia-
lysis. Nephrol Dial Transplant. 2005;20:578–584.
56. Bots CP, Brand HS, Veerman EC, et al. Interdialytic weight gain in
patients on hemodialysis is associated with dry mouth and thirst.
Kidney Int. 2004;66:1662–1668.
57. Glace BW, Murphy CA, McHugh MP. Food intake and electrolyte
status of ultramarathoners competing in extreme heat. J Am Coll
Nutr. 2002;21:553–559.
58. Gerth J, Ott U, Funfstuck R, et al. The effects of prolonged
physical exercise on renal function, electrolyte balance and muscle
cell breakdown. Clin Nephrol. 2002;57:425–431.
59. Twerenbold R, Knechtle B, Kakebeeke TH, et al. Effects of
different sodium concentrations in replacement fluids during
prolonged exercise in women. Br J Sports Med. 2003;37:300–303.
60. Hew-Butler TD, Sharwood K, Collins M, et al. Sodium
supplementation is not required to maintain serum sodium
concentrations during an Ironman triathlon. Br J Sports Med.
61. Stuempfle KJ, Lehmann DR, Case HS, et al. Change in serum
sodium concentration during a cold weather ultradistance race.
Clin J Sport Med. 2003;13:171–175.
62. Nelson PB, Ellis D, Fu F, et al. Fluid and electrolyte balance
during a cool weather marathon. Am J Sports Med. 1989;
63. Refsum HE, Tveit B, Meen HD, et al. Serum electrolyte, fluid and
acid-base balance after prolonged heavy exercise at low environ-
mental temperature. Scand J Clin Lab Invest. 1973;32:117–122.
64. Cohen I, Zimmerman AL. Changes in serum electrolyte levels
during marathon running. S Afr Med J. 1978;53:449–453.
65. Noakes TD, Carter JW. Biochemical parameters in athletes before
and after having run 160 kilometres. S Afr Med J. 1976;50:
66. Kavanagh T, Shephard RJ. On the choice of fluid for the hydration
of middle-aged marathon runners. Br J Sports Med. 1977;11:26–35.
67. Maron MB, Horvath SM, Wilkerson JE. Acute blood biochemical
alterations in response to marathon running. Eur J Appl Physiol
Occup Physiol. 1975;34:173–181.
68. Gastmann U, Dimeo F, Huonker M, et al. Ultra-triathlon-related
blood-chemical and endocrinological responses in nine athletes.
J Sports Med Phys Fitness. 1998;38:18–23.
69. Rocker L, Kirsch KA, Heyduck B, et al. Influence of prolonged
physical exercise on plasma volume, plasma proteins, electrolytes,
and fluid-regulating hormones. Int J Sports Med. 1989;10:270–274.
70. Beckner GL, Winsor T. Cardiovascular adaptations to prolonged
physical effort. Circulation. 1954;9:835–846.
71. Riley WJ, Pyke FS, Roberts AD, et al. The effect of long-distance
running on some biochemical variables. Clin Chim Acta. 1975;
72. Barr SI, Costill DL, Fink WJ. Fluid replacement during prolonged
exercise: effects of water, saline, or no fluid. Med Sci Sports Exerc.
73. McConell GK, Burge CM, Skinner SL, et al. Influence of ingested
fluid volume on physiological responses during prolonged exercise.
Acta Physiol Scand. 1997;160:149–156.
74. Vrijens DM, Rehrer NJ. Sodium-free fluid ingestion decreases
plasma sodium during exercise in the heat. J Appl Physiol.
75. Maresh CM, Bergeron MF, Kenefick RW, et al. Effect of
overhydration on time-trial swim performance. J Strength Cond
Res. 2001;15:514–518.
76. Montain SJ, Coyle EF. Fluid ingestion during exercise increases
skin blood flow independent of increases in blood volume.
J Appl Physiol. 1992;73:903–910.
77. Heaps CL, Gonzalez-Alonso J, Coyle EF. Hypohydration causes
cardiovascular drift without reducing blood volume. Int J Sports
Med. 1994;15:74–79.
78. Gonzalez-Alonso J, Mora-Rodriguez R, Coyle EF. Stroke volume
during exercise: interaction of environment and hydration.
Am J Physiol Heart Circ Physiol. 2000;278:H321–H330.
79. Gonzalez-Alonso J, Calbet JA, Nielsen B. Muscle blood flow is
reduced with dehydration during prolonged exercise in humans.
