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Perceived exertion is associated with an altered brain
activity during exercise with progressive hyperthermia
LARS NYBO AND BODIL NIELSEN
Department of Human Physiology, Institute of Exercise and Sport Sciences,
University of Copenhagen, DK-2100 Copenhagen, Denmark
Received 8 May 2001; accepted in final form 6 July 2001
Nybo, Lars, and Bodil Nielsen. Perceived exertion is
associated with an altered brain activity during exercise with
progressive hyperthermia. J Appl Physiol 91: 2017–2023,
2001.—The present study tested the hypothesis that per-
ceived exertion during prolonged exercise in hot environ-
ments is associated with changes in cerebral electrical activ-
ity rather than changes in the electromyogram (EMG) of the
exercising muscles. Therefore, electroencephalogram (EEG)
in three positions (frontal, central, and occipital cortex),
EMG, rating of perceived exertion (RPE), and core tempera-
ture were measured in 14 subjects during submaximal exer-
cise in normal (18°C, control) and hot (40°C, hyperthermia)
environments. RPE increased from 11 ⫾ 1 units at 5 min to
20 ⫾ 0 units at exhaustion (50 ⫾ 3 min) in the trial with
progressive hyperthermia, whereas exercise in the control
trial was maintained with a stable core temperature for 1 h
without exhausting the subjects. Altered EEG activity was
observed in all electrode positions, and stepwise forward-
regression analysis identified core temperature and a fre-
quency index of the EEG over the frontal cortex as the best
predictors of RPE. In contrast, there were no significant
correlations between RPE and any of the measured EMG
parameters (median spectral frequency, root mean square, or
amplitude), and the EMG parameters were not different in
hyperthermia compared with control. Thus hyperthermia
does not seem to affect the activation pattern of the muscles.
Rather, the linear correlation among core temperature, EEG
frequency index, and RPE indicates that alterations in cere-
bral activity may be associated with the hyperthermia-in-
duced development of fatigue during prolonged exercise in
hot environments.
electroencephalography; electromyography; core tempera-
ture
HEAT PRODUCTION DURING DYNAMIC exercise can elevate
core temperature rapidly, and it seems that hyperther-
mia during prolonged exercise in hot environments is
an independent cause of exhaustion (7, 10, 25). How-
ever, the mechanism(s) underlying hyperthermia-in-
duced fatigue during prolonged, dynamic exercise in
the heat is not well understood. Fatigue, defined as a
loss of force-generating capacity or an increased diffi-
culty in maintaining a required power output, may
develop for a variety of reasons and occur at various
Address for reprint requests and other correspondence: L. Nybo,
Dept. of Human Physiology, Institute of Exercise and Sport Sciences,
August Krogh Institute, Universitetsparken 13, DK-2100 Copenha-
gen Ø, Denmark (E-mail: lnnielsen@aki.ku.dk).
http://www.jap.org 8750-7587/01 $5.00 Copyright © 2001 the American Physiological Society
J Appl Physiol
91: 2017–2023, 2001.
sites along the pathway from the central nervous sys-
tem to the contractile machinery of the muscles. Det-
rimental effects of hyperthermia on muscle function
and on metabolism have been observed, but these fac-
tors cannot explain the fatigue that develops during
prolonged exercise in hot environments (4, 5, 9, 15, 20,
24). We have recently demonstrated that hyperthermia
reduces voluntary force development during a sus-
Downloaded from jap.physiology.org on June 17, 2009
tained, maximal isometric contraction, and this im-
pairment in performance could be explained by “cen-
tral fatigue” (18). In the above-mentioned study,
superimposed electrical stimulation of the femoral
nerve was used to differentiate between the contribu-
tion of central and peripheral factors to the develop-
ment of fatigue during sustained isometric contrac-
tions. The results revealed that hyperthermia did not
affect the ability of the muscles to generate force.
