Sports Medicine 2: 8-20 (1985)

0112-1642/85/0100-0008/$6.50/0
© ADIS Press Limited
All rights reserved.

Exercise, Performance and Temperature Control:

Temperature Regulation during Exercise and Implications for
Sports Performance and Training

Suzanne M. Fortney and Neil B. Vroman

Johns Hopkins University, Baltimore, and Department of Physical Education,
University of New Hampshire, Durham

Summary Thermoregulation is an important consideration not only for athletic performance but
also for the safety ofthe athlete. This article presents a broad overview ofthe mechanisms
by which body heat is dissipated in an individual exercising in a hot environment. Par-
ticularly emphasised are more recent views of body heat loss mechanisms and the influ-
ences of non-thermal inputs, such as effects due to changing blood volume or blood flow
distribution.
During exercise in a hot environment, metabolic heat produced by the exercising muscles
is transported by the circulating blood to the surface of the body where it is released to
the environment, either by radiation and convection or by evaporation ofsweat. The prim-
ary drives for both the increased skin blood flow and increased body sweating are the
thermal inputs which are sensed by receptors in the deep body core, with a lesser drive
from skin receptors. These thermal signals are integrated in the hypothalamus and proper
heat loss responses are effected. When exercise is prolonged, however, and body rehydra-
tion is not adequate, the total blood volume may be compromised. In addition, as the core
temperature increases during exercise, larger proportions of the blood volume are distrib-
uted to the cutaneous vessels, thus effectively reducing cardiac return and central blood
volume. During severe exercise, a reduction in cardiac filling may result in a fall in central
venous pressure and stimulate baroreceptor vasconstrictor reflexes. As discussed below, the
outputs from these baroreceptorscompete with and modify the thermal drives for both the
control of the skin blood flow and control of the sweat glands.
The effect of high ambient temperatures on exercise performance is most evident in
prolonged submaximal exercise. Normally, maximal exercise performance is not altered
by high temperatures unless the individual has an elevated deep body temperature before
the start ofthe exercise task. However, submaximal exercise performance is often impaired
by high ambient temperatures, but may be improved by programmes of physical training
and heat acclimatisation. Both training and heat acclimatisation significantly modify the
control systems which regulate skin blood flow and sweating. Only acclimatisation pro-
grammes, however, are effective in preventing heat stress during prolonged exercise in hot
environments.

1. Overview of the Human porting evidence is our comparatively well-devel-

Heat Loss System oped heat loss system. Along with other mammals,
humans are warm-blooded, which enables a life-
It is commonly thought that Homo sapiens style with several advantages, such as the ability to
evolved in a tropical environment, and the sup- remain active as the ambient temperature falls.
Exercise, Performance and Temperature Control 9

However, the cost of maintaining a constant body
temperature is seen by our absolute dependence
upon a steadily available food supply and the sev-
ere consequences which occur when the body tem-
perature drifts outside the narrow 4°C critical tem-
perature range. Also, our reliance upon evaporative
forms of heat loss leaves us critically dependent
upon available sources of drinking water.
Our thermoregulatory system is so efficient that
through both physiological and behavioural re-
sponses, man is able to tolerate most naturally oc-
curring ambient temperatures. Usually, the major
threat to thermoregulatory balance is derived in-
ternally from the heat produced from exercising
muscles. During severe exercise, body temperature
may rise to life-threatening levels within only 10
to 15 minutes if heat loss responses are not acti-
vated.
Heat produced by the exercising muscles is car-
ried via venous drainage to the body core, elevat-
ing deep body temperature. Input proportional to
this rise in core temperature is integrated with in-
put from peripheral thermal receptors by the ther-
moregulatory centre in the hypothalamus. In ad-
dition, non-thermal inputs (see fig. 1) are evaluated
and integrated to determine the proper efferent re-
sponse. For example, during dehydration, sweat
output is reduced, which helps to maintain central
venous filling and mean blood pressure. The exact
mechanism by which the body is kept appraised of
the total body hydration state is unknown, but
probably involves input from osmo- and/or baro-
receptors.
Rising body temperatures elicit from the ther-
moregulatory centre two effector output signals
which function to dissipate body heat - inhibition
of cutaneous vasomotor tone and increased sweat
output. Nielsen (1938) first described the linear re-
lationship between the rise in core temperature and
increasing levels of exercise. Later Saitin and Her-

Intravascular
e

~
= stretch
receptors Arterial and/or
(±)Osmolality cardiac filling
+ Osmoreceptors ~--------, pressures

Ul
:;
a. (±) Cutaneous
/
81'----8-'
.!:

8
vasomotor Exercise

•
Q; Heat (n-.
s: tone
o Thermoregulatory
./. \.+J

L-._ _) _ (±) C:r~~~al 8

Centre
(±) Sweat gland
e
activity Body
temperatures

1-- Body ~
thermoreceptors

Fig 1. Schematic representation of the human thermoregulatory system including the thermal reflex inputs (lower half of figure) and
non-thermal inputs (top half). [Adapted from Nadel, 1983.1
Exercise, Performance and Temperature Control
mansen (1966) showed that an even closer rela-
tionship exists between the exercise level and body
core temperature, when the exercise intensity is ex-
pressed in terms of relative percentage of maximal
exercise capacity, rather than the absolute level of
exercise. However, since the heat produced is pro-
portional to the absolute, and not the relative,
amount of work performed, differences in core
temperatures between individuals who are working
at similar absolute exercise intensities must be due
to differences in the efficiency of their heat loss
systems.
In this review, we will examine in greater detail
the heat loss effector systems, which are activated
during exercise. We will also discuss exercise heat
loss responses during exposure to high ambient
temperatures.
2. Control of Skin Blood Flow
2.1 Role of Vasodilatation in
Temperature Regulation
An important avenue of heat dissipation is the
increase in skin blood flow accompanying rises in
body temperature. Warm blood from the body core
is redistributed to the skin, so that heat is lost to
the ambient surroundings via radiation and con-
vection, at a rate proportional to the difference be-
tween skin and ambient temperature. This increase
in skin blood flow occurs by relaxation of the re-
sistance vessels, thereby opening new skin capillary
beds, and also by dilatation of cutaneous veins.
Venodilatation increases the transient time of blood
through the superficial tissues allowing a longer in-
terval for heat transfer from warm blood to the
cooler skin (Goetz, 1950).
At ambient temperatures below about 32 to
34"C, increasing skin blood flow is the primary
method of releasing body heat. Vasodilatation for
heat loss is limited by the ambient conditions,
however. When air temperatures are hotter than
mean skin temperature, the gradient for heat ex-
change is reversed, and heat is transferred from the
air to the skin, resulting in heat storage rather than
heat loss.
10
2.2 Competitive Interactions between
Vascular Beds and the Control of Skin
Blood Row
During exercise, especially in a hot environ-
ment, a redistribution of blood flow occurs in sev-
eral vascular beds. Blood is diverted towards ex-
ercising muscles, and away from non-exercising
muscles and splanchnic regions. Also as body tem-
perature rises, an increased skin blood flow is
needed to dissipate body heat. In conditions where
cardiac output is limited, such as during heavy ex-
ercise in the heat, competition occurs between the
muscle and skin vascular beds. On the one hand,
if skin blood flow is compromised, body temper-
atures will rise at a faster rate, and thus limit ex-
ercise endurance. Alternatively, if muscle blood
flow is inadequate, muscle fatigue and discomfort
will limit exercise performance. The final distri-
bution of whole body blood flow depends upon the
level of exercise and the ambient conditions. Other
factors, such as hydration level and posture may
also influence blood flow distribution and will be
discussed later.
2.3 Skin Blood Flow Response to Exercise
At the beginning of an exercise task, there is a
transient vasoconstriction, probably a result of a
sympathetic vasoconstrictor response associated
with the exercise. As the deep body core temper-
ature (Tc) increases however, this vasoconstrictor
effect is overridden by thermal vasodilatory re-
flexes. While Rowell(1974) reported that blood flow
to visceral regions is reduced in proportion to the
relative exercise intensity, the changes in the skin
blood flow-core temperature relationship during
exercise do not appear to be proportional to ex-
ercise intensity, (Johnson, 1979; Nadel et al., 1979;
Wenger et al., 1975).
2.4 Thermal Inputs in the Control of
Skin Blood Row
The thermal control of skin blood flow is pri-
marily accomplished by reflex mechanisms involv-
Exercise, Performance and Temperature Control II

ing afferent information from both skin and deep
body core temperature receptors. Integration of this
information occurs in the hypothalamus (Hensel,
1973).
The basic relationship describing the reflex
actions of core and skin temperatures of skin blood
flow, is depicted in figure 2. Skin blood flow is most
easily measured in a limb such as the forearm, and
thus changes in forearm blood flow (FBF) are often
represented as changes in whole body skin blood
flow. In figure 2, forearm blood flow is plotted as
a function of the core temperature, here measured
in the oesophagus (Tes) . At rest, skin blood flow is
proportional to core temperature beyond a certain
core temperature vasodilatory threshold; for the
subject in figure 2, the threshold is about 37.3°C
when skin temperature is 30.3°C. Increasing mean
skin temperature (T s) to 35SC resulted in a low-
ering of the vasodilatory threshold without signifi-
cant change in the slope of the skin blood flow-
core temperature relationship. Therefore, the over-
all skin blood flow response is proportional to a
Tforearm = 36.8°
'2
I activity; for example, active vasodilatation is ab-
E 10
0
--
0
~
combination of core and skin temperatures, with
the core temperature being the more influential
variable (Wyss et aI., 1974).
2.5 Mechanism of the Vasodilatory
Response
Vasodilatation of human skin vessels in re-
sponse to rising body temperature, is an active pro-
cess not due merely to a release of tonic sympath-
etic vasoconstrictor tone. Roddie et al. (1957)
reported only a minor passive increase of skin blood
flow following release of an elevated level of vaso-
constrictor tone. Active vasodilatation is respon-
sible for the major part of the increase in skin blood
flow during heat stress. This active vasodilatation
is believed to involve a cholinergic mechanism.
Shepherd (1963) and Edholm et al. (1957) have
shown that the blood flow response to body heat-
ing could be eliminated by sympathetic blockade.
Fox and Hilton (1958) suggested that the vasodi-
latory mechanism was related to the secretion of
bradykinin which was produced during the sweat-
ing process.
However, other investigators have found that
the vasodilatory response does not always depend
upon local activation of sweat glands, and brady-
kinin therefore cannot be the sole mediator in the
vasodilatory responses (Rowell, I977a; Wyss et aI.,
1974). In many cases, however, active vasodilata-
tion appears to be closely associated with sweating
sent in individuals with a congenital absence of