J Physiol. 1998;513 (Pt 3):895–905.
80. Maw GJ, Mackenzie IL, Taylor NA. Human body-fluid distribu-
tion during exercise in hot, temperate and cool environments.
Acta Physiol Scand. 1998;163:297–304.
81. Costill DL, Cote R, Fink W. Muscle water and electrolytes
following varied levels of dehydration in man. J Appl Physiol.
82. Sanders B, Noakes TD, Dennis SC. Sodium replacement and fluid
shifts during prolonged exercise in humans. Eur J Appl Physiol.
83. Kozlowski S, Saltin B. Effect of sweat loss on body fluids. J Appl
Physiol. 1965;19:1119–1124.
84. Pastene J, Germain M, Allevard AM, et al. Water balance during
and after marathon running. Eur J Appl Physiol Occup Physiol.
85. Rogers G, Goodman C, Rosen C. Water budget during ultra-
endurance exercise. Med Sci Sports Exerc. 1997;29:1477–1481.
86. Noakes TD, Sharwood K, Speedy D, et al. Three independent
biological mechanisms cause exercise-associated hyponatremia:
evidence from 2,135 weighed competitive athletic performances.
Proc Natl Acad Sci USA. 2005;102:18550–18555.
87. Milledge JS, Bryson EI, Catley DM, et al. Sodium balance, fluid
homeostasis and the renin-aldosterone system during the
prolonged exercise of hill walking. Clin Sci (London). 1982;62:
88. Takamata A, Mack GW, Gillen CM, et al. Sodium appetite, thirst,
and body fluid regulation in humans during rehydration without
sodium replacement. Am J Physiol. 1994;266:R1493–R1502.
89. Verbalis JG. Clinical aspects of body fluid homeostasis in humans.
In: Stricker EM, ed. Neurobiology of Food and Fluid Intake.
Handbook of Behavioral Neurobiology. New York: Plenum; 1990:
90. Beauchamp GK, Bertino M, Burke D, et al. Experimental sodium
depletion and salt taste in normal human volunteers. Am J Clin
Nutr. 1990;51:881–889.
91. McCance RA. Experimental sodium deficiency in man. Proc Royal
Soc Bri. 1936;119:245–268.
Clin J Sport Med Volume 16, Number 4, July 2006 Updated Fluid Recommendation
r2006 Lippincott Williams & Wilkins 291
92. Kochli A, Tenenbaum-Rakover Y, Leshem M. Increased salt
appetite in patients with congenital adrenal hyperplasia 21-
hydroxylase deficiency. Am J Physiol Regul Integr Comp Physiol.
93. Yeomans MR, Blundell JE, Leshem M. Palatability: response to
nutritional need or need-free stimulation of appetite? Br J Nutr.
2004;92(Suppl 1):S3–S14.
94. Wald N, Leshem M. Salt conditions a flavor preference or aversion
after exercise depending on NaCl dose and sweat loss. Appetite.
95. Leshem M, Abutbul A, Eilon R. Exercise increases the preference
for salt in humans. Appetite. 1999;32:251–260.
96. Leshem M. Salt preference in adolescence is predicted by common
prenatal and infantile mineralofluid loss. Physiol Behav. 1998;
97. Leshem M, Rudoy J. Hemodialysis increases the preference for salt
in soup. Physiol Behav. 1997;61:65–69.
98. Meyer LG, Horrigan DJ Jr, Lotz WG. Effects of three hydration
beverages on exercise performance during 60 hours of heat
exposure. Aviat Space Environ Med. 1995;66:1052–1057.
99. Goldman MB, Nash M, Blake L, et al. Do electrolyte-containing
beverages improve water imbalance in hyponatremic schizophre-
nics? J Clin Psychiatry. 1994;55:151–153.
100. Reeves RR. Worsening of hyponatremia with electrolyte-
containing beverage. Am J Psychiatry. 2004;161:374–375.
101. Vieweg WV, Rowe WT, David JJ, et al. Oral sodium chloride in the
management of schizophrenic patients with self-induced water
intoxication. J Clin Psychiatry. 1985;46:16–19.
102. Speedy DB, Thompson JM, Rodgers I, et al. Oral salt supple-
mentation during ultradistance exercise. Clin J Sport Med. 2002;
103. Pitts GC, Johnson RE, Consolazio FC. Work in the heat as
affected by intake of water, salt and glucose. Am J Physiol.