Instead, a markedly lower voluntary activation per-
centage during the hyperthermic trials indicated that
the hyperthermia-induced fatigue was located within
the central nervous system. Those results appear to
support the idea that high core temperature may in-
hibit the cerebral ability to provide an adequate neural
drive to the muscles, and this may be the explanation
why both humans and rats fatigue when high body
temperatures are reached (7, 10, 15, 25). The increas-
ing difficulty to maintain power output during pro-
longed exercise with progressive hyperthermia is also
reflected in the subjective rating of perceived exertion
(RPE), which increases concurrently with the rise in
core temperature (10, 16, 19). Furthermore, hyperther-
mia results in a marked reduction in cerebral blood
flow velocity during prolonged, submaximal exercise
(19), and alterations in the electroencephalogram
(EEG) have been found to be linearly related to in-
creasing core temperature during cycle exercise in the
heat (16). Taken together, these results indicate that
cerebral function is substantially affected by hyper-
thermia. However, the interaction among the hyper-
thermia-induced cerebral changes, the activation pat-
tern of the muscles, and the development of fatigue
during dynamic exercise has never been investigated.
Therefore, the primary purpose of the present study
The costs of publication of this article were defrayed in part by the
payment of page charges. The article must therefore be hereby
marked ‘‘advertisement’’ in accordance with 18 U.S.C. Section 1734
solely to indicate this fact.
2017
2018 EEG AND EMG WITH OR WITHOUT HYPERTHERMIA
was to elucidate whether or not hyperthermia-induced
cerebral changes during dynamic exercise were related
to an altered activation of the exercising muscles and,
secondarily, to investigate whether the subjective RPE
was correlated with changes in cerebral and/or muscu-
lar activity.
METHODS
Subjects. Age, body weight, height, and maximal oxygen
consumption of the 14 healthy endurance-trained cyclists
participating in the study were 25 ⫾ 1 (SE) yr, 71 ⫾ 2 kg,
181 ⫾ 2 cm, and 65 ⫾ 2 ml 䡠 kg⫺1 䡠 min⫺1, respectively. Max-
imal oxygen uptake was determined during an incremental
exercise protocol on a cycle ergometer using a metabolic cart
(model CPX/D, MedGraphics, St. Paul, MN). The subjects
were informed of any risks and discomforts associated with
the experiments before they gave their written consent to
participate. The study was approved by the Ethics Commit-
tee of Copenhagen and Frederiksberg (KF 01-135/00). All
subjects had previously participated in experiments involv-
ing cycling in hot environments.
Experimental protocol. On two separate occasions, subjects
cycled at ⬃60% of maximal oxygen consumption (power out-
put 188 ⫾ 7 W, 85 ⫾ 1 rpm, counterbalanced order) in a
climatic chamber. In one trial, they exercised to exhaustion
(50 ⫾ 3 min) in a hot environment (40°C, hyperthermic trial),
whereas exercise in the other trial was maintained for 1 h in
a thermoneutral environment (18°C, control trial) without
exhausting the subjects. Exhaustion was defined as either
the point at which the subject volitionally stopped exercising
or the point when power output could no longer be main-
tained. The subjects arrived at the laboratory ⬃1 h before the
start of the experiment and rested in a thermoneutral room
while the equipment was attached. The subjects then emp-
tied their bladder, were weighed, and entered the climatic
chamber. Here they were seated on the cycle ergometer
(Monark Ergomedic 818; mounted with a triathlon handlebar
to secure a steady working position) and remained in their
racing position while resting measurements of heart rate
(HR), esophageal temperature (Tes), and EEG were obtained.
After the onset of exercise, HR, Tes, EEG, electromyogram
(EMG), and RPE [the subject rated his perceived effort on the
Borg scale (3)] were recorded at 5, 10, 20, and 30 min and just
before exhaustion or at 58–60 min in the control trial.
EMG and EEG measurements. Surface EMG signals were
recorded from the right vastus lateralis 15 cm proximal to the
superior border of the patella, with the use of a pair of EMG
recording electrodes with an interelectrode distance of 3 cm
(Neuroline electrodes, type 72001-J, Medicotest). The EMG
signals were amplified (gain ⫻1,000), sampled at 1,000 Hz,
band-pass filtered [3 Hz (⫺6 dB) to 500 Hz (⫺6 dB)] by using
an IP511 alternating-current preamplifier (Astro-Med) and a
CED 1401-plus analog/digital converter, and stored to a data-
acquisition file. After additional high-pass filtering (at 10 Hz)
to minimize movement artifacts, root mean square (RMS),
median, and mean power frequency were calculated as an
average of data obtained during 10 consecutive pedal cycles.
