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Review
Rehydration during Endurance Exercise: Challenges, Research,
Options, Methods
Lawrence E. Armstrong
Citation: Armstrong, L.E.
Rehydration during Endurance
Exercise: Challenges, Research,
Options, Methods. Nutrients 2021,13,
887. https://doi.org/10.3390/
nu13030887
Academic Editor: Ajmol Ali
Received: 11 February 2021
Accepted: 1 March 2021
Published: 9 March 2021
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4.0/).
Human Performance Laboratory and Korey Stringer Institute, University of Connecticut,
Storrs, CT 06269-1110, USA; Lawrence.Armstrong@Uconn.edu
Abstract:
During endurance exercise, two problems arise from disturbed fluid–electrolyte balance:
dehydration and overhydration. The former involves water and sodium losses in sweat and urine
that are incompletely replaced, whereas the latter involves excessive consumption and retention of
dilute fluids. When experienced at low levels, both dehydration and overhydration have minor or no
performance effects and symptoms of illness, but when experienced at moderate-to-severe levels they
degrade exercise performance and/or may lead to hydration-related illnesses including hyponatremia
(low serum sodium concentration). Therefore, the present review article presents (a) relevant research
observations and consensus statements of professional organizations, (b) 5 rehydration methods in
which pre-race planning ranges from no advanced action to determination of sweat rate during a
field simulation, and (c) 9 rehydration recommendations that are relevant to endurance activities.
With this information, each athlete can select the rehydration method that best allows her/him to
achieve a hydration middle ground between dehydration and overhydration, to optimize physical
performance, and reduce the risk of illness.
Keywords:
thirst; drinking; sweat; sodium; hyponatremia; overhydration; dehydration; marathon; triathlon
1. Introduction
The essential components of central nervous system maintenance of body water volume
and concentration include perceptions, behavior, nervous system responses, and the release
of hormones (vasopressin, AVP; angiotensin II; atrial natriuretic peptide; apelin) [
1
–
4
]. Per-
turbations of whole-body water volume and concentration are monitored by the brain,
the resulting thirst and oropharyngeal sensations modulate drinking, and neuroendocrine
responses regulate water and electrolyte excretion or retention by the kidneys [
1
]. Dur-
ing typical daily activities that do not include exercise, these complex interactions act to
maintain total body water volume and serum concentration within 1–3% of baseline each
day [
5
–
7
]. However, the relative influence of these processes varies with different life activ-
ities [
8
]. Table 1explains that, during sedentary daily pursuits in a mild environment, renal
responses and thirst are the primary homeostatic regulators. During prolonged endurance
exercise at low intensities (5–24 h duration), renal responses and thirst have minor-to-large
effects on water regulation. As the duration of exercise increases, sweat losses become a
major factor in whole-body water balance [
9
], regardless of the volume of fluid consumed.
This review article considers endurance exercise from the perspectives of body water
and electrolyte balance, the negative effects that substantial fluid–electrolyte disturbances
(i.e., both water loss and gain) have on competitive performance and health, and ways
that endurance athletes can minimize performance decrements and mitigate the risk of
exercise-associated illness. This is important because an endurance athlete can lose as
much as 11–12% (7.8–8.5 kg) of body weight in the form of water, during a 12.3-h Ironman
triathlon in a cool environment (3.8-km swim, 180-km bike, 42.2-km run) [
10
]. This also
is important because day-long walking or hiking in a desert environment can result in
extreme body mass losses of 14–18% when fluids are unavailable or restricted (Figure 1).
Nutrients 2021,13, 887. https://doi.org/10.3390/nu13030887 https://www.mdpi.com/journal/nutrients
Nutrients 2021,13, 887 2 of 21
Conversely, excessive fluid intake (i.e., water retention) can result in a body mass gain of
more than 10% (7.8 kg) in 12.7 h while competing in an ultraendurance triathlon (ambient
temperature, Tamb, 20.5
◦
C) [
11
]. These vastly different changes of body mass represent
the primary problem and focus of this review paper: how to maintain a rehydration middle
ground during prolonged exercise that reliably reduces the risk of illness by avoiding
overhydration, and maintains exercise performance by avoiding significant dehydration.
Table 1.
The relative effects of thirst, drinking, and physiological responses on fluid-electrolyte balance during ordinary
daily activities and endurance exercise.
Activity
Thirst &
Drinking
Behavior
Sweat Gland
Secretion of
Hypotonic Fluid
Kidney
Regulation of Water &
Electrolytes
Neuroendocrine
Homeostatic
Responses a
Effects on Water
& Electrolyte Balance
Sedentary daily
activities (16 h) Basal bNegligible Basal bBasal b
CNS responses are
sufficient to maintain water
and electrolyte
homeostasis
Brief exercise (5–30 min) at
moderate-to-high
intensity
Minor Minor-to-moderate Minor Minor, brief Water and electrolyte losses
are minor
Endurance exercise
(0.5–5 h) at low-to-high
intensity
Minor-to-large Moderate-to-large Minor-to-moderate Minor-to-large,
prolonged
Moderate-to-large
turnover cdue to sweating
and drinking
Ultraendurance exercise
(5–24 h) at
low-to-moderate intensity
Moderate-to-large Large Moderate-to-large Large, prolonged
Water and electrolyte losses
in sweat and urine exceed
24 h dietary intake
CNS, central nervous system (i.e., brain and spinal cord); TBW, total body water.
a
, CNS effects involving nerves and hormones that regulate
whole-body water volume and concentration, blood volume/pressure/osmolality, and thirst (see [
9
] for a review of this topic).
b
, a standard
low level maintenance of whole-body fluid-electrolyte balance with small turnover (intake versus loss) and minor perturbations.
c
, turnover
refers to the sum of gains and losses of water and electrolytes.
Figure 1.
Signs and symptoms of dehydration in men who walked in the desert without drinking. The symbol which appears
to the left of each sign or symptom identifies the approximate water deficit of its first report. Based on information from [
12
].
2. Problem: Water and Salt Losses during Endurance Exercise
Most ultraendurance competitors do not meet their fluid needs during competi-
tion [
13
], due primarily to three factors that interact to influence sweat volume and body
mass during prolonged exercise [
14
]. The first of these factors is exercise intensity. Table 2
presents whole-body water balance measurements of 32 cyclists who completed a 164-km
Nutrients 2021,13, 887 3 of 21
event in the state of Texas, USA during the month of August [
15
]. Cyclists have been
grouped on the basis of time to complete 164 km: 9.6, 6.3, and 4.8 h. The total volume
of sweat lost by these groups were similar (range of 7000–7200 g), demonstrating that
the higher exercise intensities of groups 4.8 and 6.3 stimulated a greater sweat rate per
hour (p< 0.01 to 0.0001) than that of group 9.6. Exercise intensity also affected body mass
proportionally. The body mass change values for cyclist groups 9.6, 6.3, and 4.8 (columns
2–4, row 11) were
−
1800,
−
2300, and
−
2750 g. The second factor is exercise duration.
As shown in Table 2, slower cyclists may be on the course at least twice as long as faster
competitors. Not surprisingly, similar body mass losses occur commonly (Figure 2) during
ultra-running, ultra-cycling, and ultra-triathlon events [
16
]. Environmental temperature
represents a third factor that influences body water balance. During 42.2 km marathon
running, mild ambient conditions of 7, 10–12, and 20
◦
C resulted in mean sweat rates of
0.81, 0.96, and 1.52 L/h, respectively [
17
]. In addition, researchers measured the sweat rates
of athletes in a laboratory building (29
◦
C, 51% relative humidity; running and cycling
protocols), a mobile laboratory (29
◦
C, 65% rh), or field environment (25
◦
C, 55% rh) [
18
].
The majority of these athletes competed in team/skill sports (n= 1022) and individual
endurance sports (n= 255). The highest average sweat rates were observed in the sports
of American football (1.51 L/h) and Endurance Sports (1.28 L/h), whereas the lowest
occurred in baseball (0.83 L/h) and soccer (0.94 L/h).
Table 2.
Characteristics of three groups of cyclists who completed a 164 km summer road cycling event in 4.8–9.6 h (modified
from [15]). No drinking instructions or experimental interventions were involved.
Variables Average Exercise Duration (h) a
9.6 6.3 4.8
Pre-event body mass b(kg) 81.90 82.05 82.55
Number of male cyclists 11 11 10
Ground speed (km/h) 17.2 d26.6 d34.0 d
Rating of perceived exertion at finish c16 16 16
ad libitum total fluid intake e(g) +6100 +4500 +3900 f
Rate of fluid intake (g/h) +635 +715 +810
Sweat secreted g(g) −7700 −7150 −7000
Sweat rate (g/h) −800 d−1135 −1460
Urine excreted g(g) −1300 −550 −450 d
Solid food mass consumed e(g) +423 +355 +350
Body mass change b(g) −1800 −2300 −2750
Body mass change (%) −2.0 −2.9 −3.4
Note: values are means or medians; negative values represent reduced mass or loss of fluid from the body; air temperature ranged from
24.4
◦
C (08:00 h) to 41.1
◦
C (15:00 h); for the purposes of this table, 1 g = 1 mL and 1 kg = 1 L.
a
, cyclist groups 9.6 and 6.3 voluntarily
stopped at 3 roadside aid stations for research measurements, elimination, drinking, and eating. Group 4.8 rode as part of a 5-h pace
team and did not stop during the entire event.
b
, measured with a calibrated floor scale (
±
100 g).
c
, using a printed 6 (very, very light)
to 20 (very, very hard) point perceptual rating scale [
19
].
d
, significantly different from all other groups (p= 0.01 to 0.0001).
e
, based on
cyclist diet records and confirmed by interviews.
f
, significantly different from group 9.6 (p= 0.04).
g
, detailed methods are described in the
original publication [15].
Representing extreme points of reference, the following individual sweat rate values
have been observed. First, an elite marathon runner (age, 26 y; height, 185 cm; body mass,
66.9 kg) produced 3.7 L of sweat per h during the 1984 Los Angeles Summer Olympics
marathon (24–28
◦
C Tamb; time to complete 42.2-km race, 2 h 14.3 min; body mass change,
5.43 kg,
−
8.1%) [
21
]. Second, a runner (age, 30 y; height, 185 cm; body mass, 91.8 kg)
who had experienced heatstroke twice previously was observed to have a sweat loss of
4.1 L during a 70-min laboratory race simulation (25
◦
C) [
22
]. Third, the sweat rate of a
male tennis player (age, 26 y; height, 197 cm; body mass, 91.4 kg) was 4.3 L/h during a
60 min laboratory simulation (36.1
◦
C; brisk walking and jogging on a treadmill) [
23
]. The
sweat sodium losses (i.e., calculated by multiplying the measured sweat volume times
the sweat sodium concentration) during the two simulations were 5930 and 7610 mg Na+,
respectively. Additionally, as noted above, extreme body mass losses of
−
11 to
−
12% were
Nutrients 2021,13, 887 4 of 21
experienced by competitors in an Ironman triathlon that required an average of 12.3 h
to complete [10].
Figure 2.