104. Ladell WBSS. The effects of water and salt intake upon the
performance of men working in hot and humid environments.
J Physiol. 1955;127:11–46.
105. Konikoff F, Shoenfeld Y, Magazanik A, et al. Effects of salt
loading during exercise in a hot dry climate. Biomed Pharmacother.
106. Hargreaves M, Morgan TO, Snow R, et al. Exercise tolerance in
the heat on low and normal salt intakes. Clin Sci (London).
107. Robertson HT, Pellegrino R, Pini D, et al. Exercise response after
rapid intravenous infusion of saline in healthy humans. J Appl
Physiol. 2004;97:697–703.
108. Takamata A, Ito T, Yaegashi K, et al. Effect of an exercise-heat
acclimation program on body fluid regulatory responses to
dehydration in older men. Am J Physiol. 1999;277:R1041–R1050.
109. Mack GW, Weseman CA, Langhans GW, et al. Body fluid balance
in dehydrated healthy older men: thirst and renal osmoregulation.
J Appl Physiol. 1994;76:1615–1623.
110. Stachenfeld NS, DiPietro L, Nadel ER, et al. Mechanism of
attenuated thirst in aging: role of central volume receptors.
Am J Physiol. 1997;272:R148–R157.
111. Phillips PA, Bretherton M, Johnston CI, et al. Reduced osmotic
thirst in healthy elderly men. Am J Physiol. 1991;261:R166–R171.
112. Phillips PA, Rolls BJ, Ledingham JG, et al. Reduced thirst after
water deprivation in healthy elderly men. N Engl J Med. 1984;
113. Miescher E, Fortney SM. Responses to dehydration and rehydra-
tion during heat exposure in young and older men. Am J Physiol.
114. Stachenfeld NS, Mack GW, Takamata A, et al. Thirst and fluid
regulatory responses to hypertonicity in older adults. Am J Physiol.
115. Zappe DH, Bell GW, Swartzentruber H, et al. Age and regulation
of fluid and electrolyte balance during repeated exercise sessions.
Am J Physiol. 1996;270:R71–R79.
116. Kenefick RW, Hazzard MP, Mahood NV, et al. Thirst sensations
and AVP responses at rest and during exercise-cold exposure.
Med Sci Sports Exerc. 2004;36:1528–1534.
117. Smith D, Moore K, Tormey W, et al. Downward resetting of the
osmotic threshold for thirst in patients with SIADH. Am J Physiol
Endocrinol Metab. 2004;287:E1019–E1023.
118. Robertson GL. Syndrome of inappropriate antidiuresis. N Engl
J Med. 1989;321:538–539.
119. Hew T. Response to the letter to the editor by Roy J. Shephard.
Clin J Sport Med. 2003;13:192–193.
120. Moroff SV, Bass DE. Effects of overhydration on man’s
physiological responses to work in the heat. J Appl Physiol.
121. Bean WB, Eichna LW. Performance in relation to environmental
temperature. Fed Proc. 1943;2:144–158.
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... These observations suggest that endurance athletes who consume fluids at a rate < 700 mL/h have a decreased risk of EHN. This theoretical 700 mL/h fluid consumption rate threshold is consistent with the 400 to 800 mL/h recommendations of both the International Marathon Medical Directors Association [84], the American College of Sports Medicine [24], and a mathematical model that was designed to clarify the etiology of EHN [76]. ...
... Rationale: drinking when thirsty preserves serum Na + and osmolality within the normal laboratory reference range. [55,84,[104][105][106][107][108][109][110] 2. Ad libitum drinking. Consuming fluid whenever and in whatever volume desired, without specific focus on thirst. ...
... The distinction between option 1 (using perceived thirst as the only signal to drink) and option 2 (consuming fluid whenever and in whatever volume desired) is subtle [101]. In fact, some professional organizations and experts have not recognized these as distinct behaviors and some authors use these terms synonymously [6,26,84,98,99,101]. However, a 2014 field study determined that cyclists could identify whether they typically used option 1 or 2 and self-selected into one of two study groups (n = 12 in each). ...
