Pflügers Arch - Eur J Physiol (2001) 442:41–48
DOI 10.1007/s004240100515
O R I G I N A L A RT I C L E
B. Nielsen · T. Hyldig · F. Bidstrup
J. González-Alonso · G.R.J. Christoffersen
Brain activity and fatigue during prolonged exercise in the heat
Received: 14 April 2000 / Received after revision: 3 November 2000 / Accepted: 18 December 2000 / Published online: 1 March 2001
© Springer-Verlag 2001
Abstract We hypothesized that fatigue due to hyper-
thermia during prolonged exercise in the heat is in part
related to alterations in frontal cortical brain activity. The
electroencephalographic activity (EEG) of the frontal
cortex of the brain. was measured in seven cyclists [maxi-
mal O.2 uptake (VO2max) 4.8±0.1 (SE) l min–1] cycling at
60% VO2max in a hot (H, 42°C) and a cool (C, 19°C) envi-
ronment. Fast Fourier transformation of the EEG was
used to obtain power spectrum areas in the α (8–13 Hz)
and β (13–30 Hz) frequencies. The ratio α/β was calcu-
lated as an index of arousal level; an elevated α/β index
reflects suppressed arousal. In H, subjects fatigued after
34.4±1.4 min coinciding with an oesophageal tempera-
ture (Toes) of 39.8±0.1°C, an almost maximal heart rate
(HR 192±3 beats·min–1), a rating of perceived exertion
(RPE) of 19.0±0.8 and significantly elevated α/β index
(188±71% of the value after 2 min of exercise; P<0.05).
In C, subjects cycled for a similar period while Toes was
below 38°C, HR and RPE were low, and the α/β index
was not significantly elevated (59±27% of 2 min value;
P=NS). Increases in the α/β index were strongly corre-
lated to increases in Toes (r2=0.98; P=0.0001).
Keywords EEG · Hyperthermia · Oesophageal
temperature
Introduction
Endurance performance in hot environments can be
markedly reduced compared to that in cool environ-
ments. In trained subjects, impaired performance and
B. Nielsen (✉) · T. Hyldig · F. Bidstrup · J. González-Alonso
Institute of Exercise and Sport Sciences,
Department of Human Physiology, University of Copenhagen,
Universitetsparken 13, 2100, Copenhagen Ø, Denmark
e-mail: bnielsen@aki.ku.dk
Tel.: +45-35-321620, Fax: +45-353-21600
G.R.J. Christoffersen
August Krogh Institute, University of Copenhagen,
Copenhagen Ø, Denmark
earlier fatigue in the heat are generally associated with
high body temperature, cardiovascular instability and al-
tered metabolism [9, 12, 15, 16]. We have recently dem-
onstrated that combined dehydration and hyperthermia
during exercise in the heat results in marked reductions
in cardiac output, exercising muscle blood flow and con-
comitant elevations in muscle glycogen utilization and
lactate production [15, 16]. However, despite diminished
blood flow and altered muscle metabolism, fatigue ap-
pears to be largely associated with high body tempera-
ture [5, 15, 16, 17, 21, 23, 25, 26].
Support for this idea is also found in our recent obser-
vation that cyclists
. exercising at 60% maximal oxygen
consumption (VO2max) fatigued at remarkably similar core
and muscle temperatures (≅40 and 40.7°C, respectively),
regardless of the wide differences in the initial value and
the rate of rise of body temperature [17]. In the same
light, recent studies show that rats exercising in hot envi-
ronments fatigue at the same core and brain temperature
when the pre-exercise core temperature is manipulated
[13, 29]. Therefore, it is clear that fatigue during exercise
in hot environments in trained subjects is closely linked
to high body temperature (i.e. high core, muscle and brain
temperature), and not to the duration of the work, albeit
the underlying mechanisms have not been elucidated.
The possibility exists that hyperthermia causes fatigue
by a direct action of temperature on the brain and/or an
indirect effect on the brain of afferent signals originating
from skeletal muscle, cardiac muscle or internal organs
in response to rising local temperature. Such effects may
result in altered central command and/or electrical poten-
tials of some brain regions [5, 6, 17]. Indeed, previous
studies have shown that high temperature is associated
with altered brain activity in humans and animals, as re-
flected by changes in electroencephalogram (EEG) activ-
ity and sensory evoked potentials [10, 11, 22]. There is
evidence from studies of resting humans that the power
spectrum of the EEG changes in proportion to the rise in
core temperature up to ≅41.8°C [10]. At present there is
no evidence for such an effect of hyperthermia on the
EEG power spectrum in exercising humans.