The relationship between body weight change (%) and serum Na
+
after 4.0–13.3 h of exercise (n= 2135) as
modified from [
20
]. Solid circles (
•
) represent asymptomatic marathon runners and Ironman triathletes. Open circles (
#
)
depict athletes with severe symptoms including hyponatremic encephalopathy (central nervous system dysfunction due to
brain swelling). Horizontal zone abbreviations: >RR, serum Na
+
concentration above resting normal; RR, the laboratory
reference range for healthy adults (green horizontal boundaries); H
B
, biochemical hyponatremia which involves few or no
symptoms; H
SYM
, symptomatic hyponatremia. Symbols A–M were overlaid by the present author (see details below in
Section 3.2.1). Gray highlighted symbols depict individuals with fluid intake rates of
≤
700 mL/h and body mass losses of
0.1 to 2.6%. Yellow highlighted squares indicate exertional hyponatremia cases (each n= 1) with fluid intake rates ranging
from 733–2061 L/h and body mass increases of +0.1 to +5.0%. Reprinted via the PNAS Open Access option from [20].
2.1. Effects of Dehydration on Endurance Exercise Performance
The negative influences of dehydration on exercise performance are recognized by
professional sports medicine organizations [
24
–
27
] and sport governing bodies [
28
] in
position statements regarding rehydration, exertional heat illness, and physical perfor-
mance. Although the precise water deficit at which performance decrements occurs is
difficult to determine because of inter-individual differences, there is overall consensus
in the literature that dehydration of
−
2 to
−
4% represents the range in which endurance
exercise performance declines [
24
–
26
,
28
–
31
]. This effect is illustrated in Figure 3, which
presents a performance analysis of 34 published studies involving dehydration; a body
water deficit of 1–3% was less likely to impair endurance exercise performance significantly
(p< 0.05) than dehydration of 4–7% [
32
]. These 60 statistical comparisons involved outdoor
track running, trail running, outdoor road cycling, indoor treadmill running, indoor rowing
ergometry, and indoor cycle ergometry.
Nutrients 2021,13, 887 5 of 21
Figure 3.
The effects of dehydration on exercise performance. Fractions represent the number of
statistically significant (p<0.05) observations out of the number at each level of body mass loss.
Across all dehydration levels, 68% of comparisons indicated impairment. Reprinted from [
32
] via the
Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/
4.0/) accessed on 2 March 2021.
It also is relevant that controlled field studies have reported statistically significant
decrements of endurance exercise performance at lower levels of dehydration (
−
1.0 to
−
2.2%). These controlled protocols evaluated running competitions at (a) three distances
on an outdoor all-weather track [
33
] and (b) an outdoor cycling hill-climbing performance
competition [
34
]. Similar performance decrements were reported for two indoor cycling
simulations [35,36] when dehydration ranged from 1.0–1.8%.
Decrements of outdoor cycling performance which occur at
≤
4% body mass loss
have been disputed in one meta-analysis [
37
] which evaluated 5 research articles (13 effect
estimates). However, virtually all researchers agree that moderate-to-severe dehydration
(e.g., 4–7% versus 1–2% body mass loss; Figure 3) results in greater physiologic strain and
decreased aerobic exercise performance [24,26,29,30,32,38–41].
Physiologists agree that dehydration-induced aerobic performance decrements are
greater in hot versus cool environments [
24
,
29
,
41
,
42
], due to greater thermal and cardiovas-
cular strain (i.e., increased skin temperature and blood flow, greater plasma volume loss,
decreased cardiac output) that becomes physiologically impactful in the dehydration range
of 2–4% of body mass [
43
,
44
]. In terms of associated physiological effects, a summary of
8 relevant publications [
29
] noted that a 4–5% dehydration level reduced maximal oxygen
consumption (VO
2max
) more in a hot environment (
−
9 to
−
27% when Tamb
≥
30
◦
C) than
in a cool or mild environment (
−
3 to
−
7% when Tamb was 15–26
◦
C). The consequences of
this dehydration included a shorter exercise time to exhaustion, an obligatory reduction in
exercise intensity, or both.
2.2. Effects of Dehydration on Symptomatology and Illness
The classic desert field observations of Adolph and colleagues [
12
] during the mid-
1940s were among the first descriptions of exercise-induced dehydration that approached
and exceeded 10% body mass loss. Although Adolph’s systematic observations of dehy-
drated soldiers walking in the desert (Tamb > 37
◦
C) were not subject to statistical analyses,
they provide a thorough description of the detrimental health effects of prolonged de-
hydration. Figure 1presents a summary of the signs and symptoms that were reported
when dehydration exceeded 2%. The following Section 2.2.1 through Section 2.2.3 describe
disorders that result from water and salt deficiencies.
Nutrients 2021,13, 887 6 of 21
2.2.1. Exercise Associated Collapse
A patient classification and care matrix, developed after years of treating runners in the
medical tent of the Twin Cities Marathon, Minnesota, USA [
45
] facilitates clinical decision
making and expedites the transition of distressed runners through a field medical facility
near the finish line. Treatment of exercise-associated collapse centers on fluid replacement
and body cooling or warming if needed. For suspected dehydration after the marathon,
oral fluid replacement is preferred (e.g., water, fluid-electrolyte beverage, or 200–300 mL of
salty soup bouillon to aid fluid retention). Intravenous fluid is necessary when casualties
are unable to tolerate oral intake, and when there are clinical indications of severe volume
depletion or ongoing fluid losses from vomiting or diarrhea. During medical treatment, to
avoid adding water to a runner who already is overhydrated, exertional hyponatremia (see
Section 3.2) is ruled out before intravenous fluid administration by assessing the serum
Na+concentration of runners who finish after 4 h [45].
2.2.2. Exertional Heat Illnesses
Water and salt losses in sweat have implications for the health of athletes who ex-
ercise in hot environments. Water and sodium deficits are recognized as predisposing
factors for exertional heat stroke [
46
–
48
], exertional heat cramps [
49
], and exertional heat
exhaustion [
43
,
50
]. Regarding the latter illness, research has shown that (a) mild exercise
(40–50%VO
2max
) in hot environments (34–39
◦
C) does not induce heat exhaustion unless a
significant fluid-electrolyte loss and cardiovascular strain exist; (b) a moderate but cumula-
tive dehydration across 3 days can result in exertional heat exhaustion [
51
,
52
]; and (c) 85%
of heat exhaustion patients who presented at a deep metalliferous mine infirmary exhibited
a urine specific gravity of 1.020–1.040, indicating mild-to-severe dehydration [53].
2.2.3. Kidney Dysfunction and Renal Stress
Failure of the kidneys to perform essential functions (i.e., the clinical disorder named
acute renal failure) is possible but uncommon during marathon footraces of 42.2 km and
dehydration less than 4% of body mass [
54
]. However, both immediate (during and post-
race) and delayed effects (i.e., 1–5 d after the event) of dehydration have been reported as
abnormal values for urine flow rate, osmolar clearance, creatinine clearance, and protein in
the renal filtration apparatus [
54
]. When no renal dysfunction is observed, considerable
renal concentrating stress is possible. For example, 11 out of 33 cyclists who finished a
summer 164 km ultraendurance event exhibited marked urine concentration, verified with
specific gravity > 1.030 [55].
3. Problem: Overhydration during Endurance Exercise
3.1. Hyperhydration and Exercise Performance
No evidence suggests that deliberate pre-exercise consumption of excess pure water
has an ergogenic effect on exercise performance [
24
,
56
]. Glycerol, however, often is ingested
prior to exercise (e.g., 1.2 g/kg body mass with a volume of fluid equal to 26 mL/kg body
mass) to hyperhydrate athletes by increasing water retention and plasma volume while
decreasing urine volume [
57
]. This act delays reaching a level of dehydration that degrades
exercise performance. Research results are not conclusive, in that studies have shown both an
ergogenic effect and no effect on exercise performance [
58
,
59
]. However, one caveat should
be noted. As glycerol dilutes both intracellular and extracellular fluids prior to exercise, it
may predispose athletes to low serum Na
+
as described in the next paragraph, especially if
aggressive drinking occurs during exercise. A similar predisposition to low serum Na
+
has
been reported for deliberate overhydration with water and dilute fluids [24,60,61].
3.2. Exertional Hyponatremia (EHN): A Potential Medical Emergency
When overhydration during exercise dilutes blood, an osmotic pressure gradient
causes water to move into cells. The resulting cell swelling can result in EHN, one of
the few illnesses that is potentially fatal to otherwise healthy athletes during exercise.
Nutrients 2021,13, 887 7 of 21
Recognizable symptoms appear in most athletes at a serum concentration of approximately
130–135 mmol Na
+
/L [
26
,
62
] and include lightheadedness, dizziness, nausea, puffiness
(e.g., hands and feet), and body weight gain from baseline [
63
]. The majority of athletes
whose serum Na
+
is below 130 mmol/L (Figure 2) experience symptoms; these may
include headache, vomiting, frothy sputum, difficulty breathing, pulmonary edema (i.e.,
fluid accumulation with swelling), and altered mental status such as confusion or seizure
that results from cerebral edema [10,64].
The signs and symptoms of EHN do not necessarily correlate with the serum Na+ in
the range shown in Table 3(
≥
130 mmol Na
+
/L). The total symptoms score (column 10),
rated with a validated Environmental Symptoms Questionnaire [
65
], was not related to
the change of serum Na
+
(column 5). Indeed, the self-rated symptoms of hyponatremic
cyclists LC and AM (serum Na+ of 130 mmol/L) ranked among the lowest in this subject
sample [
66
]. Thus, the severity of symptoms and not the absolute value of serum Na
+
concentration guide the course of medical treatment [63].
Table 3.
Athlete physiological and perceptual responses during a summer road cycling event (7.1–10.9 h duration). Data are
rank-ordered on the basis of serum Na+change (column 5). Modified from [66] with unpublished data added.
Cyclists Total Fluid
Intake (L) a,b
Total Fluid
Intake
(ml/kg) a,b
Sodium Intake
(mg) a,b
Change of
Serum Na+
(mmol/L) a
Pre-Event
Body Mass
(kg)
Body Mass
Change (%) a
Urine
Specific
Gravity at
Finish Line
Rating of
Thirst at
Finish Line c
Environmental
Symptoms
Questionnaire
dTotal Score
at Finish Line
A 3.7 42 356 +6 88.6 −4.6 1.021 4 13
B 5.3 75 194 +4 71.0 +1.4 1.024 8 10
C 3.0 48 328 +3 61.8 −4.2 1.030 6 11
D 4.7 62 149 +1 75.2 −1.2 1.026 8 27
E 10.9 139 1166 +1 78.5 −1.5 1.020 7 25
F 4.6 54 124 −1 85.5 +0.1 1.021 6 21
G 4.1 50 261 −2 82.0 −1.8 1.030 5 13
H 3.4 41 263 −2 82.9 −0.1 1.023 4 11
I 9.5 103 823 −2 91.8 −4.6 1.034 6 25
J 9.6 124 1259 −3 77.2 −1.9 1.016 4 17
K 10.5 101 1182 −3 104.7 +1.0 1.026 5 21
L 9.2 109 1601 −6 84.7 +1.1 1.003 5 12
LC e13.7 191 1179 −11 72.0 +4.3 1.003 2 4
AM e14.7 189 3292 −11 77.5 +0.1 1.010 2 11
a
, during the 164-km ride;
b
, consumed in water, beverages, sport drinks, solid foods, bars, gels, tablets, capsules;
c
, a visual rating scale
presented thirst levels of increasing intensity, ranging from 1(not thirsty) to 9 (very, very thirsty);
d
, see reference [
65
];
e
, cyclists LC and AM
experienced exertional hyponatremia, both with a serum Na+of 130 mmol/L.
