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Does Dehydration Impair Exercise Performance?
PREVAILING VIEW
Dehydration (water deficits of >2% body mass, BM)
degrades aerobic exercise performance in temperate
and warm-hot environments. This prevailing view is
supported by:
1. observations made on individuals performing
arduous work, with limited fluids, in warm-hot
environments;
2. the vast majority of experimental data from
laboratory and field studies in temperate and
warm-hot environments;
3. paucity of experimental data indicating otherwise;
and
4. ‘expert’’ panels performing comprehensive litera-
ture reviews.
Comment
Total body water (TBW) fluctuates within ~0.5% of
BM or more, thus ‘‘euhydration’’ represents a continu-
um for which no one absolute or ‘‘true’’ TBW value can
be assigned (31). A determination must therefore be
made of body water fluctuations beyond the ‘‘normal’
range that have a consistent deleterious functional
outcome (1). Cheuvront and colleagues (16) proposed
that a water deficit of >2% of BM falls beyond the
normal TBW fluctuation and consistently demonstrates
a reduction in endurance exercise performance. Bio-
logical variation will allow some individuals to be more
or less tolerant to the adverse consequences of
dehydration; however, this is not the topic of debate.
Review of Literature
Experimental Studies—Support
Twenty-eight studies support the prevailing view
that dehydration degrades aerobic exercise perfor-
mance. These consistent findings were observed despite
the studies employing a broad range of experimental
CHALLENGING VIEW
It is definitively established that some humans who
either (i) begin an exercise test with unreplaced acute
fluid losses induced, for example, by prolonged (6 h)
exposure to either a hot environment (19) or to
prolonged (2 h) prior exercise in uncomfortable heat
during which they did not ingest any fluid (21) or after
pretreatment with a diuretic that increases urinary water
and electrolyte losses (2) by inducing the uncomfort-
able symptoms of polyuria; or who (ii) drink either
nothing or little during exercise [for example, (10,
33,59,75)], will show a measurably impaired exercise
performance. Since I am a coauthor of two studies
(23,78) showing this effect under more realistic
experimental conditions, it would be disingenuous to
deny that it exists. Indeed I have recently written that:
‘these data clearly support the conclusion that not
drinking at all during exercise is likely to impair
exercise performance especially during prolonged
exercise in the heat’ (50).
Thus there is no need to debate whether or not the
exercise performance of some individuals will be impaired
if they either begin exercise in a state in which their total
body water content (TBW) has been artificially reduced or
if they are not allowed to drink during exercise. Rather my
argument is that the results of these experiments have been
interpreted according to a simplistic model of human
physiology. Here I argue that it is the development of thirst
that impairs exercise performance so that athletes who
drink sufficiently to prevent thirst during exercise will
optimize their performance regardless of the extent to
which their TBW is reduced or the extent to which they
become ‘‘dehydrated.’’ I present my argument by address-
ing four fundamental questions:
i. Of what relevance are most of these ‘‘classically
cited studies’’ to the real world of competitive sport
and recreational exercise?
ii. What is the optimal experimental design to study
the effects of ‘‘dehydration’’ on exercise perfor-
mance?
iii. What biological mechanism(s) likely explain this
effect?
iv. On the basis of this information, how should we
advise athletes to drink during exercise?
Contrasting
Perspectives
Contrasting Perspectives in Exercise Science & Sports Medicine
0195-9131/07/3908-1209/0
MEDICINE & SCIENCE IN SPORTS & EXERCISE
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7
methods regarding dehydration/rehydration procedures,
aerobic exercise tasks and environmental conditions.
During World War II, U.S. military forces fought in hot-
tropic and hot-desert environments and it was observed
that fluid consumption influenced their operational
effectiveness. Such observations stimulated an initial
series of controlled laboratory (6,59) and field (10)
studies that demonstrated that dehydration degrades
aerobic exercise performance (outdoor hikes, treadmill
walks) in warm-hot environments.
During the next five decades, other investigators,
employing more sophisticated laboratory exercise/per-
formance tests, consistently reported that dehydration
degrades aerobic exercise performance in temperate
environments (5,7,12–14,17,25,29,37,41,46,61,63,70)
and warm-hot environments (19,33,57,58,70,78). In
addition, investigators employing fieldlike evaluations
reported that dehydration degrades aerobic exercise
performance while in temperate (2,79) and warm-hot
(43,72,75) environments. Of note are the findings that
the greater the dehydration level, the greater the
degradation in aerobic exercise performance (19,58).
