Cheuvront & Haymes (2001)

REVIEW ARTICLE
Sports Med 2001; 31 (10): 743-762

0112-1642/01/0010-0743/$22.00/0
Adis International Limited. All rights reserved.
Thermoregulation and
Marathon Running
Biological and Environmental Influences
Samuel N. Cheuvront1 and Emily M. Haymes2
1 United States Army Research Institute of Environmental Medicine, Thermal and Mountain
Medicine Division, Natick, Massachusetts, USA
2 Department of Nutrition, Food and Exercise Sciences, Florida State University, Tallahassee,
Florida, USA
Contents
Abstract
. . . . . . . . . . . . . . . . . . . .
1. Thermoregulation and the Marathon . . . .
2. The Role of the Environment . . . . . . . . .
2.1 Environmental Limitations . . . . . . . .
2.2 Performance Evidence . . . . . . . . .
3. The Role of Dehydration . . . . . . . . . . . .
3.1 Fluid Balance . . . . . . . . . . . . . . .
3.2 Distribution of Exercise Fluid Losses . . .
4. The Role of Metabolic Rate . . . . . . . . . .
4.1 Body Mass and Running Speed . . . . .
4.2 Race Strategy and Course Topography
5. The Role of Gender . . . . . . . . . . . . . .
5.1 Environment . . . . . . . . . . . . . . . .
5.2 Dehydration . . . . . . . . . . . . . . . .
5.3 Metabolic Rate . . . . . . . . . . . . . .
5.4 Menstrual Cycle . . . . . . . . . . . . . .
5.5 Summary of Gender . . . . . . . . . . .
6. Statistical Review . . . . . . . . . . . . . . . .
7. Conclusion . . . . . . . . . . . . . . . . . . .
Abstract
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The extreme physical endurance demands and varied environmental settings

of marathon footraces have provided a unique opportunity to study the limits of
human thermoregulation for more than a century. High post-race rectal temperatures (Tre) are commonly and consistently documented in marathon runners, yet
a clear divergence of thought surrounds the cause for this observation. A close
examination of the literature reveals that this phenomenon is commonly attributed
to either biological (dehydration, metabolic rate, gender) or environmental factors.
Marathon climatic conditions vary as much as their course topography and
can change considerably from year to year and even from start to finish in the
same race. The fact that climate can significantly limit temperature regulation
744
Cheuvront & Haymes
and performance is evident from the direct relationship between heat casualties
and Wet Bulb Globe Temperature (WBGT), as well as the inverse relationship
between record setting race performances and ambient temperatures. However,
the usual range of compensable racing environments actually appears to play
more of an indirect role in predicting Tre by acting to modulate heat loss and fluid
balance.
The importance of fluid balance in thermoregulation is well established.
Dehydration-mediated perturbations in blood volume and blood flow can compromise exercise heat loss and increase thermal strain. Although progressive dehydration reduces heat dissipation and increases Tre during exercise, the loss of
plasma volume contributing to this effect is not always observed for prolonged
running and may therefore complicate the predictive influence of dehydration on
Tre for marathon running.
Metabolic heat production consequent to muscle contraction creates an internal heat load proportional to exercise intensity. The correlation between running
speed and Tre, especially over the final stages of a marathon event, is often significant but fails to reliably explain more than a fraction of the variability in
post-marathon Tre. Additionally, the submaximal exercise intensities observed
throughout 42km races suggest the need for other synergistic factors or circumstances in explaining this occurrence.
There is a paucity of research on women marathon runners. Some biological
determinants of exercise thermoregulation, including body mass, surface area-tomass ratio, sweat rate, and menstrual cycle phase are gender-discrete variables
with the potential to alter the exercise-thermoregulatory response to different
environments, fluid intake, and exercise metabolism. However, these gender differences appear to be more quantitative than qualitative for most marathon road
racing environments.
1. Thermoregulation and the Marathon

Homeotherms exist within a narrow operative
range of internal body temperatures (core temperature, Tc) despite regular exposure to environmental extremes. The eloquently precise human thermoregulatory system accomplishes this task using
sensory feedback to the hypothalamus from thermoreceptors within the peripheral and central nervous system.[1] Even small fluctuations in Tc stimulate neural autonomic outflow. A cascade of reflex
vasomotor and cardiovascular responses follows to
correct a temperature change by heat loss or heat
production. Although the upper limits of thermoregulatory control are rarely tested, prolonged exercise provides a unique challenge to the multitude
of systems that maintain temperature homeostasis.
The drama of the marathon, its demanding 42km
distance and varied environmental settings have
for decades provided an excellent opportunity to

study the human capacity for temperature control
(table I). The impact of exercise on Tc is most commonly assessed in the field by the measurement of
rectal temperature (Tre). Numerous individual and
external factors can influence Tre,[36] but consensus
is lacking on which factor, or set of factors, has the
most impact during prolonged physical exertion in
marathon race-like circumstances. Environmental
conditions,[37-41] dehydration[3,5,34,42] and metabolic rate[15,16,22,23] are commonly referenced as limiting for thermoregulatory control; however, gender[31,35,43] may also contribute independently or in
conjunction with other factors. The purpose of this
review is to examine the merit of these variables as
predictors of Tre in distance running. Walking, cycling and other modes of prolonged activity will
also be referenced for comparative purposes when
Sports Med 2001; 31 (10)
Thermoregulation and the Marathon
745
Table I. Review of marathon and related distance running literature