42
Therefore, the purpose of the present study was to de-
termine whether progressive hyperthermia and ultimate-
ly fatigue during exercise in hot environments are in part
related to altered brain activity in the frontal cortex. We
measured EEG activity of the frontal area of the brain in
cyclists under two conditions: cycling at the same inten-
sity in (1) a hot environment until exhaustion occurred at
a core temperature of ≅40°C, and (2) a cool environment
for a similar period of time. In the latter condition
core temperature was maintained below 38°C. We specu-
lated that a shift in EEG from the higher frequencies
(β, 13–30 Hz) to the slower wave bands (α, 8–13 Hz) in
the frontal area of the brain reflects a reduced state of
arousal.
Subjects and methods
Subjects
The subjects were seven endurance-trained male cyclists, with
the following characteristics (mean ±SE): age 26.3±1.9 years,
height 186.1±1.7 cm, mass 78.7±2.3 kg, maximal heart rate
.
198±3 beats·min–1, and VO2max 4.83±0.12 l·min–1. The subjects
were fully informed of any risks and discomfort associated with
the experiment before giving their written consent to participate.
This study was approved by the Ethics Committee of Copenhagen
and Frederiksberg
. communities. Prior to the experimental trials
their VO2max was assessed on a cycle ergometer using an incremen-
tal protocol,
. consisting of 4 min of exercise at 60% of the predict-
ed VO2max, followed by four to five 1-min work stages, in which
the work intensity was increased each minute by 15%, 10%, 5%
and then by 5% until exhaustion was reached after 5–7 min. Fur-
thermore, subjects were familiarized
. with the experimental proto-
col by cycling for 90 min at 60% VO2max in a 20°C environment.
Procedure
.
After a preliminary test cycling at 20°C, 60% VO2max for 90 min,
subjects
. cycled on two occasions separated by 1–6 days, at
60% VO2max (power output 213±4 W, 80 rpm, counterbalanced or-
der) in a climatic chamber while wearing a water-perfused jacket.
On one trial (hyperthermic trial, H), they exercised until they
reached exhaustion (34.4±1.4 min) in a hot environment (i.e.
42°C, 18% relative humidity) while the jacket was perfused with
water at 42°C. During the other trial (control trial, C), in a cool en-
vironment (i.e. 19°C, 40% relative humidity) while 18°C water
was circulated through the jacket, they were stopped after
36.4±1.4 min. When the control experiment was performed first
the subjects exercised for 5–10 min longer than the predicted time
to fatigue in H. Measurements taken during the 5-min period clos-
est to the time of exhaustion in the following hot trial were used
for comparison. Exercise was performed on a cycle ergometer
(Monark Ergomed 818) mounted with toe clips and triathlon han-
dlebars in order to secure a steady working posture. On the day
prior to the experimental trial, subjects consumed a carbohydrate-
rich diet with copious amounts of fluid and refrained from hard
training. On both occasions subjects arrived at the laboratory at
the same time of the day after a light meal. Subjects were weighed
on a digital scale (Ohaus 1–10) to ±20 g wearing short bicycle
tights. Thereafter, an oesophageal probe was inserted through the
nose, and the skin thermocouples were attached to the skin. Heart
rate (HR) was recorded with a Polar Sports Tester (Polar Electro,
Finland). The EEG electrodes were then fixed to the scalp. Subject
rested for 30 min in a supine position in a thermally comfortable
condition. Subjects then walked quietly to the climatic chamber,
where they were fitted with the water-perfused jacket. Inside the
chamber subjects were seated on the ergometer in a forward bend
position (approx. 30° angle from the horizontal axis) while resting
their arms on the triathlon handlebars. The positions of the saddle
and the triathlon handlebars were adjusted for each subject in the
same way during both conditions. The subjects wore earplugs and
snow glasses without glass all the time in order to reduce the pe-
ripheral field of vision and decrease external disturbances of brain
activity Furthermore, they faced a white sheet. During exercise
each subject maintained the same position, with his eyes fixed on
an imaginary point in front of himself.
At rest, the EEG signals were measured for 30 s three different
times (see Methods below). Resting Toes, skin temperature (Tsk)
and HR were recorded before exercise started. At 2-, 5- and then
at 5-min intervals during exercise, a slight touch indicated that the
subjects should shut their eyes and relax the jaw for a sequence of
EEG measurements. The final EEG was taken when a sign from
subjects indicated that the point of exhaustion was close. At the
abovementioned time periods after the start of exercise, EEG was
recorded twice: the first 30 s during exercise and then during the
subsequent 30-s pause while maintaining the same body position.