Also larger and more consistent degradations in aerobic
exercise performance were observed in warm-hot
environments than temperate environments.
Supporting Exemplars
The following experimental exemplars employed differ-
ent methods, but reached conclusions supporting the
prevailing view. Two studies were selected employing
increasing intensity performance tests, one study was
conducted in a temperate environment (46) and the other
study was conducted in a hot environment (19). In
addition, three studies were selected employing constant
intensity exercise followed by volitional effort perform-
ance tests (at submaximal work rates), with one study
conducted in a temperate environment (17), and the other
studies conducted in warm-hot environments (7,78).
Nielsen et al. (46) had subjects perform cycle
exercise to exhaustion (by increasing power output to
105% V
˙O
2max
) in temperate conditions when euhy-
drated and when dehydrated by ~2.5% BM. Three
dehydration trials were conducted with water deficits
achieved by prior heat exposure, prior exercise or
diuretic administration. Dehydration reduced the total
work performed by 18%–44% for the three trials. Craig
and Cummings (19) had subjects walk to exhaustion
(by increasing treadmill grade) in hot conditions when
euhydrated and when dehydrated by ~2% BM and ~4%
BM. Subjects dehydrated by prior resting heat exposure
with restricted water intake. Total exercise time was
reduced by 22% and 48%, while V
˙O
2max
was reduced
by 10% and 22% when dehydrated by 2% and 4% BM,
respectively.
There are two features common to the conduct of
many laboratory experiments performed in applied
exercise science. First, studies are usually (and cor-
rectly) designed to establish the biological consequen-
ces of a specific intervention; for example, the effects
of a preexercise reduction in TBW or a restricted fluid
intake on physiology and exercise performance.
But the design of these experiments often enforces
behaviors that athletes would never adopt during either
competitive sport or recreational exercise. Yet the
authors of these studies usually generalize the study
findings to real-world conditions that were not simu-
lated in the original experiments.
For example, no athlete other than those involved in
sports involving weight categories, would start exercise
after spending 6 h in a hot, dry environment without
drinking as was the case in the study of Craig and
Cummings (19). Nor would they ‘‘warm up’’ by
exercising for 2 h without drinking as occurred in the
study of Dougherty et al. (21). Nor, unless they were
under treatment for hypertension, would they consider
exercising after the acute administration of a diuretic as
in the study of Armstrong et al. (2). Nor would many
modern athletes exercise with enthusiasm for any
length of time if they knew beforehand that they would
be forced to drink less than their thirst dictates, as in
many of the original classical studies (2,10,33,59,75).
Second, the findings of these studies are inevitably
interpreted according to the philosophy of reductionism
(52) and according to a simplistic model of exercise
physiology (53). So it is usually assumed that any
measured performance impairment must be caused
exclusively by the variable that is most usually measured,
namely the level of ‘dehydration’’ that develops before
or during exercise. Then the conclusion is generalized
that performance in any form of exercise, regardless of
circumstance, will always be impaired whenever that
specific (critical) level of ‘‘dehydration’’ is exceeded. But
exercise performance is a complex phenomenon that is
seldom regulated by a single variable (74).
Studies that most obviously invite this criticism of
reductionism are those in which ‘‘dehydration’’ is
induced with diuretics. One frequently referenced study
(2) failed to include controls to measure any direct
effect of the drug on exercise performance. Rather it
was presumed that the drug acts exclusively by
reducing the TBW. But athletes cannot begin an
exercise bout in an ideal frame of mind if they have
spent the previous 4 h repeatedly relieving themselves
of the uncomfortable symptoms caused by polyuria.
Similarly athletes who begin an exercise session
knowing that they will not receive any fluid, will have a
different mental attitude than if they knew beforehand
that they would be allowed to drink freely. For
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Cheuvront et al. (17) had subjects perform cycle
exercise 30 min at constant intensity (~50% V
˙O
2max
)
followed by a constant duration performance time trial
(total work completed in 30 min) in a temperate
environment. Subjects were dehydrated (3% BM) by
resting heat exposure with restricted fluid replacement.