Reference
Distance
(km)
Participants Environment
(n)
[Tdb, relative
humidity]
SR
(L/h)
DEH
(%)
FI
(L/h)
Tre
(C)
Speed
(m/min)
Adams et al.a[2]
42.2
M1
10C
0.71
2.13
0.33
39.4
256
19C
1.44
4.95
0.32
39.6
254
22C
1.25
3.65
0.47
39.9
256
3.71
8.1
0.84
Armstrong et al.a[3]
42.2
M1
23.9-27.8C
Beckner & Winsor[4]
42.2
M1
25.6C, 35%
Buskirk & Beetham[5]
42.2
M4
20.4C, 37%
1.52
Cade et al.a[6]
42.2
M 8; F 3
16.1-22.5C,
60-67%
1.17b,c
Christensen & Ruhling[7] 42.2
F1
18.1-20.5C
Cohen & Zimmermana[8] 42.2
M 18
13.1-13.7C,
99-100%
0.95
2.9
0.39
Kavanagh & Shepharda[9] 42.2
M9
21.7C, 69%
0.93
3.3
0.45
39.1
199
Kavanagh et al.[10]
42.2
M7
26C
0.70
3.5
Magazanik et al.a[11]
42.2
M6
21-26C, 50-60% 1.13
3.7
0.42
38.5
194
Maron et al.a[12]
42.2
M2
18.6C
0.86
2.9
0.54
40.5
259
Maron et al.a[13]
42.2
M2
17.9C
0.86
3.1
0.35
39.9
268
Maron et al.a[14]
42.2
M6
15-29C
0.98
4.3
0.19
39.8
257
Maughan[15]
42.2
M 59
10.8-12.1C,
70-80%
0.74
2.8
0.38
38.8
191
Maughan et al.[16]
42.2
M 62
6.6-11.8C
38.7
198
Maughan et al.[17]
42.2
M 47
10-12C
3.0
0.39
194
Muir et al.[18]
42.2
M 20
13.7-16C
4.97
0.07
303
Myhre et al.a[19]
42.2
M6
17.5-20.4C
F5
Myrhe et al.a[20]
42.2
M3
WBGT:
15.5-24.5C
Nelson et al.[21]
314
5.1
6.4
0.46b,c
39
266
39.1b,c
216b,c
39
180
203
142
0.99
3.2
0.37
39.5
194
0.67
2.92
0.28
38
169
1.24
4.7
0.37
39.2
194
0.41b
175b
42.2
M 39; F 6
7.8C
a[22]
Noakes et al.
42.2
M 30
19-22C, 68%
1.0
2.5
0.61
38.9
Noakes et al.a[23]
42.2
M 10
WBGT: 15-19C
1.27
3.1
0.45
38.3
250
M 16
1.15
2.4
0.49
38.5
213
M 32
0.94
2.3
0.47
38.8
183
M6
0.69
1.6
0.42
39
163
3.1b
0.44b
0.96
5.2
0.13
39
216
1.32
5.8
40.6
259
Pastene et al.[24]
42.2
M 5; F 1
19C, 60%
Pugh et al.a[25]
42.2
M 56
22-23.5C,
52-58%
M 4; top 4
finish
Rehrer et al.[26]
42.2
M 83
6-24C, 45-85%
3.4
F 31
Riley et al.[27]
42.2
Tsintzas et al.[28]
42.2
M7
20.5C, 51%
Wells et al.[29]
42.2
M6
10.6-15C,
48-67%
M1
F4
19.6-21.4C,
52-60%
1.0c
204
210b
0.15b
188
2.6
182
5.4
178
3.9c
0.34c
38.6c
220c
212
237
Continued over page
Sports Med 2001; 31 (10)
746
Cheuvront & Haymes
Table I. Contd
Reference
Distance
(km)
Participants Environment
(n)
[Tdb, relative
humidity]
Whiting et al.[30]
42.2
M 90
Millard-Stafford et al.[31]
40.0
M6
F6
1.25
SR
(L/h)
DEH
(%)
FI
(L/h)
Tre
(C)
Speed
(m/min)
10-12C, 70-80%
2.9
0.373
25-32C, 70-82% 1.71
4.0
0.70
40
230
3.9
0.57
39.3
217
0.79
40.0
231
187
Millard-Stafford et al.[32]
40.0
M8
25-32C, 62-82% 1.8
4.45
Wells et al.[33]
32.0
M 10
23-30C, 25-26%
6.97
Wyndham & Strydom[34] 32.0
M 31
9.1-17.0C,
29-96%
1.5-4.2
total sweat
losses
2-5
0.3-2.4
total fluid
intake
38.3-40.8
Cheuvront & Haymesa[35] 30.0
F8
14C, 64%
0.69
2.5
0.47
38.5
185
20C, 54%
0.80
2.4
0.54
38.6
185
29C, 55%
1.07
2.8
0.70
38.7
185
38.6
Ad libitum fluid intakes.
Male and female data pooled.
Combined data from 3 groups.
DEH = dehydration; F = female; FI = fluid intake; M = male; SR = sweat rate; Tdb = dry bulb (air) temperature; Tre = post-run rectal temperature;
WBGT = Wet Bulb Globe Temperature.
necessary. Despite record setting numbers of female participants in marathon races and the recent
completion of a fifth Womens Olympic Marathon,
surprisingly little research has been devoted to the
study of thermoregulation in the female marathon
runner in particular (table I). Therefore, the potential for gender to affect body temperature regulation
in long-distance running events will be hypothesised where little direct evidence is available.
2. The Role of the Environment
The milieu of intricate regulatory processes which
maintain Tre homeostasis were originally shown to
function independent of wide fluctuations in air temperature (5 to 30C).[44] However, the thermodynamic properties of the environment can significantly add to the challenge that work imposes on
human thermoregulation. Lind[45] was the first to
propose a prescriptive zone of environmental temperatures dependent on exercise intensity for the
prediction of a thermal steady state. As metabolic
heat production rises with the intensity of exercise,
the need to transfer heat away from the body becomes paramount for the maintenance of a thermal
equilibrium. Environmental extremes can severely

limit a favourable thermal gradient for heat loss,
thus imposing additional thermoregulatory strain.
The Wet Bulb Globe Temperature (WBGT) is commonly used to gauge environmental heat stress[46]
by conveying information about humidity [wet bulb
temperature (Twb)], solar radiation [globe temperature (Tg)], and dry bulb (air) temperature (Tdb).
However, all climatic temperatures referred to herein
will be air temperatures (Tdb) unless otherwise indicated.
2.1 Environmental Limitations
Heat exchange occurring between humans and

the environment is defined by the heat balance
equation:
MWRCE=S
where M is defined as the metabolic heat produced during exercise and W as the proportionally
smaller amount of heat used to perform external work.
Convection (C) and radiation (R) are bidirectional
routes of heat exchange, while E represents evaporative heat loss and S denotes heat storage. When
Sports Med 2001; 31 (10)
Tdb and Twb are lower than skin temperatures (Tsk),

a thermal gradient is created which favours heat loss
as warmed blood from the body core is transferred
to the skin by convective blood flow and emitted by
radiation, convection, and sweat evaporation. Hypothalamic control of skin blood flow and sweating results primarily from changes in Tre, although
Tsk can significantly modulate this response.[47-49]
The driving force for radiative and convective
heat loss depends on the maintenance of a large
temperature gradient between skin and air. When
Tdb exceeds 36C, the gradient for heat exchange
is reversed and heat is gained. [41,50] If storage
heat raises Tre to 38C, convective heat transfer
approaches its limits as the slope of the skin blood
flow response to continued elevations in Tre reaches
a plateau.[48,51] This is explained by blood flow
limitations involving the skin, active musculature
and the quintessential need to maintain blood pressure.[48,52-54] However, as Tdb rises, sweat rate also
increases.[2,39] Sweat evaporation becomes the primary means of heat dissipation when convective
and radiative heat exchanges are minimal. Approximately 0.6 kcal of heat are removed when 1ml of
sweat evaporates from the skin surface.[55] Therefore, the average sweat rate of 1.2 L/h, taken from the
marathon studies in table I, would result in more than
half of all the heat produced under moderate to hot
environmental conditions being lost through evaporation, even at extremely high metabolic rates.[41,56]
However, evaporative heat losses can also be limited by the environment.
When the water vapour pressure of the air approaches skin water vapour pressure, evaporation
is reduced. At any given temperature, relative humidity provides an index of the actual amount of
water vapour in the air relative to its maximal water-holding capacity.[57] Since the temperature of
the air and its water holding capacity are linearly
related,[58] hot humid weather can severely limit
the largest and final avenue of heat exchange. If the
metabolic rate during exercise in a hot, humid environment requires levels of evaporative heat exchange that exceed the capacity of the environment
to accommodate more water vapour, a critical heat
747
load may be reached which limits further exercise

