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Sports Medicine
ISSN 0112-1642
Sports Med
DOI 10.1007/s40279-013-0089-y
The Quantification of Body Fluid Allostasis
During Exercise
Nicholas Tam & Timothy D.Noakes
1 23
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REVIEW ARTICLE
The Quantification of Body Fluid Allostasis During Exercise
Nicholas Tam
•
Timothy D. Noakes
Ó Springer International Publishing Switzerland 2013
Abstract The prescription of an optimal fluid intake during
exercise has been a controversial subject in sports science for
at least the past decade. Only recently have guidelines
evolved from ‘blanket’ prescriptions to more individualised
recommendations. Currently the American College of Sports
Medicine advise that sufficient fluid should be ingested to
ensure that body mass (BM) loss during exercise does not
exceed [2 % of starting BM so that exercise-associated
medical complications will be avoided. Historically, BM
changes have been used as a surrogate for fluid loss during
exercise. It would be helpful to accurately determine fluid
shifts in the body in order to provide physiologically appro-
priate fluid intake advice. The measurement of total body
water via D
2
O is the most accurate measure to detect changes
in body fluid content; other methods, including bioelectrical
impedance, are less accurate. Thus, the aim of this review is to
convey the current understanding of body fluid allostasis
during exercise when drinking according to the dictates of
thirst (ad libitum). This review examines the basis for fluid
intake prescription with the use of BM, the concepts of
‘voluntary and involuntary dehydration’ and the major routes
by which the body gains and loses fluid during exercise.
1 Introduction
Mindful of complications such as exercise-induced heat-
stroke, those competing in ultra-endurance events are
encouraged to be careful about their fluid intake. Athletes
are advised to avoid a decrease in body mass (BM) during
exercise as this ‘dehydration’ is perceived to be detrimental
to performance and may even increase the probability that
heat-related illnesses can occur [1, 2].
In 1996 the American College of Sports Medicine
(ACSM) published a position stand providing guidelines on
exercise and fluid replacement [3]. Their recommendations
encouraged athletes to ingest fluid equivalent to the amount
of BM lost during exercise [3]. Beltrami et al. [4] reviewed
recommendations subsequent to the advent of this position
stand and noted that there was an increase in the dissemi-
nation of advice that athletes should ‘replace all the water
lost through sweating (i.e. BM loss), or consume the
maximal amount that can be tolerated’. However, this
advice conflicts with the established physiological princi-
ple that plasma osmolality (POsm) is the physiologically
protected variable which is regulated by the stimulation of
thirst [4].
Since the adoption of these guidelines there has been a
marked increase in the number of cases of exercise-asso-
ciated hyponatremia (EAH) and even death due to exer-
cise-associated hyponatremic encephalopathy (EAHE) [5].
This troubling rise and lack of consensus of the cause(s) led
to the formulation of the 1st International EAH Consensus
Statement on the aetiology and risk factors for EAH [6].
EAH is often described as a life-threatening and prevent-
able condition; its predominant aetiology is now accepted
as a dilutional hyponatremia associated with the syndrome
of inappropriate anti-diuretic hormone secretion (SIADH)
resulting from both osmotic and non-osmotic stimuli [7].
This consensus led to a greater general appreciation and a
directed focus of future research into the aetiology and
management of EAH. Subsequently, the ACSM updated
their recommendations for fluid replacement during
N. Tam (&) T. D. Noakes
UCT/MRC Research Unit for Exercise Science and Sports
Medicine, Department of Human Biology, Faculty of Health
Sciences, University of Cape Town, 3rd Floor, Sports Science
Institute of South Africa, Boundary Road, Newlands,
Cape Town, Western Cape, South Africa
e-mail: nicholas.tam@uct.ac.za
Sports Med
DOI 10.1007/s40279-013-0089-y
Author's personal copy
exercise, replacing the 1996 guidelines with new guidelines
published in 2007. These new guidelines include the advice
that athletes should drink to thirst (ad libitum) but should
drink enough to avoid a[2 % BM loss during exercise [1].
These guidelines now mirror those of the International
Marathon Medical Directors Association (IMMDA) with
the exception that the IMMDA guidelines do not set limits
for ‘safe’ levels of BM loss during exercise in those
drinking to thirst.
It is evident that recent fluid replacement guidelines
have evolved from blanket fluid replacement [3] to more
individualised prescriptions [1], even though endurance
athletes are still advised to replace fluids, based on the
extent of BM lost [8]. These prescriptions are encouraged
because data obtained from tightly controlled laboratory
trials have demonstrated that athletes who either ingest
fluid according to thirst or who restrict their fluid intake do
not maintain a constant BM during exercise [8, 9]. This is
considered inappropriate because any decrease in BM is
believed to indicate a failure of the thirst mechanism to
properly replenish the body’s water stores or return the
body to a state of euhydration. It is argued that in this
apparently dehydrated state, athletes are at increased risk of
heat illness, ill health and impaired athletic performance [1,
10].
