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The Quantification of Body Fluid Allostasis During Exercise



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 appropriate fluid intake advice. The measurement of total body water via D2O 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 23
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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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
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
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,
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 [1315].
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, 2326].
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
Author's personal copy
BM alone do not account for all the factors affecting body
fluid allostasis [2022, 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, 2834]. 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,
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
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].
N. Tam, T.D. Noakes
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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
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
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 (
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
O) has emerged as the most acceptable tracer for
the accurate measure of TBW. Other tracers that can be
considered include tritium (
H) or tritiated water (
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
H during exercise
Fluid Allostasis During Exercise
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and stated that
H might not be the best tracer to use
because of the increase in
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.
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
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
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 [7880]. Similarly,
runners in 56 and 21.1 km races, regulated both plasma
] 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
N. Tam, T.D. Noakes
Author's personal copy
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 [7881,
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
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
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
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
O[91]. Reference values for POsm
range from 273 to 317 mOsm/kgH
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, 9395].
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
][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
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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Fluid Allostasis During Exercise
Author's personal copy
... The body mass of humans is approximately 70% water. Regulation of water flow across cell membranes is essential for maintaining an appropriate fluid balance within the cells [3], which is a critical factor in health status and CE performance [4]. A novel finding related to water management at the molecular level occurred in 1988 with the identification of transmembrane water channels in erythrocytes [5]. ...
... Saunders et al. [30] hypothesized that reductions in the expression of AQP1 in the presence of the G-allele could cause a slower response to changes in osmotic gradient during exercise. That notion substantiated by the Tam and Noakes [4] observation that serum osmolality is physiologically defended during exercise. ...
... Conversely, Rivera et al. [29] determined body fluid loss from the difference between nude body weight (weight before 10 km − weight after 10 km) with adjustments for fluid intake, respiratory water loss, and urine excretion. Tam and Noakes [4] reviewed the literature pertaining to the controversy of when and why absolute body weight should be adjusted, given practical and scientific endeavors. It is beyond the present review to go further into such controversy. ...
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Background: There is abundant and mounting information related to the molecular and biological structure and function of the Aquaporin-1 (AQP1) gene and the AQP1-Aquaporin channel. Regulation of water flow across cell membranes is essential for supporting inter- and intracellular fluid balance, which is critical for health and exercise performance. The transmembrane water channel AQP1 is important for cardiorespiratory endurance (CE) because it influences fluid transfers in erythrocytes, endothelial, and pulmonary cells and is vital for transport of ammonium, bicarbonate, carbon dioxide, glycerol, nitric oxide, potassium ion, water, and trans-epithelial and renal water. Very recent publications suggest the association between a DNA sequence variant, rs1049305 (C > G), in the 3'-untranslated region of the AQP1 gene and CE performance. Other reports indicate further significant associations between AQP1 channel and CE phenotypes. The purposes of this systematic review were to examine the extent of the associations between the AQP1 rs1049305 genotype and CE exercise performance and body fluid loss in long-distance runners and AQP1 channel associations with other CE phenotypes. Methods: Data sources: A comprehensive review was conducted using PubMed, EMBASE, CINAHL, and Cochrane electronic databases. The search ranged from January 1, 1988, to December 31, 2018. Studies reported in English, French, and Spanish were considered. Eligibility criteria: The criteria for inclusion in the review were (a) case-control study; (b) unequivocal definition of cases and controls; (c) CE was defined as performance in endurance events, laboratory tests, and/or maximal oxygen consumption; (d) exclusion criteria of known causes; (e) genotyping performed by PCR or sequencing; (f) genotype frequencies reported; and (g) no deviation of genotype frequencies from