35

Thermoregulatory Adaptation in Humans and Its Modifying Factors
Narihiko KONDO1*, Nigel AS TAYLOR2, Manabu SHIBASAKI3, Ken AOKI4 andAhmad Munir Che MUHAMED5
1

Laboratory for Applied Human Physiology,
Graduate School of Human Development and Environment, Kobe University
3-11 Tsurukabuto, Nada-ku, Kobe 657-8501, Japan
2
School of Health Sciences, University of Wollongong, Australia
3
Nara Women’s University, Japan
4
Nihon University School of Medicine, Japan
5
University of Malaya, Malaysia*e-mail: kondo@kobe-u.ac.jp

Abstract
Humans have extensive abilities to adjust their thermoregulatory activities when responding to changes
in both endogenous (exercise) and exogenous (environmental) conditions and thereby maintain thermal
homeostasis. Five phenotypic adaptations may be described: reduced heart rate at a fixed work rate; expanded plasma volume; lower core temperature at an equivalent workload; superior sodium and chloride
reabsorption from sweat; and an elevated sweat secretion. Thermal factors such as core and skin temperatures are the primary afferent signals that modulate sweat rate and skin blood flow. However, it is also suggested that various non-thermal factors associated with exercise (central command, muscle mechano- andmetabo-reflexes, and baroreflexes) can modify sweat rate and skin blood flow. Thermoregulatory controls ofsweating and cutaneous vasodilation during heat stress are also modified by circadian changes in coretemperature, as well as secretion of endogenous melatonin. Moreover, high humidity reduces sweat efficiency, and therefore core temperature increases during exercise when humidity is elevated at a fixed
temperature. In this case, the ability to maintain dry heat loss at the expense of a reduced capacity ofevaporative heat loss is seen as an important contributing factor to thermoregulation in humid environments.
Key words: acclimation, adaptation, circadian rhythm, exercise, humans, skin blood flow, sweating

1. Introduction
Humans are currently facing the social, physiologicaland economic effects of global warming. Since living in“Harmony within Nature” is very important, it is essential these problems are clearly understood. We haveeffective physiological thermoregulatory mechanisms to
defend homeostasis of body temperature against bothchanging endogenous (exercise) and exogenous environmental conditions (ambient temperature, humidity,
radiation and so on). For investigating “Harmony within
Nature,” it is important to understand thermoregulatory
adaptation in humans. Heat adaptation and endurance
training induce adaptive changes of the thermoregulatory system. Furthermore, sweating and skin blood flow
responses may be modified by non-thermal factors suchas central command, muscle mechano- and metaboreflexes, baroreflexes, baroreceptor loading, changes inbody fluids (volume reduction, hyperosmolality) associated with exercise, and by the natural circadian rhythm
controlled by the hormone melatonin. Therefore, we
Global Environmental Research
13/2009: 35-41
printed in Japan

have briefly reviewed thermoregulatory adaptations toheat and endurance training and the effects of modifying
factors on thermoregulatory responses, by focusing on
the influences of four factors: 1) heat adaptation andendurance training, 2) exercise, 3) circadian rhythms,
and 4) environmental humidity.

2. The Effects of Endurance Training andHeat Adaptation on Thermoregulatory
Responses
2.1 Adaptation in the contemporary world
People live and work within a very broad range ofnaturally occurring air temperatures (–90ºC to >55ºC).
Since survival of unprotected individuals at these extremes is very brief, our capacity to live within suchenvironments is wholly dependent upon our ability todevelop protective clothing, portable life-support apparatuses and mobile habitats. Indeed, these behaviouralcapabilities far exceed our physiological capacity to resist thermal energy transfers, or to generate or dissipate©2009 AIRIES