and produces dangerous, uncompensable heat
strain.[41,59,60]
Direct solar radiation can also add significantly
to the thermal metabolic load,[58,61] and consideration for reflected and emitted solar radiation from
the ground must not be forgotten. When all of these
measurements were considered in the assessment
of climatic heat stress at the start of the 1992 Womens Olympic Marathon,[58] a WBGT measurement
of 27.7C was made that was just within the acceptable upper limit (28C) for competition judged
by the American College of Sports Medicine.[46]
The important influence and limitations that the
environment can have on thermoregulation during
prolonged exercise like the marathon is therefore
clear.
Mass participation marathons are held under significantly variable environmental conditions, even
for the same annual events. For example, race-day
air temperatures at the New York City Marathon
have ranged from 1 to 29C between 1984 and 1995,
despite a consistent annual race-day calendar (October 28 to November 12).[62] Temperatures have
even been reported to change by as much as 17C
from start to finish in the same race.[62] Not surprisingly, more medical complaints of hyperthermia
(Tre 39C)[46] occur in warm weather marathon
events,[63,64] while hypothermia (Tre 35C)[46] is
often reported for cool weather events.[65] Although
temperature ranges can be extreme, most marathons
are held under compensable climatic conditions
(table I).
Adams et al.,[2] systematically examined the effect of temperature by having an individual run 3
marathons at the same pace (255 m/min) under 3
temperatures of 10, 19 and 22C. The results from
Tre measurements were 39.4, 39.6 and 39.9C, respectively, suggesting a potential influence of environment. In the field, Maughan[15] has reported
Tre among competitors ranging from hypothermic
(35.6C) to hyperthermic (39.8C) values in the
same race held under cool conditions (10 to 12C).
Two different marathon studies, both run under mild
(19C) conditions reported Tre in runners ranging
Sports Med 2001; 31 (10)
748
from 38[22] to 41.7C.[12] The warmest runs reviewed (table I) report Tre of 40C at a WBGT between
23 to 29C.[31,32] It would, therefore, appear that
individual differences in heat loss efficiency, fluid
balance, or metabolic rate might better explain the
wide variations in Tre observed between runners
competing under the same or similar environmental conditions. The fact that typical marathon racing environments do not severely limit heat loss or
impose oppressive heat gain also supports this conclusion. However, one trend does remain clear among
the studies reviewed. Runners competing at or below 12C may be at risk for developing hypothermia rather than hyperthermia.[15,16,65]
2.2 Performance Evidence
Suping et al.[37] examined the influence of climate on marathon performance and found that actual 42km race times were 1 minute faster and 10
minutes slower than registered race times when Tdb
was 8 and 29C, respectively. Trapasso and Cooper[38] reported a correlation (r = 0.739) between
Twb and finishing times at the Boston Marathon,
with record setting performances most often characterised by a Twb below 8C. Sky cover in Boston
was 100% in 25 out of the 31 races examined and
this meteorological variable improved the explained
variance in running time to r = 0.836.[38] This obvious impact of climate on performance is further
exaggerated by fluid restriction. In the absence of
fluid intake, Galloway and Maughan[39] observed
higher Tc and shorter times to exhaustion (42 minutes) in cyclists when exercising at 30 compared
with 10C. Even when glycogen depleted, athletes
in the cold (10C) cycled 36 minutes longer than
glycogen loaded athletes in the heat (30C) when
fluid intake remained restricted.[40] Therefore, while
extremes in temperature, solar radiation and humidity add to the external heat load and limit heat
losses, more modest environmental changes still
alter time to fatigue if fluid is withheld. Since sweat
rate is proportional to air temperature when metabolic rate is held constant,[2,39] some of the detrimental effects of warmer environments on endur Adis International Limited. All rights reserved.
Cheuvront & Haymes
ance performance can be rationalised as the result

of poor fluid balance.
3. The Role of Dehydration
The integrity of the thermoregulatory system during exercise is logically determined by the maintenance of an adequate blood volume. Although research abounds to explain the proposed mechanisms
by which body water losses (dehydration) increase
thermoregulatory strain, it must be recognised that
most studies have been designed to test these effects
by dehydrating individuals before exercise (hypohydration). The methods used to create a fluid deficit often vary and include diuretic administration,
food and fluid restriction, pre-experiment exercise
and passive thermal exposure. Unfortunately, none
of these techniques is what occurs during a marathon. While these studies are desirable for an understanding of physiological phenomena, they are
probably of little practical application for runners
who are adequately hydrated (euhydrated), well nourished, rested and otherwise prepared for competition. Additionally, the method of water loss is known
to differently affect the partitioning of fluid between
the intracellular and extracellular spaces and can
produce both volume and osmotic changes that independently affect temperature regulation.[66] For
these reasons, only research involving active dehydration (process of losing water from the euhydrated state) and its effects on thermoregulation will
be reviewed.
Relatively few studies have compared the effects of active dehydration to euhydration on human thermoregulatory responses under controlled
conditions. Pitts et al.,[67] was the first to systematically demonstrate that active dehydration resulted
in a progressive and continued rise in Tre during
extended treadmill marches in the heat. The same
experiments showed convincingly how both modest and complete replacement of fluid losses attenuated the hyperthermia of dehydration. Costill et
al.,[68] measured the Tre responses of marathon runners during 2 hours of treadmill running (25C)
with and without fluid replacement. The observed
rise in Tre was ameliorated beyond 1 hour of exerSports Med 2001; 31 (10)
cise when fluid was taken. Gisolfi and Copping[69]

compared the thermoregulatory responses of 6 men
during 2 hours of treadmill running (33C) under
7 experimental conditions. Dehydration progressively elevated Tre and regular fluid replacement
dampened this response again after 1 hour of exercise. A strong correlation (r = 0.76 to 0.87) was
reported for the effect of percent bodyweight loss
on Tre, and an 0.4C rise in Tre was predicted for
each 1% of bodyweight loss incurred beyond 2%
of bodyweight.[69] Remarkably similar results were
seen by Maron et al.[13] 2 years later when comparing 2 competitive marathon runners in the field.
Both athletes finished the race within 3 minutes of
each other, ran at approximately the same velocity
and had similar bodyweights and sweat rates but
markedly different fluid intakes. Runner one had a
body water deficit of 2.6% and an overall increase
of 2.2C in Tre. The other finished with a 3.6%
bodyweight loss and a 2.6C rise in Tre. The difference between the 2 runners was 1% dehydration
and an 0.4C difference in Tre,[12,13] corroborating
the prediction of Gisolfi and Copping.[69]
More recently, in a series of cycling studies,[52,54,70]
participants were compared during 2 hours of cycling
in the heat (22 to 35C) with 80% replacement of
fluid losses versus no fluid replacement. Bodyweight
losses for the no fluid replacement groups ranged
from 3 to 5%. Tre rose under both conditions for
the first 1 hour of exercise, after which a plateau
was observed for the fluid replacement groups only,
while Tre rose continuously in the no fluid replacement groups.[52,54,70] Participants in the no fluid replacement groups consistently had higher heart rates,
lower stroke volumes and cardiac outputs,[52,54,70]
as well as reduced skin blood flow[52,70] and higher
systemic vascular resistance.[52] A 3 to 6% reduction in blood volume below fluid replacement group
values was reported for the no fluid replacement
groups in all studies. By providing fluid to replace
20, 50 and 80% of sweat losses in a similar cycling
study (at 33C), Montain and Coyle[42] showed that
the magnitude of graded dehydration was directly
related to the observed rise in both Tre (r = 0.98)
and heart rate (r = 0.99), as well as the drop in
749
stroke volume (r = 0.99). An additional 3% reduction in plasma volume below control values was
observed after 40 minutes of exercise and serum
osmolality was positively correlated (r = 0.81 to
0.98) with the rise in Tre from 20 minutes to 2 hours
of exercise.
Together, these 4 experiments support that competition for blood between the cutaneous circulation and active tissue occurs despite elevated body
temperatures. The need to maintain blood pressure
(mean arterial pressure) appears to supersede requirements for heat dissipation as evidenced by classic cardiovascular drift together with enhanced peripheral sympathetic vasoconstriction. The role of
osmotic and volume loss factors in the evolution
of hyperthermia is also demonstrable and in agreement with a comprehensive review of hypohydration studies.[71] Therefore, it is clear that active dehydration increases thermoregulatory strain under
controlled laboratory conditions. However, field studies offer more ambiguous results.
Although the study of Wyndham and Strydom[34]
is often credited as the first to suggest that dehydration is the most influential factor in determining
Tre during a marathon race, Buskirk and Beetham[5]
were the first to report a significant correlation (r
= 0.58) between dehydration and Tre following observations at the Boston Marathon. After controlling for rate of work (speed bodyweight), which
itself was poorly correlated with Tre (r = 0.11), the
correlation coefficient improved to r = 0.66. However, the average bodyweight loss incurred in this
race was considerable (6%).[5] Wyndham and Strydom[34] evaluated the Tre and dehydration levels of
runners following two 32km field efforts. Their analysis of the data indicated a similar linear relationship (r = 0.67) between percent bodyweight loss
and Tre when expressed beyond a 3% deficit in bodyweight. Adams et al.[2] reported an even stronger
overall relationship (r = 0.79) between dehydration
and Tre after a series of repeated and controlled
treadmill marathon runs resulting in a mean bodyweight loss of 3.5%. All 3 studies were performed
in temperatures (Tdb) ranging from 10 to 22C. Opposition to the predictive nature of dehydration on
Sports Med 2001; 31 (10)
750
Tre during marathon running has also been offered.