Table 3includes data regarding two recreational cyclists (LC and AM) who began
a summer 164-km event (Tamb, 34
±
5
◦
C) with normal serum electrolytes but finished
the ride with a serum sodium concentration of 130 mmol/L, indicative of mild EHN. The
data of 12 other finishers (A–L, column 1) are presented to allow comparisons. Although
they did not ride together, both cyclists consumed a large and similar relative volume of
fluid (191 and 189 mL/kg), experienced an identical 11 mmol/L decrease of serum sodium,
and reported low thirst sensations. However, one (LC) gained 3.1 kg (+4.3% of body mass)
during 8.9 h of exercise (i.e., suggesting a dilutional effect) and the other (AM) maintained
body mass (+0.1 kg, +0.1%, 10.6 h), suggesting that no excess fluid was retained. Thus,
Table 3suggests a complex, individualized EHN etiology [66].
After exercise, fluids should be consumed judiciously because symptoms of EHN
may develop hours after excess fluid consumption, as described in two published case
reports. The first involved a 21-year old man who had aggressively consumed water and
gained 5.25 kg of body weight during 5 h of treadmill exercise in a hot environment [
61
].
He was asymptomatic until he experienced nausea and malaise late that evening, and
was transferred to a nearby hospital with a serum Na
+
of 122 mmol/L. After a night of
observation, fluid restriction, and large urine output, he was released at 11:00 a.m. the
next morning without symptoms. A more serious EHN case with delayed symptom onset
involved a 49-year old runner who finished a 42.2 km marathon in 4 h 22 min then boarded
an airline flight to return home [
67
]. Approximately 5 h after he finished the race, he became
ill and experienced a grand mal seizure in the aisle of the cabin. The pilots diverted the
Nutrients 2021,13, 887 8 of 21
aircraft to a nearby city for an emergency landing. The runner was transported to a hospital,
where he experienced two additional seizures while unconscious with a serum Na
+
of
129 mmol/L. A chest x-ray indicated pulmonary edema and a brain scan revealed cerebral
edema; he also was diagnosed with renal insufficiency and liver damage. During the
ensuing 18 months, this runner learned that he was unable to mentally process information
that had previously been routine, and he was unable to perform his professional duties.
3.2.1. Predisposing Factors for EHN
Exercise duration greater than 4 h, high sweat rate, high sweat Na
+
, and small body
size have been identified as predisposing factors for EHN [
63
,
68
–
70
]. Table 4allows
consideration of other risk factors; data are rank-ordered on the basis of final serum Na
+
(column 5). As the severity of EHN increased (i.e., moving from top to bottom as serum
Na
+
decreased), both body mass change (column 6) and the rate of fluid intake (column 8)
trended toward increasing. The individuals and groups in Table 4(labeled A through M
in column 1) also are depicted in Figure 2, allowing comparisons to a large data base of
marathon runners and Ironman triathletes. The open symbols (
#
) in Figure 2represent
individuals who sought medical care for symptomatic EHN.
Table 4. Factors that influence exertional hyponatremia. Letters in column 1 refer to the symbols embedded in Figure 2.
Symbols in
Figure 2Men Women Scenario (Ambient
Temperature, ◦C)
Final Serum
Na+
(mmol/L)
Body Mass
Change (%)
Exercise
Duration (h)
Rate of
Fluid Intake
(ml/h)
Mean Initial
Body Mass
(kg)
Source
Background
data points
a a 11 endurance events aSee Figure 3See Figure 3bbb[20]
A 42 164 km cycling (34.4) 141 −0.8 9.1 649 85.9 [55]
B 31 164 km cycling (24.4–39.5) 141 −1.4 9.0 700 85.4 [66]
C 6 164 km cycling (34.4) 140 −0.1 9.0 520 67.3 [55]
D 50 100 km run (15.6–21.7) 138 −2.6 12.2 600 74.9 [71]
E 7 Treadmill walk (41.0) c136 −0.1 4.0 c640 77.9 [61]
F 5 44 km trail run (15–34) 131 −2.2 9.3 290 d81.9 [72]
G 1 Ironman triathlon
(21.0) e,f 131 +0.9 13.3 733 57.5 [73]
H 1 164 km cycling (24.4–39.5) g130 +4.3 8.9 1,500 72.0 [66]
I 1 Ironman triathlon
(21.0) e,f 130 +2.5 12.0 764 59.0 [73]
J 1 164 km cycling (24.4–39.5) g130 +0.1 10.6 1,400 77.5 [66]
K 2 5 Ironman triathlon e128 −0.5 12.3 b62.5 [74]
L 1 Treadmill walk (41.0) c122 +4.0 4.0 c2,061 h82.2 [61]
M 1 Ironman triathlon e116 +5.0 14.0 1,642 b[75]
Note: values are means or medians (columns 5–9) when the number of subjects is
≥
2.
a
, 3 Ironman triathlons, 6 marathon footraces
(42.2 km), a 109 km cycling tour, and a 160 km footrace (2,135 athletes);
b
, not reported;
c
, 5.6 km/h, 5% grade, 30 min walking and
30 min seated rest per hour;
d
, runners were allowed to drink and eat only fluids and food provided by the race organizing committee, at
11 intermediate checkpoint stations, positioned every 3–5 km; they did not drink when thirsty or ad libitum;
e
, triathlon stages were 3.8 km
swim, 180 km cycle, 42.2 km run;
f
, this athlete stopped during the cycling stage due to hyponatremic illness;
g
, identical to cyclists LC and
AM in Table 4(column 1); h, this individual purposefully overhydrated.
A few athletes possess a “perfect storm” of characteristics in which a high sweat
rate (e.g., 2.0–3.0 L/h) coexists with a high sweat sodium concentration (e.g., 40–80 mmol
Na
+
/L; 2.3–4.6 g NaCl/L). These athletes may be identified by white salt deposits on
a shirt, jersey, or shorts. Due to their relatively large sodium loss in sweat, they are at
increased risk of developing EHN. In a hypothetical calculation, Hiller [
68
] noted that
an Ironman triathlete with a sweat rate of 1.5 L/h could lose 36 g of NaCl (14,040 mg of
sodium) in 12 h. This observation is supported by the mathematical prediction model
of Montain et al. [
76
], which demonstrates that a high sweat sodium concentration is an
important etiological factor.
3.2.2. EHN Etiologies
Multiple EHN origins have been described [
20
,
61
,
66
,
67
,
71
], and consensus regarding
a single etiology is difficult to reach because some cases reportedly involve hyponatremia
with body mass gain (i.e., hypervolemic hyponatremia, water retention that exceeds sweat
and urine losses) [
10
,
77
–
79
], whereas other EHN cases involve hyponatremia with body
Nutrients 2021,13, 887 9 of 21
mass loss due to partially replaced sweat water and sodium losses (hypovolemic hypona-
tremia) [10,68,77,80]. Importantly, a 2015 consensus document noted that all known EHN
fatalities to that date had involved overconsumption of dilute fluids [63].
3.2.3. EHN Cases Involve Variable Vasopressin Responses
Vasopressin (antidiuretic hormone) is the body’s principal water-regulating hormone.
It functions to maintain body water balance, in conjunction with thirst, by regulating
serum osmolality within narrow limits [
81
]. Although dehydration with elevated serum
osmolality is the primary stimulus for the release of vasopressin from the pituitary, non-
osmotic factors also are known, including plasma volume decrease, hypoglycemia, nausea,
and vomiting [82].
In an unknown percentage of EHN cases, serum vasopressin increases abnormally
during overhydration, facilitating water retention. This inappropriately high serum vaso-
pressin also stimulates sodium excretion by the kidneys, reducing serum Na
+
. As vaso-
pressin has a brief half-life and laboratory analysis is technically difficult, this hormone
rarely is analyzed in cases of EHN. Nevertheless, this condition was verified during a
marathon field study [
83
] in which 43% of runners with a serum Na
+
< 130 mmol/L ex-
hibited inappropriately high serum vasopressin levels (range, 3–17 pg/mL), and during a
case of symptomatic EHN that developed during a laboratory investigation [
61
]. A notable
exception to these reports occurred among 7 symptomatic Ironman triathletes [
74
] who
finished 12 h of exercise with a median body weight loss of 0.5%, post-exercise plasma
Na
+
of 128 mmol/L, and a post-exercise plasma vasopressin concentration of 1.6 pmol/L;
these values represented symptomatic EHN with a low serum vasopressin concentration.
A control group of 11 asymptomatic triathletes exhibited the following comparison values:
body weight loss of 3.9%, plasma Na
+
of 141 mmol/L, and a plasma vasopressin concen-
tration of 4.6 pmol/L; these levels represented a typical hormonal response to moderate
dehydration. These variable vasopressin responses illustrate why it is difficult to attain
consensus regarding the role of arginine vasopressin in EHN.
A coherent explanation for variable vasopressin responses was published by Hew-
Butler [
82
]. Her review article distinguished intense (brief, >90% of maximal oxygen
consumption), steady state (sustained at 40–60% of maximal oxygen uptake), and pro-
longed endurance (>1 h) exercise. During the former, an obvious and statistically significant
increase of plasma vasopressin occurs that exceeds the expected increase due to increased
plasma osmolality. Steady state exercise also generally stimulates a statistically significant
vasopressin increase. During prolonged competitive endurance exercise, a similar vaso-
pressin increase occurs, with or without significant increases of serum Na
+
or osmolality;
this elevation persisted for 2 h after a 24 h competitive track race and for 31 h after a 38 km
non-competitive run. In all of these exercise types, it appears that published vasopressin
responses are difficult to interpret because of differences in exercise intensity [82].
3.2.4. Evidence for an EHN Drinking Rate Threshold
A previous analysis of 6 groups of runners and triathletes reported that no case of
symptomatic EHN occurred (serum sodium < 130 mmol/L during continuous exercise
that lasted 3.2–12.3 h) among 270 athletes who consumed less than 750 mL of fluid per
hour [
67
]. In addition, case reports of two female ultradistance triathletes [
73
] observed
that their post-race hyponatremia (130 and 131 mmol Na+/L) was accompanied by weight
gain (0.5 and 1.5 kg). They consumed fluids during competition at a rate of 730 and
760 mL/h. Figure 2also supports this drinking rate threshold for the onset of EHN, in
that all yellow highlighted square symbols represent individuals who consumed fluids
at a rate > 700 mL/h, and gained weight during their respective exercise bouts. These
individuals are clustered in the lower left quadrant of Figure 2, among symptomatic athletes
(open symbols,
#
). These observations suggest that endurance athletes who consume
fluids at a rate < 700 mL/h have a decreased risk of EHN. This theoretical 700 mL/h fluid
consumption rate threshold is consistent with the 400 to 800 mL/h recommendations of
Nutrients 2021,13, 887 10 of 21
both the International Marathon Medical Directors Association [
84
], the American College
of Sports Medicine [
24
], and a mathematical model that was designed to clarify the etiology
of EHN [76].
3.2.5. Does Sodium Intake Counteract a Low Serum Na+?
It is widely recognized that salt (sodium chloride, NaCl) capsules are consumed
during triathlons and marathons. Exploring this trend within endurance sports, Hoffman
& Stuempfle [
80
] reported that 90–96% of runners consumed sodium supplements during
a 161-km ultramarathon footrace because they believed that it prevented muscle cramps
and hyponatremia. However, there is little evidence to support this belief. For example,
Table 3shows that cyclists J, K, L, LC and AM consumed the largest amounts of sodium but
experienced the greatest decrease of serum Na
+
, whereas cyclists A, B, C and D consumed
small amounts of sodium and experienced an increased serum Na
+
[
61
]. Therefore, sodium
consumption did not prevent EHN from occurring in cyclists LC and AM, and low sodium
intake by other cyclists was not associated with EHN. Similar conclusions have been
published regarding ultramarathon competitors by Speedy et al. [
85
], Hew-Butler et al. [
86
],
Hoffman and Stuempfle [80], and Hoffman and Myers [87].