Hardy-Weinberg equilibrium in the control group. Study appraisal: The systematic review included studies examining the AQP1 gene and AQP1 channel structure and function, associations between the AQP1 gene sequence variant rs1049305 (C > G) and CE performance, body fluid loss in long-distance runners, and other studies reporting on the AQP1 gene and channel CE phenotype associations. Synthesis methods: For each selected study, the following data were extracted: authors, year of publication, sample size and number of cases and controls, CE definition, exclusion criteria, inclusion criteria for cases and controls, methods used for genotyping, genotype, allele frequencies and HWE for genotype frequencies in cases and control groups, and method of AQP1 gene and AQP1 channel analysis. Results: The initial databases search found 172 pertinent studies. Of those, 46 studies were utilized in the final synthesis of the systematic review. The most relevant findings were (a) the identification of an independent replication of the association between AQP1 gene sequence variant rs1049305 (C > G) and CE performance; (b) the association of the rs1049305 C-allele with faster CE running performance; (c) in knockout model, using a linear regression analysis of distance run as a function of Aqp1 status (Aqp1-null vs. wild-type mice) and conditions of hypoxia (ambient [O2] = 16%), normoxia (21%), and hyperoxia (40%) indicated that the Aqp1 knockout ran less distance than the wild-type mice (p < 0.001); (d) in vitro, a reduced AQP1 expression was associated with the presence of the rs1049305 G-allele; (e) AQP1 null humans led normal lives and were entirely unaware of any physical limitations. However, they could not support fluid homeostasis when exposed to chronic fluid overload. The limited number of studies with "adequate sample sizes" in various racial and ethnic groups precluding to perform proper in-depth statistical analysis. Conclusions: The AQP1 gene and AQP1 channel seems to support homeostatic mechanisms, yet to be totally understood, that are auxiliary in achieving an advantage during endurance exercise. AQP1 functions are vital during exercise and have a profound influence on endurance running performance. AQP1s are underappreciated structures that play vital roles in cellular homeostasis at rest and during CE endurance running exercise. The outcome of the present systematic review provide support to the statement of hypotheses and further research endeavors on the likely influence of AQP1 gene and AQP1 channel on CE performance. Registration: The protocol is not registered.
... Terms & Conditions of access and use can be found at http:// Introduction There has previously been controversy surrounding the prescription of fluid intake during prolonged exercise (Tam & Noakes, 2013). However, current guidelines suggest that ad libitum drinking to thirst during exercise will sufficiently protect healthy athletes from the risks of either over-or under-hydration (Hew-Butler, Verbalis, & Noakes, 2006;Sawka et al., 2007). ...
... Percentage body weight lost or gained was calculated as the difference between the pre-and post-race weights divided by the pre-race weight and expressed as a percentage. Although changes in body weight during exercise are significantly influenced by fuel utilisation and likely overestimate true changes in total body water (Tam & Noakes, 2013), weight changes during the Ironman were nevertheless used as an indirect measure of changes in total body water during the event, as the group of athletes with the greatest percentage weight loss would also, presumably, have been the most dehydrated (Armstrong et al., 2014;Saunders et al., 2006). As previously described (Saunders et al., 2006), triathletes who gained weight during the event were considered to be overhydrated, those who lost between 0% and 3% body weight were considered to be euhydrated, while those who lost more than 3% of their pre-race body 2 C. J. Saunders et al. ...
... The CC genotype has also been associated with lower serum sodium concentration (P = 0.003) and lower serum osmolality (P = 0.03) in patients with liver cirrhosis than that observed in patients with a CG or GG genotype. As serum osmolality is physiologically defended during exercise (Tam & Noakes, 2013), we hypothesise that decreased expression of AQP1 in the presence of the G allele may result in a slower response to changes in osmotic gradients during exercise. A number of previously published observations may allude to the mechanism by which this variant influences running performance. ...
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Abstract The objective of this study was to test the association of the rs1049305 (G > C) variant within the 3'-untranslated region of the aquaporin 1 gene, AQP1, with changes in body weight, post-race serum sodium concentration and performance in Ironman triathletes. Five hundred and four male Ironman triathletes were genotyped for the rs1049305 variant within the AQP1 gene. Change in pre- and post-race body weight was calculated for 470 triathletes and used as a proxy for changes in body fluid during the race, as well as to divide triathletes into biologically relevant weight-loss groups (0-3%, 3-5% and >5%). There were no rs1049305 genotype effects on post-race serum sodium concentrations (P = 0.647), pre-race weight (P = 0.610) nor relative weight change during the Ironman Triathlons (P = 0.705). In addition, there were no significant differences in genotype (P = 0.640) nor allele (P = 0.643) distributions between the weight loss groups. However, triathletes who carry a C-allele were found to complete the 42.2-km run stage faster (mean 286, s = 49 min) than triathletes with a GG genotype (mean 296, s = 47 min; P = 0.032). The AQP1 rs1049305 variant is associated with running performance, but not relative body weight change, during the 2000, 2001 and 2006 South African Ironman Triathlons.