Dehydration reduced the total work completed by 8%.
Below et al. (7) had subjects perform cycle exercise
for 50 min at constant intensity (~80% V
˙O
2max
)
followed by a constant work performance test (time to
complete a set amount of work) in warm-hot conditions.
Subjects either replaced (0.5% BM loss) or under-
replaced (2% BM loss) their sweat losses during
these exercise sessions. Dehydration reduced the total
work completed by 7%. Walsh and colleagues (78)
had subjects perform cycle exercise (70% V
˙O
2max
)
for 60 min followed by a performance test (time to
exhaustion at 90% V
˙O
2max
) in a warm-hot environ-
ment. Subjects either replaced or underreplaced (2%
BM loss) sweat losses during these exercise sessions.
Dehydration reduced the time to exhaustion by 31%.
Experimental Studies—Nonsupport
No study disagreed with the prevailing view in
warm-hot environments. Seven studies found that
dehydration did not degrade aerobic exercise perform-
ance in temperate environments. Four of these studies
employed marginal (G2% BM) dehydration levels
(3,9,36,38). Therefore, only three studies (30,62,71)
report data that may refute the prevailing view. One of
those studies (71) employed an activity with a
substantial anaerobic component (~4 min of high-
intensity rowing) and dehydration does not degrade
anaerobic exercise performance (31). Another study
(62) reported that subjects complained of stomach
fullness during the fluid replacement trials so discom-
fort may have confounded their results.
The last study (30) not support the prevailing view
employed maximal aerobic power (V
˙O
2max
) as their only
index of aerobic exercise performance. Dehydration
consistently degrades V
˙O
2max
in warm-hot environments
(19,57), but in temperate environments V
˙O
2max
either may
(9,13,14) or may not (9,13,14) be degraded. However,
investigators who observed no change in V
˙O
2max
with
dehydration but who included other indices of aerobic
exercise performance, have all reported that dehydration
degraded that other index (2,14,63). Therefore, the data
from Houston and colleagues (30) does not necessarily
refute the prevailing view.
Expert Panels—Support
Three ‘‘expert’’ panels have been established to
evaluate scientific evidence regarding several hydration
example, our as yet unpublished study (22) found that
subjects aware at the start of exercise that their fluid
intakes during exercise would be restricted, began the
exercise bout at a lower exercise intensity than when
they knew they could drink without restriction. Since
this effect was present at the outset of exercise, it could
not be due to ‘‘dehydration’’ but was due to a
behavioral change ‘‘in anticipation’’ of the exercise
bout. We have indeed shown that exercise performance
in the heat is regulated ‘‘in anticipation’’ (77).
If we do not understand all the factors that alter
exercise behavior ‘‘in anticipation,’’ it is presumptuous
to assume that alterations in exercise performance
produced by interventions imposed before the exercise
bout, can all be explained by a single variable,
‘dehydration,’’ measured during exercise.
Since we cannot separate the effect on subsequent
exercise performance of the interventions that produce
the ‘‘dehydration’’ from any effects resulting directly
from that ‘‘dehydration,’’ it follows that only studies in
which the ‘‘dehydration’’ develops during exercise
provide a valid measure of the direct effects of
‘dehydration.’’ Furthermore, since the natural behavior
is to drink ad libitum during exercise, that is, in
response to the dictates of thirst, it follows that the
control drinking condition in all experiments must be
the ad libitum condition.
Whereas such experiments will establish the drinking
behavior that optimizes exercise performance, yet they
cannot easily determine the exact mechanism explaining
this effect. For it is difficult to exclude the possibility
that the impaired exercise performance is part of the
thirst mechanism regulated centrally in the brain as part
of a complex and intelligent control system (74).
For example, our model of exercise regulation
(52,74) theorizes that sensory feedback from multiple
organs and tissues regulates the extent of skeletal
muscle recruitment during exercise and in this way
the exercise intensity that can be sustained. According
to this model, thirst, like the rating of perceived
exertion (73), acts as the conscious perception of a
developing cellular homeostatic disturbance (in this
case an unacceptable increase in plasma osmolality due
to a large reduction in TBW) to induce two crucial
behavioral changes, the goal of which are to limit the
extent of this disturbance. These behavior changes are
(i) an increase in drinking and (ii) a reduction in the
exercise intensity (until the moment the athlete
addresses the cause of the homeostatic disturbance by
starting too drink appropriately).