It is commonly stated that a [2 % of BM loss during
any bout of exercise is associated with a decreased mental/
cognitive performance [1]. But this conflicts with the his-
torical findings that athletes regularly lose 5–6 % of their
BM during ultra-endurance exercise lasting 5–24 h, whilst
maintaining proper fluid allostasis and without developing
any medical complications [11, 12].
This suggests that fluid regulation is far more complex
than can be assessed purely on the basis of gross BM
changes during endurance exercise. It appears that BM
changes during exercise may overestimate the real extent
of changes in body fluid allostasis [13–15].
2 Concepts in Hydration
Defining euhydration is complex because the body’s water
content shows diurnal variation. A common definition for
euhydration is the following [9, 10]: a BM that is relatively
stable (within B1 % from day to day) with the maintenance
of an adequate fluid intake to sustain normal urine volume
and concentration. To this definition may be added more
physiologically appropriate terms such as a relatively sta-
ble total body water (TBW) content together with the
maintenance of plasma sodium concentration ([Na
?
]) and
POsm, although these parameters are not as easily mea-
sured as BM [10]. A majority of these variables seem
appropriate to define euhydration during daily sedentary
activity but during endurance exercise some variables may
be altered allostatically in order to maintain the milieu
interior [16].
The use of BM as a marker of hydration status during
exercise begins perhaps with Adolph and Dill [17] who
reported that humans walking in desert heat for several
hours all developed some degree of BM loss during the
exercise bout. The presumption was that they had failed to
drink adequately. As a result of this observation the term
‘voluntary dehydration’ was advanced to describe a state of
BM loss in the presence of an adequate fluid supply [18].
This was explained as a temporary reduction in TBW
caused by a delay before sweat losses are fully replaced. As
a result it is argued that even a ‘normal’ thirst mechanism
is unable to maintain body fluid allostasis during exercise
[10, 19].
More recently, Greenleaf [9] used the term ‘involuntary
dehydration’ to describe the failure of the thirst mechanism
to maintain baseline BM [1]. Laboratory experiments have
demonstrated that ‘voluntary dehydration’ ([2 % BM loss)
is associated with impaired aerobic exercise performance
in temperate conditions [1]. In contrast to these laboratory
findings, studies of ultra-endurance events have found that
the best performing athletes are usually the most ‘dehy-
drated’, with some incurring BM losses [6%[13, 20, 21].
Hew-Butler et al. [22] have argued that ‘‘to assume the
thirst drive would be an ‘inaccurate index’ of fluid balance
during exercise would seem contradictory to the evolution
of our species’’. Their point is that some may have failed to
consider the complex integration of the brain, specifically
the hypothalamus, which governs the body’s milieu inte-
rior by maintaining POsm and plasma [Na
?
], utilizing
mechanisms developed during our evolution into terrestrial
creatures [16]. These evolutionary adaptations have liber-
ated humans from having to continually seek water every
moment of the day [16].
It seems that fluid-associated BM loss could be defined
as a voluntary dehydration such that the level of water loss
alters the milieu interior causing the termination of exer-
cise as occurs in the more severe stages of dehydration (and
thirst) documented by Adolph [11]. Whilst severe dehy-
dration should be avoided to prevent a decrease in exercise
performance and to maintain overall health, it is evident
that strictly adhering to replacing all BM loss with fluid
intake during exercise will contribute to a state of body
fluid overload, resulting in a number of potential problems
such as gastric discomfort, nausea, impaired performance
and, ultimately, EAH and EAHE [5, 23–26].
The life-threatening conditions EAH and EAHE have
arisen because some researchers have not questioned crit-
ically the use of BM as an absolute indicator of body
hydration status during exercise. This has long been a
contentious issue highlighted by the finding that changes in
N. Tam, T.D. Noakes
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BM alone do not account for all the factors affecting body
fluid allostasis [20–22, 26, 27].
There are many factors that can influence the body’s
hydration status during exercise and that would contribute
to changes in the TBW pool. These include gains in TBW
through eating, drinking, metabolic water formation (water
as a product of fuel metabolism) and glycogen-associated
water liberation (water bound when glycogen is stored in
muscle and liver and released during glycogenolysis) or
factors associated with the loss of TBW such as respiratory
and cutaneous water loss, gastrointestinal loss and renal
water clearance [1, 10, 14, 28–34]. All need to be con-
sidered if the changes in TBW during exercise are to be
understood properly.