Two controlled laboratory studies also have quantified the effects of sodium consump-
tion on serum Na
+
. The first provided 3911 mg of sodium during 6 h of exercise in a 34
◦
C
environment [
88
], and the second provided 1409 mg sodium during 3 h of exercise at
30
◦
C [
89
]. Post-exercise measurements detected a mean serum Na
+
increase of 3 mmol/L
(i.e., supplemented versus control experiments) in both studies, indicating that sodium
supplementation had a minor influence on serum Na+levels.
4. The Complexity of Thirst and Drinking
Thirst prompts seeking and consuming water, and is measured with a subjective
rating scale. Drinking behavior is distinct from thirst, is measured as the volume of
fluid consumed, and may involve fluid selection on the basis of preferred or required
characteristics (i.e., temperature, palatability, ingredients, energy content) [90].
During sedentary daily activities (i.e., producing a small 24-h water turnover), the
perception of thirst, the act of drinking, renal regulation of water and electrolytes, and neu-
roendocrine responses (Table 1) adequately regulate total body water volume and serum
concentration within 1–3% of each individual’s baseline, from one day to the next [
5
–
7
].
During prolonged endurance exercise, however, the relationship between perception of
thirst and whole-body fluid–electrolyte balance can be distorted by physiological chal-
lenges [
32
,
91
] such as sizeable water and sodium losses in sweat, movement of water
between the intracellular and extracellular spaces, or plasma volume depletion [6].
4.1. Multiple Factors Influence Drinking during Endurance Exercise
Figure 4presents several factors that influence thirst and drinking behavior, each
of which is monitored and regulated continuously by the central nervous system. Thus,
the phrase dynamic complexity applies to the vast, integrated, brain-wide network of
nerve circuits and brain regions that regulate thirst, drinking, body water volume, and
fluid concentration [
92
]. The findings of two recent human studies [
93
,
94
] suggest that
thirst is one of multiple conscious perceptions and subconscious autonomic responses
(Figure 4) that evolve simultaneously during dehydration and rehydration to influence
drinking behavior. Simply stated, the internal motivation to consume water is influenced
by multiple factors that reinforce the perception of thirst.
Nutrients 2021,13, 887 11 of 21
Figure 4.
Influences on thirst and drinking behavior during endurance exercise. All factors in this
diagram are perceived, monitored, and/or regulated by the brain.
As dehydration concentrates extracellular fluid, plasma osmolality (P
osm
) is rec-
ognized as the primary factor that stimulates thirst [
2
,
81
,
95
]. However, as shown in
Figure 5, the P
osm
threshold at which thirst is perceived varies greatly across individuals
(range, 274–293 mOsm/kg) and may be lower than the range of laboratory reference values
for P
osm
(285–295 mOsm/kg) [
96
]. The data in Figure 5were compiled from 5 published
human studies; the shape of this frequency distribution implies that the thirst threshold
is a multifactorial (polygenic) characteristic [
97
]. Although inter-individual differences of
the P
osm
threshold for thirst have not been studied during exercise, Figure 5suggests that
the level of dehydration (i.e., increased P
osm
) that initiates drinking during exercise might
differ considerably among athletes.
Figure 5.
Frequency distribution of the plasma osmolality (P
osm
) threshold for the onset of thirst.
The horizontal gray bar delineates the laboratory reference range of P
osm
values (285–295 mOsm/kg)
for healthy adults. Reprinted under the terms and conditions of the Creative Commons Attribu-
tion (CC BY) license (http://creativecommons.org/licenses/by/4.0/) accessed on 2 March 2021.
Modified from [97].
Nutrients 2021,13, 887 12 of 21
4.2. Inter-Individual Differences
Figure 6illustrates six factors that influence the change of body mass and serum
Na
+
. Interactions of these factors with inherited characteristics and endurance training
regimens produce great differences among athletes. In Figure 2, for example, if a male
athlete experienced a body mass change of only—0.5% (0.35 kg) during a 13 h Ironman
triathlon, his serum Na
+
could range from 119 (symptomatic EHN) to 157 mmol/L (severe
hypernatremia). Conversely, if a male athlete finished with a serum Na
+
of 140 mmol/L (i.e.,
in the center of the reference range for healthy adults), his body weight change could range
from +5.5% (+3.9 kg) to
−
12.5% (
−
8.8 kg). These large serum Na
+
and body mass ranges
represent the effects of numerous perceptual, behavioral, hereditary and fluid-electrolyte
variables (Figures 4–6), but are influenced mostly by the total volume of sweat produced
(e.g., 15.6 L/13 h at a sweat rate of 1.2 L/h) and the total volume of fluid consumed (e.g.,
9.1 L/13 h at a drinking rate of 700 mL/h).
Figure 6.
Factors that influence the relationship between body weight gain/loss and serum Na
+
during endurance exercise.
The largest effects on whole body fluid–electrolyte balance are the volume of sweat lost and the volume of fluid consumed.
Notes:
a
, water and low-sodium fluids promote dilution of body fluids;
b
, physical training and heat acclimatization increase
sweat rate and decrease sweat sodium concentration;
c
, urine production decreases during exercise;
d
, increased dietary
sodium encourages water retention but affects only a minor increase of serum Na+.
Large inter-individual differences also exist among elite runners. Fluid intake rates
were determined for 10 men who placed 1st or 2nd (range of finish times, 2:03:59 to 2:10:55)
during prestigious city marathons [
98
]. Each runner ’s drinking behavior was recorded on
videotape and fluid intake was estimated by multiplying drinking time by 45.2 mL/s (i.e.,
a value determined by laboratory drinking simulations). Half of these runners consumed
fluids at rates that ranged from 30–300 mL/h (73–631 mL total), whereas the rate of
fluid intake of the other 5 elite runners ranged from 420–1040 mL/h (886–2205 mL total).
Clearly, these data indicate that elite marathon runners (a) ingest fluid at rates that span a
wide range during competition (30–1040 mL/h), and (b) some individuals greatly exceed
Nutrients 2021,13, 887 13 of 21
the proposed drinking rate threshold at which symptomatic EHN appears (700 mL/h),
described above in Section 3.2.4.
4.3. Personal Beliefs and Sources of Rehydration Information
Personal beliefs about drinking may predispose an athlete to EHN, according to the
findings of two case reports. The first [
66
] involved cyclists LC and AM in Table 3(who also
are designated as athletes H and J in Table 4). Their urine specific gravity measurements on
Day-1 (LC, 1.006; AM, 1.004; 31 control cyclists, 1.017) and the morning of the road ride (LC,
1.003; AM, 1.005; controls, 1.019) indicated that both had overhydrated before prolonged
exercise. The authors suggested that their pre-event hydration behavior, coupled with
high rates of fluid intake during the ride (LC, 1500 mL/h; AM, 1400 mL/h), resulted in
both cyclists experiencing asymptomatic EHN. The second publication [
61
] involved a
controlled case report of EHN (serum Na
+
, 122 mmol/L) observed during 5 h of intermittent
treadmill walking in a hot environment (Tamb, 41
◦
C). A physically fit, 21 year-old male
began exercise with blood values (serum Na
+
, 134 mmol/L; osmolality, 282 mOsm/kg)
slightly below the laboratory reference ranges for healthy males, because he had voluntarily
overhydrated throughout the previous day. Overhydration prior to exercise is known to
lower serum Na
+
and therefore increase the risk of dilutional hyponatremia if fluids are
aggressively consumed during exercise [
24
]. This man acknowledged that his pre-exercise
overhydrated state, and his high rate of fluid intake during exercise (2061 mL/h; 10.31 L
total), were purposeful. He believed that drinking a large volume of water would decrease
his risk of exertional heat exhaustion and heatstroke.
To understand the factors that guide drinking behavior, Winger and colleagues [
99
]
surveyed 106 female and 97 male runners who had competed in road races (average
experience, 13.0 and 8.3 y, respectively) at distances ranging from 5 to 42.2 km. Seven
years later, Wilson [
100
] surveyed 223 female and 199 male marathon runners (average
number completed by both groups, 4). Both studies focused on runner perceptions of
fluid replacement, their beliefs about rehydration during exercise, and drinking behaviors.
Winger et al. [
99
] observed that the most important influences on the drinking behavior of
runners were: trial and error/personal history, recommendations from running groups or
clubs, and advice from friends; sport drink companies were the least influential sources of
information. Among marathon runners, Wilson [
100
] reported that the following sources
of information were considered to be the most reliable: social media, print magazines,
a personal trainer, and a fellow runner; scientific journals, dietitians/nutritionists, and
running coaches were rated as the least reliable sources of information.
4.4. Unique Characteristics of Competitive Events
Distinctive aspects of different sporting events also can influence an athlete’s rate of
fluid intake; three examples follow. First, the possibility of inhaling water when respiratory
ventilation rate is high (e.g., 120–155 L/min), and potentially having to stop to clear both
lungs [
21
], may deter runners from drinking. Second, whereas fluid intake during endurance
footraces is generally limited to the number of aid stations along a race course or a water
bottle in hand, cyclists can consume fluids whenever desired because containers are attached
to the bicycle frame or held in jersey pockets. Third, during the water stage of a triathlon,
endurance swimmers have no access to fluids except the water they inadvertently consume
during competition. These factors explain, in part, the consistent observation that endurance
competitors replace ≤50% of sweat losses when allowed liquids ad libitum [101–103].
5. Rehydration Options
Table 5describes five approaches to rehydration that endurance athletes employ:
drink when thirsty, ad libitum drinking, individualized planned drinking, drink nothing,
and drink as much as possible. In the following paragraphs, these approaches will be
named options 1 through 5. The percentage of athletes who employ each option during
endurance exercise is unknown.
Nutrients 2021,13, 887 14 of 21
Table 5. Five options for rehydration during endurance exercise.
Description Objective/Rationale Relevant
Publications
1. Drink when thirsty. Fluid intake occurs only
when thirst is sensed.
Primary focus: to prevent exertional hyponatremia. Secondary goal: to
prevent a level of dehydration that impairs exercise performance.
Proponents of this method assert that increased extracellular concentration
triggers thirst to naturally protect athletes from the negative consequences
of both fluid excess and severe dehydration. However, no randomized,
controlled study confirms that drinking when thirsty successfully prevents
exertional hyponatremia. Rationale: drinking when thirsty preserves serum
Na+and osmolality within the normal laboratory reference range.
[55,84,104–110]
2. Ad libitum drinking. Consuming fluid whenever
and in whatever volume desired, without specific
focus on thirst.
Primary focus: to prevent exertional hyponatremia. Secondary goal: to
prevent a level of dehydration that impairs exercise performance. Ad
libitum drinking often is viewed as being identical to drinking when thirsty
(above), however it is subtly different. See text for details.
[6,55,101,110,111]
3. Individualized planned drinking. This involves
drinking a predetermined fluid volume that is
determined by measuring sweat rate.
Primary focus: to prevent excessive dehydration that impairs exercise
performance and to prevent exertional hyponatremia. Secondary goals: to
decrease the risk of heat illness (heat exhaustion, heat stroke), and reduce
cardiovascular/thermoregulatory strain associated with dehydration.