36

N. KONDO et al.

body heat. Most people from advanced, contemporarysocieties now have such broad access to these technological advances, that few rarely encounter skin temperatures outside the thermal comfort zone (~33ºC).
Daily use of such technology has largely removed
modern man from the stresses of life. As a result,contemporary humans have become increasingly moresedentary, and less able to tolerate the stresses of life.
Thermal adaptation occurs through behavioural,morphological, biochemical and physiological adjustments superimposed upon the genetic, phenotypic andphysiological status of the individual, thereby improving
the relationship between an organism and its surrounding environment. Six stages of heat adaptation may be
identified (Taylor & Cotter, 2006), and since cardiovascular and thermal regulatory mechanisms share somecommon effectors (vascular smooth muscle) and sensors(baroreceptors), many external stresses elicit similar
integrated physiological adaptations. For example, repeated endurance exercise and heat exposures elevatecore temperature, and stimulate blood flow redistribution and sweat secretion.
2.2 Endurance training
Habitual endurance training is associated with anarray of cardiovascular, pulmonary and metabolic adaptations. However, of principal relevance to temperature
regulation are changes that facilitate increased peripheral blood flow, since these support metabolic heat removal without compromising blood pressure regulation.
In this regard, research indicates that endurance training
increases arterial calibre, improves whole-body vasodilatory function and lowers vasomotor tone (Green et al.,2004, 2008). These changes combine to elevate peripheral vascular conductance. An expansion of the blood
volume is often observed following endurance training,with increments in plasma volume facilitating heat loss
(Tipton et al., 2008). In addition, endurance exercise
elevates the body tissue temperatures, and runners willroutinely complete marathons with a core temperature>40ºC. Such high temperatures are a function of exercise intensity and duration, and endurance athletes produce enough heat, and on such a regular basis, that theymust also adapt to training by improving heat dissipation.
2.3 Heat adaptation
Repeated thermal stress elicits adaptations evident
within the neural networks and integrating regulatory
systems (controller adaptations), that appear as morphological changes (e.g., sweat gland hypertrophy), andmay be expressed as adjustments within effector processes (e.g., altered vasomotor or sudomotor sensitivities).
The most common functional effect of heat acclimation
is a change in the effector thresholds, with the mean
body temperature for effector activation being shifted
downwards (Tipton et al., 2008). One can also observe
effector adaptations, evident from changes in the gain of
the effector response. Thus, for a given thermal stimulus,

acclimatised individuals frequently display an increased
effector sensitivity, such as a greater sweating response
for an equivalent change in body temperature. Fivephenotypic adaptations may be described: reduced heart
rate at a fixed work rate; expanded plasma volume;
lower core temperature at an equivalent workload; superior sodium and chloride reabsorption from sweat; andan elevated sweat secretion. However, whilst perhaps
the most commonly reported, and certainly the most
readily recognised change, is the elevated sweating response, it is possible that this represents only a transitional state as one progresses towards becoming more
completely heat adapted (Taylor, 2006).
2.4 Challenging old concepts
Four tenets of heat adaptation physiology may bequestioned. First, the nature of the forcing function
applied determines the level of adaptation achieved.
Traditional heat adaptation protocols use constant thermal and metabolic stresses to elicit adaptation. However,superior physiological adaptation can be achieved by
gradually increasing the stress applied as adaptation
occurs (Taylor & Cotter, 2006). Second, heat adaptationinduced increases in plasma volume are not transitory,
but can be sustained if the forcing function is elevated as
adaptation progresses (Patterson et al., 2004b). Third,
heat adaptation is not accompanied by a peripheral
redistribution of sweat (Patterson et al., 2004a). Finally,it has been considered that a low sweat rate is indicativeof an inferior state of heat adaptation. While this may becorrect in many cases, it is not a correct interpretation
for those who live in tropical climates. For suchindividuals, the ultimate level of heat adaptation isassociated with reduced and very efficient sweat secretion during thermal loading (Taylor, 2006).

3. Neural Control of Sweating and Skin Blood
Flow during Exercise
3.1 Factors associated with exercise that modify
thermoregulatory responses
Thermal factors such as core and skin temperatures
are the primary feedback signals for sweat rate and skinblood flow, and thus these responses are typically expressed as a function of internal or mean body temperatures (Nadel et al., 1971). However, van Beaumont andBullard (1963) first reported that sweating occurred immediately (within 1.5-2 sec) with the onset of dynamic
exercise in warmed subjects, and these responses occurred prior to any measurable elevation of core temperature. They concluded that non-thermal factors associated with exercise contributed to this increase. It issuggested that a number of non-thermal factors associated with exercise (central command, muscle mechanoand metabo-reflexes, and baroreflexes) can modify the
aforementioned thermoregulatory responses (Fig. 1). In
addition, the effect of body fluid regulation on thermoregulatory responses should also be considered.

Thermoregulatory Adaptation in Humans and Its Modifying Factors

37(Nadel et al., 1980; Fortney et al., 1981). Plasma
hyperosmolality inhibits the core temperature thresholdfor the onset of sweating but not the aforementioned
slope (Takamata et al., 1997).

Fig. 1 Effects of non-thermal factors on cutaneous vascular andsweat gland responses.