3 Dynamics of Body Fluid Balance
3.1 What is Lost?
3.1.1 Renal Water Clearance
This is the loss of water through the process of filtration in
the kidneys which are the primary controllers of water
balance in the body. The kidneys are controlled by various
systems including the renin–angiotensin–aldosterone sys-
tem and anti-diuretic hormones including arginine vaso-
pressin (AVP) and atrial natriuretic peptide (ANP) [35, 36].
These hormones either increase or decrease the re-uptake
of filtrate passing through the kidney tubules resulting in an
increase or decrease in the concentration of urine excreted.
This wholly depends on the state of whole-body
hydration, the greater the fluid intake the greater the fluid
volume excreted as urine and vice versa. This is tightly
controlled in order to maintain body fluid allostasis to
prevent either overhydration or excessive urine loss
resulting in severe dehydration [22].
It has been observed that the body is unable to maxi-
mally suppress AVP secretion during exercise so that a
state of relative fluid retention occurs during and for some
time after exercise [37]. Under these circumstances any
relative overdrinking combined with unsuppressed AVP
secretion will greatly influence the probability for the
development of dilutional EAH [7].
The average urine clearance for normal individuals is
1–2 L/day but can range from 0.5 to 4 L [14, 38], with
maximum rates of ±800 mL/h in males [39]. There is little
reduction in urine flow rate during prolonged exercise but
in more strenuous exercise a reduction of 20–60 % has
been reported [40]. Thus, renal water clearance during
prolonged exercise could be considered to be highly indi-
vidual but is suppressed during prolonged exercise through
elevated AVP secretion. In addition, the kidneys are unable
to excrete more than ±800 mL/h to prevent fluid overload
in those who overdrink at rest.
3.1.2 Respiratory Water Loss
Respiratory water loss (RWL) is the loss of water associ-
ated with respiration. Daily RWL for individuals at rest in
temperate climates is approximately 400 mL and can reach
1500 mL/day when performing hard work in dry air [31].
Mitchell et al. [31] described the rate of water loss
through the respiratory tract as roughly 2–5 g/min during
exercise at a ventilatory rate of 1.5 L/min in a dry envi-
ronment with a vapour pressure of 10 mmHg. There is no
associated solute (electrolyte) loss [14, 31]. This loss is
said to roughly match the release of metabolic water as a
result of substrate metabolism [1, 14].
3.1.3 Gastrointestinal Water Loss
The normal loss of water through faecal excretion is
*100–200 mL a day, excluding the gross mass of the
actual stool. Most fluid ingested is reabsorbed by the small
intestine and the colon [1, 14, 41]. Faecal water loss does
not usually occur in ‘healthy’ individuals during exercise
[1, 41]. Thus, fluid loss via this route during prolonged
exercise should be minimal unless diarrhoea develops.
Interestingly, Ladell [12] first hypothesized a possible
bodily fluid reserve of up to 2 L that may not require fluid
replacement for whole-body fluid allostasis to be main-
tained. This has led to the hypothesis of a possible fluid
volume that exists in the gut and can be drawn upon to
offset some fluid losses from the body. This might explain
why, in some, BM losses of up to 3 % may not influence
physiological function or performance during prolonged
exercise [14, 21, 42].
3.1.4 Cutaneous Water Loss
Cutaneous water loss plays a major thermoregulatory role
during exercise due its cooling effect through evaporation.
This occurs at the cost of fluid loss [2]. Sweat is fluid
secreted through sweat glands as a hypotonic fluid (when
compared with plasma). The secretion of sweat consists
mainly of water, urea and sodium at a concentration that
varies depending on the habitual sodium intake and the rate
of urinary sodium loss (since losses in sweat and urine
must balance the sodium intake) [43].
The average person sweats between 0.5 and 2.0 L/h
during exercise. Total sweat loss is related to a variety of
factors, the most important being metabolic rate which is a
function of the athlete’s mass and intensity of effort and the
environmental temperature and humidity [1].
Fluid Allostasis During Exercise
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Collection of sweat and measurement of sweat rate is
difficult due to the function of sweat as a thermoregulatory
control mechanism utilizing evaporative heat loss [44].
Thus, in order to collect sweat it is necessary to prevent
evaporation of the sweat (thus hampering cooling) and to
prevent contamination of sampling [44, 45]. Various
techniques have been used but none has been shown to be
scientifically sound for measuring whole-body sweat rates.
Methods that have been used include closed-pouch col-
lection [46], sweat patches, whole-body wash downs,
whole-body sweat collection in a large plastic frame [44]
and, more recently, collection via technical absorbent
materials that can define regional sweat rates and sweat
electrolyte concentrations [47].