I sweat glands (Brengelmann et aI., 1981). Thus, the

i: active vasodilatation in skin appears to be pri-
0
;;::
'0
5 marily a sympathetic response, with modifying in-
0
0 fluences exerted by factors associated with rising
:0
E body temperature and activation of sweat glands.
:0
e
0
u, 0 2.6 Non-Thermal Modifiers of
36 37 38 39
Skin Blood Flow
r., rC)
Many non-thermal reflexes modify skin blood
Fig 2. Skin blood flow (measured in the forearm) to oesophageal
temperature relationship (Te s ) in a typical subject performing
flow regulation. Cutaneous vasomotor tone, or skin
moderate exercise at 2 mean skin temperatures (Ts )' [From blood flow, is acted upon by efferent input from
Wenger et al., 1975.] both the thermoregulatory centre to maintain ther-
Exercise, Performance and Temperature Control
mal homeostasis, and by the vasomotor centre to
maintain arterial blood pressure (fig. 1). The final
level of skin blood flow then represents the sum of
several reflexes which interact competitively with
each other.
2.6.1 Severe Exercise
When exercise is severe or prolonged, so that
cardiac filling is not adequate, several authors
(Brengelmann et al., 1977;Nadel et al., 1980) have
noted an attenuation of the skin blood flow-core
temperature relationship, as seen by the decrease
in slope of the response in figure 3. The attenuated
skin blood flow-core temperature slope at higher
body temperatures is believed to occur in response
to both the reduction in absolute blood volume
during exercise, and to blood flow redistribution to
the skin. The reduction in blood volume occurs
because of the fluid losses associated with sweat-
ing, and also because of the net movement of fluid
from the vascular compartment into the interstitial
spaces surrounding the exercising muscles. Blood
flow redistribution occurs in response to the rising
body temperatures.
2.6.2 Hypovolaemia
As also seen in figure 3, hypovolaemia prior to
exercise significantly alters the skin blood flow re-
sponse. In this study (Nadel et aI., 1980), subjects
were made hypovolaemic by ingestion of diuretic
tablets, so that blood volume was reduced an av-
erage 11%, without significant alteration in plasma
osmolality. Blood flow measurements were then
compared when these same subjects began exercise
in a euhydrated state (triangles), to measurements
obtained in the hypohydrated state (squares).
Hypovolaemia resulted in an elevation in the va-
sodilatory threshold, resulting in a greater heat
storage and higher exercise body temperatures. In-
creasing blood volume through ingestion of water
before exercise (circles) had little effect on the fore-
arm blood flow-oesophagus temperature relation-
ship. The authors suggested that the attenuation in
the skin blood flow response during hypovolaemic
exercise was caused by the stimulation of barore-
ceptors (see fig. I), which were activated by a re-
12
.. Control ± S.E.
25-
• Hypohydration ± S.E.
• Hyperhydration ± S.E.
:s 20
.§.
E
o
~ 15
§.
g 10
"0
0
0
:0
5
E
ttl
~
0
u, 0
37 38 39
Oesophageal temperature (OC)
Fig 3. Effect of hydration state on the forearm blood flow-oeso-
phageal temperature relationship. Results are mean data from
5 subjects during moderate exercise in euhydrated (control), hy-
perhydrated (water ingestion) and hypohydrated (diuretics) con-
ditions. [From Nadel et aI., 1980.1
duction in central venous filling or by a fall in mean
arterial blood pressure. The baroreceptor signals
travelled to the vasomotor centre which then had
an inhibitory influence on the thermoregulatory
centre, causing a vasoconstrictor response.
2.6.3 Positive Pressure Breathing
Further evidence that a reduction in skin blood
flow-core temperature relationship results when
cardiac return is impeded and thus central blood
volume is reduced, was recently reported by Vro-
man et ai. (1985). The addition of positive pressure
breathing (CPAP) during exercise impaired normal
thermoregulatory responses. The higher body tem-
peratures were because of an increase in the core
temperature vasodilatory threshold, and a reduc-
tion in the peak forearm blood flow during CPAP,
as compared to control breathing. Positive pres-
sure breathing reduces venous return and depletes
central blood volume, presumably stimulating low
pressure cardiopulmonary baroreceptors. Thus,
positive pressure breathing is yet another example
where competition occurs between the thermore-
Exercise, Performance and Temperature Control
gulatory system and the system controlling blood
pressure. In conditions where cardiac filling is
compromised, such as positive pressure breathing,
blood pressure maintenance prevails at the ex-
pense of temperature regulation.
2.6.4 Postural Considerations
The effect of blood pooling on the control of
skin blood flow is evident when skin blood flow
responses are compared for the same individuals
in different postures. In the upright posture, over
70%of the blood volume is located in vessels below
heart level, primarily in the veins. Thus, upright
humans have a particularly difficult time ensuring
adequate venous return under conditions of high
body temperatures, and must rely on the muscle
pump action of the legs to maintain venous return
(Rowell, I977b). The influence of posture at rest
and during exercise on the skin blood flow-core
temperature relationship is illustrated in figure 4.
Johnson et al. (1974) demonstrated that at rest
for any given core temperature, a lower slope of
the skin blood flow response occurred in the up-
21
18
15
12
C et aI., 1972).
I However, the contribution of respiratory water
E 9
-I
0
0
6 ercise, or exercise in a warm environment is al-
u.
CD
u,
3 through sweating, or sensible perspiration. For ex-
0
36.5 37.0 37.5 38.0 38.5
r., 1°C)
Fig 4. Effect of posture on the forearm blood flow (FBF)-oeso-
phageal temperature (Tos) relationship. Regression lines are
drawn from data from one typical subject during supine and
upright rest and exercise. [Adapted from Johnson et al.• 1974.]
13
right position than in the supine position. The ef-
fect of exercise was to exaggerate these postural dif-
ferences. Thus, in the upright position, the greater
blood pooling in the lower extremities also reduces
cardiac return. An increased vasoconstrictor baro-
receptor output may then contribute to the de-
crease in slope of the forearm blood flow-core tem-
perature relationship in the upright posture.
One factor which may aid in the maintenance
of cardiac return during upright exercise in the heat,
was described by Bevegard et al. (1977). They
showed that decreases in right atrial pressure may
increase the sensitivity of the arterial barorecep-
tors. Thus, cutaneous vasodilatation and reduc-
tions in plasma volume during exercise in the heat
may result in an increased sensitivity of the skin
vasculature to high-pressure baroreceptor-induced
vasoconstriction.
3. Control of Evaporative Heat Loss
3.1 Contribution of Insensible Perspiration
to Total Evaporation during Exercise
At rest in a comfortable environment, evapor-
ative heat loss accounts for approximately 20 to
25% of the total heat loss. Evaporative heat is lost
via two channels of insensible perspiration; cutan-
eous evaporation resulting in water losses of about
4 to 13 g/h, and respiratory evaporation, resulting
in a further loss of 10 to 15 g/h. During exercise,
respiratory water loss increases by up to 10-fold in
proportion to increases in metabolic rate (Mitchell
loss to the overall heat balance during severe ex-
most negligible compared to the water loss
ample, during exercise at an intensity requiring 2
litres of oxygen uptake per minute, in a 30°C en-
vironment with a water vapour pressure of
IOmm Hg, the water loss through the respiratory
tract would be calculated at 78 g/h. Total water
losses under similar conditions for subjects exer-
cising in our laboratory average between 1000 g/h
and 2000 g/h.
Exercise, Performance and Temperature Control
3.2 The Sweat Gland
Apocrine and eccrine sweat glands have been
identified in the human, and they differ both mor-
phologically and functionally. Apocrine glands are
derived from hair follicles, and their secretion rate
is slow and contains relatively large quantities of
organic substances. They do not become functional
until puberty, suggesting a secondary sexual func-
tion (Elizondo, 1977).
Eccrine sweat glands on the other hand are the
true thermal sweat glands, and are therefore the
focus of discussion for the remainder of this article.
There are 2 to 5 million eccrine glands distributed
on the body surface. They develop from the epi-
dermis and are functional from infancy (Kuno,
1956). Each gland consists of a simple tubular
structure containing a single-layered secretory coil
and a double-layered duct. The secretory coil is
composed of 3 primary cell types - clear (secretory
cells), dark (mucoid cells), and myoepithelial cells.
Clear cells are believed to be involved in the active
secretion of the precursor fluid of sweat, while the
function of the dark cells is still unknown. The role
of the myoepithelial cells in sweat secretion is still
debated. Their contraction is not believed to be ne-
cessary for sweat secretion (Sato, 1977). The sweat
gland duct is coiled at first, but becomes straighter
as it reaches the epidermis. It appears that the
proximal (coiled) area of the duct is the more ac-
tive region, containing high Na/K ATPase activity.
3.3 Eccrine Gland Innervation
Efferent nerves involved in the sweating reflex
originate in the hypothalamus and descend through
the brain stem and spinal tract, crossing at various
heights and ending in the lateral hom where new
neurons start. Non-myelinated class C, sympath-
etic cholinergic fibres, are involved in sweating and
were first described by Dale and Feldberg (1934).
In addition, there is evidence of the presence of a
network of sympathetic adrenergic nerve fibres