3.2 Sweating
Shibasaki et al. (2003) measured sweat rate during
2 min. of isometric handgrip exercise with and without
augmented central command, via administration of apartial neuromuscular blocking agent. After administration of the agent, force generation could not be maintained; however, the sweat rate during this period
remained elevated similar to the response to the exercise
bout without neuromuscular blockage. These findings
provide evidence that central command can modulate
sweat rate.
Circulatory occlusion just prior to the end of exercise
stimulates muscle metaboreceptors while central command and muscle mechanoreceptor activity are removed.
During circulatory arrest after isometric handgrip exercise, the sweat rate remains elevated and then decreases
upon release of the ischemic challenge (Crandall et al.,
1998; Kondo et al., 1999; Shibasaki et al., 2001) without any effect of baroreceptors on sweating (Shibasaki
et al., 2003). Furthermore sweating is augmented during
dynamic exercise with leg compression (Kacin et al.,2005). Together these findings suggest that muscle
metaboreceptor stimulation is capable of modulating thesweat rate during both isometric and dynamic exercise.
Passive cycling or limb movement is one of several
methods used to selectively stimulate muscle mechanoreceptors. Kondo et al. (1997) adopted passive limb
movement in subjects exposed to a warm environment,
which caused slight elevations in the sweat rate at theonset of limb movement. In addition, Shibasaki et al.
(2004) had subjects perform passive cycling after
moderate exercise. During the recovery following
moderate exercise, the sweat rate was greater when thesubjects’ legs were passively cycled relative to when thesubjects rested. These studies demonstrated that muscle
mechanoreceptors are capable of modulating sweat rateduring exercise.
Finally, hypovolemia reduced the slope of the relationship between the increase in core temperature relative to the increase in sweating, but did not change thecore temperature threshold for the onset of sweating

3.3 Skin blood flow
Friedman et al. (1991) found that a reduction in
cutaneous vascular conductance (CVC) observed at theonset of dynamic exercise in normothermic subjects was
not mediated by central command, in that CVC did notdecrease when the subjects tried to perform exercise
during partial neuromuscular blockade. In contrast,
recent data suggest that during isometric exercise of heatstressed subjects, central command can contribute to the
reduction in CVC observed during this form of exercise(Shibasaki et al., 2005), and is primarily due to withdrawal of cutaneous active vasodilator activity.
During a period of post-isometric-exercise ischemiaof heat stressed subjects, Crandall et al. (1998) foundthat CVC remained reduced, and upon release of ischemia returned to pre-exercise levels. They concluded thatthe reduction in CVC during isometric exercise in heatstressed subjects can be mediated by muscle metaboreceptor stimulation resulting from withdraw of cutaneous
active vasodilation (Crandall et al., 1995, 1998).
Shibasaki et al. (2004) showed that CVC response
during semi-recumbent passive cycling (i.e., primarily
muscle mechanoreceptor stimulation) after moderate
exercise was similar to that in subjects not cycling during recovery. This result indicated that stimulation ofmuscle mechanoreceptors does not modulate CVC
Johnson and Park (1981) showed that upright postureand exercise each contributed to an increased thresholdfor cutaneous vasodilation. Moreover, numerous observations show that baroreceptor unloading due to lowerbody negative pressure and head-up tilt in heat stressedsubjects is capable of reducing cutaneous vasodilator
activity. Hypovolemia also reduced the slope of therelationship between the increase in cutaneous vasodilation and the increase in core temperature (Nadel
et al., 1980). When core temperature approaches ~38°C
during dynamic exercise, the rate of increase in CVC issubstantially attenuated (Brengelmann et al., 1977). The
feedback mechanism to maintain cardiac filling pressure
may be the mechanism resulting in an attenuated rise in
CVC when core temperature is substantially elevated(Nose et al., 1990). Similar to that observed with sweating, elevated plasma osmolality increases the core temperature threshold for the onset of cutaneous vasodilation (Takamata et al., 1997).