Furthermore, EMG data during the same 10 pedal cycles
were full-wave rectified and smoothed by using a fourth-
order Butterworth low-pass filter with a cutoff frequency of 6
Hz. The amplitude of the smoothed, rectified EMG is ex-
pressed as a percentage of maximum EMG, which was mea-
sured pre- and postexercise as an average of 1 s of smoothed,
rectified EMG obtained during a maximal knee extension.
Because of technical problems, EMG measurements from five
J Appl Physiol • VOL
subjects were rejected, and the EMG data, therefore, only
represent nine subjects.
EEG Beckmann Ag-AgCl electrodes were affixed to the
scalp with conductive electrode paste (Bentonite paste, Dan-
tec) and secured with Omnifix stretch tape. The electrodes
were positioned 1 cm in front of CZ, at F3, and at OZ [accord-
ing to the ten-twenty system (12)] chosen to represent the
motor areas of the legs, the prefrontal cortex, and the visual
cortex, respectively. A paired mastoid reference was used.
Pilot studies showed that signals from the right and left
hemisphere had similar power spectrum responses to exer-
cise and hyperthermia, thus rendering the basis for recording
EEG from just one hemisphere. Surface potentials were am-
plified (gain ⫻10,000) and sampled at 1,000 Hz in each
electrode using a CED 1401-plus analog/digital converter.
EEG measurements in three subjects were rejected because
of movement-related artifacts. The data analysis of the EEG
was similar to the method previously described by Nielsen et
al. (16). In short, fast-Fourier transformation of the EEG was
made with a CED software package (Spike2) using steps of
0.2 Hz for the power spectrum. The areas of the power
spectrum between 8 and 13 Hz (A␣) and between 13 and 30
Downloaded from jap.physiology.org on June 17, 2009
Hz (A␤) were calculated as quantitative indexes of the activ-
ity in the ␣- and ␤-bands, respectively. Furthermore, an
A␣/A␤ index was calculated by dividing A␣ by A␤, and the
index was expressed as a percentage of the preexercise rest-
ing value obtained on the trial day, thus reducing interindi-
vidual and day-to-day variations. The described analysis
allows us to focus on possible changes in relative amplitudes
between ␣- and ␤-waves occurring during exercise, rather
than on changes in absolute EEG power amplitudes.
Middle cerebral artery (MCA) mean blood velocity (Vmean)
was measured with ultrasound Doppler sonography in 8 of
the 14 subjects in a parallel study, with an identical exercise
protocol (see Ref. 19 for further details).
Core temperature and degree of dehydration. Tes was mea-
sured in the deep esophagus with a thermocouple (model
MOV-A, Ellab) inserted through the nasal passage at a
distance equal to one-fourth of the subject’s standing height.
HR was measured with a Polar HR recorder (Polar Electro).
To avoid differences in the degree of dehydration between
trials, subjects drank 0.6 ⫾ 0.1 liter of prewarmed water
(adjusted to core temperature) in the hyperthermic trial and
0.2 ⫾ 0.1 liter in the control trial. The degree of dehydration
(estimated from the difference between pre- and postexercise
body weights) was thereby restricted to 0.9 ⫾ 0.2% in the
hyperthermic trial and 0.8 ⫾ 0.1% in the control trial [P ⫽
not significant (NS)]. Body weight was determined on a
platform scale (model 1–10, Ohaus).
Statistical analysis. Two-way (time-by-trial) repeated-
measures ANOVA was performed to evaluate differences
between and within trials. After a significant F test, pairwise
differences were identified using Tukey’s significance (hon-
estly significant difference) post hoc procedure. Furthermore,
simple linear regression was used to test the strength of the
association between variables. Stepwise forward-regression
analysis was also used to test the strength of the association
between RPE as the dependent variable and HR, core tem-
perature, A␣/A␤ index of the EEG, RMS, and median spectral
frequency of the EMG as independent variables. All regres-
sion analyses are made on the basis of the average values
from subjects when all parameters (included in the analysis)
are present. Data are presented as means ⫾ SE, unless
otherwise indicated.