(Sato, 1977). Both a- and {3-adrenergic receptors are
present in the human sweat gland, and there is con-
siderable controversy over the interaction between
14
the cholinergic and adrenergic controls.
Kuno (1965) reported that adrenergic input po-
tentiates cholinergic actions, while Terada (1966)
reported inhibition of sweating by adrenergic fibres.
However, both authors agree that during exercise,
adrenergic input increases total sweat output. Cal-
cium is required for both cholinergic and e-adre-
nergically-mediated sweating. One hypothesis sug-
gests that acetylcholine (ACH), may function to
increase calcium permeability into the sweat gland
clear cell. {3-Receptor sweating is believed to work
through release of cyclic-AMP which is thought to
increase intracellular stores of calcium (Sato and
Sato, 1981).
3.4 Mechanism of Sweat Secretion
Sweat secretion is an active 2-stage process, in-
volving secretion and reabsorption of sodium ions.
First, sodium ions are actively transported into the
secretory coil and water passively follows, resulting
in an isotonic precursor fluid in the coil. This fluid
is then transported into the sweat gland duct where
sodium is actively reabsorbed in an excess of water.
The slower the sweat rate, the longer the transit
time of the fluid in the sweat gland duct and the
1.0
E0
c- 0.8
'E
Ci
oS
:c- 0.6
E
Cl
~
~ 0.4
0;
Q)
~
en 0.2
0
37.0 37.6 38.2 38.8
r., lOG)
Fig 5. Effect of mean skin temperature (Ts ) and oesophageal
temperature (Te s ) on local sweat rate, with the skin temperature
under the sweat capsule being 34.8°C. Data is taken from one
typical subject. [From Nadel et aI., 1971.]
Exercise, Performance and Temperature Control
greater the amount of sodium reabsorbed, resulting
in a more hypotonic sweat (Sato, 1977).
3.5 Factors Affecting Sweat Output
3.5.1 Neural, Hormonal and
Mechanical Factors
Neural, hormonal, and mechanical factors all
interact to regulate the volume and composition of
sweat. The principal efferent signal which stimu-
lates sweat production is sympathetic cholinergic
output from the anterior hypothalamus. This neural
output is largely initiated in response to afferent
input, proportional to the deep body temperature.
Above a threshold core temperature, a linear re-
lationship exists between sweat output and the rise
in core temperature (see fig. 5). The sensors for this
core temperature signal have been postulated to
exist in the anterior hypothalamus, in other areas
of the brain, in the spinal cord, and in the viscera.
Also shown in figure 5, is the effect of changes in
mean skin temperature (Ts) , on the sweating re-
sponse. Increasing ambient temperature will in-
crease mean skin temperature, resulting in a par-
allel shift in the sweat rate to core temperature
relationship.
3.5.2 Adrenergic Innervation
Adrenergic innervation alters sweat output, but
as mentioned above, the effect is controversial.
Circulating adrenergic substances such as adrena-
line (epinephrine) also alter sweat output, and are
involved in the total exercise sweat response. Sato
(1973) reported that in the isolated in vitro sweat
gland, both methylcholine and adrenaline pro-
duced precursor sweat at comparable rates. They
postulated that the low, in vivo secretory response
to adrenaline, which is reported to be only one-
tenth that of acetylcholine, can probably be ex-
plained by the strong vasoconstrictor effect of ad-
renaline on the periglandular blood vessels.
3.5.3 Other Humoral Agents
Other humoral agents which have been shown
to alter sweat output include bradykinin, aldoster-
one, antidiuretic hormone (ADH), and prostaglan-
15
din E 1• Bradykinin was once postulated to be an
important mediator in sweat production (Fox,
1958). Although locally released bradykinin may
increase local blood flow and thus increase sweat
output, increases in sweating have been described
without an increase in bradykinin (Brengelmann et
aI., 1981). Aldosterone affects sweat secretion by
altering sodium reabsorption in the sweat duct. Its
role in sodium secretion in the sweat coil is still
uncertain (Sato, 1977).
Antidiuretic hormone is often postulated to im-
pair sweat output. However, most efforts to dem-
onstrate a direct local action of ADH on either iso-
lated glands or on in vivo glands have failed to
demonstrate an inhibitory action. A central action
of ADH in the hypothalamus has also been hy-
pothesised (Fortney et aI., 1981, Senay, 1979), and
alterations in hypothalamic ADH concentrations
have been reported following conditions of heat
stress in animals (Epstein, 1983). Definitive studies
proving a direct central action of ADH on sweating
are required. Prostaglandin E) has been shown to
have an inhibitory effect on sweat secretion (Eli-
zondo, 1977) but its physiological role is still un-
defined.
3.5.4 Specific Ions and Osmolality
Specific ions and/or changes in blood or cere-
brospinal fluid osmolality have been postulated to
alter sweat production. Nielsen (1974a) suggested
that either sodium ions alone or the sodium: cal-
cium ratio alters sweating in humans. The author
reported that sweating was inhibited after drinking
hypertonic saline solutions, and increased after
drinking l.5litres of water (Nielson, 1974b). Sweat
rate changes were attributed to the peripheral ac-
tion of plasma osmolality or specific ions in either
altering the sensitivity of the sweat glands to a given
neural input, or the secretion-absorption process in
the sweat gland. A direct central action of osmo-
lality on the hypothalamus was also suggested.
Nielsen (1974a) next studied whether the
changes in sweat rate following ingestion of hy-
pertonic saline, were caused by the change in os-
molality per se, or by a direct action of specific
ions. Subjects drank solutions of either hypertonic
Exercise, Performance and Temperature Control
sodium chloride or calcium chloride. Although
plasma osmolality was increased after subjects
drank both solutions, only after drinking sodium
chloride was sweating inhibited, suggesting a direct
action of the sodium ions. Feldberg et al. (1970)
suggested that alteration in temperature regulation
may occur through changes in the sodium : cal-
cium ratio. Doris and Baker (1982) recently pub-
lished a study which supports a role for central os-
moreceptors in evaporative cooling. Water was
infused into the lateral cerebral ventricle of heat-
stressed cats. Evaporative cooling increased, de-
spite no alteration in the sodium : calcium ratio.
Therefore, the role of specific ions and/or osmo-
lality on temperature regulation is still an ongoing
research problem.
3.6 Mechanical Factors in Alteration of
Sweat Rate
When an individual is abruptly exposed to a hot
environment or performs severe exercise, the
sweating rate increases and reaches maximal val-
ues within 1 to 3 hours, but then progressively de-
creases with continued exposure, even though both
rectal and skin temperatures remain elevated. This
decline in sweating has been defined as the phen-
omenon of hidromeiosis. Previously, it was thought
that this sweat rate depression was due to a
'fatigue' of the sweat glands, possibly due to a lack
of neurotransmitters or fuel needed for the sweat-
ing process.
However, hidromeiosis is now thought to occur
because of a mechanical blockage of the sweat ducts
caused by a swelling of epidermal cells. Evidence
to support the mechanical blockage theory was
provided by Brown and Sargent (1965). First they
exercised subjects in a hot humid environment un-
til sweat depression was evident. When these sub-
jects were then transferred to a hot dry environ-
ment their sweat rate recovered, presumably
because sweat was now able to evaporate from the
skin surface, because of drying of the epidermal
cells. Candas et al. (1983) and Nadel et al. (1973a)
also presented evidence that sweating efficiency is
related to the degree of skin wetness, and Frye and
16
Kamon (1983) showed that hidromeiosis was ac-
companied by decreases in the number of active
sweat glands and also in the average output of ac-
tive sweat glands, suggestinga progressive blockage
of sweat gland pores as the epidermal cells increase
in size.
Another unproven theory is that hidromeiosis
is caused by an alteration in central neural pro-
cesses whereby a prolonged elevation of body core
temperature results in depression in the sensitivity
or effectiveness of the sweating reflex (Collins et
aI., 1965).
4. Effects of Physical Training on
Thermoregulation
Although it is generally accepted that physical
training improves heat tolerance, it is often diffi-
cult to separate the effects of training from heat
acclimatisation, since most individuals experience
pronounced elevation in body temperatures during
training. A controversy exists. as to whether re-
peated elevation in core temperature during exer-
cise in a cool environment may result in heat ac-
climatisation, as suggested by Piwonka et al. (1965).
Although training may reduce thermoregulatory
strain during short heat exposures, Strydom et a1.
(1966) showed that during exposures to hot wet
conditions for longer than about 2 hours, the bene-
ficial effects of training on heat tolerance were no
longer adequate.
4.1. Mechanisms of Thermoregulatory
Balance
The mechanisms by which physical training im-
proves thermoregulatory balance are 2-fold; through
improved sweating and improved skin perfusion.
Firstly, as illustrated in figure 6, sweat output in-
creases. Nadel et a1. (1974) and Henane et a1. (1977)
reported that sweat output increased with training
both through reductions in the core temperature
threshold for sweating and through increased
sweatingsensitivity, as evidenced by a steeper slope
of the sweat rate-core temperature relationship. In
a study comparing athletes to untrained non-ath-
Exercise, Performance and Temperature Control 17