4. Modification of Circadian Variation in
Human Thermoregulatory Responses
4.1 Circadian variation of sweating and skin bloodflow responses during heat stress
It is well recognized that the circadian rhythm in
resting core temperature in humans shows a nadir in theearly morning and a peak in the evening. This rhythm in

38

N. KONDO et al.

core temperature results from an endogenous circadianrhythm in heat production and heat dissipation (Aschoff& Heise, 1972). A resting individual is in a heat-gain
mode in the morning and in a heat-loss mode in the lateevening (Waterhouse et al., 2005). Effector responses tothermoregulatory challenges also show diurnal or nocturnal variation during cycling exercise (Wenger et al.,
1976; Stephenson et al., 1984). For example, thecircadian variation in core temperature thresholds forthe onset of sweating and active cutaneous vasodilation
during dynamic exercise clearly shifted in parallel to thecircadian rhythm in the resting core temperature(Stephenson et al., 1984). However, these variations inthermoregulatory sweating and cutaneous vasodilation
during dynamic exercise are modulated by both thermal
and non-thermal factors as mentioned in the previous
chapter.
Aoki et al. (2001) compared the thermoregulatory
sweating and cutaneous vasodilation evoked by passive
heating in the early morning and evening. The coretemperature thresholds for the onset of sweating andactive cutaneous vasodilation shifted to higher coretemperatures in the evening compared with thresholds
observed in the early morning (Figs. 2 and 3). The slopeof the relationship between the increase in coretemperature relative to the increase in sweating did not
differ between the early morning and evening. On theother hand, the slope of the relationship between theincrease in core temperature and the increase in
cutaneous vasodilation declined in the early morningcompared with the slopes observed in the evening.
4.2 Modification of exogenous and endogenous
melatonin on thermoregulatory responses
In humans, the nadir in core temperature occurs
during the phase from midnight to early morning andskin blood flow in the distal limbs peaks during thisphase (Smolander et al., 1993) when endogenous melatonin levels rise to their nocturnal maximum (Kräuchi
et al., 2006). Time courses suggest a causal relationshipbetween the nocturnal increase in endogenous melatonin
and the nocturnal decrease in core temperature. On theother hand, melatonin secretion is typically suppressedby bright light and, thus, endogenous melatonin levels
are almost zero during daytime.
An oral dose of melatonin (3 mg) administered in thedaytime induced a decrease in resting core temperature.
Also, core temperature thresholds for the onset of sweating and active cutaneous vasodilation during passive
heating in the evening were shifted to lower coretemperatures by exogenous melatonin (Figs. 2 and 3)(Aoki et al., 2006). Moreover, exogenous melatonin
administration reduced the slope of the relationshipbetween the increase in core temperature and theincrease in cutaneous vasodilation, but did not change
the slope of the relationship between the increase in coretemperature relative to the increase in sweating.
It is well known that the circadian rhythms in
endogenous melatonin and resting core temperature canFig. 2 Sweating response to passive heating from theonset of sweating up to the time of achieving a
steady state. SR is shown as a function of Tc.
The regression lines are means from all subjects.
SR; sweat rate, Tc; core temperature.

Fig. 3 Cutaneous vasodilator response to passive heating from the beginning of vasodilation up to thetime of achieving a steady state. CVC, expressed
as a percentage of maximal CVC (%CVCmax), isshown as a function of Tc. The regression lines
are means from all subjects.
CVC; cutaneous vascular conductance, Tc; coretemperature. *; The slope of relationship between
the increase in core temperature relative to theincrease in cutaneous vasodilation significantly
declined (P<0.05).

be entrained or phase-shifted by artificial bright light
exposure (Czeisler et al., 1989; Strassman et al., 1991).
For example, bright light (BL) exposure (>2,000 lx) fora single night suppressed secretion of melatonin andattenuated the fall in core temperature from the night tothe early morning (Strassman et al., 1991). Indeed, BL
exposure (2,800 lx) at night suppressed melatonin andattenuated the fall in core temperature during the night.
Also, the core temperature thresholds for the onset ofsweating and active cutaneous vasodilation duringThermoregulatory Adaptation in Humans and Its Modifying Factors

5.2 Effect of humidity in earlier studies
The current understanding of the physiologicalresponses during prolonged exercise in humid envi& O 2 25% max) andronments has been limited to low (≤ V&
moderate (40% to 50% V O 2 max) exercise (Pandolf
et al., 1974; Nielsen et al., 1997; Gonzalez et al., 1974;
Kobayashi et al., 1980) involving sedentary to moderately trained subjects. Highly trained athletes have beenshown to have generally superior capability to cope withheat stress due to their higher sweat rates and higher
skin blood flow rates (Tipton et al., 2008).
3.5

30.0

3.0

25.0

2.5

20.0

2.0

15.0

1.5

10.0

1.0
H20

H30

H40

H50

H60

H70

38.7

38.9

39

39.1

39.2

39.5

Body Weight Deficit(%)