It seems all have their shortcomings but the ability to
collect the whole-body sweat to measure rates is logically
the most reproducible because it does not rely on sampling
from a specific area to estimate whole-body sweat rates. It
is known that regional sweat rates vary. New advances in
this field have prompted interest in the neuro-humoral
control of sweating [48]. Further investigations should be
conducted to elucidate the precise regulatory factors that
regulate sweat production and whole-body fluid allostasis
during exercise.
3.2 What is Gained?
3.2.1 Food and Fluid Consumption
Maintaining adequate hydration and energy replacement is
considered necessary for optimizing sporting performance
and health during prolonged exercise [49]. Specifically for
ultra-endurance exercise, athletes should consume enough
energy and fluid to maintain and prevent decrements in
performance at the same time, minimizing their risk of
developing heat-illness or EAH or EAHE, the latter due to
overzealous fluid consumption associated with SIADH [7,
50].
As mentioned, the prevention of both extremes (no fluid
intake and overconsumption) should be avoided. The most
probable explanation for the recent appearance of EAH and
EAHE in ultra-endurance sporting events has been the
promotion of fluid replacement equal to BM loss or to
drink to ‘stay ahead of thirst’ or ‘as much as tolerable’
based on the theory that only by drinking in this way is it
possible to maintain health and prevent any decrements in
performance [51].
Monitoring fluid and food consumption in race settings
is difficult and potentially inaccurate due to the competitive
nature of events in which subjects are participating. This
introduces psychological and logistical factors that hamper
data collection. These include the difficulty of determining
exact quantities of fluid consumed because not all the fluid
in a measured volume may be ingested, but could be used
for cooling of the head and body. A similar difficulty is
experienced when large numbers of athletes participate.
This makes it difficult to identify subjects in an experiment
and to monitor their fluid usage.
It is often easier to use the post-race fluid recall method
which involves the recall of the total amount of fluid
ingested once a race has been completed [20, 21]. This is
an indirect and subjective report and thus not totally reli-
able but it is practically useful for both the clinician and
researcher.
Interestingly, recent research has found that adopting an
ad libitum approach to general food and fluid consumption
adequately maintains day-to-day euhydration in elite
Kenyan athletes with high daily-training demands [52].
Often research has found that POsm can be maintained in
sedentary humans drinking \1.2 L/day [53].
3.2.2 Metabolic Water Formation
Metabolic water is the inevitable end-product of the oxi-
dation of fats, carbohydrates and proteins metabolized to
produce the energy needed to perform work. Metabolic
water formation is most commonly calculated using stoi-
chiometric equations for substrate oxidation such that 1 g
of carbohydrate oxidised will produce 0.6 mL water [14],
whereas the oxidation of 1 g of fat will generate 1.3 mL of
water [14, 54]. An important consideration when consid-
ering metabolic water formation is that the rate of substrate
oxidation is dependent on the work intensity and that the
type of fuel used is an individual response [33].
Pivarnik et al. [33] calculated that metabolic water
formation during endurance exercise is of little value in
maintaining the plasma volume. However, the researchers
did not consider whether metabolic water formation might
restore the intracellular volume without contributing
directly to extracellular fluid re-hydration [14]. Although
metabolic water production did not replenish the extra-
cellular volume this does not mean that it does not con-
tribute to a net gain in the TBW pool [33].
Additionally, a study of a 90 km cross-country ski race
calculated that 2 L of fluid was added to the TBW pool
during exercise [55]. This included 1 kg of water from fat
and carbohydrate oxidation and 1 kg as water released
when stored glycogen was metabolized.
The 2007 ACSM Guidelines for Exercise and Fluid
Replacement state that metabolic water formation does not
produce a net water gain since it merely offsets RWL [1]. It
would be incorrect to ignore the contribution these sources
contribute to body fluid allostasis during competition
because environmental and individual factors change and
so will RWL along with the extent of metabolic water
production [15, 27, 55].
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3.2.3 Glycogen-Associated Water Stores
Widely acknowledged as a possible source of additional
water release during exercise is the water associated with
glycogen storage. However, there is uncertainty about the
exact amount of water associated with glycogen storage in
muscle and liver.
It is, however, clear that glycogen storage produces an
insignificant osmotic effect because of the very large size
of the glycogen molecule. Thus, water released from gly-
cogen breakdown could contribute to offset the fluid lost
from the body without producing any threat to osmotic
allostasis.
In 1906, Zuntz et al. [56] proposed the widely accepted
but perhaps still uncertain theory that 3 g of water is still
associated with each gram of stored glycogen. However,
they did not directly measure this ratio but their statement
has been accepted as fact for the past 100 years. Instead
they calculated the relationship from data presented by
Pavy [57] who at the time was experimenting on sugar
(carbohydrate) formation in the liver [56]. It would take
some years until methods were developed that could pro-
vide a greater degree of precision to address this question.