The essential component of this model is that it
predicts behavior change (increased drinking and
altered exercise intensity) before a catastrophic failure
of homeostasis develops (53). We have shown that this
Contrasting
Perspectives
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issues. The Institute of Medicine, National Academies
of Science appointed a panel on dietary reference
intakes for water and electrolytes that concluded that
dehydration ‘‘adversely influences aerobic exercise
tasks’’ (31). The American College of Sports Medicine
appointed two panels to conduct Strength of Recom-
mendation Taxonomy analyses on hydration issues, and
those panels both concluded (with highest strength of
support rating) that dehydration degrades aerobic
exercise performance (1,15).
Summary
There is overwhelming support from experimental
studies demonstrating that dehydration (>2% BM)
degrades aerobic exercise performance in temperate
and warm-hot environments. Any effective argument
against this prevailing view must be supported by
sound experimental studies demonstrating otherwise.
REPLY TO CHALLENGING VIEW
Dr. Noakes makes two points: 1) he concedes that
‘some’’ humans who dehydrate before or during
exercise will suffer impaired performance and con-
cludes there is ‘‘no need to debate’’ that issue, and 2) he
then argues that dehydration experiments should not be
interpreted ‘‘according to a simplistic model of human
physiology,’’ and it is ‘‘the development of thirst that
impairs exercise performance.’
Concession that Dehydration Impairs
Exercise Performance
Regarding the first point, use of the adjective
‘some’’ subjects implies less than the vast majority
and unfairly understates the overwhelming conclusion
of experimental studies that dehydration (>2% BM)
degrades aerobic exercise performance. In addition,
performance degradation was consistently demonstrat-
ed in studies employing a broad range of fluid loss and
rehydration (including drinking during exercise) meth-
odologies, which only strengthens the prevailing view.
‘Simplistic Model of Human Physiology’’?
Physiological mechanisms explaining dehydration-
mediated performance decrements are not simplistic
and they include augmented hyperthermia (18),
increased cardiovascular strain (39,40), reduced skele-
tal muscle blood flow (27), altered skeletal muscle
metabolism (increased glycogen utilization and lactate
accumulation) (28), altered EMG patterns (8), and
increased perception of effort (39) during exercise.
Though each physiological mechanism is unique,
evidence suggests they contribute in an integrated and
multifactorial manner to degrade performance (67). The
complex, intelligent model adequately explains the brain_s
behavioral response to the stress of exercise in the heat
(77). But traditionally taught exercise physiologists who
fail to understand the anticipatory nature of these controls
will conclude incorrectly that the very endpoint that the
brain wishes to avoid—in this case a marked rise in
plasma osmolality consequent to a large reduction in
TBW (‘‘dehydration’’)—is, in their interpretation, the
singular cause of the altered exercise performance.
Presently the published literature includes six studies
[Table II in (50)] with an appropriate experimental
design (4,7,20,22,37,38) to distinguish (i) the direct
effects of dehydration from those potentially due to the
techniques inducing the ‘‘dehydration’’ and (ii) the
possible role of thirst as a regulator of the exercise
response. These studies allow a precise conclusion: In
no study did drinking more fluid than that dictated by
thirst (and which result in lower levels of ‘‘dehydra-
tion’’) produce a superior performance than did ad
libitum drinking (according to the dictates of thirst).
Hence, these studies support the predictions of the
model that holds that thirst functions also to modulate
the exercise performance as part of an anticipatory
control and that drinking ‘‘beyond thirst’’ to prevent
‘dehydration’’ will not produce a superior response.
The finding that drinking according to the dictates of
thirst optimizes exercise performance (50) suggests that
the absolute level of ‘‘dehydration’’ does not explain
why underdrinking during exercise impairs perform-
ance. Were this the case then all athletes would develop
an identical level of ‘‘dehydration’’ when ingesting
fluid ad libitum during exercise. This level would be
somewhat less than the critical value that some believe
impairs exercise performance (21). But this is clearly
not the case. Rather our study [Fig. 1 in (15)] found that
athletes competing in endurance events in which fluids
are provided ad libitum, finish with body weight (BW)
changes that vary from a loss of -11% BW to a gain of
+6% BW. We have also provided evidence that genetic
factors regulating the thirst response might explain this
highly individualistic response (64).