Exercise was resumed upon completion of the EEG measurement.
During exercise, Toes, Tsk and HR were recorded continuously. A
rating of perceived exertion (RPE) was recorded after 13 min of
exercise and at exhaustion after the final EEG measurement, using
a Borg scale [4]. After exercise subjects were weighed again. The
degree of dehydration was estimated from the difference in body
mass before and after exercise.
Measurements
Temperatures
Temperature measurements were recorded using thermocouples
connected to electrical thermometers with an accuracy of ±0.1°C
(Ellab, Copenhagen: CTF 9008, and CTD 85). Toes was measured
in the deep oesophagus at a depth, measured from the nostril, cor-
responding to 1/4 of the subject’s standing height (Ellab probe
MOV-05005-A). Skin temperature was measured at the centre of
the forehead (Tfsk) in all subjects. Furthermore, in four subjects
mean Tsk was calculated from the skin temperatures (Ellab probe
MHC-40050-A) measured at six sites (i.e. chest, back, upper arm,
forearm, thigh, lower leg).
EEG recordings
Beckmann Ag/AgCl electrodes (11 mm diameter) were affixed in
two positions on the scalp (i.e. positions F3 and F4 according to
the international “ten-twenty system” [19]) with conductive
electrode paste (Bentonite paste, Dantec). Paired mastoid refer-
ences were used. In addition, the electrodes were secured with
OMNIFIX stretch tape and a specially made elastic “helmet”. The
inter-electrode resistance was below 5 kΩ. Signal conditioners
(CED1902, Cambridge Electronic Design) set at a gain of 1000
and –3 dB bandwidth between 0.15 Hz and 40 Hz (roll-off
12 dB/octave) were used. Scalp potentials were sampled at
1000 Hz for each electrode, using a CED 1401-plus A/D con-
verter. An oscilloscope was used for continuous visual inspection
of the EEG signals. Signals from only F4 are presented, as they
were not different from those from F3.
Data analysis
Fast Fourier transformation of recorded potentials of EEG was
made with CED Spike2 software using steps of 0.2 Hz for the
power spectrum. In the power spectrum the composite EEG is bro-
ken down into component waves of narrow frequency bands along
the entire EEG frequency spectrum, and the square of the ampli-
tudes of these components calculated. As a representative re-
sponse, Figure 1A shows an EEG recording from a subject exer-

Fig. 1 A Electroencephalographic activity (EEG) recording from
F4 in an exercising subject. B Power spectrum calculated from
EEG recording after 5 min of work, and C after 25 min of work
cising with closed eyes. Panels B and C show the power spectrum
of a 30-s EEG recording after 5 and 25 min, respectively, of cy-
cling in the hot environment.
The focus of the present analysis was primarily on possible
changes in relative amplitude between the α-bands and β-bands,
rather than on changes in absolute EEG amplitude within each fre-
quency. Thus, data are presented as percent changes to correct for
day-to-day and between-subject variability. The changes in α-
bands and β-bands were calculated: (1) as a percentage of the rest-
ing measurement obtained while sitting on the ergometer on the
particular experimental day to describe differences between rest
and exercise, and (2) as a percentage of the first exercise measure-
ment (2 min) to describe the effect of hyperthermia during exer-
cise. In preliminary experiments the effects of isolated motor ac-
tivities, e.g. eye movements, swallowing and chewing, were stud-
ied. All had considerable and characteristic effects on the EEG re-
cording, and sections including such noise were excluded from the
analysis. During sitting rest immediately before the onset of exer-
cise, three 30-s recordings of the EEG signal were sampled. The
highest and lowest power spectra were discarded to exclude ex-
tremes, and the remainder was selected as the best representation
of the brain activity at rest. At rest and during exercise, the area
under the power spectrum between 8 Hz and 13 Hz (α) and be-
tween 13 Hz and 30 Hz (β) was calculated, as was the ratio α/β
(α/β index).
43
Statistical analysis
Data were analysed using a two-way (trial by time) analysis of
variance with repeated measures. Following a significant F-test,
pair-wise differences were identified using Tukey’s honestly sig-
nificant difference (HSD). Significance was set at the 5% level.
Results are presented as means ±SE. Furthermore, simple linear
regression analysis was used to describe the relationship between
the rise in core temperature and the alterations in brain activity oc-
curring during exercise.