... Acutely, the necessity to drink (in excess of fluid losses) may lead to hyperhydration (Bargh et al. 2016). The balance of mechanisms acting on regulated variables as well as controlled variables operating to an apparent set point of osmolality usually affects a mild oscillation around a specific body water content (Tam and Noakes 2013). ...
... Hypotonic losses (i.e., sweat, Buono et al. 2008) increase ECF osmolality, and consequently, fluid moves from ICF to equilibrate the change, known as intracellular dehydration (Cheuvront and Kenefick 2014). However, the suggestion has also been made that glycogen and its associated water (1:3 on g per g basis) may represent an important store of available water to combat such dehydration, presumably "released" as glycogen is oxidised during exercise (Maughan et al. 2007;Tam and Noakes 2013). It has been suggested that approximately 1.2 L may become available during a marathon (Maughan et al. 2007). ...
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PurposeThis study evaluated whether glycogen-associated water is a protected entity not subject to normal osmotic homeostasis. An investigation into practical and theoretical aspects of the functionality of this water as a determinant of osmolality, dehydration, and glycogen concentration was undertaken. Methods In vitro experiments were conducted to determine the intrinsic osmolality of glycogen–potassium phosphate mixtures as would be found intra-cellularly at glycogen concentrations of 2% for muscle and 5 and 10% for liver. Protected water would not be available to ionic and osmotic considerations, whereas free water would obey normal osmotic constraints. In addition, the impact of 2 L of sweat loss in situations of muscle glycogen repletion and depletion was computed to establish whether water associated with glycogen is of practical benefit (e.g., to increase “available total body water”). ResultsThe osmolality of glycogen–potassium phosphate mixtures is predictable at 2% glycogen concentration (predicted 267, measured 265.0 ± 4.7 mOsmol kg−1) indicating that glycogen-associated water is completely available to all ions and is likely part of the greater osmotic system of the body. At higher glycogen concentrations (5 and 10%), there was a small amount of glycogen water (~ 10–20%) that could be considered protected. However, the majority of the glycogen-associated water behaved to normal osmotic considerations. The theoretical exercise of selective dehydration (2 L) indicated a marginal advantage to components of total body water such as plasma volume (1.57% or 55 mL) when starting exercise glycogen replete. Conclusion Glycogen-associated water does not appear to be a separate reservoir and is not able to uniquely replete water loss during dehydration.
... Furthermore, observational studies of this nature (O'Hara et al. 2010;Jones et al. 2015;Jones et al. 2016a;Jones et al. 2016b) fail to accurately determine body fluid balance due to the absence of measurement of appropriate physiologically controlled variables (viz. POsm) (Tam and Noakes 2013), thus the cause of potential over-drinking is not known. ...
... However, it is apparent within these data that change in BM did not reflect the changes in POsm due to the observation of some BM loss arising without the occurrence of an increase in POsm (Table 1). This observation is likely due to the acknowledged dissociation between BM loss and total body water due to alternative sources for body water gain and BM loss (Maughan et al. 2007;King et al. 2008;Nolte et al. 2011;Tam and Noakes 2013). Consequently, this finding reflects that some degree of BM loss may be essential to maintain POsm (Nolte et al. 2011), given that other (e.g. ...