Rationale: because there is considerable inter-individual variability of sweat
rate and sweat electrolyte concentration, a customized fluid replacement
plan meets each athlete’s individual rehydration needs.
[24,26,32,66,108,112,113]
4. Purposefully drink nothing during exercise. No professional sport medicine or sport nutrition organization recommends
this extreme option for prolonged endurance exercise.
5. Purposefully drink as much as possible, in excess
of thirst.
No professional sport medicine or sport nutrition organization recommends
this extreme option for prolonged endurance exercise. Nevertheless, a 2011
survey of runners (5 to 42.2 km finishers) determined that 8.9% plan to
drink as much as possible during racing and training.
[99]
5.1. Options 1 and 2
The distinction between option 1 (using perceived thirst as the only signal to drink)
and option 2 (consuming fluid whenever and in whatever volume desired) is subtle [
101
].
In fact, some professional organizations and experts have not recognized these as distinct
behaviors and some authors use these terms synonymously [
6
,
26
,
84
,
98
,
99
,
101
]. However, a
2014 field study determined that cyclists could identify whether they typically used option
1 or 2 and self-selected into one of two study groups (n= 12 in each). Despite the fact that
cyclists understood options 1 and 2 as distinct rehydration behaviors, no between-group
differences were observed in the following measurements: total fluid intake (L), body
mass change (%), time to ride 164 km (h), urine specific gravity, and rating of thirst at the
finish line [
110
]. Thus, the greatest value of distinguishing options 1 and 2 may exist in
communications among athletes.
During prolonged endurance exercise, the effectiveness of thirst and drinking in
maintaining whole-body fluid–electrolyte balance is challenged [
32
] by large water and
sodium losses in sweat, perturbations of intracellular volume or concentration, and plasma
volume depletion [
6
]. As one example of several in the literature, Greenleaf et al. [
91
]
reported that test subjects who drank ad libitum during exercise-heat stress, were not
thirsty and felt fully recovered despite a body water deficit of 4–5 L. This phenomenon was
named involuntary dehydration [
6
,
12
] because thirst was not sufficient to maintain body
water and fluid intake did not match the level of dehydration. Voluntary dehydration is
observed in most endurance athletes [17,102].
A field study involving 26 ultraendurance cyclists explored thirst during exercise [
114
].
Ratings of thirst were statistically compared to several other variables during 7 h of exercise
(mean ground speed, 25.4 km/h; Tamb, 35.5
◦
C). The total fluid intake of these male cyclists
varied greatly, ranging from 2.1 to 10.5 L during the 164 km ride. Post-event ratings of
thirst were not significantly correlated with any measured variable, including total fluid
intake (i.e., a measure of drinking behavior), body mass index, height, ground speed,
body water balance (ingested fluid volume—volume of fluid lost), and change of body
mass. In other words, the intensity of thirst did not represent the degree of dehydration
or the volume of fluid consumed. This observation is consistent with the known effects
of oropharyngeal sensations on drinking behavior. These sensory signals (e.g., mouth
dryness, swallowing fluid) rapidly reduce and limit fluid intake by modulating satiety
and opposing overdrinking [
115
]. Thus, whenever fluid is consumed, even if the volume
Nutrients 2021,13, 887 15 of 21
is small, oropharyngeal signals diminish the sensation of thirst [
93
,
115
] and theoretically
reduce the risk of EHN by reducing fluid intake.
5.2. Option 3
Individualized planned drinking appeals to athletes who prefer to design their exercise
rehydration systematically. This approach to rehydration is recommended by the National
Athletic Trainer’s Association [
26
] and the American College of Sports Medicine [
24
].
The accuracy of this method relies on an objective measurement of sweat rate during
outdoor exercise. After sweat rate is determined, the athlete can design a customized fluid
replacement plan for use during endurance exercise, realizing that the predetermined rate
of fluid intake always should be less than sweat rate, to avoid overhydration and body
weight gain.
5.2.1. Determining Sweat Rate
The method to determine sweat rate involves voiding the bowel and bladder, weighing
body mass before exercise on a digital floor scale with a precision of 0.1 kg (i.e., 0.2 lb),
simulating a future competitive event (i.e., considering environmental conditions, exercise
intensity), and measuring body weight after exercise [
116
,
117
]. Sweat rate equals the
body mass change per hour. If fluid is consumed or if urine is excreted between the pre-
and post-exercise body weight measurements, the final sweat rate should be corrected as
follows: sweat rate (L/h) = body weight difference (1 kg = 1 L) + water intake (L)—urine
volume (L). All factors are measured over a 1-h or half-hour period; the latter is corrected
to 1 h mathematically.
5.2.2. Determining a Morning Baseline Body Mass
As body mass measurements may be impractical or impossible at the event site,
it is valuable for each athlete to determine his/her baseline body mass approximately
1 week before an event. This is done by measuring body weight upon waking, on
3–5 consecutive days, using an accurate digital floor scale (
±
0.1 kg or lb). The median
(middle) or average body mass serves as a useful baseline [
116
]. The important comparison
is made between this baseline value and the body mass measured on the morning after
an endurance event [
118
,
119
]. If the post-event body mass is notably less or greater than
baseline, fluid intake should be adjusted accordingly (i.e., avoiding overconsumption and
underconsumption) for 1–2 days; thirst and urine color changes will assist this adjustment
of fluid intake [
5
,
118
,
119
]. Three other details are important. First, wear little or no clothing
each time that body mass is recorded. Second, if dietary carbohydrate “loading” is used
during the days prior to competition, body mass may increase (0.5–1.5 kg) because water is
stored with glycogen in skeletal muscles. This extra water temporarily inflates body mass
measurements, and these values should not be used to determine one’s baseline. Third,
this technique may not be valid after an event lasting 7–24 h because loss of muscle mass
and/or fat mass may confound interpretation of body water status for several days after
an ultraendurance event [16].
5.2.3. Interpreting Body Mass Changes
During exercise lasting 0.5–4.0 h, body mass change (
∆
M
b
) is the most commonly
used representation of body water change [
120
,
121
] because most of body weight loss is
water loss, muscle and adipose tissue losses are negligible, and
∆
M
b
has a measurement
resolution of
±
0.1 L (e.g., 100 mL out of a 42–47 L total body water volume) when using a
floor scale that reads to
±
100 g. Within the time frame of 0.5–4.0 h,
∆
M
b
essentially equals
water loss (i.e., when corrected for the mass of fluid and food intake, urine output, and
sweat loss), because no other body constituent is lost at a similar rate [
120
,
122
]. Option 3
in Table 5is the only approach to rehydration that incorporates a known sweat rate
value (calculated using
∆
M
b
measurements) and a planned rate of fluid intake (personally
monitored during competition).
Nutrients 2021,13, 887 16 of 21
When endurance exercise lasts longer than 4 h, the contributions of other factors
confound the interpretation of
∆
M
b
[
13
]. These include mass loss due to carbohydrate or
fat oxidation, cellular water generated during metabolic reactions, and skeletal muscle
and/or adipose tissue catabolism [
15
,
16
,
71
]. However, because athletes seldom know the
technical methods to calculate these internal gains and losses of water, measurements of
∆
M
b
remain the only realistic surrogate measure of dehydration for athletes and field-based
practitioners [15,77,119,122].
5.3. Options 4 and 5
The practices of drinking as much as possible (i.e., increasing the risk of EHN) and
drinking nothing (i.e., increasing the likelihood of a performance decrement) are discour-
aged. No professional sports medicine or sports nutrition organization recommends these
extreme options during endurance exercise.
6. Rehydration Recommendations for Endurance Athletes
Attempting to control all of the factors that influence thirst, drinking behavior, ex-
ercise performance, and health (described in the paragraphs above) is a formidable and
unreasonable task. Nevertheless, the aim of rehydration should be to consume a volume of
fluid that not only avoids dehydration greater than 2–4% of body mass, but also avoids
overhydration. Although no single recommendation will suffice for all individuals (e.g.,
across a range of ambient temperatures, and with varied sweat rates, body masses, and
exercise durations/intensities) [
123
], the following 9 recommendations are appropriate for
most endurance and ultraendurance activities.
1.
Measure body weight before and after exercise (Section 5.2.1). Change of body mass
during exercise is a reasonable, albeit not perfect, surrogate measure of water gain
or loss [
15
,
77
,
119
,
122
]. If body weight cannot be assessed on the day of endurance
exercise, measure body weight on the morning after and compare this weight to a
pre-determined baseline morning body weight [
119
]. Detailed methods are described
above in Sections 5.2.2 and 5.2.3.
2. Do not gain weight during endurance exercise. Weight gain typically indicates fluid
retention and increased risk of EHN [32,63].
3.
Consume fluid at a rate less than 700 mL/h to reduce the risk of EHN. The proposed
rationale for this recommendation is described in Section 3.2.4, Table 4(column 8, sym-
bols A–E), and Figure 2(gray and yellow highlighted symbols). This recommendation
is consistent with the 2001 guidelines of the International Marathon Medical Direc-
tors Association [
84
], and the 2007 fluid replacement position stand of the American
College of Sports Medicine [
24
]. Both organizations recommend a 400 to 800 mL/h
rate of fluid intake during endurance exercise.
4.
Be alert for physiologic and perceptual cues that discourage drinking. When stomach
fullness, bloating, or vomiting are experienced, decrease fluid intake [84].
5.
Guide drinking behavior with this in mind: modest levels of dehydration up to 2–3%
of body weight are tolerated well, with little risk of morbidity, symptoms, or a decline
in exercise performance (Figure 1; Figure 3) [77].
6.
According to the International Marathon Medical Directors Association [
84
], a weight
loss that exceeds 4% of body mass justifies a medical consultation. The number of
athletes affected by at least a 4% loss of body mass during prolonged endurance
exercise is considerable, as shown in Figure 2.
7.
After endurance exercise, white salt deposits on a shirt, jersey, or shorts indicate both
a high sweat rate and a high sweat sodium concentration [
124
]. Consecutive days of
profuse sweating (e.g., during lengthy training sessions) or a day-long utraendurance
event in a hot environment may lead to whole-body salt deficiency [
125
,
126
] due to
large sweat sodium losses, inadequate sodium intake, or both [
46
]. If salt depletion
is suspected (e.g., increased salt appetite or salt craving), it is prudent to consider
adding specific dietary food items to ensure that daily sodium intake replaces exercise-
Nutrients 2021,13, 887 17 of 21
induced sodium loss. Refer to [
97
] to identify the amount of sodium in common
food items. Sodium supplementation during meals should be guided by dietary
recommendations for daily sodium intake [
127
], and by considering the potential
negative health effects of chronic high dietary salt intake [128].
8.
Sodium consumption in solid food or capsules has a minor influence on serum Na
+
and
whole-body sodium balance during endurance exercise (Section 3.2.5) [
88
,
89
]. Athletes
should be aware that sodium intake, while not discouraged, may provide little or
no defense against EHN during prolonged exercise and the effects are unpredictable
(see Table 3). This recommendation is supported by observations of ultramarathon
runners [
80
]. Multiple regression analysis indicated that the amount of sodium
consumed during a 161 km race accounted for only 6–8% of the variance in post-
race serum Na
+
. This recommendation also is supported by the Wilderness Medical
Society Clinical Practice Guidelines [
123
], which advise that sodium and/or salty
snacks be consumed along with an appropriate fluid volume. Salt intake should not
be combined with overdrinking, which increases the risk of EHN despite sodium
consumption; see recommendations 2–4 above.