letes, Kobayashi et a1. (1980) reported only lower perature is elevated significantly through a reduc-
sweating thresholds in the athletes, with no differ- tion in the vasodilatory threshold without signifi-
ences in the sweat rate slope. cant change in the slope of the skin blood flow-
Isolated sweat glands from individuals who de- core temperature relationship (see fig. 6).
scribed themselves as fit and good sweaters, were
found to be larger, and to show a greater sensitivity 4.2. Effects of Heat Acclimatisation on
to methacholine administration than the sweat Thermoregulation
glands from non-fit subjects (Sato and Sato, 1983).
These results suggest that physical training may Two of the classic indices of heat acclimatisa-
structurally modify sweat glands, increasing their tion are a reduction in deep body temperature, and
sweat output. Addditionally, it is possible that reduced skin temperatures for a given absolute level
training may alter central neural processes which of exercise. Kuno (1956) argued that the enhanced
control sweating, although such a mechanism has sweat output following heat acclimatisation was
not been described. caused by a central modification of the sweating
The second mechanism by which physical train- response. However, Ito and Adachi (1934),and Fox
ing improves heat tolerance is through alteration et a1. (1964) supported a local peripheral modifi-
in the control of skin blood flow. Following phy- cation of the sweat glands following heat exposure.
sical training, skin blood flow at a given core tem- Both peripheral and central changes in sweat gland
function probably occur during heat acclimatisa-
tion.
_ Pre-training
Another problem is whether the increase in
s: 0.8
E
.-- Post-training sweat output during heat acclimatisation is a result
._.- Post-acclimatisation
~
c: I of an increase in the number of active sweat glands,
'E 0.6 i
i , or an increase in the output of individual glands.
I
Ci i I
~ i
i
I
I
I
Accordingto the work of Collins et a1. (1965), sweat
~ 0.4 i I
I
output increases solely as a result of an increased
CD i I
s: i
.8. i I
I
output, without significant recruitment of glands.
I
i
~ 0.2 i I
I
Kuno (1956) reported that recruitment of active
i I
i I
I sweat glands is possible only in the first 2 years of
i
o/ life.
10 , Dobson (1960) presented morphological evi-
,/ ,/ dence of a change in sweat gland function follow-
8 ing heat acclimatisation. Prior to heat acclimatis-
'2 /i / ' "
I ./ ,/
.'
ation depletion of glycogen occurs in the secretory
E
0
6 I I cells of sweat glands after a single bout of vigorous
--~
0
~
.I " I I
sweating and glycogen levels are rapidly restored
4 .i/
during recovery. After heat acclimatisation, gly-
• I
I
u.
m
u, cogen depletion was no longer observed even after
2
very vigorous sweating, suggesting a metabolic al-
0 teration in sweat gland function.
37.0 38.0 38.5
While physical training increased the slope of
the sweat rate-core temperature relationship and
tended to reduce the sweating threshold, the com-
Fig 6. Representation of the data from local sweatingand fore-
arm blood flow (FBF) responses during exercise: (a) before
bination of training and heat acclimatisation re-
training (-), (b) after training (----), and (c) after acclimatis- sulted in further slight increases in slope and a sig-
ation (_....._._J. [After Roberts et aI., 1977]. nificant decrease in threshold (Nadel et al., 1973b).
Exercise, Performance and Temperature Control 18