In 42km races held under similar ranges in environmental temperatures (Tdb = 8 to 19C), neither
Noakes et al.[22,23] nor Maughan[15] could establish
any significant relationship between the level of
dehydration and Tre. Noakes et al.[22] reported a
low, nonsignificant correlation coefficient (r =
0.18).
The studies that argue against any effect of dehydration on Tre report bodyweight losses ranging
from 1.6 to 3.1%, with an overall mean of <2.5%
(table I). All research showing positive relationships between dehydration and Tre incurred a 3%
bodyweight deficit. According to Wyndham and
Strydom,[34] a true linear relationship between those
variables occurs only beyond 3% dehydration. The
reduction in plasma volume that occurs with increasing dehydration may provide an explanation
since losses in plasma volume, even in the absence
of osmotic changes, can impair heat loss.[66] In the
field, Myhre et al.[19] observed a maintenance in
plasma volume in marathon runners provided dehydration was <4% bodyweight. These losses did
not impair cardiovascular or thermoregulatory function as plasma volumes were kept constant beyond
initial drops at the onset of exercise. [19] Similar
plasma volume stability has been observed by others for marathon[72] and treadmill[73] running despite even larger reductions (4 to 7%) in total body
water.
Because cycling imparts a comparatively greater
haemoconcentration than running,[74] the mode of
exercise may explain differences in plasma volume
losses and thermoregulatory sensitivity to dehydration. Indeed, when compared with marathon data
with similar levels of dehydration, plasma volume
losses were larger and declined progressively in the
cycling study[42] while the sensitivity of Tre to these
graded deficits in body water was also clearly demonstrated.[42] Therefore, Tre responds to active dehydration (1 to 4%) in a graded fashion under controlled
laboratory cycling conditions. Alternatively, plasma
volume appears well defended when running and
may require that some threshold of dehydration
Cheuvront & Haymes
be exceeded before reliable correlations with Tre

can be observed.
3.1 Fluid Balance
A review of fluid balance data from the distance

running literature (table I) provides valuable insight into typical fluid losses, intakes and body temperature responses to marathon racing events. When
divided into races run in cool weather (<15C =
CW)[2,8,15-18,21,29,30,32] and warm weather (>15C =
WW),[2-7,9-14,19,20,22,24-28,31-33] average dehydration
values of 3.2% (CW) to 4% (WW) are observed
with corresponding Tc of 39.0 and 39.3C, respectively. Sweat rates range from 0.83 L/h (CW) to 1.2
L/h (WW).
Research using active dehydration while cycling has made it clear that replacing 50 to 80% of
sweat losses will maintain plasma volume and Tre
throughout exercise.[42,70] When drinking low volumes (50% of sweat losses), significantly higher
Tre are only apparent after 2 hours of exercise when
compared with drinking larger fluid volumes. Interestingly, similar results were observed more than
50 years ago.[67] For an individual marching in the
heat, ad libitum fluid intakes equal to 66% of sweat
losses maintained Tc within a zone of comfort
(38.3C) almost as well as 100% replacement
(38.1C) for up to 4 hours of light exercise.
Fluid intakes that produce a Tre plateau in male
runners are 0.6 to 1.2 L/h.[42,68,69] However, abdominal discomfort was noted at 1.2 L/h in one study.[68]
A lower tolerance to high fluid volumes is seen
more commonly when running at intensities approaching those seen in marathon races and probably relates to a reduction in gastric emptying.[75,76]
This fact may explain in part the poor ad libitum
fluid intake practices observed for runners in table
I, who replaced 43% (0.36 L/h, CW) and 36% (0.43
L/h, WW) of sweat losses (0.83 L/h, CW and 1.2
L/h, WW) in those studies.[2,3,6,8,9,11-14,19,20,22,23,25]
Noakes et al.[22,23] have argued that 0.5 to 0.6
L/h fluid consumption is all that is necessary to
maintain Tre in cool or moderate environments.
This appears accurate for fair weather marathons
since these volumes would replace 63 to 75% of
Sports Med 2001; 31 (10)
average sweat losses (0.83 L/h) previously calculated from table I CW studies. Also, this volume
(%) has already been shown to maintain plasma
volume and supports a plateau in exercise Tre. The
same authors additionally contend that this volume
is adequate because an overestimate of eccrine sweat
production occurs when failing to account for respiratory and metabolic bodyweight losses.
3.2 Distribution of Exercise Fluid Losses
The hypothesis that current fluid intake recommendations (ideally replace 100% of sweat losses)[77]
may overestimate fluid replacement needs by failing to consider that bodyweight loss (dehydration)
is not synonymous with sweat loss[22,23] is a noteworthy observation. The weight in question can
be divided into eccrine sweat loss, metabolic bodyweight loss (CO2-O2 exchange)[78] and respiratory
bodyweight loss.[79] The relative contribution of
each variable mentioned to total bodyweight loss
has recently been examined in female marathon
runners. Respiratory and metabolic bodyweight loss
combined represented 15, 13 and 7% of total bodyweight loss at 12, 17 and 25C (WBGT) during
each of three 30km treadmill runs.[35] Theoretical calculations for a man [maximal oxygen up.
take (VO 2max) = 4.55 L/min], race pace = 70%
.
VO2max, respiratory exchange ratio (RER) = 0.90,
at 20C, 50% relative humidity) would result in a
combined 17% of total bodyweight loss (assuming
1.2 L/h sweat rate). Therefore, failure to calculate
respiratory and metabolic bodyweight losses in the
field may overestimate eccrine sweat losses by 7
to 15% in women, or by 17% in men depending
on metabolic rate, sweat rate and the environment.
However, athletes are usually weighed clothed
before and after exercise in the field. Since the
amount of sweat trapped in clothing represented
roughly 8% of total bodyweight losses in each condition for the female marathon runners[35], failing
to account for this factor would underestimate sweat
loss by 0 to 8%. Males have higher sweat rates than
females and might therefore be expected to retain
more sweat in their clothing, thus appearing even
heavier. Collectively, field evaluations of sweat
751
loss that do not account for either of these factors