Thus we have proposed that correct drinking during
exercise influences performance by preventing thirst,
the development of which alters the exercise behavior
in an anticipatory manner as part of a regulatory
process. Provided the athlete is not thirsty, we speculate
that a level of ‘‘dehydration’’ even up to -11% BW
might not impair exercise performance (68,69).
This is simple: Drink according to the dictates of
thirst. If you are thirsty, drink; if not, do not. All the
rest is detail.
Imprecise experimental design and the interpretation
of research studies according to a simplistic model of
human physiological function during exercise, do not
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relative contribution of each mechanism likely differs
depending on the exercise task, environment, and
athlete_s biomedical state, but augmented hyperthermia
appears critical to performance degradation.
Dehydration augments hyperthermia (at a given
metabolic rate) during aerobic exercise in temperate
and warm-hot environments (11,65). The augmented
hyperthermia is proportionate to the magnitude of water
deficit (39,40,66). Dehydration augments hyperthermia
by reducing heat dissipation, as both sweating (42,66)
and skin blood flow (32,45) are reduced for a given
core temperature. Dehydration from sweat losses will
increase plasma osmolality and decrease plasma vol-
ume in proportion to the magnitude of body water
deficit (31). Hyperosmolality and hypovolemia both
exert separate and combined effects on reducing heat
dissipation and thus augmenting hyperthermia when
dehydrated (18).
Hyperthermia alone increases cardiovascular strain,
alters skeletal muscle metabolism (26), reduces cerebral
blood flow and alters brain metabolism (56), alters
CNS activity (55), attenuates muscular force genera-
tion (54), and increases perception of effort. These
physiological events elicited by hyperthermia alone
are similar to the physiological events elicited by
dehydration, which augments hyperthermia. Finally,
experimental evidence on hyperthermia mediated phys-
iological events and associated laboratory performance
test degradation are supported by analyses demonstrat-
ing that actual marathon race performance is progres-
sively degraded with increasing environmental heat
stress (24).
‘Thirst Impairs Exercise Performance’’?
Dr. Noakes notion that ‘‘it is the development of
thirst that impairs exercise performance—as part of an
anticipatory control’’ is not necessarily consistent with
known physiology and lacks experimental support.
First, many key physiological signals (hyperosmolality,
hypovolemia) for thirst are the same signals mediating
augmented hyperthermia and cardiovascular strain from
dehydration (34). Second, I am unaware of data
supporting that thirst is a feed-forward process that
either precedes any osmotic-volume signals or dehy-
dration, or if occurring alone will mediate physiological
events consistent with performance degradation. Third,
of the six studies claimed to support the ‘‘thirst impairs
performance’’ notion, no study measured thirst, three
studies (4,7,38) did not achieve dehydration >2% BM,
three studies (7,37,38) did not employ ad libitum
drinking trials, and two studies (4,20) had overdrinking
causing uncomfortable gastric fullness, likely impact-
ing performance. Fourth, it is difficult to be convinced
that 11% BM dehydration does not degrade aerobic
allow the conclusion that the level of ‘‘dehydration’’ is
the exclusive cause of any impaired exercise perfor-
mance measured in subjects who begin exercise with
either a reduced TBW or who drink less than their thirst
dictates during exercise. A more defendable conclusion
is that any impairment may be a component of the thirst
mechanism, regulated centrally in the brain, the goal of
which is to ensure that athletes do not damage their
health by continuing to exercise while drinking too
little during exercise. In which case the prevention of
thirst rather than ‘‘dehydration’’ will optimize exercise
performance.
REPLY TO PREVAILING VIEW
The key point in my challenging perspective was
that scientists have used a simplistic (reductionistic)
model of exercise physiology to interpret the results of
studies to determine whether ‘‘dehydration’’ alters
exercise performance. But when interpreted according
to a complex model of human exercise performance
(74), their usual experimental designs cannot prove that
a specific level of ‘‘dehydration’’ is the direct cause of
impaired exercise performance in all humans. These
designs cannot disprove the alternate theory that the
sensation of thirst, acting as part of an anticipatory
regulatory system, alters the exercise behavior in those
who either begin exercise in a ‘‘dehydrated’’ state or
who drink less than their thirst dictates.