91 • NOVEMBER 2001 • www.jap.org
 EEG AND EMG WITH OR WITHOUT HYPERTHERMIA 2019

RESULTS

The core temperature increased continuously during

the exercise period in the uncompensable hot environ-
ment and reached a peak value of 40.0 ⫾ 0.1°C at
exhaustion after 50 ⫾ 3 min of exercise. HR increased
from 140 ⫾ 4 beats/min at 5 min to 179 ⫾ 3 beats/min
at exhaustion, and in the same period RPE increased
from 11 ⫾ 1 to 20 ⫾ 0 units (both P ⬍ 0.001). In the
control trial, exercise was maintained for 1 h with only
a modest increase in RPE from 10 ⫾ 1 at the beginning
of exercise to 12 ⫾ 1 at 60 min and with Tes and HR
stabilized at 38.0 ⫾ 0.1°C and 140 ⫾ 4 beats/min,
respectively, after ⬃20 min of exercise.
EMG and EEG measurements. A representative ex-
ample of raw and smoothed rectified EMG obtained at
the beginning and at the end of a hyperthermic exer-
cise trial is shown in Fig. 1. The amplitudes of the
smoothed rectified EMG were in the range of 40–60%
of maximum EMG in all subjects, and the average
amplitude of 10 pedal cycles remained unchanged dur-

Downloaded from jap.physiology.org on June 17, 2009

ing the exercise period, both in the hyperthermic trial
(45 ⫾ 6% at 5 min vs. 48 ⫾ 5% at 50 ⫾ 3 min; P ⫽ NS)
and in the control trial (48 ⫾ 4% at 5 min vs. 47 ⫾ 3%
at 60 min; P ⫽ NS). RMS was also similar in the
hyperthermic and normothermic condition and re-
mained constant over time in both trials. Furthermore,
neither mean nor median spectral frequency of the
EMG changed significantly over time within either of
the two exercise conditions, and there were no signifi-
cant differences between hyperthermia and control.
In all three EEG electrode positions, the A␣/A␤ index
increased significantly during the hyperthermic trial.
During the control trial, A␣/A␤ indexes only increased
insignificantly (P ⫽ NS), and the A␣/A␤ indexes were
significantly higher in hyperthermia compared with
control at the end of exercise (see Fig. 2). The increase
in the A␣/A␤ indexes during the hyperthermic trial was
caused by a significant reduction in the A␤ by ⬃50%
(P ⬍ 0.05), whereas the A␣ remained unchanged. All
subjects had a similar pattern of response; however,
large interindividual variations in the magnitude of
the changes in the A␣/A␤ indexes were observed. When
the A␣/A␤ indexes were plotted against Tes, it appeared
that, in all three electrode positions, there was a good
linear relationship between the changes in A␣/A␤ index
Fig. 1. Raw (A and C) and smoothed rectified (B and D) electromyo-
and the changes in core temperature (r ⫽ 0.94–0.95; gram (EMG) in 1 representative subject measured at the beginning
P ⬍ 0.001; see Fig. 3). of exercise (5th min) in the hyperthermic trial when the core tem-
RPE. RPE was plotted against the changes in EEG, perature was normal (37.2°C) (A and B) and at the end of the same
EMG, HR, Tes, and MCA Vmean (see Fig. 4), and step- cycle trial when core temperature had increased to 39.8°C (C and D).
wise forward-regression analysis identified core tem- max, Maximum.
perature and the A␣/A␤ index of F3 as the best predic-
tors of RPE. Simple linear regression analysis revealed 7). In contrast, there were no significant correlations
that RPE also was strongly associated with the between RPE and any of the measured muscle param-
changes in MCA Vmean (r ⫽ 0.98), HR (r ⫽ 0.97), and eters (see Fig. 4, E and F), and the EEG frequency
A␣/A␤ indexes of CZ and OZ (r ⫽ 0.95 and 0.94, respec- changes were not correlated with any of the measured
tively); however, these variables did not increase the muscle parameters.