may overestimate sweat loss in moderate and cool
conditions by 5 to 10%, but would probably be
accurate for estimates made in the heat. Therefore,
sweat rates reported in the literature for field observations can probably be considered accurate to
within a 10% margin of error.
It has also been suggested that metabolic water,
the water liberated from glycogen storage (water
decomplexing), or both may help offset body water
losses during exercise, thus overestimating the need
for fluid yet again.[9,10,20,22-24] Metabolic water production can be determined from the caloric equivalents of oxygen consumption and the respiratory
exchange ratio.[78] An average metabolic water production of 80 g/h during prolonged treadmill
.
exercise (71% VO2max) has been calculated for
women (unpublished observations from Cheuvront and Haymes[35]). This is less than the 144 g/h
reported by Pivarnik et al.[80] for men exercising at
.
74% of VO2max. The difference is easily explained
by a larger active tissue mass and absolute work
load (32% greater bodyweight, and 32% higher
.
VO2max) in the males. Pivarnik et al.[80] speculated
that metabolic water is probably distributed evenly
among body compartments, leaving no more than
10% to be added to the vascular volume. This would
equate to an addition of 8 to 14ml of extracellular
water during each hour of exercise for women and
men, respectively. The potential fluid sparing benefit of gaining such a small volume of extracellular
water every hour during strenuous exercise is obviously overstated if given as a reason to drink
less.
Whether or not the estimated 3 to 4g of water
hygroscopically bound to each gram of glycogen[81]
can act as a hydration reservoir is plausible, but
unknown. Observations of marathon runners gaining 2 to 4kg after carbohydrate loading[27] and reductions in intracellular muscle water content following prolonged exercise[82] are consistent with
this notion, but evidence in support of a direct thermoregulatory benefit is lacking. Therefore, taking
CO2-O2 exchange and respiratory water loss into
consideration is more than adequate when assessSports Med 2001; 31 (10)
752
ing the eccrine sweat contribution to bodyweight

loss. If clothing is not weighed separately after exercise in the field, errors in failing to consider CO2O2 exchange and respiratory water loss are likely
to be minimal. Laboratory studies regularly account
for metabolic and respiratory bodyweight losses and
most field observations that do not are probably
still within a 10% margin of error. Therefore, typical sweat losses reported in the literature appear
accurate. Runners replacing 50 to 80% (or more if
tolerable) of these losses should successfully minimise the detrimental effects of dehydration on thermoregulation.
4. The Role of Metabolic Rate
Exercise imparts a large internal heat load caused
by the inefficiency with which chemical energy is
converted to mechanical work. Even at maximal
mechanical efficiency, more than 75% of the energy liberated during exercise is transferred to the
surrounding tissues and environment as heat, while
the remainder is used to perform external work.[83-85]
In fact, the specific heat of body tissues (3.47 kJ
C kg)[86] predicts that heat storage would limit
exercise to mere minutes if human thermoregulation was adiabatic.
4.1 Body Mass and Running Speed
The energetic cost of running is known to be

constant, largely independent of running speed and
directly proportional to body mass (1 kcal/kg/
km).[83,87,88] However, the rate of metabolic heat
production is clearly a function of running speed.
In vitro, the application of myothermic and biochemical analyses to theoretical models of muscle
contraction predict a rise in energy liberation proportional to the number of activated muscle fibres.[89]
In addition, the efficiency with which energy is
converted to work declines as the intrinsic velocity
of cross-bridge cycling increases.[90] As a result,
less energy is used for work and even more liberated as heat with increasing speed of movement. It
is not surprising then that relative exercise intensity
.
(%VO2max) correlates very well with Tre and that
this relationship appears to hold true for both men
Cheuvront & Haymes
and women.[91,92] The high Tre achieved by athletes

in shorter distance races (5 to 10km) not limited by
dehydration have been used to defend the notion
that metabolic rate is most predictive of a rise in Tre
during exercise. However, these events require a
relatively larger anaerobic component than marathon races and should elicit higher Tre since they
.
are run at a higher %VO2max.[93] Mixed findings
prevail for longer races.
Several field investigations report the highest
post-race Tre in the fastest marathon finishers,[14,22,25]
which is consistent with evidence that competitive
marathon runners compete at higher percentages of
.
VO2max than recreational runners.[94,95] The average metabolic rate for a 42km race effort, estimated
from running speed, has been reported to significantly correlate with post-run Tre (r = 0.39).[22] However, the predictability of elevated post-run Tre from
running speed time to finish (r = 0.35) over the
final stages (6 to 21km) of a marathon are more
consistent observations.[15,16,22] In opposition to these
findings, Maughan[15] has reported disparate Tre of
39.8 and 35.6C for 2 marathon runners finishing
in the same time of 3 hours 45 minutes. In the 1983
Dundee Marathon,[16] a Tre difference of only 0.8C
separated first place (2 hours 17 minutes) from last
(5 hours 11 minutes). The highest Tre recorded on
the same day was 40.3C (3 hours 33 minutes).
Maron et al.[12] also observed very different temperatures of 41.7 and 39.3C for 2 competitive runners finishing within 2 minutes of each other.
4.2 Race Strategy and Course Topography
According to Maughan,[96] the hypothermia exhibited by some runners in cool weather marathons
is explained by a fast, early pace coupled with significant heat production, followed by a gradual slowing of running speed and excessive convective and
radiative heat losses. Cade et al.[6] reported a 0.5C
drop in Tre for marathon runners forced to slow to
a walk from 29 to 42km under mild (16 to 23C)
conditions. It is logical then that an accelerated running speed toward the end of a marathon would
result in an added heat load, which might be further
exacerbated by progressive dehydration or changSports Med 2001; 31 (10)
ing environmental conditions. Competitive runners

may also challenge each other with interval bursts
along any portion of a 42km event, thus producing
progressively more metabolic heat. Additionally, a
single female runner followed throughout the length
of a marathon race exhibited Tre spikes in direct
response to hill running.[7] Therefore, it is apparent
that metabolic rate, race strategy and course topography can all influence Tre in a marathon event.
Furthermore, laboratory treadmill marathon simulations only provide a piece of the puzzle in predicting Tre from average marathon racing speeds.
5. The Role of Gender
Many early studies comparing the male and female response to prolonged exercise, especially in
hot environments, concluded that women were more
susceptible than men to thermal stress and physical
harm.[97] Shortcomings in early research methodology and a historical social sports bias combined
to keep women from legally competing in marathons until 1972.[98] In contrast with the 8 female
competitors who toed the line at the 1972 Boston
marathon, almost 3500 female participants competed in the 1998 race and nearly 9000 female runners ran in the New York City Marathon the same
year.[62,98,99] The establishment of a Womens Olympic Marathon in 1984 and the mere 15 minutes that
presently separate the best mens and womens performances over 42km clearly illustrate a coming of
age in womens marathon running.
Although science and the study of female athletes has progressed markedly over the past 30 years,
a limited number of studies offer firm conclusions
on the qualitative meaning behind many quantitative gender differences, especially when comparing the male and female response to prolonged exercise and environmental stress.
5.1 Environment
Females generally have a smaller body mass and

body surface area when compared with males, but
larger surface area-to-mass ratios (SA/M).[43] Since
exercise heat production is proportional to body
mass and heat loss a function of body surface
753
area,[56] women marathon runners will produce