9.
Experiment with rehydration options (Table 5) during training sessions, before using
them in competition or in hot environments.
Funding: This research received no external funding.
Institutional Review Board Statement: Not applicable.
Informed Consent Statement: Not applicable.
Data Availability Statement:
No new data were created or analyzed in this study. Data sharing is
not applicable to this article.
Conflicts of Interest: The author declares no conflict of interest.
References
1.
Thornton, S.N. Thirst and hydration: Physiology and consequences of dysfunction. Physiol. Behav.
2010
,100, 15–21. [CrossRef]
[PubMed]
2. Fitzsimons, J.T. The physiological basis of thirst. Kidney Int. 1976,10, 3–11. [CrossRef]
3.
Galanth, C.; Hus-Citharel, A.; Li, B.; Llorens-Cortes, C. Apelin in the control of body fluid homeostasis and cardiovascular
functions. Curr. Pharm. Des. 2012,18, 789–798. [CrossRef] [PubMed]
4.
Azizi, M.; Iturrioz, X.; Blanchard, A.; Peyrard, S.; De Mota, N.; Chartrel, N.; Vaudry, H.; Corvol, P.; Llorens-Cortes, C. Reciprocal
regulation of plasma apelin and vasopressin by osmotic stimuli. J. Am. Soc. Nephrol. 2008,19, 1015–1024. [CrossRef] [PubMed]
5.
Cheuvront, S.N.; Kenefick, R.W. Am I drinking enough? Yes, no, and maybe. J. Am. Coll. Nutr.
2016
,35, 185–192. [CrossRef]
[PubMed]
6.
Greenleaf, J.E. Problem: Thirst, drinking behavior, and involuntary dehydration. Med. Sci. Sports Exerc.
1992
,24, 645–656.
[CrossRef]
7.
Bartoli, W.P.; Davis, J.M.; Pate, R.R.; Ward, D.S.; Watson, P.D. Weekly variability in total body water using
2
H
2
O dilution in
college-age males. Med. Sci. Sports Exerc. 1993,25, 1422–1428. [CrossRef]
8. Armstrong, L.E. Assessing hydration status: The elusive gold standard. J. Am. Coll. Nutr. 2007,26, 575S–584S. [CrossRef]
9.
Armstrong, L.E.; Johnson, E.C. Water Intake, Water Balance, and the Elusive Daily Water Requirement. Nutrients
2018
,10, 1928.
[CrossRef]
10.
Speedy, D.B.; Noakes, T.D.; Rogers, I.R.; Thompson, J.M.; Campbell, R.G.; Kuttner, J.A.; Boswell, D.R.; Wright, S.; Hamlin, M.A.
Hyponatremia in ultradistance triathletes. Med. Sci. Sports Exerc. 1999,31, 809–815. [CrossRef]
11.
Hew-Butler, T.; Collins, M.; Bosch, A.; Sharwood, K.; Wilson, G.; Armstrong, M.; Jennings, C.; Swart, J.; Noakes, T. Maintenance of
plasma volume and serum sodium concentration despite body weight loss in ironman triathletes. Clin. J. Sport Med.
2007
,17, 116–122.
[CrossRef]
12.
Adolph, E.F. Signs and symptoms of desert dehydration. In Physiology of Man in the Desert; Adolf, E.F., Ed.; Interscience Publishers:
Cummings Park, MA, USA, 1947.
13. Rehrer, N.J. Fluid and electrolyte balance in ultra-endurance sport. Sports Med. 2001,31, 701–715. [CrossRef]
14. Barr, S.I.; Costill, D.L. Water: Can the endurance athlete get too much of a good thing? J. Am. Diet. Assoc. 1989,89, 1629.
15.
Armstrong, L.E.; Johnson, E.C.; Ganio, M.S.; Judelson, D.A.; Vingren, J.L.; Kupchak, B.R.; Kunces, L.J.; Muñoz, C.X.; McKenzie, A.L.;
Williamson, K.H. Effective body water and body mass changes during summer ultra-endurance road cycling. J. Sports Sci.
2015,33, 125–135. [CrossRef] [PubMed]
Nutrients 2021,13, 887 18 of 21
16.
Knechtle, B.; Knechtle, P.; Wirth, A.; Rüst, C.A.; Rosemann, T. A faster running speed is associated with a greater body weight
loss in 100-km ultramarathoners. J. Sports Sci. 2012,30, 1131–1140. [CrossRef]
17. Rehrer, N.J.; Burke, L.M. Sweat losses during various sports. Nutr. Diet. 1996,53 (Suppl. S4), S13–S16.
18.
Barnes, K.A.; Anderson, M.L.; Stofan, J.R.; Dalrymple, K.J.; Reimel, A.J.; Roberts, T.J.; Randell, R.K.; Ungaro, C.T.; Baker, L.B.
Normative data for sweating rate, sweat sodium concentration, and sweat sodium loss in athletes: An update and analysis by
sport. J. Sports Sci. 2019,37, 2356–2366. [CrossRef] [PubMed]
19. Borg, G. Perceived exertion as an indicator of somatic stress. Scand. J. Rehabil. Med. 1970,2, 92–98.
20.
Noakes, T.D.; Sharwood, K.; Speedy, D.; Hew, T.; Reid, S.; Dugas, J.; Almond, C.; Wharam, P.; Weschler, L. Three independent
biological mechanisms cause exercise-associated hyponatremia: Evidence from 2135 weighed competitive athletic performances.
Proc. Natl. Acad. Sci. USA 2005,102, 18550–18555. [CrossRef]
21.
Armstrong, L.E.; Hubbard, R.W.; Jones, B.; Daniels, J.T. Preparing Alberto Salazar for the Heat of the 1984 Olympic Marathon.
Phys. Sportsmed. 1986,14, 73–81. [CrossRef]
22.
Roberts, W.O.; Dorman, J.C.; Bergeron, M.F. Recurrent Heat Stroke in a Runner: Race Simulation Testing for Return to Activity.
Med. Sci. Sports Exerc. 2016,48, 785–789. [CrossRef] [PubMed]
23. Bergeron, M.F.; SIVOTEC Analytics, Boca Raton, FL, USA. Personal communication, 2021.
24.
Sawka, M.N.; Burke, L.M.; Eichner, E.R.; Maughan, R.J.; Montain, S.J.; Stachenfeld, N.S. American College of Sports Medicine
position stand. Exercise and fluid replacement. Med. Sci. Sports Exerc. 2007,39, 377–390. [PubMed]
25.
Armstrong, L.E.; Casa, D.J.; Millard-Stafford, M.; Moran, D.S.; Pyne, S.W.; Roberts, W.O. Exertional heat illness during training
and competition. Med. Sci. Sports Exerc. 2007,39, 556–572. [CrossRef] [PubMed]
26.
McDermott, B.P.; Anderson, S.A.; Armstrong, L.E.; Casa, D.J.; Cheuvront, S.N.; Cooper, L.; Kenney, W.L.; O’Connor, F.G.;
Roberts, W.O. National athletic trainers’ association position statement: Fluid replacement for the physically active. J. Athl. Train.
2017,52, 877–895. [CrossRef]
27.
Casa, D.J.; DeMartini, J.K.; Bergeron, M.F.; Csillan, D.; Eichner, E.R.; Lopez, R.M.; Ferrara, M.S.; Miller, K.C.; O’Connor, F.; Sawka, M.N.; et al.
National Athletic Trainers’ Association position statement: Exertional heat illnesses. J. Athl. Train.
2015
,50, 986–1000. [CrossRef]
28.
Collins, J.; Maughan, R.J.; Gleeson, M.; Bilsborough, J.; Jeukendrup, A.; Morton, J.P.; Phillips, S.M.; Armstrong, L.; Burke, L.M.;
Close, G.L.; et al. UEFA expert group statement on nutrition in elite football. Current evidence to inform practical recommenda-
tions and guide future research. Br. J. Sports Med. 2020, 01961. [CrossRef]
29.
Cheuvront, S.N.; Kenefick, R.W. Dehydration: Physiology, assessment, and performance effects. Compr. Physiol.
2014
,4, 257–285.
30.
Judelson, D.A.; Maresh, C.M.; Anderson, J.M.; Armstrong, L.E.; Casa, D.J.; Kraemer, W.J.; Volek, J.S. Hydration and muscular
performance: Does fluid balance affect strength, power and high-intensity endurance? Sports Med.
2007
,37, 907–921. [CrossRef]
31.
Sawka, M.N. Physiological consequences of hypohydration: Exercise performance and thermoregulation. Med. Sci. Sports Exerc.
1992,24, 657–670. [CrossRef] [PubMed]
32. Kenefick, R.W. Drinking strategies: Planned drinking versus drinking to thirst. Sports Med. 2018,48, S31–S37. [CrossRef]
33.
Armstrong, L.; Costill, D.; Fink, W. Influence of diuretic-induced dehydration on competitive running performance. Med. Sci.
Sports Exerc. 1985,17, 456–461. [CrossRef]
34.
Bardis, C.N.; Kavouras, S.A.; Arnaoutis, G.; Panagiotakos, D.B.; Sidossis, L.S. Mild dehydration and cycling performance during
5-kilometer hill climbing. J. Athl. Train. 2013,48, 741–747. [CrossRef]
35.
Bardis, C.N.; Kavouras, S.A.; Kosti, L.; Markousi, M.; Sidossis, L.S. Mild hypohydration decreases cycling performance in the
heat. Med. Sci. Sports Exerc. 2013,45, 1782–1789. [CrossRef]
36.
Walsh, R.M.; Noakes, T.D.; Hawley, J.A.; Dennis, S.C. Impaired High-Intensity Cycling Performance Time at Low Levels of
Dehydration. Int. J. Sports Med. 1994,15, 392–398. [CrossRef] [PubMed]
37.
Goulet, E.D. Effect of exercise-induced dehydration on time-trial exercise performance: A meta-analysis. Br. J. Sports Med.
2011,45, 1149–1156. [CrossRef] [PubMed]
38.
Sawka, M.N.; Pandolf, K.B. Effects of body water loss on physiological function and exercise performance. In Fluid Homeostasis
during Exercise; Gisolfi, C.V., Lamb, D.R., Eds.; Benchmark Press: Carmel, IN, USA, 1990; pp. 1–38. ISBN 0-936157-52-6.
39.
Sawka, M.N.; Young, A.J.; Francesconi, R.P.; Muza, S.R.; Pandolf, K.B. Thermoregulatory and blood responses during exercise at
graded hypohydration levels. J. Appl. Physiol. 1985,59, 1394–1401. [CrossRef]
40.
Armstrong, L.E.; Maresh, C.M.; Gabaree, C.V.; Hoffman, J.R.; Kavouras, S.A.; Kenefick, R.W.; Castellani, J.W.; Ahlquist, L.E.
Thermal and circulatory responses during exercise: Effects of hypohydration, dehydration, and water intake. J. Appl. Physiol.
1997,82, 2028–2035. [CrossRef]
41.
Cheuvront, S.N.; Carter, R.I.; Castellani, J.W.; Sawka, M.N. Hypohydration impairs endurance exercise performance in temperate
but not cold air. J. Appl. Physiol. 2005,99, 1972–1976. [CrossRef]
42.