Results
Body temperature, heart rate and rating
of perceived exertion
Measurements of Toes, mean Tsk and HR during the hy-
perthermic and control trials are presented in Fig. 2A–C.
In the hyperthermic trial, Toes was 36.8±0.1°C at the on-
set of exercise and rose steadily throughout exercise, un-
til exhaustion occurred after 34.4±1.4 min at Toes
39.8±0.1 °C. From the onset of exercise, mean Tsk rose
progressively from 36.0±0.1°C to 38.4±0.4°C, whereas
forehead temperature (Tfsk) was 36.7±0.1°C and in-
creased to 37.8±0.2°C. HR at 2 min was 150±4 beats
min–1 and thereafter rose gradually to a nearly maximal
value of 192±3 beats min–1 (97%HRmax). RPE was
44

Fig. 2 Mean oesophageal temperature, mean skin temperature

(n=4) and heart rate during exercise in the hyperthermic and con-
trol trials. Mean ±SE for 7 (or 4) subjects. *Significantly higher
than the initial rest value (P<0.05). †Significantly different from
control (P<0.05)

13±0.4 units after 13 min of exercise and 19.0±0.8 units

at exhaustion. The degree of dehydration due to sweat
loss represented 1.7±0.1% of body mass.
In the control trial, Toes increased from 36.8±0.0°C at
rest to 37.8±0.1°C after 15 min of exercise reaching a
plateau thereafter. Mean Tsk was 34.8±0.2°C at the start
and 35.6±0.2°C after 35 min, whereas Tfsk increased
from 33.9±0.2°C at rest to 35.1±0.1 at 10 min when it
levelled off. Therefore, at the end of the hyperthermic
compared to the control trial, Toes was ≅2°C higher and
mean Tsk and Tfsk were ≅3°C greater. In the control trial,
HR rose to 140±3 beats·min–1 after 2 min, increasing
thereafter up to 159±6 beats·min–1 at the end of the C
trial. RPE was 10.9±0.8 units at 13 min of exercise and
13.7±0.7 units at the end of exercise. The degree of de-
hydration in the C trial represented 1.0±0.1% of body
mass.
Fig. 3 Mean (±SE) percentage change from resting values in the
EEG power spectra in the α frequency (A) and β frequency range
(B), when exercising and paused for 30 s during 35 min of exer-
cise in a hot (42°C) environment. C α power spectrum and D β
power spectrum in the control (18°C) environment. *Exercise and
pause significantly higher than the initial rest value (P<0.05). †Ex-
ercise significantly different from pause (P<0.05)
Electroencephalographic activity
Figure 3 depicts the EEG activity during exercise and the
subsequent 30-s rest intervals in both the hyperthermic
(Fig. 3A, B) and control (Fig. 3C, D) trials. In the transi-
tion from rest to exercise, the α power spectrum area, α,

Fig. 4 α power spectrum areas (A), β power spectrum areas (B)
and exercise α/β index (C), all as a percentage of the first measure-
ment made after 2 min of exercise in the hot and control conditions.
Mean ±SE for 7 subjects. *Significantly different from 2-min value
(P<0.05). †Significantly different from control (P<0.05)
increased significantly, both in H and C. After 2 min of
exercise α rose 131±73% above the resting value in the
hot condition (see Fig. 3A) and 36±22% in the control
trial (Fig. 3C). The difference between trials was not sta-
tistically significant. After 2 min of exercise the β power
spectrum area, β, increased 109±30% and 115±30%
(P<0.05) at the onset of exercise in H and C, respective-
ly (Fig. 3B, D). During the initial 20 min, β was higher
during exercise than during the subsequent 30-s pauses
(Fig. 3B, D). For α (Fig. 3A, C) the difference between
exercise and rest was not statistically different.
Figure 4 depicts power spectrum data during exercise
expressed as a percent change from the value obtained
after 2 min of exercise. α levelled off after the first 5 min
at 15–25% in both H and C (Fig. 4A). In contrast, β de-
clined significantly throughout the hyperthermic trial,
being 50±5% and 59±5% lower (P<0.05) after 25 and
45
Fig. 5 α/β index from the exercise measurements versus oesopha-
geal temperature (A) and α/β index versus heart rate (B) during
the hot and control trials. Correlation for α/β index versus heart
rate: Hot y=4.2–645x, r2=0.94; Control y=3.1–421x, r2=0.89.