less, while dissipating more, heat than men for the
same relative exercise intensity. However, this morphological advantage is often referenced with a
strong environmental contingency. Hot, dry conditions with an air temperature exceeding Tsk should
result in faster heat gain and more thermal strain
for female bodies with a larger SA/M. However,
this is not the general finding when comparing men
and women if heat acclimatisation state and relative work intensity are controlled and matched.[43]
When the environment is warm and humid, but air
temperature is lower than Tsk, the larger SA/M in
women actually confers a thermoregulatory advantage over males in the form of lower heart rates, Tsk
and Tre, but this gender difference also disappears
if men and women are matched for metabolic rate
and SA/M.[43] Careful analysis of this second example is warranted. The matching of relative, rather
than absolute, exercise intensity is essential when
comparing heat production and thermoregulation,
but characteristic height and bodyweight differences
between men and women are fundamental. Therefore, any advantage or disadvantage incurred by
differences in morphology should be considered as
a genuine gender difference.
Since tissue insulation has been shown to be
directly proportional to skinfold thickness,[100] the
higher body fat levels of female athletes imparts
a logical thermoregulatory advantage in the cold.
However, this does not typically translate into differences in heat storage or Tre when comparing men
and women at equal relative exercise intensities in
the cold,[101] possibly because more heat is simultaneously lost by women because of their larger
SA/M. It has also been suggested that womens
greater percentage body fat might be a disadvantage in the heat if working at equal relative exercise
intensities to men. Others[36] contend that body fat
is only active as an insulator when skin blood flow
is low. Millard-Stafford et al.[31] compared the thermoregulatory responses of men and women while
running 40km in hot weather. The women experienced lower post-run Tre despite having twice the
.
body fat of the men, similar VO2max (ml/kg fat-free
Sports Med 2001; 31 (10)
754
mass (FFM)/min) values and equal relative race

.
efforts (75% VO2max). However, this observation
may be explained by the smaller body mass in the
women (see section 5.3). The only study to examine the Tre response of women to distance running
in different environments[35] reported no difference
in post-run Tre or mean Tre during three 30km runs
at 12, 17 and 25C (WBGT).
Therefore, it is concluded that a gender difference in SA/M may convey an advantage for
women marathon runners competing in warm, humid weather conditions when compared with men
of similar competitive ability. Although data are
limited, differences in body fat do not appear to
make any direct, insulative impact on thermoregulation. Related issues regarding body water,
dehydration, sweat rate and metabolic rate raise additional questions concerning gender-specific differences in exercise temperature regulation.
5.2 Dehydration
Active dehydration, fluid replacement and thermoregulation in women during distance running
have been largely unstudied. However, there is reason to suspect that gender can significantly affect
dehydration and Tre regulation. Anatomically, females have a larger number of heat activated sweat
glands per unit of surface area than males but produce less sweat per gland.[102] In fact, whether heat
acclimatised or not, men produce more sweat than
women in both absolute (L/h) and relative (g m2/h)
terms during exercise in warm, humid conditions.[43]
This fact, in addition to the larger SA/M in women
that encourages convective and radiative heat exchange (sections 2.1, 5.1), results in a combined
thermoregulatory advantage over males in hot, humid conditions. Recall that high humidity limits
sweat evaporation, which makes excessive sweating counterproductive and may even reduce sweat
production by hidromeiosis.[103] Together, these characteristics reduce cardiovascular strain[104] and result
in a lower Tre per unit volume of sweat produced
in women.[105] Similar race completion percentages (male = 78%, female = 79%) during the Barcelona mens and womens Olympic Marathons,
Cheuvront & Haymes
despite more humid and severe weather during the

womens race,[58] may be explained in part by this
phenomenon.
When the environment is hot and dry, the sweat
rates in heat acclimatised men and women are usually similar if matched for metabolic rate.[43] However, because women have a lower total body water
content than men, any loss of body water expressed
as a percentage of total body mass will be relatively
larger in women.[43,106,107] As a result, but in direct
contrast to humid environments, women may be
more susceptible than men to heat strain and performance decrements if competing in a hot, dry
marathon event because of greater relative dehydration. Unfortunately, direct evidence in support
or in refute of this effect is lacking.
Sweat rates for female marathon runners have
ranged from 0.67 to 1.25 L/h in temperatures from
14 to 32C (table I). These losses represent only
68 to 73% of the absolute sweat rates of males in
the same studies. This absolute difference may be
caused by higher relative sweat rates in men (humid conditions), but is more likely the result of
higher absolute metabolic rates (section 5.3).[91] Gender comparisons of sweat rates, fluid losses and responses to dry or humid environments introduces
the rationale for a potential gender difference in
optimal fluid replacement strategies.[31]
It is generally observed that women complain of
more gastric distress than men when attempting to
consume the same absolute fluid volumes. Com.
petitive female runners matched for VO2max (ml/
kgFFM/min) to males complained of gastric fullness after 20km of a 40km run in the heat when
asked to consume 250ml/5km (0.57 L/h).[31] Myhre
et al.[20] reported vomiting in a recreational female
marathon runner after 35km while trying to consume ~ 290ml/5km interval. In contrast, ad libitum
intakes of 0.47 to 0.70 L/h have recently been reported for female marathon runners (205-288ml/
5km) without a single incident of gastrointestinal
discomfort.[35] These same intakes replaced 60 to
70% of sweat losses and maintained a plateau in Tre
well below 39C for more than 2 hours of continuous running at 42km race pace in temperature
Sports Med 2001; 31 (10)
conditions ranging from 12 to 25C (WBGT). Others[31] have shown that from 20 to 40km in the heat
(25 to 32C), fluid intakes representing 46% of sweat
losses were inadequate to prevent a continued rise
in Tre throughout exercise. Under true race conditions, Myhre et al.[19] showed that recreational female marathon runners generally replaced 42% of
fluid losses under moderate environmental conditions (17 to 20C), but Tre was only measured in a
single female.
Therefore, it is apparent that, primarily because
of absolute differences in sweat losses, women may
require smaller absolute fluid intakes than men but
must still replace a similar percentage of sweat losses
to maintain thermal balance in response to prolonged
exercise, especially in warm environments.[31,35,42]
It is also obvious from the table I review that neither men nor women drink enough to compensate
for even 50% of sweat losses when fluid intakes
are voluntary, although slightly higher intakes have
been reported for women.[35] Because inadequate
hydration progressively raises T re during extended exercise,[42,68] elevated post-marathon Tre are
logically related to poor fluid balance in men and
women.
5.3 Metabolic Rate
When post-race Tre were compared in males and

females following the completion of a near marathon (40km) distance, women demonstrated lower
Tre (in the order of 0.5 to 1.0C lower) over the
final 10km despite similar finishing times, relative
efforts and relative dehydration.[31] As previously
mentioned, heat production rises as more muscle
is made active and metabolic rate is directly proportional to the mass supported during movement.
Although both men and women were closely match.
ed for VO2max (ml/kgFFM/min), the men in this
study were 20% heavier than the women, which
may partially explain the higher Tre seen in the men.
This gender-specific bodyweight difference is commonly seen between male and female marathon runners.[108-111] Although correlation coefficients for
the effect of bodyweight on Tre in a marathon range
from only 0.18 to 0.58,[22,34] the mathematical pre Adis International Limited. All rights reserved.
755
dictions for the energy cost of movement (kcal/kg/km)