Sawka, M.N.; Leon, L.R.; Montain, S.J.; Sonna, L.A. Integrated physiological mechanisms of exercise performance, adaptation,
and maladaptation to heat stress. Compr. Physiol. 2011,1, 1883–1928. [PubMed]
43.
Armstrong, L.E. Heat Exhaustion. In Exertional Heat Illness: A Clinical and Evidence-Based Guide; Adams, W.M., Jardine, J., Eds.;
Springer Nature: New York, NY, USA, 2020; pp. 81–115. ISBN 978-3-030-27804-5.
44.
Kenefick, R.W.; Cheuvront, S.N.; Palombo, L.J.; Ely, B.R.; Sawka, M.N. Skin temperature modifies the impact of hypohydration on
aerobic performance. J. Appl. Physiol. 2010,109, 79–86. [CrossRef]
45. Roberts, W.O. Exercise-associated collapse care matrix in the marathon. Sports Med. 2007,37, 431–433. [CrossRef]
Nutrients 2021,13, 887 19 of 21
46.
Gaffin, S.L.; Hubbard, R.W. Pathophysiology of heatstroke. In Medical Aspects of Harsh Environments; Pandolf, K.B., Burr, R.E., Eds.;
Office of the Surgeon General, U.S. Army: Washington, DC, USA, 2001; Volume 1, pp. 161–209. ISBN 978-0-160-51071-7.
47.
Lambert, G.P.; Lang, J.; Bull, A.; Pfeifer, P.C.; Eckerson, J.; Moore, G.; Lanspa, S.; O’Brien, J. Fluid restriction during running
increases GI permeability. Int. J. Sports Med. 2008,29, 194–198. [CrossRef] [PubMed]
48.
Armstrong, L.E.; Lee, E.C.; Armstrong, E.M. Interactions of gut microbiota, endotoxemia, immune function, and diet in exertional
heatstroke. J. Sports Med. 2018, 5724575. [CrossRef] [PubMed]
49.
Bergeron, M.F. Heat cramps: Fluid and electrolyte challenges during tennis in the heat. J. Sci. Med. Sport
2003
,6, 19–27. [CrossRef]
50.
King, B.A.; Barry, M.E. The physiological adaptations to heat-stress with a classification of heat illness and a description of the
features of heat exhaustion. S. Afr. Med. J. 1962,36, 451–455.
51.
Armstrong, L.E.; Hubbard, R.W.; Szlyk, P.C.; Sills, I.V.; Kraemer, W.J. Heat intolerance, heat exhaustion monitored: A case report.
Aviat. Space Environ. Med. 1988,59, 262–266.
52.
Sawka, M.N.; Young, A.J.; Latke, W.A.; Neufer, P.D.; Quigley, M.D.; Pandolf, K.B. Human tolerance to heat strain during exercise:
Influence of hydration. J. Appl. Physiol. 1992,73, 368–375. [CrossRef]
53.
Donoghue, A.M.; Sinclair, M.J.; Bates, G.P. Heat exhaustion in a deep underground metalliferous mine. Occup. Environ. Med.
2000,57, 165–174. [CrossRef]
54.
Irving, R.A.; Noakes, T.D.; Irving, G.A.; Van Zyl-Smit, R. The immediate and delayed effects of marathon running on renal
function. J. Urol. 1986,136, 1176–1180. [CrossRef]
55.
Armstrong, L.E.; Casa, D.J.; Emmanuel, H.; Ganio, M.S.; Klau, J.F.; Lee, E.C.; Maresh, C.M.; McDermott, B.P.; Stearns, R.L.;
Vingren, J.L.; et al. Nutritional, Physiological and Perceptual Responses During a Summer Ultra-Endurance Cycling Event. J.
Strength Cond. Res. 2012,26, 307–318. [CrossRef]
56.
Hillman, A.R.; Turner, M.C.; Peart, D.J.; Bray, J.W.; Taylor, L.; McNaughton, L.R.; Siegler, J.C. A comparison of hyperhydration
versus ad libitum fluid intake strategies on measures of oxidative stress, thermoregulation, and performance. Res. Sports Med.
2013,21, 305–317. [CrossRef]
57.
Kavouras, S.A.; Armstrong, L.E.; Maresh, C.M.; Casa, D.J.; Herrera-Soto, J.A.; Scheett, T.P.; Stoppani, J.; Mack, G.W.; Kraemer, W.J.
Rehydration with glycerol: Endocrine, cardiovascular, and thermoregulatory responses during exercise in the heat. J. Appl.
Physiol. 2006,100, 442–450. [CrossRef] [PubMed]
58.
Van Rosendal, S.P.; Osborne, M.A.; Fassett, R.G.; Coombes, J.S. Guidelines for glycerol use in hyperhydration and rehydration
associated with exercise. Sports Med. 2010,40, 113–139. [CrossRef] [PubMed]
59.
Kerksick, C.M.; Wilborn, C.D.; Roberts, M.D.; Smith-Ryan, A.; Kleiner, S.M.; Jäger, R.; Collins, R.; Cooke, M.; Davis, J.N.; Galvan, E.; et al.
ISSN Exercise & Sports Nutrition Review Update: Research & Recommendations. J. Int. Soc. Sports Nutr. 2018,15, 1–57.
60. Montain, S.J. Strategies to prevent hyponatremia during prolonged exercise. Curr. Sports Med. Rep. 2008,7, S28–S35. [CrossRef]
61.
Armstrong, L.E.; Curtis, W.C.; Hubbard, R.W.; Francesconi, R.P.; Moore, R.O.; Askew, E.W. Symptomatic hyponatremia during
prolonged exercise in heat. Med. Sci. Sports Exerc. 1993,25, 543–549. [CrossRef]
62.
Armstrong, L.E.; McDermott, B.P. Exertional hyponatremia. In Emergency Management for Sport and Physical Activity; Casa, D.J.,
Stearns, R., Eds.; Jones & Bartlett Learning: Burlington, MA, USA, 2015; pp. 169–180. ISBN 978-1-284-02216-2.
63.
Hew-Butler, T.; Rosner, M.H.; Fowkes-Godek, S.; Dugas, J.P.; Hoffman, M.D.; Lewis, D.P.; Maughan, R.J.; Miller, K.C.; Montain, S.J.;
Rehrer, N.J.; et al. Statement of the Third International Exercise-Associated Hyponatremia Consensus Development Conference,
Carlsbad, California, 2015. Clin. J. Sport Med. 2015,25, 303–320. [CrossRef] [PubMed]
64. Weschler, L.B. Exercise-associated hyponatraemia. Sports Med. 2005,35, 899–922. [CrossRef] [PubMed]
65.
Kobrick, J.L.; Sampson, J.B. New inventory for the assessment of symptom occurrence and severity at high altitude. Aviat. Space
Environ. Med. 1979,50, 925–929.
66.
Armstrong, L.E.; Lee, E.C.; Casa, D.; Johnson, E.C.; Ganio, M.S.; McDermott, B.; Vingren, J.; Oh, H.M.; Williamson, K.H. Exertional
Hyponatremia and Serum Sodium Change During Ultraendurance Cycling. Int. J. Sport Nutr. Exerc. Metab.
2017
,27, 139–147.
[CrossRef]
67.
Armstrong, L.E. Exertional hyponatremia. In Exertional Heat Illnesses; Armstrong, L.E., Ed.; Human Kinetics: Champaign, IL,
USA, 2003; pp. 103–136. ISBN 0-7360-3771-3.
68. Hiller, W.D. Dehydration and hyponatremia during triathlons. Med. Sci. Sports Exerc. 1989,21 (Suppl. S5), S219–S221.
69.
Armstrong, L.E.; Casa, D.J. Predisposing Factors for Exertional Heat Illnesses. In Exertional Heat Illnesses; Armstrong, L.E., Ed.;
Human Kinetics: Champaign, IL, USA, 2003; pp. 162–167. ISBN 0-7360-3771-3.
70.
Seal, A.D.; Anastasiou, C.A.; Skenderi, K.P.; Echegaray, M.; Yiannakouris, N.; Tsekouras, Y.E.; Matalas, A.L.; Yannakoulia, M.;
Pechlivani, F.; Kavouras, S.A. Incidence of hyponatremia during a continuous 246-km ultramarathon running race. Front. Nutr.
2019,6, 161. [CrossRef]
71.
Rüst, C.A.; Knechtle, B.; Knechtle, P.; Wirth, A.; Rosemann, T. Body mass change and ultraendurance performance: A decrease in
body mass is associated with an increased running speed in male 100-km ultramarathoners. J. Strength Cond. Res. 2012,26, 1505–1516.
[CrossRef] [PubMed]
72.
Arnaoutis, G.; Anastasiou, C.A.; Suh, H.; Maraki, M.; Tsekouras, Y.; Dimitroulis, E.; Echegaray, M.; Papamichalopoulou, D.;
Methenitis, S.; Sidossis, L.S.; et al. Exercise-Associated Hyponatremia during the Olympus Marathon Ultra-Endurance Trail Run.
Nutrients 2020,12, 997. [CrossRef] [PubMed]
Nutrients 2021,13, 887 20 of 21
73.
Speedy, D.B.; Noakes, T.D.; Rogers, I.R.; Hellemans, I.; Kimber, N.E.; Boswell, D.R.; Campbell, R.; Kuttner, J.A. A prospective
study of exercise-associated hyponatremia in two ultradistance triathletes. Clin. J. Sport Med. 2000,10, 136–141. [CrossRef]
74.
Speedy, D.B.; Rogers, I.R.; Noakes, T.D.; Wright, S.; Thompson, J.M.; Campbell, R.; Hellemans, I.; Kimber, N.E.; Boswell, D.R.;
Kuttner, J.A.; et al. Exercise-induced hyponatremia in ultradistance triathletes is caused by inappropriate fluid retention. Clin. J.
Sport Med. 2000,10, 272–278.
75.
Speedy, D.B.; Rogers, I.; Safih, S.; Foley, B. Hyponatremia and seizures in an ultradistance triathlete. J. Emerg. Med.
2000
,18, 41–44.
[CrossRef]
76.
Montain, S.J.; Cheuvront, S.N.; Sawka, M.N. Exercise associated hyponatremia: Quantitative analysis for understand the aetiology.
Br. J. Sports Med. 2006,40, 98–106. [CrossRef]
77. Hew-Butler, T.; Loi, V.; Pani, A.; Rosner, M.H. Exercise-associated hyponatremia: 2017 update. Front. Med. 2017,4. [CrossRef]
78.
Noakes, T.D.; Goodwin, N.; Rayner, B.L.; Branken, T.R.; Taylor, R.K. Water intoxication: A possible complication during endurance
exercise. Med. Sci. Sports Exerc. 1985,17, 370–375. [CrossRef] [PubMed]
79.
Frizzell, R.T.; Lang, G.H.; Lowance, D.C.; Lathan, S.R. Hyponatremia and ultramarathon running. JAMA
1986
,255, 772–774.
[CrossRef]
80.
Hoffman, M.D.; Stuempfle, K.J. Sodium Supplementation and Exercise-Associated Hyponatremia during Prolonged Exercise.
Med. Sci. Sports Exerc. 2015,47, 1781–1787. [CrossRef] [PubMed]
81.
Bankir, L.; Bichet, D.G.; Morgenthaler, N.G. Vasopressin: Physiology, assessment and osmosensation. J. Intern. Med.
2017
,282, 284–297.
[CrossRef] [PubMed]
82. Hew-Butler, T. Arginine vasopressin, fluid balance and exercise. Sports Med. 2010,40, 459–479. [CrossRef]
83.