Mean ±SE for 7 subjects
34.4±1.4 min of exercise, respectively, compared to the
2-min value (Fig. 4B). In the control trial, however, β
did not decline significantly over time (Fig. 4B).
The calculated α/β index rose steadily throughout the
hyperthermic trial until exhaustion, largely due to the de-
cline in β activity, becoming significantly elevated after
25 min with a final value of 188±71% (Fig. 4C). In the
control trial, the α/β index tended to increase up to
59±27% at 20 min when it reached a plateau of 58±28%.
The difference between H and C was significant after
25 min of exercise (Fig. 4C). The same pattern of re-
sponse was observed in the α/β index estimated during
the pauses between exercise bouts (not shown).
A close to linear correlation between Toes and the α/β
index measured during exercise was observed up to Toes
of 38°C for both C and H, continuing to 39.8°C in H
(r2=0.98, P=0.0001; Fig. 5A). Such tight, common corre-
46
lation for both C and H was not found between HR and
the α/β index (Fig. 5B).
Discussion
The main finding of this study was that during prolonged
exercise in the heat the electrical activity of the prefron-
tal cortex initially increased in the transition from rest to
exercise, and thereafter showed a progressive decline in
the high frequency β band, in association with the pro-
gressive rise in body temperature until exhaustion oc-
curred at ≅40°C. Conversely, the electrical activity of the
prefrontal area of the brain reached a plateau when body
temperature levelled off at ≅38°C during the control
trial. These results indicate that these alterations in EEG
activity in the frontal cortex reflect activity changes in
parts of the brain involved in the hyperthermia-associat-
ed reduced ability to exercise.
The present study is, to our knowledge, the first to re-
port EEG recordings during ongoing exercise in humans.
The present observation that EEG activity during ongo-
ing cycling in essence displayed the same pattern of re-
sponse as during the subsequent 30-s pauses supports the
validity of our exercise EEG measurements. Further-
more, the major finding that EEG activity during exer-
cise in the heat differs significantly from that in a cool
environment indicates that EEG is sensitive enough to
record alterations in brain activity with large differences
in body temperature. The small number of electrodes and
the positions were chosen merely to investigate a possi-
ble shift of general frontal cortical arousal. It is impor-
tant to note that great care was taken to reduce the exter-
nal disturbances of brain activity by having subjects
wear earplugs and snow glasses. In addition, subjects
maintained “relaxed” body and face positions while fac-
ing a white sheet.
The previous observation that the maximal isometric
force of the exercised leg and the rested arm was un-
changed at the point of exhaustion in hyperthermic sub-
jects suggests that the reduced capacity for dynamic ex-
ercise with hyperthermia might not be mediated by pro-
cesses located in the primary motor cortex or the pyrami-
dal tract [25]. The abrupt increases in α and β found in
this study at the onset of cycling in both environments
suggest that the frontal area is activated at the start of ex-
ercise (Fig. 3). However, the activity of the prefrontal ar-
ea further on during exercise and subsequent pauses de-
pended on whether the subject was hyperthermic, as
judged by the significant decline in β frequencies only
with high body temperature.
The present results from exercising humans are con-
sistent with earlier reports of animals and human patients
indicating that hyperthermia alters brain activity as re-
flected by EEG recordings and sensory-evoked poten-
tials [10, 11, 22, 27]. In a study of heat stroke patients,
Mustafa et al. [22] showed that brain stem auditory-
evoked potentials displayed characteristic changes in
their mid-latency response at critical high temperatures.
Dubois et al. [11] also observed that the late components
of somatosensory-evoked potentials to electrical stimula-
tion during hyperthermia treatment to Toes 41–42°C dis-
appeared at the high plateau temperature, but returned to
baseline with cooling. In another study, Dubois et al.
[10] found a progressive decrease in the higher frequen-
cies of the EEG spectra with increasing Toes with passive
heating in cancer patients, to the point that they disap-
peared completely at ≅39°C and reappeared when cool-
ing was applied. They demonstrated a direct inverse rela-
tionship between spectral power and temperature, in
agreement with the present findings [10]. In these stud-
ies, however, the patients were sedated and at various
levels of consciousness, which in itself could affect cor-
tical activity [10, 11, 22]. Together, the previous and
present evidence suggests that a high body temperature
has the potential to alter the function of the central ner-
vous system at rest and during exercise.