suggest that the lower bodyweight of women match.
ed to men of similar VO2max (ml/kgFFM/min) may
confer a thermoregulatory advantage because of a
lower metabolic heat producing potential.[56] The
high correlation between metabolic rate and sweat
rate[91] probably also explains the lower absolute
sweat losses in females which may act to preserve
a lower level of total body water. Whether or not
this combined body mass and metabolic rate advantage in women is qualitatively meaningful probably depends most on the environment[56] (see sections 5.1, 5.2).
5.4 Menstrual Cycle
The study of thermoregulation in women is

unique because of the effects of the female reproductive cycle on Tre and skin blood flow. It is well
established that Tre is 0.5C higher in the luteal
phase of the menstrual cycle than in the follicular
phase.[112-114] This temperature change also produces
a higher threshold for the initiation of sweating and
cutaneous vasodilation.[113,114] Therefore, heat loss
may be delayed and more heat stored for the same
work effort. These phenomena have made the control of menstrual cycle phase imperative for comparative gender studies of thermoregulation. By convention, most research is conducted within the first
10 days of the follicular phase. However, it has
recently been reported that Tre and the sweating
threshold decrease below baseline in the immediate pre-ovulatory phase (days 9 to 12), presumably
because of the pre-ovulation estrogen surge.[115] This
suggests testing in the first 8 days of the follicular
phase to avoid any overt Tre fluctuations.
Among the few studies of women marathon runners, only 2 have reported menstrual cycle phase.
Immediate post-run Tre for women running 30km
at 30C in the follicular phase were 38.7,[35] and
39.3C[31] for women running 40km at 25 to 32C
in the mid-luteal phase. Although it is tempting to
attribute the 0.5C difference to menstrual phase,
participants were also more (1.5%) dehydrated in
the 40km run and ran at slightly higher (5%) relative exercise intensities. What remains clear, howSports Med 2001; 31 (10)
756
Cheuvront & Haymes
ever, is that menstrual cycle phase does affect thermoregulation and must, therefore, be considered in
the assessment of gender-specific differences between male and female marathon runners. How much
these changes reduce heat tolerance is questionable, though the heat stress of exercise and environment probably mask any subtle effects of the
ovarian hormones.[43]
5.5 Summary of Gender
Based on limited marathon data, but ample

laboratory research, it is concluded that, for the environmental conditions common to mass participation marathon events (table I), women will respond
to and be limited by similar thermal stressors during prolonged work when compared with men. Quantitative morphological advantages (lower body mass,
larger SA/M) or physiological disadvantages (lower
total body water, higher resting luteal phase Tre and
sweating/blood flow thresholds) might only produce qualitative gender differences in thermoregulation under extreme heat or cold stress circumstances.
6. Statistical Review
Table II is a summary of correlations between
metabolic rate or dehydration and Tre reported in
the distance running literature. In an effort to fur-
ther explore the relationships between Tre and common candidate predictors of post-marathon Tre,
table III was compiled using studies of male marathon runners (table I) that reported post-race
Tre. Simple linear regression analysis of more than
10 independent variables was performed with Tre
.
as the modelled dependent variable. Both VO2max
(ml/kg/min) [r = 0.777; p < 0.001] and running
speed (m/min) [r = 0.585; p < 0.001] were significantly correlated with Tre, while dehydration (percentage bodyweight) was not (r = 0.157; p = 0.475).
Wyndham and Strydom,[34] some of the first researchers to put forth the predictive nature of dehydration on Tre, suggested the relationship would
be linear beyond 3% of bodyweight losses. The
mean percentage of dehydration incurred in the table III studies was 3.8% of bodyweight. However,
a closer look at the relationship (r = 0.157) between
dehydration and Tre (fig. 1) illustrates how, under
almost identical levels of dehydration (3 to 4%),
differences in metabolic rate or environment may
confound the prediction and potentially explain the
observed differences in Tre. When correlations were
calculated with percentage dehydration as the dependent variable, ambient temperature (Tdb) [r =
0.532], sweat rate (L/h) [r = 0.772] and relative
rehydration (percentage sweat losses replaced) [r =
Table II. Statistical correlations reported to evaluate one or more predictors of rectal temperature in distance running research (32-42km)a
Study
Predictor variable
Correlation
Significance
Adams et al.[2]
% dehydration
r = 0.79
Not stated
Buskirk & Beetham[5]
% dehydration
r = 0.58
p < 0.01
Work rate
r = 0.11
NS
Maughan[15]
Maughan et al.[16]
Noakes et al.[22]
Wyndham & Strydom[34]
59
62
30
31
Time to complete 42km
r = 0.234
NS
Time to complete final 21km
r = 0.348
p < 0.01
Time to complete 42km
r = 0.23
NS
Time to complete final 10km
r = 0.33
p < 0.01
p < 0.01
Metabolic rate over final 6km
r = 0.53
Metabolic rate over final 21km
r = 0.44
p < 0.02
Metabolic rate (0-42km) and running velocity

over final 6km
r = 0.39
p < 0.05
% dehydration
r = 0.18
NS
% dehydration
r = 0.67
p < 0.05
a Only research observing ad libitum fluid intakes were reviewed.

NS = not significant.
Sports Med 2001; 31 (10)
757
Table III. Physiological and performance factors affecting thermoregulation during prolonged running: analyses using simple linear regression
(predicting rectal temperature or dehydration)
Independent variable
Dependent variable
ra
p-Value
References
Ambient temperature (Tdb)
Rectal temperature
0.277
0.223
2,5-7,9,11-16,22,25,28,31-33
Bodyweight (kg)
Rectal temperature
0.338
0.114
2,6,9,11-15,19,20,22,23,25,28,31-33
Relative rehydration (%)
Rectal temperature
0.036
0.879
2,9,11,12-15,19,20,25,28,31,32
Dehydration (%)
Rectal temperature
0.157
0.475
2,5,9,11-15,19,20,22,23,25,28,31-33
Running speed (m/min)
Rectal temperature
0.585
0.003
2,5-7,9,11-16,19,20,22,23,25,28,31,32
Sweat rate (L/h)

.
VO2max (ml/kg/min)
Rectal temperature
0.276
0.202
2,5,6,9,11-15,19,20,22,23,25,28,31,32
Rectal temperature
0.777
0.000
2,6,9,11-14,20,22,31-33
Ambient temperature (Tdb)
Dehydration
0.532
0.004
2-5,8-15,17-19,22,24-28,31-33
Bodyweight (kg)
Dehydration
0.175
0.392
2-4,8,11-15,18-20,22-25,27,31-33
Relative rehydration (%)
Dehydration
0.739
0.000
2,3,8,9,11-15,19,20,22,23,25,28,31,32
Fluid intake (L/h)
Dehydration
0.138
0.511
2,3,8,9,11-15,17-20,22-25,28,31,32
Running speed (m/min)
Dehydration
0.499
0.007
2,3,5,8-15,17-20,22-25,27,28,31,32
Sweat rate (L/h)

.
VO2max (ml/kg/min)
Dehydration
0.772
0.000
2,3,5,8-15,19,20,22,23,25,28,31,32
Dehydration
0.124
0.623
2,3,9-14,20,22,24,27,28,31-33
Bold indicates statistical significance.