But it was researchers studying glycogen storage in the
liver (Puckett and Wiley [58], McBride et al. [59], MacKay
and Bergman [60, 61], and Bridge and Bridges [62, 63])
who propelled the field forward by measuring changes in
liver glycogen concentrations and associated water storage.
Puckett and Wiley found that 2.4 g of water was stored
with each gram of glycogen in rats with varying liver
glycogen contents. They concluded that the liver should be
considered a possible site for water exchange when fluid
balance is studied [58]. MacKay and Bergman also estab-
lished the direct proportion in which water is stored with
glycogen in rabbit liver. They concluded that although their
results did not directly support the 3:1 water glycogen
ratio, their data did not oppose it either [60]. Similarly,
McBride and colleagues [59] concluded that during gly-
cogenesis in rats, as long as non-glycogen solids in the liver
do not change, 2.7 g of water are stored with each gram of
glycogen.
The only study to investigate this relationship in humans
was that of Olsson and Saltin [29], who found a 2.4 kg
increase in BM and a 2.2 L increase in TBW [measured
with tritium (
3
H) labelled water] in response to an
increased carbohydrate intake. They assumed that the
increase in TBW was the result of glycogen storage in the
muscles and liver and amounted to approximately 500 g.
As a result they concluded that 3–4 g of water would be
associated with each gram of glycogen stored in liver and
muscle [29].
This was disputed by Sherman et al. [34] who found an
inconsistent ratio between the storage of muscle glycogen
and water in rats. Although they disagreed with the findings
of Olsson and Saltin [29], their study investigated only
muscle glycogen concentrations, used a different experi-
mental model and did not investigate change in TBW and
whole-body glycogen storage in muscle and liver, as had
the study of Olsson and Saltin.
4 Total Body Water
In the ‘normal’ (70 kg) human, 60 % of BM (approxi-
mately 42 L), with a range from 45 to 75 % of BM,
comprises the TBW [64, 65]. TBW is the measure of the
body’s entire water content representing what would be
considered the true hydration state at the time of sampling,
assuming the subjects have normal blood reference values
and are in good health. Body fluids composed of the largest
amount of water are cerebrospinal fluid and bone marrow
fluid (99 % water), blood plasma (85 %) and the brain
(75 %) [64].
Body fluid allostasis is essential for electrolyte, acid-
base and thermal balance, and is the medium in which
bodily processes take place [32, 38, 64]. Water turnover by
the body ranges from 5 to 10 % (2–5 l) of TBW daily and
is influenced by the level of habitual activity [66, 67]. TBW
is regulated within ±0.2 to 0.5 % of BM at rest [65]. It has
been stated that no one true absolute value for TBW can be
assigned [68], although it has been proposed that a water
deficit of [2 % of BM falls outside the ‘normal’ TBW
fluctuations. This statement might hold true for short
exercise durations (\2 h) and at rest but there has been
little direct research to support this statement.
The use of isotopic tracer methodology to measure the
body’s total water content has become the accepted gold
standard [38]. The use of the stable isotope deuterium
oxide (D
2
O) has emerged as the most acceptable tracer for
the accurate measure of TBW. Other tracers that can be
considered include tritium (
3
H) or tritiated water (
3
H
2
O)
which is used less commonly because of its radioactive
nature and a half-life spanning 12 years which could render
it potentially hazardous [54].
Initial studies found the optimum tracer equilibration
period to be longer than the 4–6 h when sampling from
urine [69]. More recent research has found that tracers are
distributed quite rapidly throughout the body water spaces.
Thus, an equilibration period of 2–4 h is adequate when
sampling with saliva, 2.5–5 h for urine and 1.5–6 h for
blood [66, 69, 70].
Samples are usually corrected for the exchange with
non-aqueous hydrogen [71]. Analysis is carried out with
the use of a ratio mass spectrometer [72] for the stable
isotopes, and with a scintillation counter for tritiated
samples [54, 73]. Colt et al. [54] utilized
3
H during exercise
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and stated that
3
H might not be the best tracer to use
because of the increase in
3
H space as the result of an
increase in non-aqueous hydrogen-exchange in the post-
exercise period. But the pre-run measurement in that study
occurred 10–20 days prior to the second measurement.
Thus, any differences in TBW between the resting and
post-run conditions could be explained by either the run
itself or by other activities taking place during the
10–20 days between measurements. The authors of that
paper also utilized an incorrect value for metabolic water
production during exercise.
D
2
O tracers used to measure TBW have an accuracy of
0.5 % [72]. Bartoli et al. [65] found that TBW measure-
ments are repeatable with an *4 % coefficient of variation
(CV), of which 60 % is inherent in the dilution technique.