Environmental Humidity
Humidity
Environmental
35.0

Body Weight Deficit (%)

RectalTemperature(0C)(°C)
Rectal Temperature
Whole Body
Body Sweat
Sweat Rate
Rate

Body Weight
Weight Deficit
Body
DeficitFig. 4 Whole body sweat rate (WBSR) at the end of 60
minutes exercise across different levels of relative
humidity (n=11). WBSR was not reduced with risinghumidity in highly trained men.
#
#

50

#

550

#

60

40

#

30

500

20

450

10
*

400
H20

H30

H40

H50

H60

Dry Heat Loss
(W.m-2)600

Dry Heat Loss
(W.m-2)

5.1 How does humidity affect thermoregulatory
responses?
Prolonged exercise in warm to hot ambient temperatures inevitably results in thermoregulatory strain as the
body seeks to maintain homeostasis. The addition ofhighly humid conditions exacerbates physiological strain,a fact that is recognized by the weight given to relative
humidity in the wet bulb globe temperature (WBGT)
heat stress index.
Perhaps the most comprehensive study examining
the influence of relative humidity on the human thermal
environment was performed by Winslow and colleagues(1937) who passively exposed their subjects to varying
levels of ambient temperature and relative humidity. It
was concluded that when environmental temperature
was above 25ºC, the relative humidity of the atmospherewould have a detrimental influence upon physiologicalresponses. Since then, there have been various experiments examining the influence of humidity on exercise
performance (Pandolf et al., 1974; Nielsen et al., 1997;
Gonzalez et al., 1974; Kobayashi et al., 1980; Frye &Kamon, 1983). A common observation from these experiments was that greater thermoregulatory strain was
experienced at higher levels of environmental humidity.
Compared with lower humidity levels, exercise at highenvironmental humidity in these studies caused a steadyrise in core temperature with no sign of thermal equilibrium and mean skin temperature rising to a higher level.
With rising skin temperature at elevated rectal temperature, the ability to transfer heat from the core to the skinis reduced, thus causing an increase in body heat storage
which ultimately results in fatigue as core temperaturereaches a critical level of around 40ºC (Nielsen et al.,1997). This increased thermoregulatory strain during
exercise in humid environments is attributed to a limited
capacity to evaporate sweat due to the decline in the
maximal evaporative capacity of the environment.
A distinct feature of thermoregulatory responses inhumid environments is a reduced rate of sweating withincreasing core temperature during prolonged exposure(Candas et al., 1983), a phenomenon referred to as
hidromeiosis (Brown & Sargeant, 1965). Hidromeiosis
refers to a condition associated with increased skinwettedness that leads to a reduction in sweat secretion.
However, this phenomenon and the underlying proposedmechanism remain controversial.
In addition to a reduced sweat rate, earlier observations have highlighted a decline in sweating efficiency

WholeWhole
BodyBody
Sweating
Sweating–1
Rate (g-mm) -1)
Rate (g.min

5. The Effect of Humidity on Thermoregulatory Responses during Prolonged Intense
Exercisewith increasing level of humidity (Libert et al., 1975;
Candas et al., 1979). Sweating efficiency, defined as theratio between evaporative rate and sweat rate, is an
important index that evaluates the effect of the sweat
rate on thermal regulation. A decline in sweating efficiency indicates that sweat produced during exercise ina humid environment is rendered relatively ineffective
in contributing to heat dissipation as it merely drips
from the skin surface, resulting in an increased area ofskin covered with sweat (skin wettedness).

Evaporative
Heat
Loss
Evaporative
Heat
Loss
(W.m–2)(W.m-2)

passive heating in the early morning were shifted tohigher core temperatures by BL exposure (Figs. 2 and 3)(Aoki et al., 2005). However, there was BL exposurethat had no effect on the slope of the relationshipbetween the increase in core temperature relative to theincrease in sweating or cutaneous vasodilation.

39

0

H70

Environmental Humidity
Evaporative Heat Loss
Dry Heat Loss

Fig. 5 Evaporative and dry heat loss values at 60 minutes of
exercise under increasing level of environmental
humidity, relative humidities from 20% (H20) to 70%(H70): n=10. Evaporative heat loss decreased graduallywhile dry heat loss was increased with rising humidity.
# indicates significant difference from the H20
environmental condition (P<0.05).