Rather, I proposed that exercise performance is
maximized by drinking according to the dictates of
thirst (ad libitum) (50). Since ad libitum drinking which
optimizes performance does not produce identical
levels of dehydration in all humans during exercise,
but can lead to changes in per cent body weight (BW)
ranging from a gain of 6% to a loss of 11% (51), then
the conclusion that a specific level of dehydration, say
a BW loss of 2%, will always cause an impaired
exercise performance in all humans cannot be correct.
Instead I argue that any impaired exercise performance
in ‘‘dehydrated’’ subjects must be causally linked to the
thirst mechanism, not to the level of ‘‘dehydration’
(since in the absence of thirst exercise performance
may not be impaired, regardless of the level of
‘dehydration’’ that is present).
I also argue that the level of ‘‘dehydration’’ (detected
as a change in plasma osmolality) will be one of the key
homeostatic variables that a complex system will actively
regulate during exercise. According to this interpretation,
‘dehydration’’ is not the direct ‘‘cause’’ of an impaired
exercise performance. Rather, exercise performance is
modified (impaired) under certain stressful conditions in
order to ensure that the osmolality of the brain remains
within the homeostatic range. To restate the argument:
Contrasting
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exercise when it is unclear if hydration levels were
carefully determined and when there are no experi-
mental controls to verify that performance was pre-
served (68,69).
CONCLUDING STATEMENT
Dehydration (water deficits of >2% BM) consis-
tently degrades aerobic exercise performance in tem-
perate and warm-hot environments. Physiological
mechanisms contributing to dehydration-mediated per-
formance degradation include augmented hyperthermia,
increased cardiovascular strain, altered metabolic and
central nervous system functions, and increased per-
ception of effort. Dr. Noakes may not agree with
conventional physiological models explaining dehydra-
tion mediated performance degradation, but his alter-
nate notion awaits supportive experimental evidence.
An unacceptable reduction in the total body water
content is the endpoint that the brain must avoid if it is
not to be damaged by a profound rise in intracellular
osmolality. Thus, the brain must regulate the athlete_s
behaviors ‘‘in anticipation’’ to ensure that only accept-
able levels of ‘‘dehydration’’ develop during exercise.
Progressively more severe thirst will increase the
athlete_s discomfort leading to an involuntary reduction
in the work rate. Ultimately the athlete will chose to
stop exercising and to seek fluids.
Finally, this interpretation explains two phenomena
that the promoters of the ‘‘dehydration hypothesis’’ (48)
chose to ignore that: 1) elite athletes appear not to drink
very much during exercise (44,47) and 2) the fastest
finishers in endurance events are often among the most
dehydrated (17,44,60,68,69,80). If these athletes are less
likely to become thirsty as a result of genetic variance
(64), then this paradox is more easily understood.
Dr. Sawka_s prevailing perspective is carefully con-
structed and accurately reviews the state of knowledge in
this field. But the data have been interpreted according
to the conventional reductionistic model of exercise
physiology that I consider simplistic. Thus, it is not
the findings that are wrong, merely how they have
been interpreted. For when interpreted according to the
predictions of a complex regulatory system, nothing in
Dr. Sawka_s review disputes my conclusions.
Thus, his first three exemplar studies (16,19,46) all
show that exercise performance is impaired in those
who begin exercise in a ‘‘dehydrated’’ state induced by
different interventions. Logically, neither these nor any
other experimental design can determine whether it is
the development of thirst or the ‘‘dehydration’’ produced
by these interventions that impairs subsequent exercise
performance.
However, the finding by Dr. Sawka and his colleagues
(16) that prior ‘‘dehydration’’ impairs subsequent exercise
performance in the heat but not in the cold, is more easily
explained by a complex intelligent system that uses the
thirst mechanism to regulate the exercise performance.
For the measured biological responses to exercise in
that study were remarkably similar in both the heat and
the cold, regardless of each subject_s level of hydration.
This proves that the impaired exercise performance in
the ‘‘dehydrated’’ condition was not caused by those
commonly measured variables, such as increased
cardiovascular ‘‘strain’’ or accelerated hyperthermia,
which are usually invoked to explain how ‘‘dehydra-
tion’’ impairs exercise performance (17).