Although the use of D
2
O is possibly the best method to
measure TBW, the ability to attain instantaneous (quick)
measurements is problematic. Currently, accurate TBW
measurements are acquired through the use of an isotope
ratio mass spectrometer that determines the tracer’s mass
compared with the rest of the solution in which it is diluted.
But this method is costly and not widely available [69].
Fusch et al. [67] examined TBW and TBW turnover
during a 7-day mountain trek at moderate altitude. They
found TBW decreased by 2 L and then stabilized over the
first few days of the trek. This was associated with a
decrease of 0.8 kg of BM over the entire trial [67].
O’Brien et al. [74] measured TBW with D
2
O before and
after an 8-day, moderately cold-weather (1–3 °C), military
training exercise. They observed a significant decrease in
TBW over the study, which they believed was due to a
noticeable decrease in lean BM and fat mass. They con-
cluded that body fluid balance was maintained during this
experiment despite high activity levels, significant BM loss
and negative energy balance.
Similar findings were reported by Knechtle et al. [75]
who used bio-electrical impedance to monitor athletes
during a 1200 km multi-day stage running race. Despite a
significant loss in BM there was a noted increase in
%TBW, despite a decrease in skeletal muscle and fat mass.
They confirmed this finding in a cohort of female runners
during a 100 km ultra-endurance run. Despite a 2.2 %
decrease in BM, %TBW increased [75].
Baker et al. [76] measured TBW utilizing the tracer
methodology for pre-exercise TBW determination and con-
cluded that TBW changes accurately track BM changes
during exercise. But a number of concerns undermine the
certainty of that conclusion [77]. Thus, Nolte and Noakes [77]
argue that Baker et al. [76] failed to prove conclusively that
changes in BM track changes in TBW during exercise in a
ratio of 1 kg of BM loss equals a 1 L loss of TBW.
Most recently, Nolte and colleagues found that ad libi-
tum drinking was sufficient to prevent large changes in
TBW during exercise in both extreme dry heat and cool
conditions. TBW, POsm and plasma [Na
?
] were main-
tained despite significant BM loss [78–80]. Similarly,
runners in 56 and 21.1 km races, regulated both plasma
[Na
?
] and POsm regardless of BM loss [81]. These studies
show that appropriate fluid allostasis is possible during
such demanding activities, even when in the face of sig-
nificant changes in BM.
5 Changes in Body Mass as a Measure of Changes
in Fluid Balance During Exercise
BM change is the most popular proxy for TBW balance
during exercise because it is non-invasive and easy to
measure [1, 38, 41]. This is based on the assumption that a
BM loss of 1 g is equivalent to the loss of 1 mL of water
[14]. The use of BM changes has become the accepted
practice because numerous studies have established that
most of the water lost during exercise occurs through
excretory mechanisms such as urination and sweat loss.
The latter is the major source of fluid loss given its role in
body temperature regulation during exercise.
Other clinically applicable reasons are the use of BM in
hospitalized patient populations. In such conditions the use
of BM is considered an accurate and reliable day-to-day
measure of changes in TBW. But it seems that these
changes in BM are more closely associated with changes in
fat and muscle mass than changes in fluid balance [82, 83].
Similarly, it is assumed that during exercise, changes in
BM and TBW are directly proportional. This may not
necessarily be true during ultra-endurance exercise if
(i) there is a store of *2 L of fluid in the intestine and (ii)
water is released, as glycogen is metabolized during
exercise [14, 20, 21, 26].
Since BM usually falls during exercise it is assumed that
TBW must also have been reduced. As a result, it is argued
that the athlete has drunk too little, has become ‘voluntary
dehydrated’ and is at risk of developing heatstroke and
other medical complications of exercise [3]. But this is
predicated on the assumption that all the BM lost during
exercise is the result of fluid loss alone without any com-
pensation from internal body water stores. This may be true
for acute and intermittent bouts of exercise but not neces-
sarily for prolonged exercise. When this assumption is used
to develop guidelines for endurance exercise, it may lead to
errors in an estimation of hydration status, possibly
encouraging overzealous fluid consumption especially
during prolonged exercise [13].
Similarly, caution should be used when BM alone is
considered as a surrogate for TBW changes, especially
during prolonged endurance exercise. Physiologically the
body is unable to track changes in BM but rather regulates
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serum [Na
?
] and POsm, both of which influence thirst. As
a result, these are the proper indicators of body fluid al-
lostasis [27, 84, 85]. We need to remember that Dill et al.
[86] already hypothesized that humans do not defend BM
during exercise but rather protect POsm.