For the skin blood flow response, both physical Table I. Effect of varying skin temperatures on maximum oxy-
training and/or heat acclimatisation lowered the gen uptake- (\102 max)

vasodilatory threshold without significantly alter- Water perfusion 0.5 28 45

ing the slope of the skin blood-flow-core temper- temperature (0C)
ature relationship (Roberts et al., 1977). Figure 6
\10 2 rna, 3.05 ± 0.34 3.03 ± 0.37 2.98 ± 0.31
summarises the thermoregulatory changes follow- (L/min)
ing training and acclimatisation.
Mean skin 30.9 ± 0.6 34.6 ± 0.3 36.6 ± 0.2
temperature
5. Effects of a Hot Environment on (0C)
Maximal Exercise Performance Oesophageal 37.9 ± 0.3 38.0 ± 0.1 38.3 ± 0.3
temperature
Rowell (1974) extensively reviewed the adjust- at \10 2 max (0C)
ments in the central circulation accompanying ex- Heart rate at 175 ± 4 177 ± 4 178 ± 4
ercise in the heat. Maximal oxygen uptake is gen- \10 2 rna,
erally unaffected when ambient temperature is (beats/min)
elevated and table I presents data from an experi-
a All values are mean ± SO; n = 4.
ment in our laboratory supporting this point.
Treadmill maximal oxygen uptake was determined
in 4 subjects who wore suits perfused from head higher heart rate for a given exercise intensity and
to foot with OSC, 28.0·C and 45.0·C water. De- greater subjective feelings of fatigue. When exercise
spite the varying skin temperatures, maximum is prolonged in a hot environment, heart rate val-
oxygen uptake was not significantly different in ues may reach nearly maximal levels and increases
these 3 conditions. Thus, in short-lasting severe ex- in heart rate can no longer compensate for the re-
ercise,ambient temperatures in this range have little duced cardiac filling. When this happens, the nor-
effect on maximal exercise performance. The in- mal linear relationship between oxygen uptake and
tense vasoconstrictor response during maximal ex- cardiac output is no longer maintained and an in-
ercise probably counteracts the vasodilatory action tense vasoconstriction occurs in a last-ditch effort
induced in high ambient conditions, preventing a to maintain central blood volume. Skin blanching,
decreased exercise tolerance because of increased expecially around the mouth is evident, and col-
blood volume in the skin. However, in exercise of lapse is imminent unless the exercise is stopped.
longer duration, or during exercise in which body These detrimental effects of heat on submaximal
core temperatures are elevated before the onset of exercise performance are even more pronounced in
testing, exercise tolerance decreases (Rowell, 1974). subjects who begin exercising in a hypohydrated
This is probably due to the increased distribution state.
of blood away from the central blood volume, thus
reducing the maximum cardiac output. 7. Conclusion