40

N. KONDO et al.

In a study examining the systematic changes inhumidity involving a group of highly trained, male dis& O 2 max = 62.9 ml/kg/min),tance runners (mean V
Che Muhamed and colleagues found that subjects wereable to complete a 60 minutes intense running (70%
V& O 2 max) exercise despite experiencing thermoregulatory stress. While earlier studies have shown adecline in sweating during prolonged exercise in humid
environments, highly trained endurance athletes wereable to maintain sweating rate across varying levelsof relative humidity as demonstrated in Fig. 4 (Che
Muhamed et al., unpublished data). In addition to theability to maintain sweat rate in highly trained subjects
during prolonged exercise, the ability to maintain dryheat loss at the expense of a reduced evaporative heatloss capacity is seen as an important contributing factor
to thermoregulation in humid environments (Fig. 5).

Acknowledgement
In this paper, we have summarised four invited
presentations from the 2008 International Conference on
Biometeriology, Tokyo.
References
Aoki, K., D.P. Stephens and J.M. Johnson (2001) Diurnal variation in cutaneous vasodilator and vasoconstrictor systems during heat stress. Am. J. Physiol. Regul. Integr. Comp. Physiol.,
281: R591-R595.
Aoki, K., M. Yokoi, R. Masago, K. Iwanaga, N. Kondo and T.
Katsuura (2005) Modification of core temperature regulation
for cutaneous vasodilation and sweating by bright light
exposure at night. Eur. J. Appl. Physiol., 95: 57-64.
Aoki, K., D.P. Stephens, K. Zhao, W.A. Kosiba and J.M. Johnson(2006) Modification of cutaneous vasodilator response to heatstress by daytime exogenous melatonin administration. Am. J.
Physiol. Regul. Integr. Comp. Physiol., 291: R619-R624.
Aschoff, J. and A. Heise (1972) Thermal conductance in man: Its
dependence on time of day and on ambient temperature. In:
S. Itoh, K. Ogata and H. Yoshimura, eds, Advances in Climatic
Physiology. Igaku shoin, Tokyo, chapter 20, 334-348.
Brengelmann, G.L., J.M. Johnson, L. Hermansen and L.B.
Rowell (1977) Altered control of skin blood flow during exercise at high core temperature. J. Appl. Physiol., 43: 790-794.
Brown, W.K. and F. Sargent (1965) Hidromeiosis. Arch. Environ.
Health., 11: 442-453.
Candas, V., J.P Libert and J.J. Vogt (1983) Sweating and sweat
decline of resting men in hot humid environment. Eur. J. Appl.
Physiol., 50: 223-234.
Candas, V., J.P. Libert and J.J. Vogt (1979) Human skin wettedness and evaporative efficiency of sweating. J. Appl. Physiol.,
46: 522-528.
Che Muhamed, A.M., T. Heap, W. Chen and M.W. Thompson
Sweating rate is maintained during high intensity exercise in
hot humid environment (submitted).
Crandall, C.G., J. Musick, J.P. Hatch, D.L. Jr. Kellogg and J.M.
Johnson (1995) Cutaneous vascular and sudomotor responses
to isometric exercise in humans. J. Appl. Physiol., 79:
1946-1950.
Crandall, C.G., D.P. Stephens and J.M. Johnson (1998) Muscle
metaboreceptor modulation of cutaneous active vasodilation.
Med. Sci. Sports. Exerc., 30: 490-496.