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This study assessed the potential physiological and perceptual drivers of fluid intake and thirst sensation during intermittent exercise. Ten male rugby players (17 ± 1 years, stature: 179.1 ± 4.2 cm, body mass (BM): 81.9 ± 8.1 kg) participated in six 6-min small-sided games, interspersed with 2 min rest, where fluid intake was ad libitum during rest periods. Pre- and postmeasurements of BM, subjective ratings (thirst, thermal comfort, thermal sensation, mouth dryness), plasma osmolality (POsm), serum sodium concentration (S[Na(+)]), haematocrit and haemoglobin (to calculate plasma volume change; PV) were taken. Fluid intake was measured during rest periods. BM change was -0.17 ± 0.59% and fluid intake was 0.88 ± 0.38 L. Pre- to post-POsm decreased (-3.1 ± 2.3 mOsm·kg(-1); p = 0.002) and S[Na(+)] remained similar (-0.3 ± 0.7 mmol·L(-1), p = 0.193). ΔPV was 5.84 ± 3.65%. Fluid intake displayed a relationship with pre-POsm (r = -0.640, p = 0.046), prethermal comfort (r = 0.651; p = -0.041), ΔS[Na(+)] (r = 0.816, p = 0.004), and ΔPV (r = 0.740; p = 0.014). ΔThirst sensation displayed a relationship with premouth dryness (r = 0.861, p = 0.006) and Δmouth dryness (r = 0.878, p = 0.004). Yet a weak positive relationship between Δthirst sensation and fluid intake was observed (r = 0.085, p = 0.841). These data observed in an ambient temperature of 13.6 ± 0.9 °C, suggest team-sport athletes drink in excess of fluid homeostasis requirements and thirst sensation in cool conditions; however, this was not influenced by thermal discomfort.
... According to the cutoff of ≥ 1.2 mg/dl serum creatinine, no significant differences were observed in weight loss immediately after the race (P > 0.05) between G1 and G2. After a marathon, body weight loss is at around 2-3% (Sawka et al., 2007;Thomas et al., 2016) and at 5-6% after ultra-endurance events without clinical implications (Tam and Noakes, 2013). G1 showed a weight loss of 2-4% and G2 of 2-5% without renal implications. ...
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Purpose: This study investigates the relationship between whole-body bioimpedance vector displacement, using bioelectrical impedance vector analysis (BIVA), and renal function through serum biomarkers [creatinine, urea, sodium, C-reactive protein (CRP), and creatine kinase] and urine biomarkers after a marathon. Methods: Bioimpedance measurements were taken among 19 non-elite runners at 24 h pre-race, immediately post-race, and at 48 h post-race. The bioimpedance measurements were analyzed by BIVA using the Hotelling’s T2 test. The runners were divided according to a cutoff of serum creatinine level immediately post-race in G1 (<1.2 mg/dl of serum creatinine level) and G2 (≥1.2 mg/dl of serum creatinine level). The increase of the serum creatinine levels in 83% of G2 runners was related to acute kidney injury (AKI) stage 1. Results: Neither G1 nor G2 showed a creatinine clearance rate (CCr) lower than 60 ml/min. G2 showed a significant increase in CRP values at 48 h post-race vs baseline compared to G1 (P < 0.05), with over 5 mg/L (6.8–15.2) in 92% of the runners, and in CK values with over 215 U/L (282–1,882) at 48 h post-race in 100% of the runners. By BIVA, the 95% confidence ellipses of G2 showed shorter bioimpedance vectors than G1, with a noticeable minor Xc/H (P < 0.01), indicating an expansion on extracellular water and inflammation. The runners with 48 h post-race Xc/H values ≤30.5 Ω, with a decrease from −3 to −12% with respect to the Xc/H value at 24 h pre-race, indicated AKI stage 1 with 85.7% sensitivity and 91.7% specificity, with a direct correlation between AKI stage 1 with greater CRP values at 48 h post-race and bioimpedance vector displacement, but not with CK values at 48 h post-race. Conclusion: Through this data collection, it was evidenced that a transient reduction in renal function is more related to inflammatory factors than muscle damage. The BIVA method along with serum biomarkers could be used to follow up the kidney function in runners.