Instead the ratings of perceived exertion (RPE) were
identical in all exercise conditions despite differences in
exercise performance. But since ‘‘dehydrated’’ subjects
exercised at a lower work rate in the heat, their RPE
must have been ‘‘upregulated’ by the presence of thirst
Contrasting
Perspectives
Michael N. Sawka
U.S. Army Research Institute of
Environmental Medicine
Natick, MA
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7
or by ‘‘dehydration,’’ or by both. This regulatory
mechanism insures that the exercise work rate is reduced
‘in anticipation’’ (35), presumably to ensure that the
brain is protected from a large change in its osmolality.
We have repeatedly argued that the RPE is used by
the complex intelligent system to ensure that humans
terminate exercise while still in homeostasis (49,76,77).
Thus, the study of Dr. Sawka and his colleagues (16)
confirms that ‘‘dehydration’’ modifies the RPE
response to exercise as would be expected if a complex
system regulates human exercise performance.
During the other two exemplar studies invoked by
Dr. Sawka, subjects drank either nothing (78) or less
than the usual ad libitum volumes (5) during exercise.
Thus, neither conflicts with our hypothesis that it is
thirst acting ‘‘in anticipation’’ that modifies exercise
performance specifically to limit the extent to which
the brain_s osmolality changes during exercise.
CONCLUDING STATEMENT
We propose that, as part of a complex system of
exercise regulation (74), the symptom of thirst acts ‘‘in
anticipation’’ to regulate the exercise performance in
those who drink less than is necessary to maintain an
acceptable level of homeostasis. According to this
interpretation, it is not the level of ‘‘dehydration’’ that
impairs exercise performance; rather, the exercise
performance is altered to limit the extent to which the
osmolality of the brain increases. As a result, damaging
levels of ‘‘dehydration’’ are not reached by those who
drink according to the dictates of their thirst during
exercise. Nor will their performance be altered.
Contrasting
Perspectives
Timothy D. Noakes
University of Cape Town
Department of Human Biology
Sports Science Institute of South Africa
South Africa
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libitum?’
... In addition to water loss, sweating also leads to significant losses of electrolytes such as sodium and potassium, which are critical for nerve and muscle function. Imbalances in electrolyte levels can disrupt the electrical activity of nerves and muscles, impairing muscle contraction [33] . Sodium depletion, in particular, has been associated with muscle cramping and weakness during prolonged exercise. ...
... Shirreffs et al. (2007) suggested that consuming fluids with electrolytes, particularly sodium, is more effective at preserving neuromuscular function than water alone, as it better compensates for electrolyte losses through sweat. Previous research has demonstrated the positive effects of hydration on overall performance during endurance sports Cheung, Sleivert, & McLellan, 1998) [33,8] . However, the specific impact of hydration on neuromuscular function, particularly during prolonged bouts of exercise, is still being explored. ...
... Our findings build on this knowledge, demonstrating that fluid ingestion helps mitigate the decline in MVC by maintaining hydration, supporting blood flow, and preserving thermoregulation. The greater reduction in MVC in the DEHYD condition also suggests that dehydration impairs muscle contractility by disrupting the balance of electrolytes, such as sodium and potassium, which are essential for generating action potentials and muscle contractions [33] . Dehydration-induced electrolyte imbalances can result in muscle cramps, a common symptom of fatigue during endurance exercise, further reducing performance. ...
... For athletes of any age, negative effects on athletic performance have been demonstrated even with modest dehydration (2%) [5]. With dehydration, the sweat rate decreases, and thermoregulation and cardiovascular function are impaired, leading to increased heart rate, subjective perception of effort, and core body temperature [6]. ...