Czeisler, C.A., R.E. Kronauer, J.S. Allan, J.F. Duffy, M.E. Jewett,
E.N. Brown and J.M. Ronda (1989) Bright light induction ofstrong (Type 0) resetting of the human circadian pacemaker.
Science, 244: 1328-1333.
Fortney, S.M., E.R. Nadel, C.B. Wenger and J.R. Bove (1981)
Effect of blood volume on sweating rate and body fluids inexercising humans. J. Appl. Physiol., 51: 1594-1600.
Friedman, D.B., J.M. Johnson, J.H. Mitchell and N.H. Secher(1991) Neural control of the forearm cutaneous vasoconstrictor
response to dynamic exercise. J. Appl. Physiol., 71: 1892-1896.
Frye, A.J. and E. Kamon (1983) Sweating efficiency in acclimated men and women exercising in humid and dry heat. J.
Appl. Physiol., 54: 972-977.
Gonzalez, R.R., K.B. Pandolf and A.P. Gagge (1974) Heatacclimation and decline in sweating during humidity transients.
J. Appl. Physiol., 36: 419-425.
Green, D.J., A.J. Maiorana, G. O’Driscoll and R. Taylor (2004)
Effects of exercise training on vascular endothelial nitric oxide
function in humans. J. Physiol., 561:1-25.
Green, D.J., L.H. Naylor, K. George, J.A. Dempsey, M.K.
Stickland and K. Katayama, (2008) Cardiovascular and pulmonary adaptations to endurance training. In: N.A.S. Taylor and
H. Groeller, eds., Physiological Bases of Human Performance
during Work and Exercise. Churchill Livingstone Elsevier,
Edinburgh, 49-70.
Johnson, J.M. and M.K. Park (1981) Effect of upright exercise on
threshold for cutaneous vasodilation and sweating. J. Appl.
Physiol., 50: 814-818.
Kacin, A., P. Golja, O. Eiken, M.J. Tipton, J. Gorjanc and I.B.
Mekjavic (2005) Human temperature regulation during cycling
with moderate leg ischaemia. Eur. J. Appl. Physiol., 95:
213-220.
Kobayashi, K., S.M. Horvath, F.J. Diaz, D.R. Bransford and B.L.
Drinkwater (1980) Thermoregulation during rest and exercise
in different postures in a hot humid environment. J. Appl.
Physiol., 48: 999-1007.
Kondo, N., H. Tominaga, T. Shiojiri, M. Shibasaki, K. Aoki, S.
Takano, S. Koga and T. Nishiyasu (1997) Sweating responses
to passive and active limb movements. J. Therm. Biol., 22:351-356.
Kondo, N., H. Tominaga, M. Shibasaki, K. Aoki, S. Koga and T.
Nishiyasu (1999) Modulation of the thermoregulatory sweating
response to mild hyperthermia during activation of the muscle
metaboreflex in humans. J. Physiol., 515: 591-598.
Kräuchi, K., C. Cajochen, M. Pache, J. Flammer and A.
Wirz-Justice (2006) Thermoregulatory effects of melatonin in
relation to sleepiness. Chronobiol. Int., 23: 475-484.
Libert, J.P., J.J. Vogt, V. Candas and A. Hoeft (1975) Influence
des conditions hygrothermiques ambiantes sur le rendement
evaporatoire de la sudation thermique. J. Physiol., 70: 717-735.
Nadel, E.R., J.W. Mitchell, B. Saltin and J.A.J. Stolwojk (1971)
Peripheral modifications to the central drive for sweating. J.
Appl. Physiol., 31: 828-833.
Nadel, E.R., S.M. Fortney and C.B. Wenger (1980) Effect ofhydration state of circulatory and thermal regulations. J. Appl.
Physiol., 49: 715-721.
Nielsen, B., S. Strange, N.J. Christensen, J. Warberg and B. Saltin(1997) Acute and adaptive responses in humans to exercise in a
warm, humid environment. Pflugers. Arch., 434: 49-56.
Nose, H., G.W. Mack, X.R. Shi, K. Morimoto and E.R. Nadel(1990) Effect of saline infusion during exercise on thermal andcirculatory regulations. J. Appl. Physiol., 69: 609-616.
Pandolf, K.B., R.R. Gonzalez and A.P. Gagge (1974) Physiological strain during light exercise in hot-humid environments.
Aerospace. Med., 45: 359-365.
Patterson, M.J., J.M. Stocks and N.A.S. Taylor (2004a) Humid
heat acclimation does not elicit a preferential sweat redistribution towards the limbs. Am. J. Physiol., 286: R512-R518.
Patterson, M.J., J.M. Stocks and N.A.S. Taylor (2004b) SustainedThermoregulatory Adaptation in Humans and Its Modifying Factors
and generalised extracellular fluid expansion following heatacclimation. J. Physiol., 559: 327-334.
Shibasaki, M., N. Kondo and C.G. Crandall (2001) Evidence formetaboreceptor stimulation of sweating in normothermic andheat-stressed humans. J. Physiol., 538; 605-611.
Shibasaki, M., N.H. Secher, C. Selmer, N. Kondo and C.G.
Crandall (2003) Central command is capable of modulating
sweating from non-glabrous human skin. J. Physiol., 553:
999-1004.
Shibasaki, M., M. Sakai, M. Oda and CG. Crandall (2004) Muscle
mechanoreceptor modulation of sweat rate during recovery
from moderate exercise. J. Appl. Physiol., 96: 2115-2119.
Shibasaki, M., N.H. Secher, J.M. Johnson and C.G. Crandall(2005) Central command and the cutaneous vascular response
to isometric exercise in heated humans. J. Physiol., 565:
667-673.
Smolander, J., M. Härmä, A. Lindqvist, P. Kolari and L.A.
Laitinen (1993) Circadian variation in peripheral blood flow inrelation to core temperature at rest. Eur. J. Appl. Physiol., 67:
192-196.
Stephenson, L.A., C.B. Wenger, B.H. O’Donovan and E.R. Nadel(1984) Circadian rhythm in sweating and cutaneous blood flow.
Am. J. Physiol. Regul. Integr. Comp. Physiol., 246: R321-R324.
Strassman, R.J., C.R. Qualls, E.J. Lisansky and G.T. Peake(1991) Elevated rectal temperature produced by all-night bright
light is reversed by melatonin infusion in men. J. Appl. Physiol.,71: 2178-2182.
Takamata, A., K. Nagashima, H. Nose and T. Morimoto (1997)
Osmoregulatory inhibition of thermally induced cutaneous
vasodilation in passively heated humans. Am. J. Physiol., 273:
R197-R204.
Taylor, N.A.S. (2006) Ethnic differences in thermoregulation:
genotypic versus phenotypic heat adaptation. J. Thermal. Biol.,
31: 90-104.
Taylor, N.A.S. and J.D. Cotter (2006) Heat adaptation: guidelines
for the optimisation of human performance. Int. SportMed. J.,
7: 33-57.
Tipton, M.J., K.B. Pandolf, M.N. Sawka, J, Werner and N.A.S.
Taylor (2008) Physiological adaptation to hot and cold environments. In: N.A.S. Taylor and H. Groeller, eds., Physiological
Bases of Human Performance during Work and Exercise.
Churchill Livingstone Elsevier, Edinburgh, 379-400.
van Beaumont, W. and R.W. Bullard (1963) Sweating: its rapid
responses to muscular work. Science, 141: 643-646.
Waterhouse, J., B. Drust, D. Weinert, B. Edwards, W. Gregson, G.
Atkinson, S. Kao, S. Aizawa and T. Reilly (2005) The circadianrhythm of core temperature: Origin and some implications forexercise performance. Chronobiol. Int., 22: 207-225.
Wenger, C.B., M.F. Roberts, J.A.J. Stolwijk and E.R. Nadel(1976) Nocturnal lowering of thresholds for sweating andvasodilation. J. Appl. Physiol., 41: 15-19.
Winslow, C.E., L.P. Herrington and A.P. Gagge (1937)
Physiological reactions of the human body to various atmospheric humidities. Am. J. Physiol., 120: 288-229.