EEG frequencies normally shift from high frequen-
cies, β-bands, towards slower wave α-bands with
changes in arousal from fully alert to drowsiness or sleep
[20]. In our study the calculated α/β index increased, but
only β changed significantly as hyperthermia developed
and exhaustion was reached. The reason for this may be
that the measurements were made during exercise in
contrast to earlier rest studies. In this context changes in
the cat EEG with fatigue have been reported during fa-
tiguing treadmill exercise [1]. High-amplitude slow
waves occurred at the time that the animals reduced their
speed because of fatigue. However, no temperature mea-
surements were made, and thus a plausible influence of
temperature could not be assessed. In contrast, in our hy-
perthermic condition no abrupt changes in the EEG oc-
curred at the point of exhaustion. Fatigue, defined as the
inability to maintain the same work output, could reflect
a state of reduced alertness. In the present study the cal-
culated α/β index was used as an indicator of “alert-
ness”. A significantly higher α/β index developed in the
hyperthermic compared to the control trial during both
exercise and the subsequent pauses. This may be as-
cribed to the different core temperatures between the two
conditions (see Fig. 5A) and not to fatigue due to exer-
cise as such, since the exercise conditions and duration
were the same.
Furthermore, the α/β index did not correlate as well
with heart rate, indicated by a clear separation between the
calculated regression lines between the two conditions
(Fig. 5B). The RPE in the hyperthermic and control trials
also appeared to be more closely correlated than heart rate
to core temperature. A tight correlation between RPE and
core temperature is not surprising, and agrees with previ-
ous results obtained during prolonged exercise with com-
bined dehydration and hyperthermia or hyperthermia
alone [15, 16, 17, 18, 25, 26]. The differences in heart rate
and RPE between the hyperthermic and control trials are
probably associated with the different skin temperature
[18]. Taken as a whole, the present reduction in β activity
and increase in α/β index appears to be most closely asso-
ciated with increases in body temperature.

The mechanism by which hyperthermia might act on
brain activity appears to be complex, possibly involving
local signals as well as afferent reflexes originating in
the skeletal muscle, cardiac muscle and internal organs.
We measured Toes, which is an index of the arterial blood
temperature that supplies the brain [7]. Therefore, it is
reasonable to expect that the temperature of the hypo-
thalamus and the rest of the brain of exercising humans
increases in parallel to Toes and reaches the same or a
higher value than core temperature, since humans do not
have a functional, selective brain-cooling mechanism
[24, 28]. The observations that rats exercising until ex-
haustion on a treadmill fatigued at the same core and hy-
pothalamic temperature support this notion [13, 29].
Caputa and co-workers [6] cleverly demonstrated that
brain temperature has an independent effect on behavior-
al responses in a goat exercising on a treadmill. When
independently increasing hypothalamic temperature to
≅43°C, they showed that the goat decreased its running
speed despite the fact that the temperature of the rest of
its body remained clamped at 40°C [6]. This compelling
evidence clearly points to hypothalamic temperature be-
ing a source of signals mediating the lowering of power
output and motor activity in the goat. The temperature
centres in the hypothalamus integrate efferent and affer-
ent signals for the control of both the autonomic and the
behavioral thermoregulatory responses in animals and
humans [2, 3]. Efferent signals could involve inhibitory
reflexes in response to local high temperatures, metabo-
lite accumulation, substrate depletion or other chemical
changes (neurohormones, neuromodulators, cytokines,
heat shock protein) [8, 14]. In the present study, signals
arising in the hypothalamus could have led to a change
in frontal cortex activity, reflected in the decline in β ac-
tivity and increased α/β index, which could possibly un-
derlie an important physiological mechanism of fatigue
in hyperthermic subjects.
We cannot rule out the possibility that other mecha-
nisms sensing cardiovascular, metabolic, chemical and
thermal reflexes from the exercising muscles or other in-
ternal organs could also be involved in the earlier fatigue
with hyperthermia [8, 12, 14, 15, 16]. Based on previous
studies [17, 18], marked differences in circulatory as
well as metabolic parameters between the hyperthermic
and control trials could be expected after 20–30 min of
exercise. This points to the possibility of an interaction
between peripheral and local brain factors in the devel-
opment of the generally observed fatigue at high body
temperatures.
In conclusion, the present findings indicate that dur-
ing exercise in the heat, the core temperature rises and
that there is a concomitant shift in the EEG power distri-
bution, a decrease in β and a steady increase in the α/β
index. These observations suggest that alterations in the
electrical activity of the brain’s frontal area indicate hy-
perthermia-associated fatigue.
Acknowledgement This study belongs to a series of studies that
were supported by grants from Team Denmark.
47
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