Full-text available
During endurance exercise, two problems arise from disturbed fluid–electrolyte balance: dehydration and overhydration. The former involves water and sodium losses in sweat and urine that are incompletely replaced, whereas the latter involves excessive consumption and retention of dilute fluids. When experienced at low levels, both dehydration and overhydration have minor or no performance effects and symptoms of illness, but when experienced at moderate-to-severe levels they degrade exercise performance and/or may lead to hydration-related illnesses including hyponatremia (low serum sodium concentration). Therefore, the present review article presents (a) relevant research observations and consensus statements of professional organizations, (b) 5 rehydration methods in which pre-race planning ranges from no advanced action to determination of sweat rate during a field simulation, and (c) 9 rehydration recommendations that are relevant to endurance activities. With this information, each athlete can select the rehydration method that best allows her/him to achieve a hydration middle ground between dehydration and overhydration, to optimize physical performance, and reduce the risk of illness.
... The median FI of the athletes was 800 ml/h in GTPfin, and 900 ml/h in VGIfin, ranging from 400 to 1,500 ml/h and 500-1,500 ml/h, respectively. No athlete drank more than 1,500 ml/h, a risk factor for hyponatremia (27). However, athletes are often told to drink more than what thirst indicates. ...
... FI should be based on thirst, the physiological mechanism that determines the volume of liquid to be ingested. Thirst, together with AVP, exert a control of water homeostasis so precise (22) that EPOsm is normally maintained within strict limits (27). In fact, in the current study, no athlete had a post-race EPOsm ≥308 mOsm/kg. ...
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Introduction Hyponatremia often occurs during the practice of endurance sports. We evaluated the impact on hyponatremia of the hydration recommendations of the Third International Exercise-Associated Hyponatremia Consensus Development Conference 2015 (3IE-AHCD) during the 2017 Gran Trail de Peñalara marathon (GTP) and the Vitoria Gasteiz Ironman triathlon (VGI). Methods Prospective study of GTP and VGI athletes participating in four information sessions in the months prior to the events, to explain that hydration should only be according to their level of thirst, per the recommendations of the 3IE-AHCD. Consenting event finishers were included in final analysis. Pre- and post-race anthropometric and biochemical parameters were compared. Results Thirty-six GTP (33 male) and 94 VGI (88 male) finishers were evaluated. GTP race median fluid intake was 800 ml/h, with 900 ml/h in the VGI race. 83.3% GTPfin and 77.6% VGIfin remained eunatremic (blood sodium 135–145 mmol/L). Only 1/36 GTP and 1/94 VGI participant finished in hyponatremia, both with a sodium level of 134 mmol/L. Fourteen percent of GTP, and 21.2% of VGI participants finished in hypernatremia, with no increase in race completion times. No participating athlete required medical attention, except for musculoskeletal complaints. Pro-BNP and Copeptin levels rose significantly. Changes in copeptin levels did not correlate with changes in plasma osmolality, nor total body water content in impedance analysis. Conclusions Recommending that athletes' fluid intake in endurance events be a function of their thirst almost entirely prevented development of hyponatremia, without induction of clinically significant hypernatremia, or a negative repercussion on race completion times.
... In 2003, the International Marathon Medical Directors Association (IMMDA) adopted more restrictive fluid guidelines of up to 400-800 ml/h of race. Despite implementation of these guidelines, studies in marathon runners have reported an incidence of hyponatraemia of 6-13% [20,21] and of hypernatraemia of 25% [21]with a range of 123-152 mmol/l [21] Current guidelines are to drink according to thirst, suggesting that the body regulates its salt and water balance accurately [22]. Even with these guidelines, the incidence of hyponatraemia is reported as between 8.2% [6] and 12.5%, even in asymptomatic volunteers [23]. ...
... Hyponatraemia in runners is thought to be dilutional secondary to increased water consumption during running, or to inappropriate vasopressin secretion [50]; current guidelines to drink only to thirst [22,47] may have reduced the incidence of clinically important hyponatraemia. It is generally accepted that the body has good homeostatic mechanisms to maintain accurate salt and water balance, and other methods of assessing hydration during exercise, for example, calculating fluid loss, or assessing the colour of urine, may be over-complicated or less accurate than simply drinking to thirst. ...