... Water remaining in the gut has been identified as a factor affecting the risk for EAH. During high water intake, water remains in the intestinal tract which leads to sodium being transferred from the blood into the gut [32,66,78]. Considering these effects, studies show that water alone is absorbed into the bloodstream slower than beverages with carbohydrates [79]. ...
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Exercise-associated hyponatremia (EAH) is defined as a plasma sodium concentration of <135 mmol/l during or after endurance and ultra-endurance performance and was first described by Timothy Noakes when observed in ultra-marathoners competing in the Comrades Marathon in South Africa in the mid-1980s. It is well-established that a decrease in plasma sodium concentration < 135 mmol/l occurs with excessive fluid intake. In this review, we present new findings about the aspects of sex, race location, sports discipline and length of performance. Clinically, a mild hyponatremia will lead to no or very unspecific symptoms. A pronounced hyponatremia (<120 mmol/l) will lead to central nervous symptoms due to cerebral edema, and respiratory failure can lead to death when plasma sodium concentration reaches values of <110-115 mmol/l. The prevalence of EAH depends on the duration of an endurance performance (i.e. low in marathon running, high to very high in ultra-marathon running), the sports discipline (i.e. rather rare in cycling, more frequent in running and triathlon, and very frequent in swimming), sex (i.e. increased in women with several reported deaths), the ambient temperature (i.e. very high in hot temperatures) and the country where competition takes place (i.e. very common in the USA, very little in Europe, practically never in Africa, Asia and Oceania). A possible explanation for the increased prevalence of EAH in women could be the so-called Varon-Ayus syndrome with severe hyponatremia, lung and cerebral edema, which was first observed in marathon runners. Regarding the race location, races in Europe seemed to be held under rather moderate conditions whereas races held in the USA were often performed under thermally stressing conditions (i.e. greater heat or greater cold). Keywords: Cold, heat, cerebral edema, prolonged exercise, swimming, cycling, running
... Gomes, Silami-García & Carneiro, 2006). Por otro lado, existen autores que defienden a la sed como un mecanismo óptimo durante el ejercicio (Noakes, 2010;Tam & Noakes, 2013) aunque los resultados de este tema siguen sin ser contundentes. ...
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Este estudio experimental fue diseñado para evaluar durante el ejercicio y la rehidratación ad libitum post-ejercicio, si las percepciones subjetivas de sed y calor, así como la ingesta voluntaria de agua, son distintas en dos condiciones ambientales diferentes pero equivalentes en cuanto al índice de estrés térmico. Métodos: 14 participantes se ejercitaron en dos ocasiones en un cuarto de clima controlado (WBGT≈28.5° C): una vez para el calor seco (SECO, TBS = 33.8°C, HR = 53%) y una para el calor húmedo (HUM, TBS = 32.1°C y HR = 67%) sin ingesta de fluidos, hasta alcanzar una deshidratación equivalente al 4% MC. Las percepciones de sed, calor, llenura y cólico se midieron cada 30 min durante el ejercicio. Posteriormente ingirieron agua ad libitum durante 90 minutos. También se midió la ingesta voluntaria de agua. Resultados: Durante el ejercicio, la percepción de sed fue la misma para ambas condiciones (SECO 64.44±23.38, HUM 67.32±20.41mm; p=0.409), pero aumentó con el tiempo (p = 0.0001). Lo mismo ocurrió con la percepción de calor: no hubo diferencia entre las condiciones (SECO 6.34±0.50, HUM 6.40±0.37ua; p=0.423), pero aumentó a través del tiempo (p=0.001). Al final de la rehidratación, la percepción de calor fue mayor para el calor seco (5.3 ± 0.2ua) que para el calor húmedo (4.7 ± 0.2ua, p=0.006). La sed al final del ejercicio (85.8 ± 19.4mm) no mostró correlación significativa con la deshidratación real (3.82 ± 0.18% MC, r = -0.14, p = 0.48) ni con el consumo voluntario de agua (1843 ± 587 mL, r = -0.04, p = 0.85). No hubo correlación entre la pérdida de sudor real (2766 ± 700 ml) y la ingesta voluntaria de agua (r = 0.16, p = 0.42). La asociación entre el balance neto de fluidos y la percepción de la sed fue de R2a= 0.70 (p = 0.001) Conclusiones: la percepción de sed y calor fue la misma cuando se realizó ejercicio en dos condiciones ambientales diferentes con el mismo nivel de estrés térmico. La escala de percepción de la sed fue capaz de detectar la deshidratación progresiva consistentemente: cuanto mayor fue la deshidratación en el tiempo, mayor fue la sed. Sin embargo, los resultados de este estudio no apoyan la teoría de que la ingesta voluntaria de agua es adecuada para reponer las pérdidas de sudor después del ejercicio.