6. Effects of a Hot Environment on Prolonged exercise in hot environments im-

Submaximal Exercise Performance
The more rapid rise in deep body and skin tem-
peratures in a hot environment will result in a
greater loss of plasma volume through increased
sweat losses and also a greater redistribution of the
central blood volume towards the skin. Both ef-
fects act to reduce cardiac filling, resulting in a
poses an added risk of heat-induced injury, espe-
cially for unfit or unacclimatised individuals.
The ACSM has recently revised its position
stand on the prevention of thermal injuries during
distance running (ACSM, 1984). The new position
statement has been expanded to include recom-
mendations to prevent heat strain in a general
community of 'fun joggers' rather than the hard
Exercise, Performance and Temperature Control
core athlete. The new guidelines recommend that
an individual be aware of possible heat stress con-
ditions when ambient conditions approach 28°C
(82°F wet bulb globe temperature heat stress in-
dex). Prolonged exercise in such conditions should
be avoided if possible. However, if exercise is per-
formed, then fluid intake should be encouraged at
a ratio of about 100 to 200ml for every 2 to 3 km
run, and athletic competition officials should be
alert for persons who present with heat-related
symptoms. The officials should not rely on the
competitor to stop exercise, as rational judgement
is often impaired under conditions of heat strain.
Although research in the field of sports medi-
cine has greatly expanded in the last few years, there
are several areas where further research is needed.
Additional work is needed to understand the endo-
crine changes associated with long term adapta-
tions to chronic heat or exercise exposure, and how
such changes might alter heat tolerance. A second
area where further research is needed involves an
understanding of the central neural responses to
exercise and possible alterations in the regulation
of blood pressure and respiration with long term
exercise or elevated body temperature.
Acknowledgement
We thank Dr Ajay Carpenter, Dr John Davis, and Dr
Baruch Bromberger-Barnea for their criticisms and sug-
gestions in the preparation of this manuscript, Ms Mary
Ann Driscoll for her help in the typing of the manuscript,
and Dr Matthew Brakora for his help with the experi-
ments shown in table l.
References
ACSM Position Statement: Prevention of thermal injuries during
distance running. Physician and Sportsmedicine 12: 43-51 (Jul
1984).
Bevegard, S,; Castenfors, J.; Linbald, L.E. and Tranesjo, J.: Blood
pressure and heart rate regulating capacity of the carotid sinus
during changes in blood volume distribution in man. Acta
Physiologica Scandinavica 99: 300-312 (1977).
Brengelmann. G.L.; Freund. P.R.; Rowell. L.B.; Oleurd, J.E. and
Kranning, K.K.: Absence of active cutaneous vasodilation as-
sociated with the congenital absence of sweat glands in man.
American Journal of Physiology 240: H571-H575 (1981).
Brengelmann, G.L.; Johnson, J.M.; Hermansen. L. and Rowell.
L.B.: Altered control of skin blood flow during exercise at high
19
internal temperatures. Journal of Applied Physiology: Respir-
ation. Environmental and Exercise Physiology 43: 790-794
(1977).
Brown. W.K. and Sargent, F.: Hidrorneiosis. Archives of Envi-
ronmental Health II: 442-452 (1965).
Candas. V.; Libert, J.P. and Vogt, U.: Sweating and sweat decline
of resting man in hot humid environments. European Journal
of Applied Physiology 50: 223-234 (1983).
Collins. KJ.; Crockford. G.W. and Weiner, J.S.: Sweat gland
training by drugs and thermal stress. Archives of Environ-
mental Health 2: 407-422 (1965).
Dale. H.H. and Feldberg. W.: The chemical transmission of se-
cretory impulses to the sweat glands of cat. Journal of Physi-
ology (London) 82: 121-128 (1934).
Dobson, R.L.: The effect of repeated episodes of profuse sweating
on the eccrine sweat glands. Journal of Investigative Derma-
tology 35: 195-198 (1960).
Doris. P.A. and Baker, M.A.: Intracranial osmoreceptors control
evaporation in heat stressed cat. Brain Research 239: 644-648
(1982).
Edholm. O.G.; Fox, R.H. and Macf'herson, R.K.: Vasomotor
control of the cutaneous blood vessels in the human forearm.
Journal of Physiology (London) 139: 455-465 (1957).
Elizondo. R.: Temperature regulation in primates; in Robertshaw
(Ed.) International Review of Physiology: Environmental
Physiology II. vol. 15. pp. 71-118 (University Park Press. Bal-
timore 1977).
Epstein, Y.; Horowitz. M.; Bosin, E.; Shapiro. Y. and Glick. S.M.:
Changes in vasopressin distribution in brain of heat stressed
and heat acclimated rats; in Hales (Ed.) Thermal Physiology.
pp. 137-140 (Raven Press. New York (983).
Feldberg. W.; Myers. R.O. and Veale. W.L.: Perfusion from cere-
bral ventricle to cisterna magna in the unanaesthetized cat.
Journal of Physiology (London) 207: 405-416 (1970).
Fortney. S.M.; Nadel. E.R.; Wenger, c.B. and Bove, J.R.: Effect
of blood volume on sweating rate and body fluids in exercising
humans. Journal of Applied Physiology: Respiration. Environ-
mental and Exercise Physiology 51: 1594-1600 (1981).
Fox. R.H.; Goldsmith. R.: Hampton. I.F.G. and Lewis. H.E.: The
nature of the increase in sweating capacity produced by heat
acclimatision. Journal of Physiology (London) 171: 368-376
(1964).
Fox. R.H. and Hilton. S.M.: Bradykinin formation in human skin
as a factor in heat vasodilation. Journal of Physiology (Lon-
don) 142: 219-232 (1958).
Frye. AJ. and Kamon. E.: Sweating efficiency in acclimated men
and women exercising in humid and dry heat. Journal of Ap-
plied Physiology: Respiration. Environmental and Exercise
Physiology 54: 972-977 (1983).
Goetz. R.H.: Effect of changes in posture on peripheral circula-
tion. with special reference to skin temperature readings and
the plethysmogram. Circulation 1: 56-75 (1950).
Henane. R.; Flandrois, R. and Charbonnier, J.P.: Increase in
sweating sensitivity by endurance conditioning in man. Jour-
nal of Applied Physiology: Respiration. Environmental and
Exercise Physiology 43: 822-828 (1977).
Hensel. H.: Neural processes in thermoregulation. Physiological
Reviews 53: 948-\017 (1973).
Ito. S. and Adachi. J.: The influence of repeated application of a