41

Narihiko KONDO
Narihiko KONDO is a Professor of
Graduate School of Human Development
and Environment, Kobe University. He
is interested in the integrated control ofsweating and skin blood flow during
exercise in humans. He also focuses on
the effects of aging, gender, physicaltraining, mental stress on human thermoregulatory system associated with international collaboration research of Environmental Physiology and
Ergonomics Research Exchange.

Nigel AS TAYLOR
Nigel TAYLOR is a human stressphysiologist (University of Wollongong)with research emphases in exercise
physiology and temperature regulation.
He participates in a five-way researchcollaboration: Environmental Physiology
and Ergonomics Research Exchange(Australia, France, Japan, Slovenia,
United Kingdom).

Manabu SHIBASAKI
Manabu Shibasaki is an exercise andenvironmental
physiologist
at theDepartment of Environmental Health,Nara Women’s University. He isinterested in control of thermoregulatory
and cardiovascular responses during
exercise and heat stress. He got PhD at
Graduate School of Science andTechnology, Kobe University in 1998.

Ken AOKI
Ken AOKI is an applied physiologist at
the Division of Hygiene, Nihon University
School of Medicine. He is interested incircadian variation of physiological
functions in humans. He got PhD at
Graduate School of Science and Technology, Chiba University in 1999. He hasstudied thermal and exercise physiology
with Professor Narihiko Kondo at Kobe
University from 1993 to 1996.

Ahmad Munir Che MUHAMED
Dr. Ahmad Munir graduated with a
Bachelor and Master of Science Degree in
Exercise Science from Indiana State
University in 1994 and 1996, respectively.
He then received Doctor of Philosophy
Degree in Exercise Physiology from The
University of Sydney in 2005. His
research’s interest is examining the influence of relative humidity on sports performance.

(Received 14 January 2009, Accepted 9 February 2009)