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Objective: Abnormal biochemical measurements have previously been described in runners following marathons. The incidence of plasma sodium levels outside the normal range has been reported as 31%, and the incidence of raised creatinine at 30%. This study describes the changes seen in electrolytes and creatinine in collapsed (2010-2019 events) and noncollapsed (during the 2019 event) runners during a UK marathon. Methods: Point-of-care sodium, potassium, urea and creatinine estimates were obtained from any collapsed runner treated by the medical team during the Brighton Marathons, as part of their clinical care, and laboratory measurements from control subjects. Results: Results from 224 collapsed runners were available. Serum creatinine was greater than the normal range in 68.9%. About 6% of sodium results were below, and 3% above the normal range, with the lowest 132 mmol/l. Seventeen percent of potassium readings were above the normal range; the maximum result was 8.4 mmol/l, but 97% were below 6.0 mmol/l. In the control group, mean creatinine was significantly raised in both the collapse and control groups, with 55.4% meeting the criteria for acute kidney injury, but had resolved to baseline after 24 h. Sodium concentration but not the potassium was significantly raised after the race compared with baseline, but only 15% were outside the normal range. Conclusion: In this study, incidence of a raised creatinine was higher than previously reported. However, the significance of such a rise remains unclear with a similar rise seen in collapsed and noncollapsed runners, and resolution noted within 24 h. Abnormal sodium concentrations were observed infrequently, and severely abnormal results were not seen, potentially reflecting current advice to drink enough fluid to quench thirst.
... Limitations of this study include the lack of information regarding athletes (i.e., nutrition, hydration during the race, runners' experience, previous strategy) and environmental characteristics (i.e., altimetry changes along the race, hydration stations). A further limitation is that we have no data about food (Burke, 2007) and fluid (Hew-Butler et al., 2006) intake during the marathon. Both fluid overload and hyponatremia (Mettler et al., 2008) and dehydration (Knechtle et al., 2011) might impair marathon running performance. ...
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Background: The two aspects of the influence of environmental conditions on marathon running performance and pacing during a marathon have been separately and widely investigated. The influence of environmental conditions on the pacing of age group marathoners has, however, not been considered yet. Objective: The aim of the present study was to investigate the association between environmental conditions (i.e., temperature, barometric pressure, humidity, precipitation, sunshine, and cloud cover), gender and pacing of age group marathoners in the “New York City Marathon”. Methodology: Between 1999 and 2019, a total of 830,255 finishes (526,500 males and 303,755 females) were recorded. Time-adjusted averages of weather conditions for temperature, barometric pressure, humidity, and sunshine duration during the race were correlated with running speed in 5 km-intervals for age group runners in 10 years-intervals. Results: The running speed decreased with increasing temperatures in athletes of age groups 20–59 with a pronounced negative effect for men aged 30–64 years and women aged 40–64 years. Higher levels of humidity were associated with faster running speeds for both sexes. Sunshine duration and barometric pressure showed no association with running speed. Conclusion: In summary, temperature and humidity affect pacing in age group marathoners differently. Specifically, increasing temperature slowed down runners of both sexes aged between 20 and 59 years, whereas increasing humidity slowed down runners of <20 and >80 years old.
... Advice given by guidelines is not consistent: According to The American College of Sports Medicine Recommendations, appropriate fluid intake is 400 -800 ml/h, but International Marathon Medical Directors Association highlights that fixed ranges of fluid intake is not always appropriate, and drinking to thirst may be the best option, while signs of overhydration (increased urination, bloating, weight gain) must be looked for [22,23]. Special beverages containing electrolytes and carbohydrates can provide benefits, but only in certain circumstances [23]. ...
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A popularity of marathons and ultramarathons is growing every year. Attending a marathon can cause a variety of biochemical changes. It is crucial to determine which changes in blood tests are of clinical significance, and what recommendations should be given to the patient. Here the most frequent changes are presented, as described in literature. Keywords: Marathon, Ultramarathon, Troponin, Blood count, Hyponatremia, Endurance, ALT, AST, Creatinine, Serum
... Caffeine's diuretic effect can lead to luid-electrolyte imbalance and renal impairment [16]. Individuals who do not typically consume large amounts of caffeine may be more prone to increased diuresis leading to dehydration [17]. ...