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(1) Background: Since older adults are more susceptible to dehydration and there is a lack of information on older athletes, this study observed a group of 12 male padel players in this age group (70.42 ± 3.50 years) to characterize their hydration habits, physiological demands, and psychological responses before and during a 90 min padel training (PT). (2) Methods: After approval from the Ethics Committee (CE/FCDEF-UC/00022023) and the provision of signed informed consent, participants’ body mass, height, waist and hip circumferences, body mass index, waist-to-hip ratio, and waist-to-height ratio were measured. Habitual fluid intake was monitored by diary from the evening until before the PT; the subjects completed a Profile of Mood States questionnaire (POMS) and a satiety scale (SLIM). To assess hydration levels at different moments, we used a portable osmometer and an eight-point urine color chart and weighed the participants immediately before and after the PT. During the PT, heart rate (HR) and hydration were monitored. After the PT, subjects completed another POMS and SLIM. (3) Results: Subjects trained at 73.2 ± 12.3% of their maximum HR, with brief peaks at the anaerobic threshold or higher (130.00 ± 18.78 bpm). The mean urine osmolality indicated normal hydration or minimal dehydration. However, the urine color values indicated dehydration after the training. Subjects drank 438 mL of liquids at night, 333 mL before PT, and 900 mL during the PT, with a good repartition of the liquids. POMS and SLIM were not affected by the training. (4) Conclusions: Older male padel athletes achieved challenging yet safe training, staying within healthy intensity zones; their hydration patterns nearly met the recommendations for exercise and should be slightly increased.
... The interaction between myosin and actin proteins is enabled by calcium, a key component of muscle contraction [25]. As a result, an efficient hydration strategy must be developed to avoid a significant negative impact on both aerobic performance [26] and athlete health [27] as a result of progressive dehydration [28]. In light of this, our study hypothesis is that DSW contains a significant amount of minerals, which are essential for physical exercise; therefore, its consumption during sports events may preserve muscle functional capacity after exercise. ...
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(1) Background: Trainers and athletes have always sought to reduce the failure of muscle function during long endurance events. However, nowadays, it is a topic that is generating much debate in the scientific field. Currently, deep-sea water (DSW) intake seems to be a suitable hydration alternative for this type of endurance event. Therefore, the aim of this study was to determine whether DSW consumption during a triathlon event could preserve muscle function after exercise. (2) Methods: Nineteen trained male triathletes (age = 39.0 ± 4.25 years; BMI = 23.67 ± 1.81 kg/m²) randomly performed three triathlons, one of them consuming DSW (Totum SPORT 30 AB, Laboratories Quinton International, S.L., Spain), the other consuming isotonic placebo and the last with tap water-hydration. A vertical jump test with countermovement and an isometric muscle strength test were conducted before and after the triathlon test. (3) Results: There was a significant difference between treatment × time during the isometric muscle strength test. Based on the Tukey post hoc analysis, the peak net force decreased statistically in the placebo (p = 0.045) and control conditions (p = 0.026), but not in the experimental condition (p = 0.121). In addition, all of the conditions studied obtained similar results in the countermovement vertical jump after exercise. (4) Conclusions: As a result, consumption of DSW seems to delay the failure of muscle function specifically in isometric exercises but does not improve performance in sports. Thus, DSW does not alter muscle capacity in a negative way; therefore, its consumption may be recommended.
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Background To mitigate health risks associated with occupational heat stress, workers are advised to adhere to a work‐rest regimen, and hydrate regularly. However, it remains unclear if beverage temperature influences whole‐body heat exchange during work‐rest cycles, and if responses differ in older workers who have a blunted heat loss capacity. Methods Ten young (mean [SD]: 22 [3] years) and 10 older (60 [4] years) males performed four 15‐min bouts of moderate‐intensity cycling at a fixed rate of metabolic heat production (200 W·m ⁻² ), each interspersed by 15‐min rest in dry heat (40°C, ~12% relative humidity). On separate days, participants consumed either ice‐slurry (~0°C), standardized to provide a heat transfer capacity of 75 kJ·m ⁻² , or an identical mass of warm fluid (37.5°C) before the first and third exercise bouts. Evaporative and dry heat exchange (direct calorimetry) and metabolic heat production (indirect calorimetry) were measured continuously to determine cumulative heat storage (summation of heat loss and heat gain) over the entire protocol. Rectal temperature was also measured continuously. Results Relative to warm fluid, ice‐slurry ingestion reduced cumulative heat storage in young (69 [181] vs. 216 [94] kJ) and older males (90 [104] vs. 254 [140] kJ, main effect: p < 0.01), but was unaffected by age ( p = 0.49). However, rectal temperature was unaffected by beverage temperature in both groups (all p ≥ 0.15). Conclusion We show that cold fluid ingestion is an appropriate administrative control for both young and older males as it can mitigate increases in body heat content during moderate‐intensity work‐rest cycles in dry heat.
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