... 25 When large samples are studied, self-report is generally the most frequently used method to evaluate fluid intake. 26 Currently, there are few epidemiological data available on fluid habits in ecologically-valid scenarios stratified by sex, age, sport mode and competitive level, and none exist for the Italian population. Therefore, the aim of this investigation was to determine current hydration practices across a range of athletes during their regular training session, and to investigate which factors may affect the fluid volumes ingested. ...
BACKGROUND: Hydration habits during training may differ depending on sports mode and individual characteristics. The aim of this study was to assess fluid intake behaviour in a wide sample of Italian athletes during their regular training. METHODS: Data on hydration habits during training were collected from a random sample of competitive athletes. Hydration strategies and personal characteristics were queried via questionnaire, including athletes' quantity and type of fluid ingested during a typical training bout, sport characteristics (e.g. mode and training duration), and whether their coach encouraged them to drink during trainings. RESULTS: Three hundred fifty-two competitive athletes participated to the study; two hundred eighty-nine athletes correctly completed all survey items (age: 8-63 y, median: 21±13 y). Athletes were involved in international (3.1%), national (34.1%) and regional (44.9%) competitions. Median fluid intakes during training were 0.25 L∙h-1; 150 athletes reported fluid intake below the median, whilst 23 athletes (6.5% of total sample) reported fluid intake at or above currently published exercise hydration guidelines (NATA and ACSM). Binary logistic regression indicated that the number of pauses to drink (B: 0.771, significance: 0.000), duration of a typical training bout (B: -2.237, significance: 0.000), and a coach's encouragement to drink (B: 0.601, significance: 0.030) were each associated with fluid consumption above or below the median value. CONCLUSIONS: Athletes across all disciplines reported drinking less fluid during training than currently espoused in hydration guidelines. A coach's encouragement to drink, the number of pauses during training, and bout duration each influence total fluid volume consumed, regardless of competition level, sex or the age of an athlete.
... Self-report (SR) has been the primary method used to assess fluid intake during endurance events, primarily because of the difficulties associated with assessing hydration practices for a large group of people. 11 While some studies have assessed fluid consumption directly or via researcher observation, [12][13][14][15] sample sizes have generally been small and these studies did not compare their methodology with SR. We are aware of only 1 study that compared direct measurement (DM) to perceived fluid consumption that occurred during a simulated 10-mile running race. ...
Self-report (SR) has been the primary method used to assess fluid intake during endurance events, but unfortunately, little is known about the validity of SR. The purpose of this study was to compare SR fluid intake to direct-measurement (DM) during the run of a 70.3-mile triathlon. Fifty-three (42 men, 11 women) individuals competing in a 70.3-mile triathlon participated in the study. On the 13.1-mile run, 11 research stations provided fluid in bottles filled with 163 ml of water or carbohydrate-electrolyte beverage (CEB). Participants submitted bottles 25 meters past aid stations to be reweighed post-race. Participants also answered questions regarding fluid intake post-race. Bland-Altman plots and 95% limits of agreement (LOA) were used to assess precision of the measures, while least-squares regression assessed linear agreement. SR intakes during the run ranged from 0-1793, 0-1837, and 0-2628 ml for water, CEB, and total fluid, with corresponding DM intakes of 0-1599, 0-1642, and 0-2250 ml. DM and SR showed strong linear agreement for water, CEB, and total fluid (R2 = 0.71, 0.80, and 0.80). Mean differences between the measures on the Bland-Altman plots were small (13-41 ml), but relatively large differences (± 500 ml) between the measures were apparent for some participants. SR is the predominant methodology used in field studies assessing hydration, despite little-to-no data confirming its validity. The results herein suggest that choosing a fluid intake assessment methodology should be done on a case-by-case basis and that caution should be utilized when interpreting data based on SR.