hot-air bath on the activity of sweat glands. Journal of Oriental
Medicine 21: 93 (1934).
Johnson. J.M.: Responses of forearm blood flow to graded leg
exercise in man. Journal of Applied Physiology: Respiration.
Environmental and Exercise Physiology 46: 457-462 (1979).
Johnson. lM.: Rowell. L.B. and Brengelmann, G.L.: Modifica-
tion of the skin blood flow-body temperature relationship by
upright exercise. Journal of Applied Physiology 37: 880-886
(1974).
Exercise, Performance and Temperature Control
Kobayashi, Y,: Ando, Y,; Okuda, N.; Takaba, S. and Ohara, K.:
Effects of endurance training on thermoregulation in females.
Medicine and Science in Sports and Exercise 12: 361-364 (1980).
Kuno, Y.: Human Perspiration (C.C Thomas, Springfield, Illinois
1956).
Kuno, Y.: The mechanism of human sweat secretion. Proceedings
International Congress Physiological Sciences (23rd. Tokyo,
Japan) 5: 8-22 (1965).
Mitchell, J.w.: Nadel, E.R. and Stolwijk, J.AJ.: Respiratory weight
losses during exercise. Journal of Applied Physiology 32: 474-
476 (1972).
Nadel, E.R.: Circulatory and thermal regulations during exercise.
Federation Proceedings 39: 1491-1497 (1980).
Nadel, E.R.: Factors affecting the regulation of body temperature
during exercise. Journal of Thermal Biology 8: 165-169 (1983).
Nadel, E.R.; Bullard, R.W. and Stolwijk, J.AJ.: Importance of
skin temperature in the regulation of sweating. Journal of Ap-
plied Physiology 31: 80-87 (1971).
Nadel, E.R.: Cafarelli, E.: Roberts, M.F. and Wenger, c.B.: Cir-
culatory regulation during exercise in different ambient tem-
peratures. Journal of Applied Physiology: Respiration, Envi-
ronmental and Exercise Physiology 46: 430-437 (1979).
Nadel, E.R.: Fortney, S.M. and Wenger, CB, Effect of hydration
state on circulatory and thermal regulations. Journal of Ap-
plied Physiology: Respiration, Environmental and Exercise
Physiology 49: 715-721 (1980).
Nadel, E.R.; Pandolf, K.B.; Roberts, M.F. and Stolwijk, J.AJ.:
Mechanisms of thermal acclimatision to exercise and heat.
Journal of Applied Physiology 37: 515-520 (1974).
Nadel, E.R and Stolwijk, J.AJ.: Effect of skin wetness on sweat
gland response. Journal of Applied Physiology 35: 689-694
(I 973a).
Nadel, E.R. and Stolwijk, J.A.J.: Sweat gland response to the ef-
ferent thermoregulatory signal. Extrait des Archives des Sci-
ences Physiologiques 27: A67-A77 (l973b).
Nielsen, B.: Effect of changes in plasma Na" and Cat" ion con-
centration on body temperature during exercise. Acta Phy-
siologica Scandinavica 91: 123-129 (l974a).
Nielsen, B.L.: Effect of changes in plasma volume and osmolality
on thermoregulation during exercise. Acta Physiologica Scan-
dinavica 91: 123-129 (l974b).
Nielsen, M.: Die regulation der korpertemperatur bei muskelar-
beit, Scandinavian Archives of Physiology 79: 193-230 (1938).
Piwonka, R.W.: Robinson, S.; Gay, V.L. and Manalis, R.S.:
Preacclimatizion of men to heat by training. Journal of Ap-
plied Physiology 20: 379-383 (1965).
Roberts, M.F.; Wenger, CB.: Stolwijk, J.AJ. and Nadel, E.R.:
Skin blood flow and sweating changes following exercise train-
ing and heat acclimatizion. Journal of Applied Physiology:
Respiration, Environmental and Exercise Physiology 43: 133-
137 (1977).
Roddie, I.C: Shepherd, J.T. and Whelan, R.F.: The contribution
of constrictor and dilator nerves to the skin vasodilation dur-
ing body heating. Journal of Physiology (London) 136: 489-
497 (1957).
20
Rowell, L.B.: Human cardiovascular adjustments to exercise and
thermal stress. Physiological Reviews 54: 75-159 (1974).
Rowell, L.B.: Reflex control of the cutaneous vasculature. Journal
of Investigative Dermatology 69: 154-166 (l977a).
Rowell, L.B.: Competition between skin and muscle for blood
flow during exercise; in Nadel (Ed.) Problems with Temper-
ature Regulation during Exercise, pp. 73-92 (Academic Press,
New York I 977b).
Saltin, B. and Hermansen, L.: Esophageal, rectal and muscle tem-
perature during exercise. Journal of Applied Physiology 21:
1757-1762 (1966).
Sato, K.: Sweat induction from an isolated eccrine sweat gland.
American Journal of Physiology 225: 1147-1151 (1973).
Sato, K.: The physiology, pharmacology and biochemistry of the
eccrine sweat gland. Reviews of Physiology Biochemistry and
Pharmacology 79: 51-131 (1977).
Sato, K. and Sato, F.: Role of calcium in cholinergic and adren-
ergic mechanisms of eccrine sweat secretion. American Journal
of Physiology 241: (Cell Physiology) 10: C113-120 (1981).
Sato, K. and Sato, F.: Individual variations in structure and func-
tion in human eccrine sweat gland. American Journal of Phys-
iology (Regulatory Integrative Comparative Physiology) 14:
R203-R208 (1983).
Senay, L.c.: Temperature regulation and hypohydration: A sin-
gular view. Journal of Applied Physiology: Respiratory, En-
vironmental and Exercise Physiology 47: 1-7 (1979).
Shepherd. J.T.: Nervous control of the blood vessels in the skin:
in Shepherd (Ed.) Physiology of Circulation in Human Limbs
in Health and Disease, pp.29-34 (W.B. Saunders, Philadelphia
1963).
Strydom, N.B.: Wyndham, CH.: Williams, CG.; Morrison, J.F.;
Breddell, G.A.G.; Benade, A.J.S. and Von Rahden, M.: Accli-
matizion to humid heat and the role of physical conditioning.
Journal of Applied Physiology 21: 636-642 (1966).
Terada, E.: Effects of adrenaline on human sweating. Journal of
the Physiological Society (Japan) 28: 176-184 (1966).
Vroman, N.B.: Beckett, W.S.; Permutt, S. and Fortney, S.: Effect
of positive pressure breathing on the cardiovascular and ther-
moregulatory responses to exercise. Journal of Applied Phys-
iology: Respiration, Environmental and Exercise Physiology
(Inpress, 1985).
Wenger, CB.; Roberts, M.F.; Stolwijk, J.AJ. and Nadel, E.R.:
Forearm blood flow during body temperature transients pro-
duced by leg exercise. Journal of Applied Physiology 38: 58-
63 (1975).
Wyss, CR.: Brengelmann, G.L.; Johnson, J.M.: Rowell, .L.B. and
Niederberger, M.: Control of skin blood flow, sweating, and
heart rate: Role of skin vs. core temperature. Journal of Ap-
plied Physiology 36: 726-733 (1974).
Address for correspondence and reprints: Dr Suzanne Fortney,
Johns Hopkins University, School of Hygiene and Public Health,
615 North Wolfe Street, Room 7032, Baltimore, Maryland 21205
(USA).