In laboratory studies it is often observed that a [2%
BM loss is associated with decrements in exercise perfor-
mance. However, BM changes tracked over 12- and 24-h
ultra-endurance events showed a significant decrease in
BM of 2.9 % (ranging from 0 to -6.5 %) for the 12-h race
and 5.1 % (ranging from -0.8 to -11.4 %) for the 24-h
race. BM fell during the first 8 h of exercise where after it
fluctuated about a new ‘baseline’ value [13].
That study, amongst many others, should discourage the
concern that BM must be maintained during all forms of
exercise regardless of their intensity or duration [78–81,
87]. Rather, it has been observed that BM loss can occur
without a decrease in TBW [80, 81]. This contradicts the
advice that the maintenance of BM is necessary to maintain
fluid allostasis during endurance exercise [86].
Yet the use of BM changes as an absolute indicator of
hydration status is still widely advocated because it is such a
practical and convenient measurement both in the laboratory
and field setting [1, 14, 38, 41]. But the evidence is clear that
changes in BM alone cannot be justified as the sole measure
on which to base fluid replacement guidelines for body fluid
allostasis for athletes during all forms of exercise.
6 Fluid Balance Controls
Classically, the main fluid balance controls in the human
body are the hormone AVP, aldosterone and ANP. Recently,
interleukin-6 and oxytocin have also been found to poten-
tially play a role in control of fluid balance during exercise in
humans [88, 89]. AVP predominately affects the rate of fluid
reabsorption in the loop of Henle in the kidney [85], whereas
aldosterone regulates the extent of sodium reabsorption and
concomitant fluid reuptake in the kidney in response to
changes in blood pressure and blood volume, thus ensuring
body fluid allostasis with the maintenance of the blood bio-
chemical markers POsm and plasma [Na
?
][36].
Hormone collection and analysis is costly. Hence, it is
more practical and less expensive to assess body fluid al-
lostasis according to the proxies to which these hormones
respond. A variety of blood biochemical measures are often
used to assess body fluid allostasis, including blood POsm
and blood sodium and potassium concentrations. These
markers are often measured because their concentrations
reflect the actual state of hydration that the body uses to
assess the net flux of fluid into and out of the extra-cellular
fluid (ECF), thereby maintaining the body in an optimum
functional state.
Kratz et al. [90] have updated reference values for
various haematological and blood biochemical markers in
athletes completing endurance events [91]. They have
proposed values that differ somewhat from standard clini-
cal values [90]. This allows us to understand the accepted
deviations from the normal resting values in athletes
competing in prolonged exercise.
6.1 Plasma Osmolality
POsm is defined as the concentration of a specific solution
expressed in milliosmoles of solute particles per kilogram of
water (mOsm/kgH
2
O); in this case it is the concentration of
solute particles present in plasma [92]. Sodium is the main
electrolyte present in the ECF; thus plasma [Na
?
] largely
dictates POsm, which in turn regulates cell size. Body fluid
allostasis is achieved through neuroendocrine regulation in
which osmoreceptors located in the organum vasculosum of
the lamina terminalis and the subfornical organ in the hypo-
thalamus detect changes in POsm (1–2 %) [85].
During exercise, POsm increases as a curvilinear function
of exercise intensity and of change in plasma volume [35, 36].
Thus, AVP concentrations rise as a linear function of
increases in POsm, increasing the stimulus for thirst con-
comitantly with an increase in renal sodium reabsorption to
maintain fluid allostasis. This occurs when the POsm rises
5–10 mOsm/kgH
2
O above normal or when TBW decreases
by 1.7–3.5 %.
The measurement of POsm is the most valid measure of
hydration status compared with urine osmolality, which is a
delayed marker of changes in hydration [27, 92]. POsm
accurately reflects acute changes in hydration status mea-
sured as BM loss, whereas urine osmolality lags behind
changes in POsm during acute dehydration. The mean
reference value for a normal person at rest ranges from 280
to 296 mOsm/kgH
2
O[91]. Reference values for POsm
range from 273 to 317 mOsm/kgH
2
O immediately after
endurance exercise, such as completing a marathon [90].
6.2 Plasma Sodium Concentration (Plasma [Na
?
])
Since plasma [Na
?
] is largely responsible for dictating the
osmotic pressure of the body, any significant disturbances
during rest and specifically during long-distance endurance
events can produce significant illness [24, 84, 93–95].
Dysnatremias can be the result of overdrinking or excessive
sodium consumption in response to fears of severe dehydra-
tion and decreases in performance. These dysnatremias are
also associated with delayed recovery in runners who col-
lapse after prolonged exercise [84].
Although sodium is lost in urine and sweat during
exercise, it is hypothesized that the body is able to activate
or inactivate various endogenous stores of sodium in order
Fluid Allostasis During Exercise
Author's personal copy
to maintain allostasis of plasma [Na
?