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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.
Participants in marathon races may require medical attention and the performance of laboratory assays. We report the changes in basic biochemical parameters, cardiac markers, CBC counts, and WBC differentials observed in participants in a marathon before, within 4 hours, and 24 hours after a race. The concentrations of glucose, total protein, albumin, uric acid, calcium, phosphorus, serum urea nitrogen, creatinine, bilirubin, alkaline phosphatase, alanine aminotransferase, aspartate aminotransferase, total creatine kinase, creatine kinase-MB, myoglobin, and the anion gap were increased after the race, consistent with the effects of exertional rhabdomyolysis and hemolysis. The increase in WBC counts was due mainly to neutrophilia and monocytosis, with a relative decrease in circulating lymphocytes, consistent with an inflammatory reaction to tissue injury. A significant percentage of laboratory results were outside the standard reference ranges, indicating that modified reference ranges derived from marathon runners might be more appropriate for this population. We provide a table of modified reference ranges (or expected ranges) for basic biochemical, cardiac, and hematologic laboratory parameters for marathon runners.
Early human ancestors evolved hunting in the midday heat on the dry African savannah and developed favourable biological adaptations that permit prolonged running in the heat. These physiological adaptations must have included the capacity to sweat profusely to maintain a low body temperature when running for 4–6 hours in dry heat, an absence of adverse consequences from developing mild to moderate fluid deficits caused by sweat losses during the hunt, a serum osmolality based thirst mechanism and the ability to ‘outrun their thirst’ (to resist the deleterious psychological and other effects of severe thirst). Until the early 1970s, the guidelines for fluid ingestion during exercise were not to drink and are consistent with this interpretation. By 1996, guidelines stated, “individuals should be encouraged to consume the maximal amount of fluids during exercise that can be tolerated without gastrointestinal discomfort up to a rate equal to that lost from sweating,” and this was interpreted by some as “to drink as much as tolerable.” This article argues that humans are designed to drink just enough to maintain plasma osmolality, not necessarily bodyweight, both at rest and during exercise. Drinking to maintain bodyweight may impair exercise performance by inducing a weight penalty and may increase the probability of exercise-associated hyponatraemia in slow marathon runners.
Four athletes developed water intoxication (hyponatremia) during endurance events lasting more than 7 h. The etiology of the condition appears to be voluntary hyperhydration with hypotonic solutions combined with moderate sweat sodium chloride losses. The reason why the fluid excess in these runners was not corrected by increased urinary losses is unknown. When advised to drink less during prolonged exercise, three of the athletes have subsequently completed prolonged endurance events uneventfully. (C)1985The American College of Sports Medicine
Background: Disorders of body fluids are among the most commonly encountered problems in the practice of clinical medicine. This is in large part because many different disease states can potentially disrupt the finely balanced mechanisms that control the intake and output of water and solute. It therefore behooves all clinicians treating such patients to have a good understanding of the pathophysiology, the differential diagnosis and the management of these disorders. Since body water is the primary determinant of the osmolality of extracellular fluid, disorders of body water homeostasis can be divided into hypoosmolar disorders, in which there is an excess of body water relative to body solute, and hyperosmolar disorders, in which there is a deficiency of body water relative to body solute. The classic hyperosmolar disorder is diabetes insipidus, and the classic hypoosmolar disorder is the syndrome of inappropriate antidiuretic hormone secretion. Conclusions: Despite the complexity of this regulatory system, most disorders of water homeostasis can be understood by applying knowledge of the physiology and pathophysiology of arginine vasopressin (AVP) secretion and effects, as summarized in the ten essential points of this review. Understanding therapy for disorders of water homeostasis, including appropriate use of the new AVP receptor antagonists, can similarly be best understood by appreciating these same essential points.