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Rhabdomyolysis is a syndrome characterized by muscle injury involving the release of potentially toxic intracellular contents into plasma, which in turn may cause extreme enzyme elevations, electrolyte imbalances and acute kidney injury. The typical causes for rhabdomyolysis include but not limited to muscle trauma or crush injury, prolonged immobilization, in lammatory myopathies, medications, drug use and severe physical exertion. We present a 24-year-old African American male with a past medical history signi icant for thalassemia minor and sickle cell trait admitted for severe rhabdomyolysis with a creatinine kinase (CK)> 650,000 precipitated by the consumption of energy drinks. Energy drinks are known to contain higher levels of caffeine whose diuretic effect can lead to hypokalemia, elevation of CK and renal impairment. Patients with sickle-cell trait are known to be more predisposed to dehydration secondary to a renal concentrating defect. This in turn can exacerbate a state of dehydration caused by caffeine, infections or excessive perspiration. Our case is the only reported presentation of severe non-traumatic rhabdomyolysis in a patient with sickle cell trait precipitated by the use of caffeine containing energy drink. Therefore, it may be prudent to avoid the consumption of energy drinks in patients with sickle cell trait.
... In addition, they are essential for regulating the osmolality of the extracellular fluid during exercise by reabsorbing some of the sodium traveling through the ducts (Amano et al. 2017). Thus, during exercise, eccrine glands are involved in the control of thirst, fluid balance, electrolyte balance and thermoregulation (Hew-Butler et al. 2006;Brown et al. 2011;Nose et al. 1988). ...
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Purposes: This study investigated the impact of permanently tattooed skin on local sweat rate, sweat sodium concentration and skin temperature and determined whether tattoos alter the relationship between local and whole-body sweat sodium concentration. Methods: Thirteen tattooed men (27 ± 6 years) completed a 1 h (66 ± 4% of VO2peak) cycling trial at 32 °C, 35% relative humidity. Sweat rate and sweat sodium concentration were measured using the whole-body washdown and local absorbent patch techniques. Patches and skin-temperature probes were applied over the right/left thighs and tattooed/non-tattooed (contralateral) regions. Results: Local sweat rates did not differ (p > 0.05) between the right (1.11 ± 0.38) and left (1.21 ± 0.37) thighs and the permanently tattooed (1.93 ± 0.82) and non-tattooed (1.72 ± 0.81 mg cm −2 min −1) regions. There were no differences in local sweat sodium concentration between the right (58.2 ± 19.4) and left (55.4 ± 20.3) thighs and the permanently tattooed (73.0 ± 22.9) and non-tattooed (70.2 ± 18.9 mmol L −1) regions. Difference in local skin temperature between the right and left thighs (− 0.043) was similar to that between the permanently tattooed and non-tattooed (− 0.023 °C) regions. Prediction of whole-body sweat sodium concentration for the permanently tattooed (41.0 ± 6.7) and the non-tattooed (40.2 ± 5.3 mmol L −1) regions did not differ. Conclusion: Permanent tattoos do not alter local sweat rate, sweat sodium concentration or local skin temperature during moderate-intensity cycling exercise in a warm environment. Results from a patch placed over a tattooed surface correctly predicts whole-body sweat sodium concentration from an equation developed from a non-tattooed region.
... In this sense, what we eat influences our body's ability to adapt to training and postexercise recovery [4,5]. Several sports medicineand nutrition-related organizations recommend specific amounts of energy and macro-and micronutrients for sustained physical activity events to maintain body weight, replenish glycogen stores, and provide sufficient proteins to build and repair working tissues [2,6,7]. Optimal carbohydrates are needed before, during, and after intense and prolonged exercise, both during training and competition, for proper performance [7]. ...
Objective : The aim of this study was to analyze, in recreational marathon runners, the intake of specific macronutrients and minerals that could influence cardiovascular health. Methods : 37 males were grouped in two groups according to their 50% percentile race time (3.39 h), dividing into fast (G1: 3.18 ± 0.18 h) and slow runners (G2: 3.84 ± 0.42 h). Anthropometric parameters, macronutrients and mineral records were collected before the race. Minerals (Na⁺, K⁺ and Mg²⁺), lipid profile (triglycerides, LDL, HDL and cholesterol), muscle damage (creatine kinase), inflammation (C-reactive protein), and cardiovascular health (high-sensitive troponin-T, ST2 and N-terminal pro-B-type natriuretic peptide) were analyzed in blood 24 h before, immediately after, and 48 h post-race. Results : Weight (G1: 74.70 ± 7.76 kg, G2: 79.58 ± 6.72 kg; p < 0.05) and body mass index (G1: 23.01 ± 1.81 kg/m², G2: 25.30 ± 2.02 kg/m²; p < 0.01) were significantly different between the groups. Moreover, G1 consumed significantly (p < 0.01) more mono- and poly-unsaturated fatty acids than G2, and presented significantly higher iron, potassium, and magnesium intake. Regarding blood lipid profile, G2 presented significantly higher triglyceride values and lower levels of high-density lipoprotein (p < 0.01). The Hs-TnT marker of cardiac myocyte stress/injury was significantly higher (p < 0.05) in G2 reaching values above 250 ng/L, and 81% of the runners (30 from 37) presented higher post-race values. Conclusions Marathon runners consuming adequate amounts of unsaturated fat, iron, potassium and magnesium, performed better and presented better cardiovascular health.