][96]. Normal ref-
erence values for plasma [Na
?
] have been established as
135–145 mmol/L for the general population [90]. Imme-
diately after prolonged exercise the values have been
established to range from 134 to 149 mmol/L, but much
lower values occur in EAH, and especially in EAHE [90].
Many researchers have insisted that sodium should be
replaced during exercise in order to correct for any sweat
and urine sodium losses [1, 2]. But significant decreases in
plasma [Na
?
] are due to the increase in fluid consumption
resulting in fluid retention during prolonged exercise
diluting the plasma [Na
?
][97]. Consequently, it has been
found that the use of oral sodium supplementation during
prolonged exercise is unnecessary to maintain the plasma
[Na
?
][97, 98]. Rather it is important to avoid overdrinking
during exercise. It is not the loss of sodium through sweat
but the dilution of the body’s sodium content due to
overhydration concomitantly with the inability to maxi-
mally suppress AVP, together with positive sequestration
of Na
?
into internal Na
?
stores that causes EAH and
EAHE [99].
6.3 Hypovolemia and Baroreceptor Activation
Haemodynamic influences may affect the defense of body
fluid allostasis. As such, isotonic volume contraction, in
particular as a result of haemorrhage, causes hypovolemia
with the maintenance of POsm and plasma [Na
?
] within
the normal range. Once a threshold has been reached a
clear stimulus for AVP secretion and thirst is triggered. In
this example, neither POsm nor plasma [Na
?
] would be
accurate surrogates for the prediction of body fluid
allostasis.
The activation of these defenses against hypovolemia
requires larger changes in blood volume and blood pressure
than do the much smaller changes in POsm that activate the
same responses for example during exercise. Further, the
shunting of blood flow away from certain vascular beds,
most notably the splanchnic bed, may maintain effective
circulating blood volume even with large decreases in
extracellular fluid volume.
Hence, whilst these measures of body fluid control may
be powerful, they likely do not come into play under non-
pathological situations such as endurance exercise. How-
ever, their existence clearly illustrates that there are fluid
balance controls other than POsm that act to protect the
body from severe dehydration.
7 Conclusion
The safety and efficacy of past and present ACSM
Guidelines for Fluid Replacement have been questioned
[1, 3]. After presenting the current understanding of
euhydration [9, 18], a more appropriate definition of
euhydration in relation to physiological variables such as
POsm have been suggested [22]. Having considered the
general gains and losses of water throughout the human
body we have argued that water may be released from
internal stores during exercise. This would add to the
body’s overall hydration status even in the face of
reductions in BM. Potentially large internal body water
stores exist in the gut and perhaps in association with
liver and muscle glycogen stores. These ideas should
establish a more physiologically appropriate model for
fluid replacement during exercise [22, 100, 101].
Current evidence establishes that it is normal to lose
[2 % BM, and that BM losses within this range are not
necessarily associated with clinically relevant reductions
in TBW [13, 20, 21]. It seems that performance may also
not be compromised despite even large BM losses since
athletes losing the greatest BM tend to perform better
than their counterparts who lose the least or even gain
BM during exercise. Thus, the term ‘involuntary dehy-
dration’’’ may be based on the erroneous belief that BM
is an accurate surrogate for body fluid allostasis. It is
largely the state of plasma [Na
?
] which determines
POsm, thus stimulating AVP release and other hormones
that regulate fluid excretion, and not a change in BM that
dictates the body’s response to fluid overload or dehy-
dration [22, 36, 102]. Thus, numerous studies have
established that markers of fluid balance pre- and post-
exercise do not usually change as dramatically as does
the BM [15].
It should be acknowledged that fluid replacement
guidelines have evolved for the better since the 1996
ACSM Guidelines for Exercise and Fluid Replacement.
Drinking to thirst (ad libitum) during exercise in races as
short as 21.1 km or in more punishing ultra-endurance
races lasting up to 12–24 h ensures that athletes will
maintain body fluid allostasis and achieve their race goals
without encountering avoidable medical complications.
Hopefully this review encourages the scientific com-
munity to disseminate practical, realistic and physiologi-
cally sound evidence further to advance fluid replacement
prescription for all athletes participating in athletic com-
petitions regardless of intensity or duration.
Acknowledgments The authors would like to thank Discovery
Health, the University of Cape Town Staff Research Fund, the
Medical Research Council of South Africa, Deutsche Akadimischer
Austache Dienst and the National Research Foundation of South
Africa for general funding.
Conflicts of interest No sources of funding were used to assist in
the preparation of this review. The authors have no conflicts of
interest that are directly relevant to the content of this review.
N. Tam, T.D. Noakes
Author's personal copy
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