.
Tdb = dry bulb (air) temperature; VO2max = maximal oxygen uptake.
0.739] were all significantly predictive of dehydration (p < 0.01) [table III].
Thus, there is ample evidence that intercorrelated factors such as these could significantly affect the predictive capacity of other variables related to Tre. Furthermore, although simple linear
Similar environments, dissimilar run speeds (m/min): difference in metabolic rate only
Similar run speeds, dissimilar environments: difference in dry bulb (air) temperature, Tdb
41
Rectal temperature (C)
regression affords a look at the strength of a relationship between 2 variables, it is a common mistake to directly compare one correlation coefficient
with another. Others[36] have acknowledged that
this fact must be properly considered when predicting Tre or when generally applying similar statistical
29C Tdb, 230 m/min
22C Tdb, 256 m/min

40
r = 0.157
39
20C Tdb, 220 m/min
22C Tdb, 194 m/min

38
0
Dehydration (%)
Fig. 1. Scatter-plot of the relationship between dehydration and rectal temperature (Tre) based upon references provided in table III.
Even with almost identical levels of dehydration, like symbols provide examples of how other variables may confound the predictive
capacity of dehydration on Tre.
Sports Med 2001; 31 (10)
758
Cheuvront & Haymes
methods.[116] Although multiple regression analysis was not an appropriate tool for the assessment
of the data in this literature review,[116] the relative
importance of different predictive variables and each
variables unique contribution to the explained variance can be determined when circumstances allow
the use of multiple regression analysis and standardised regression coefficients.[36,116] Havenith et
al.[36] applied this type of multiple regression analysis to the prediction of Tre in a heterogenous group
of exercising men and women. Over a range of climates, it was concluded that the human response to
heat stress is multifaceted and must be interpreted
while taking into account the heat transfer potential
of the environment and the effect of exercise intensity on metabolic heat production.[36] Unfortunately, fluid balance was not considered in their study
design.
7. Conclusion
Figure 2 illustrates that at the onset of exercise,
heat production exceeds heat loss and significant
heat storage occurs. A new Tre plateau is achieved
when heat loss and heat gain reach a thermal equilibrium (phase I). The expected rise in Tre and plateau will be proportional to metabolic rate, but will
generally approach between 1.0 to 1.5C above resting values (fig. 2)[35,42,54,68,69] for exercise intensities common to those in a marathon effort.[93-95,117]
This steady state in heat-gain/heat-loss will occur
in endurance races as long as: (i) the climate is
compensable, which is the norm for most marathon
races (table I); and (ii) exercise is submaximal, which
is also the norm for prolonged bouts of exercise
like the marathon.[93-95,117] Tre is most influenced
by dehydration (fluid balance) in phase II. The environment and fluid intake practices will determine
to what extent dehydration occurs (sweat loss >
fluid intake) and, therefore, how much Tre will drift
upward or remain stable. Any changes in course
topography or racing speed will modulate this response; however, dehydration will make adjustments
to additional metabolic or environmental heat loads
more difficult.[53] Five possible scenarios have been
offered to explain phase III (fig. 2). At the extremes,
runners who slow the most in the coolest conditions
40
Rectal temperature (C)
1
2
3
39
4
38
37
Phase I
Phase II
Phase III
36
Start
42km
Finish
Fig. 2. Theoretical influence of metabolic rate and dehydration on rectal temperature (Tre) during a marathon. In phase I, metabolic
heat gain exceeds environmental heat loss until a thermal equilibrium (steady state) is reached. Dehydration (sweat loss > fluid
intake) results in an incremental rise in Tre throughout phase II. Effects on Tre observed in phase III include 5 possibilities: (1) poor
hydration, fast finish; (2) poor hydration, steady finish; (3) adequate hydration, fast finish; (4) adequate hydration, steady finish; (5)
adequate hydration, slow finish (cool weather only).
Sports Med 2001; 31 (10)
are likely to experience the most severe drop in

Tre,[96] while runners competing at the fastest speeds,
in competitive situations, and who drink the least
will experience the highest post-run Tre.[18,34,118]
This is corroborated by data showing that the highest post-marathon Tre are usually recorded in the
fastest runners, who also happen to have the poorest documented fluid intake practices.[18,34,93,118] This
model applies equally for both men and women since
it was constructed with the consideration that mass
participation marathons are usually run in compensable climates that lack temperature and humidity
extremes (table I and section 5.5).
In conclusion, metabolic rate, hydration and the
environment can all play a significant, integrated
role in influencing post-marathon Tre. Metabolic
rate will elevate Tre at the start of exercise (phase
I) until a new thermal equilibrium is reached. Fluid
balance (sweat loss versus fluid intake) will dictate
the slope of the line in phase II, thus setting the
limit on the degree of change expected in Tre between phase I and III. Significant fluctuations in
metabolic rate during the shorter final segment of
phase III will further alter (plus or minus) any incurred heat load. Therefore, final post-run Tre are
probably best explained (fig. 2) by fluid balance
(scenario 2 and 4), metabolic rate (scenario 3 and
5) or a synergy between both (scenario 1). The discrepancies among research studies examining the
relative influence of these factors on Tre are invariably explained by differences in individual fluid
intake practices, climatic conditions and racing strategies. Application of these conclusions appears
suitable for both male and female marathon runners.
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(9): 1024-9
Correspondence and offprints: Dr Emily M. Haymes, 430

Sandels Building, Department of Nutrition, Food and Exercise Sciences, Florida State University, Tallahassee, FL
32306-1493, USA.
E-Mail: ehaymes@mailer.fsu.edu
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The extreme physical endurance demands and varied environmental settings

Cheuvront & Haymes

1. Thermoregulation and the Marathon

for decades provided an excellent opportunity to

Thermoregulation and the Marathon

Table I. Review of marathon and related distance running literature

Beckner & Winsor[4]

Buskirk & Beetham[5]

Christensen & Ruhling[7] 42.2

Cohen & Zimmermana[8] 42.2

Kavanagh & Shepharda[9] 42.2

21-26C, 50-60% 1.13

Continued over page

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Sports Med 2001; 31 (10)

Cheuvront & Haymes

25-32C, 70-82% 1.71

25-32C, 62-82% 1.8

Wyndham & Strydom[34] 32.0

Cheuvront & Haymesa[35] 30.0

Ad libitum fluid intakes.

Male and female data pooled.

Combined data from 3 groups.

equilibrium. Environmental extremes can severely

Heat exchange occurring between humans and

Thermoregulation and the Marathon

Tdb and Twb are lower than skin temperatures (Tsk),

load may be reached which limits further exercise

Cheuvront & Haymes

ance performance can be rationalised as the result

Thermoregulation and the Marathon

cise when fluid was taken. Gisolfi and Copping[69]

Tre during marathon running has also been offered.

Cheuvront & Haymes

be exceeded before reliable correlations with Tre

A review of fluid balance data from the distance

Thermoregulation and the Marathon

loss that do not account for either of these factors

ing the eccrine sweat contribution to bodyweight

The energetic cost of running is known to be

Cheuvront & Haymes

and women.[91,92] The high Tre achieved by athletes

Thermoregulation and the Marathon

ing environmental conditions. Competitive runners

Females generally have a smaller body mass and

area,[56] women marathon runners will produce

mass (FFM)/min) values and equal relative race

Cheuvront & Haymes

despite more humid and severe weather during the

Thermoregulation and the Marathon

When post-race Tre were compared in males and

dictions for the energy cost of movement (kcal/kg/km)

The study of thermoregulation in women is

Cheuvront & Haymes

Based on limited marathon data, but ample

Buskirk & Beetham[5]

Wyndham & Strydom[34]

Time to complete 42km

Time to complete final 21km

Time to complete 42km

Time to complete final 10km

Metabolic rate over final 6km

Cheuvront & Haymes (2001)

Cheuvront & Haymes (2001)