... 70 Supplemental sodium has no effect on blood sodium concentration when exercising individuals drink according to thirst, 70,71 although those who drink the least amount of fluid during exercise will often finish the activity with elevated blood sodium concentrations. [72][73][74][75] Collectively, these observations demonstrate that it is the amount of fluid ingested during exercise rather than the amount of sodium that has the more pronounced effect on blood sodium concentrations. Studies suggest that sweat sodium losses augment the palatability of salty beverages, 76,77 which may support the utility of having sodium-rich foods and beverages available during long and hot activities. ...
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Exercise-associated hyponatremia (EAH) is defined by a serum or plasma sodium concentration below the normal reference range of 135 mmol·L-1 that occurs during or up to 24 h after prolonged physical activity. It is reported to occur in individual physical activities or during organized endurance events conducted in environments in which medical care is limited and often not available, and patient evacuation to definitive care is often greatly delayed. Rapid recognition and appropriate treatment are essential in the severe form to increase the likelihood of a positive outcome. To mitigate the risk of EAH mismanagement, care providers in the prehospital and in hospital settings must differentiate from other causes that present with similar signs and symptoms. EAH most commonly has overlapping signs and symptoms with heat exhaustion and exertional heat stroke. Failure in this regard is a recognized cause of worsened morbidity and mortality. In an effort to produce best practice guidelines for EAH management, the Wilderness Medical Society convened an expert panel in May 2018. The panel was charged with updating the WMS Practice Guidelines for Treatment of Exercise-Associated Hyponatremia published in 2014 using evidence-based guidelines for the prevention, recognition, and treatment of EAH. Recommendations are made based on presenting with symptomatic EAH, particularly when point-of-care blood sodium testing is unavailable in the field. These recommendations are graded on the basis of the quality of supporting evidence and balanced between the benefits and risks/burdens for each parameter according to the methodology stipulated by the American College of Chest Physicians.
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A rise in body core temperature and loss of body water via sweating are natural consequences of prolonged exercise in the heat. This review provides a comprehensive and integrative overview of how the human body responds to exercise under heat stress and the countermeasures that can be adopted to enhance aerobic performance under such environmental conditions. The fundamental concepts and physiological processes associated with thermoregulation and fluid balance are initially described, followed by a summary of methods to determine thermal strain and hydration status. An outline is provided on how exercise-heat stress disrupts these homeostatic processes, leading to hyperthermia, hypohydration, sodium disturbances and in some cases exertional heat illness. The impact of heat stress on human performance is also examined, including the underlying physiological mechanisms that mediate the impairment of exercise performance. Similarly, the influence of hydration status on performance in the heat and how systemic and peripheral hemodynamic adjustments contribute to fatigue development is elucidated. This review also discusses strategies to mitigate the effects of hyperthermia and hypohydration on exercise performance in the heat, by examining the benefits of heat acclimation, cooling strategies and hyperhydration. Finally, contemporary controversies are summarized and future research directions provided.