Siegel, A.J.; Verbalis, J.G.; Clement, S.; Mendelson, J.H.; Mello, N.K.; Adner, M.; Shirey, T.; Glowacki, J.; Lee-Lewandrowski, E.;
Lewandrowski, K.B. Hyponatremia in marathon runners due to inappropriate arginine vasopressin secretion. Am. J. Med.
2007,120, 461.e11–461.e17. [CrossRef]
84.
Hew-Butler, T.; Verbalis, J.G.; Noakes, T.D. Updated fluid recommendation: Position statement from the International Marathon
Medical Directors Association (IMMDA). Clin. J. Sport Med. 2006,16, 283–292. [CrossRef] [PubMed]
85.
Speedy, D.B.; Thompson, J.M.; Rodgers, I.; Collins, M.; Sharwood, K. Oral salt supplementation during ultradistance exercise.
Clin. J. Sport Med. 2002,12, 279–284. [CrossRef]
86.
Hew-Butler, T.D.; Sharwood, K.; Collins, M.; Speedy, D.; Noakes, T. Sodium supplementation is not required to maintain serum
sodium concentrations during an Ironman triathlon. Br. J. Sports Med. 2006,40, 255–259. [CrossRef]
87.
Hoffman, M.D.; Myers, T.M. Symptomatic Exercise-Associated Hyponatremia in an Endurance Runner Despite Sodium Supple-
mentation. Int. J. Sport Nutr. Exerc. Metab. 2015,25, 603–606. [CrossRef]
88.
Barr, S.I.; Costill, D.L.; Fink, W.J. Fluid replacement during prolonged exercise: Effects of water, saline, or no fluid. Med. Sci.
Sports Exerc. 1991,23, 811–817. [CrossRef]
89.
Vrijens, D.M.J.; Rehrer, N.J. Sodium-free fluid ingestion decreases plasma sodium during exercise in the heat. J. Appl. Physiol.
1999,86, 1847–1851. [CrossRef]
90.
Armstrong, L.E.; Kavouras, S.A. Thirst and drinking paradigms: Evolution from single factor effects to brainwide dynamic
networks. Nutrients 2019,12, 2864. [CrossRef]
91. Greenleaf, J.E.; Sargent, F. Voluntary dehydration in man. J. Appl. Physiol. 1965,20, 719–724. [CrossRef]
92.
Allen, W.E.; Chen, M.Z.; Pichamoorthy, N.; Tien, R.H.; Pachitariu, M.; Luo, L.; Deisseroth, K. Thirst regulates motivated behavior
through modulation of brainwide neural population dynamics. Science 2019,364, 6437. [CrossRef]
93.
Armstrong, L.E.; Giersch, G.E.W.; Dunn, L.; Fiol, A.; Muñoz, C.X.; Lee, E.C. Inputs to Thirst and Drinking during Water Restriction
and Rehydration. Nutrients 2020,12, 2554. [CrossRef]
94.
Armstrong, L.E.; Giersch, G.E.; Colburn, A.T.; Lopez, V.; Sekiguchi, Y.; Muñoz, C.X.; Lee, E.C. Progression of human subjective
perceptions during euhydration, mild dehydration, and drinking. Physiol. Behav. 2021,229, 113211. [CrossRef] [PubMed]
95. Fitzsimons, J.T. Angiotensin, thirst, and sodium appetite. Physiol. Rev. 1998,78, 583–686. [CrossRef] [PubMed]
96.
Kratz, A.; Ferraro, M.; Sluss, P.M.; Lewandrowski, K.B. Laboratory Reference Values. N. Engl. J. Med.
2004
,35, 1548–1563.
[CrossRef]
97.
Armstrong, L.E.; Muˇnoz, C.X.; Armstrong, E.M. Distinguishing Low and High Water Consumers: A Paradigm of Disease Risk.
Nutrients 2020,12, 858. [CrossRef]
98.
Beis, L.Y.; Wright-Whyte, M.; Fudge, B.; Noakes, T.; Pitsiladis, Y.P. Drinking behaviors of elite male runners during marathon
competition. Clin. J. Sport Med. 2012,22, 254–261. [CrossRef] [PubMed]
99.
Winger, J.M.; Dugas, J.P.; Dugas, L.R. Beliefs about hydration and physiology drive drinking behaviours in runners. Br. J. Sports
Med. 2011,45, 646–649. [CrossRef] [PubMed]
100.
Wilson, P.B. Nutrition behaviors, perceptions, and beliefs of recent marathon finishers. Phys. Sportsmed.
2016
,44, 242–251.
[CrossRef] [PubMed]
101.
Cheuvront, S.N.; Haymes, E.M. Ad libitum fluid intakes and thermoregulatory responses of female distance runners in three
environments. J. Sports Sci. 2001,19, 845–854. [CrossRef]
102.
Cheuvront, S.N.; Haymes, E.M. Thermoregulation and marathon running: Biological and environmental influences. Sports Med.
2001,31, 743–762. [CrossRef]
Nutrients 2021,13, 887 21 of 21
103.
Noakes, T.D. Fluid replacement during exercise. In Exercise and Sport Science Reviews, Holloszy, J., Ed.; Williams & Wilkins:
Philadelphia, PA, USA, 1993; Volume 21, pp. 297–330. ISBN 978-0-683-00035-1.
104.
Hoffman, M.D.; Cotter, J.D.; Goulet, É.D.; Laursen, P.B. View: Is drinking to thirst adequate to appropriately maintain hydration
status during prolonged endurance exercise? Yes. Wilderness Environ. Med. 2016,27, 192–195. [CrossRef]
105.
Hoffman, M.D.; Cotter, J.D.; Goulet, É.D.; Laursen, P.B. Rebuttal from “Yes”. Wilderness Environ. Med.
2016
,27, 198–200. [CrossRef]
106.
Hoffman, M.D. Comment on “Drinking Strategies: Planned Drinking Versus Drinking to Thirst”. Sports Med.
2019
,49, 1133–1134.
[CrossRef]
107.
Noakes, T.D. Hydration in the Marathon. Using Thirst to Gauge Safe Fluid Replacement. Sports Med.
2007
,37, 463–466. [CrossRef]
[PubMed]
108.
Kenefick, R.W. Author’s Reply to Goulet: Comment on: “Drinking Strategies: Planned Drinking Versus Drinking to Thirst”.
Sports Med. 2019,49, 635–636. [CrossRef]
109.
Dion, T.; Savoie, F.A.; Asselin, A.; Gariepy, C.; Goulet, E.D. Half-marathon running performance is not improved by a rate of fluid
intake above that dictated by thirst sensation in trained distance runners. Eur. J. Appl. Physiol. 2013,113, 3011–3020. [CrossRef]
110.
Armstrong, L.E.; Johnson, E.C.; Kunces, L.J.; Ganio, M.S.; Judelson, D.A.; Kupchak, B.R.; Vingren, J.L.; Munoz, C.X.; Huggins, R.A.;
Hydren, J.R.; et al. Drinking to thirst versus drinking ad libitum during road cycling. J. Athl. Train.
2014
,49, 624–631. [CrossRef]
[PubMed]
111.
Hubbard, R.W.; Szlyk, P.C.; Armstrong, L.E. Influence of thirst and fluid palatability on fluid ingestion during exercise. In Perspec-
tives in Exercise Sciences and Sports Medicine. Fluid Homeostasis during Exercise; Gisolfi, C.V., Lamb, D.R., Eds.; Benchmark Press:
Indianapolis, IN, USA, 1990; Volume 1, pp. 39–95. ISBN 978-0-697-14816-2.
112.
Armstrong, L.E.; Johnson, E.C.; Bergeron, M.F. Counterview: Is drinking to thirst adequate to appropriately maintain hydration
status during prolonged endurance exercise? No. Wilderness Environ. Med. 2016,27, 195–198. [CrossRef] [PubMed]
113.
Armstrong, L.E.; Johnson, E.C.; Bergeron, M.F. Rebuttal from “No”. Wilderness Environ. Med.
2016
,27, 200–202. [CrossRef]
[PubMed]
114.
Armstrong, L.E.; Johnson, E.C.; McKenzie, A.L.; Ellis, L.A.; Williamson, K.H. Ultraendurance Cycling in a Hot Environment:
Thirst, Fluid Consumption and Water Balance. J. Strength Cond. Res. 2015,29, 869–876. [CrossRef]
115.
Figaro, M.K.; Mack, G.W. Regulation of fluid intake in dehydrated humans: Role of oropharyngeal stimulation. Am. J. Physiol.
Regul. Integr. Comp. Physiol. 1997,272, R1740–R1746. [CrossRef]
116.
Armstrong, L.E.; Casa, D.J. Methods to evaluate electrolyte and water turnover of athletes. Athl. Train. Sports Health Care
2009
,1, 169–179.
[CrossRef]
117. Casa, D.J. Proper hydration for distance running: Identifying individual fluid needs. Track Coach 2004,167, 5321–5328.
118. Armstrong, L.E. Hydration assessment techniques. Nutr. Rev. 2005,63 Pt 2 (Suppl. S6), S40–S54. [CrossRef]
119.
Ganio, M.S.; Armstrong, L.E.; Kavouras, S.A. Hydration. In Sport and Physical Activity in the Heat; Casa, D.J., Ed.; Springer: Cham,
Switzerland, 2018; pp. 83–100. ISBN 978-3-319-70216-2.
120. Kavouras, S. Assessing hydration status. Curr. Opin. Clin. Nutr. Metab. Care. 2002,5, 519–524. [CrossRef] [PubMed]
121. Shirreffs, S.M. Markers of hydration status. Eur. J. Clin. Nutr. 2003,57 (Suppl. S2), S6–S9. [CrossRef]
122.
Maughan, R.J.; Shirreffs, S.M.; Leiper, J.B. 2007. Errors in the estimation of sweat loss and changes in hydration status from
changes in body mass during exercise. J. Sports Sci. 2007,25, 797–804. [CrossRef] [PubMed]
123.
Bennett, B.L.; Hew-Butler, T.; Rosner, M.H.; Myers, T.; Lipman, G.S. Wilderness Medical Society clinical practice guidelines for the
management of exercise-associated hyponatremia: 2019 update. Wilderness Environ. Med. 2020,31, 50–62. [CrossRef] [PubMed]
124.
Kavouras, S.A. Sodium balance during exercise and hyponatremia. In Fluid Balance, Hydration, and Athletic Performance; Meyer, F.,
Szygula, Z., Wilk, B., Eds.; CRC Press: Boca Raton, FL, USA, 2015; pp. 23–31. ISBN 978-1-4822-2328-6.
125. Marriott, H. Water and salt depletion. Br. Med. J. 1942,2, 285–290.
126.
Taylor, H.L.; Henschel, A.; Mickelsen, O.; Keys, A. The effect of the sodium chloride intake on the work performance of man
during exposure to dry heat and experimental heat exhaustion. Am. J. Physiol. 1943,140, 439–451. [CrossRef]
127.
National Academies of Sciences, Engineering, and Medicine. Dietary Reference Intakes for Sodium and Potassium; The National
Academies Press: Washington, DC, USA, 2019. [CrossRef]
128.
Diet, Nutrition and the Prevention of Chronic Diseases: Report of a Joint WHO/FAO Expert Consultation. Geneva, 28 January–
1 February 2002. Available online: https://www.who.int/publications-detail-redirect/924120916X (accessed on 10 February 2021).
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