Context.—Recommendations for prevention and treatment of medical emergencies in participants in marathon races center on maintenance of adequate hydration status and administration of fluids. Recently, new recommendations for fluid replacement for marathon runners were promulgated by medical and athletic societies. These new guidelines encourage runners to drink ad libitum between 400 and 800 mL/h as opposed to the previous “as much as possible” advice. Objective.—To assess the sodium and hydration (plasma osmolality) status of collapsed marathon runners after the promulgation of new hydration guidelines. Design.—Plasma sodium and osmolality values of runners who presented to the medical tent at the finish line of the 2003 Boston Marathon were measured. Results.—Using reference ranges derived from the general population, of 140 collapsed runners, 35 (25%) were hypernatremic (sodium, >146 mEq/L) and 6 (12%) were hyperosmolar (osmolality, >296 mOsm/kg H2O), whereas 9 (6%) were hyponatremic (sodium, <135 mEq/L) and 8 (16%) were hypo-osmolar (osmolality, <280 mOsm/kg H2O). Compared with a population of marathon runners who had experienced no medical difficulties, 9% of the runners were hypernatremic, 5% were hyponatremic, 8% were hypo-osmolar, and none were hyperosmolar. Conclusions.—Our findings indicate a significant incidence of hypernatremia with hyperosmolality and hyponatremia with hypo-osmolality among collapsed runners despite the new fluid intake recommendations, suggesting that either further educational measures are required or that the new guidelines are not entirely adequate to prevent abnormalities in fluid balance. Furthermore, the immediate medical management of hypernatremia and hyponatremia is different. Administration of fluids to severely hyponatremic patients may result in fatal cerebral edema. Our findings caution against institution of treatment until laboratory tests determine the patient's sodium status.
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.
Exercise capacity and exercise performance are reduced when the ambient temperature is high. This has mainly been attributed to the large sweat losses which lead to hypohydration, a failure of thermoregulation, and eventually circulatory collapse. Exercising athletes rarefy drink enough before or during exercise to replace the ongoing fluid losses, especially in hot conditions. In order to combat dehydration hyperthermia, and impending circulatory collapse, athletes should drink fluids before, during, and after exercise. Preexercise strategies include attempts to maintain euhydration but also to hyperhydrate. Hyperhydration is relatively easy to achieve but thermoregulatory benefits during prolonged exercise have not been observed in comparison to euhydration. In prolonged continuous exercise, fluid and carbohydrate (CHO) ingestion has clearly been shown to improve performance, but the evidence is not so clear for high-intensity intermittent exercise over a prolonged period The general consensus is that fluid ingestion should match sweat losses during exercise and that the drink should contain CHO and electrolytes to assist water transport in the intestine and to improve palatability. Postexercise rehydration is essential when the strategies adopted before or during exercise hat not been effective. The best postexercise rehydration strategy would be to ingest a large volume of a beverage that contains a CHO source and a high sodium content.
After a 7-h H2O and Na+ depletion period (DP), produced by intermittent light exercise (8 bouts) at 35 degrees C, we examined thirst and taste palatability responses to 10 different NaCl solutions during 23 h of rehydration (RH) at 25 degrees C. During DP, net H2O and Na+ loss were 27.2 +/- 2.9 ml/kg and 3.29 +/- 0.45 meq/kg, respectively. Plasma osmolality (P-Osm) and plasma Na+ concentration ([Na+](p)) increased significantly during DP by 3.4 +/- 1.2 mosmol/kgH(2)O and 3.0 +/- 1.0 meq/kgH(2)O, respectively. Plasma volume (PV) decreased by 6.5 +/- 1.9%. Thirst rating, renal fractional reabsorption of H2O, and plasma arginine vasopressin concentration (P-AVP) increased as P-Osm increased. This increased thirst was accompanied by increased palatability ratings to H2O. During RH, subjects drank deionized H2O ad libitum and ate a Na+-free diet for 23 h. P-Osm and [Na+](p) returned to control levels within 1 h RH and remained at or below the control thereafter. PV remained reduced by similar to 5% throughout RH. The increased thirst and P-AVP returned to their respective control levels within 1 h of RH as P-Osm decreased, but thirst rating increased again between 17 and 23 h of RH without an increase in P-Osm or P-AVP. Palatability ratings to a 1 M NaCl solution at and after 3 h RH and palatability ratings to 0.3 M at 17 and 23 h RH were significantly higher than control. Plasma aldosterone concentration (P-Aldo) increased after DP, decreased with drinking, and increased again between 6 and 23 h of RH, accompanied by a marked decrease in fractional Na+ excretion to <0.07%. Thus both Na+ preference and thirst in humans are influenced by body fluid and electrolyte status. The increased Na+ palatability (Na+ appetite) was preceded by osmotically induced thirst, and accompanied by nonosmotically driven thirst [extracellular fluid (ECF) thirst] and increased P-Aldo. The ''Na+ appetite'' and ''ECF thirst'' along with increased renal Na+ retention could contribute to ECF volume regulation after thermally induced H2O and Na+ depletion.
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.