predicting power of the F3 A␣/A␤ index and Tes, because DISCUSSION
they were all significantly correlated with Tes. A linear
association between the three A␣/A␤ indexes and MCA In the present study, we observed that, during pro-
Vmean was also observed (r ⫽ 0.93–0.97; P ⬍ 0.001; n ⫽ longed exercise with progressive hyperthermia, EMG
J Appl Physiol • VOL 91 • NOVEMBER 2001 • www.jap.org
2020 EEG AND EMG WITH OR WITHOUT HYPERTHERMIA
Fig. 2. Area of power spectrum between 8 and 13 Hz (A␣)/area of
power spectrum between 13 and 30 Hz (A␤) index of the electroen-
cephalogram (EEG) measured at F3 (frontal cortex; A), 1 cm in front
of CZ (motor cortex; B), and at OZ (visual cortex; C) during submaxi-
mal cycling with and without hyperthermia. Values are expressed as
percentages of resting values and represent means ⫾ SE for 11
subjects. Significantly different from * 5-min value and from † control
(P ⬍ 0.05).
amplitudes and frequencies of the exercising muscles
remained unaltered, whereas a calculated frequency
index of the EEG (A␣/A␤ index in all three electrode
positions) increased linearly with increasing core tem-
J Appl Physiol • VOL 91 • NOVEMBER 2001 •
perature. Stepwise forward-regression analysis indi-
cated that the A␣/A␤ index of F3 (prefrontal cortex) and
core temperature were the best predictors of the sub-
jects’ RPE, whereas there was no correlation between
RPE and any of the measured EMG parameters.
The unaltered RMS of the raw EMG and amplitudes
of the smoothed rectified EMG indicate that the level of
muscular activation was constant throughout the ex-
Downloaded from jap.physiology.org on June 17, 2009
Fig. 3. A␣/A␤ index of the EEG measured at F3 (frontal cortex; A), 1
cm in front of CZ (motor cortex; B), and at OZ (visual cortex; C)
plotted against core temperature responses during submaximal cycle
exercise with and without hyperthermia. Values are means for 11
subjects. Solid line, line of best fit.
www.jap.org
 EEG AND EMG WITH OR WITHOUT HYPERTHERMIA
ercise periods in both the control and hyperthermic
trial. Unchanged EMG amplitude and RMS during
moderate-intensity cycling in a thermoneutral envi-
ronment is in accordance with previous findings (11,
22), and the present results demonstrate that hyper-
thermia does not affect the electrical activation pattern
of the active skeletal muscles. Corroborating this ob-
servation, Ftaiti et al. (6) recently observed that EMG
amplitude measured during running was unchanged
during an exercise bout with progressively developing
dehydration and hyperthermia. If hyperthermia had
J Appl Physiol • VOL
2021
Fig. 4. Rating of perceived exertion
(RPE) plotted against the A␣/A␤ in-
dex measured at F3 (n ⫽ 11; A); core
temperature (n ⫽ 14; B); heart rate
(n ⫽ 14; C); middle cerebral artery
Downloaded from jap.physiology.org on June 17, 2009
(MCA) mean blood velocity (Vmean)
(n ⫽ 8; D); root mean square (RMS) of
the EMG from vastus lateralis as a
percentage of the 5-min control trial
value (n ⫽ 9; E); and median spectral
frequency of the EMG from vastus
lateralis (n ⫽ 9; F) measured during
prolonged, submaximal exercise with
hyperthermia (E) and during control
(F). Values are means for 11 subjects.
Solid line, line of best fit. NS, not
significant.
resulted in fatigue-induced changes in motor unit re-
cruitment and/or discharge rates, it would be expected
that, similar to high-intensity cycle exercise, there
would have been a progressive increase in the RMS
and an increase in the amplitude of the smoothed
rectified EMG (11, 22, 23), as well as a shift in the
median spectral frequency (8, 14). The absence of hy-
perthermia-induced signs of muscular fatigue during
submaximal exercise is in accordance with the results
from our recent study (18), in which maximal force of
the knee extensors was evaluated immediately after
91 • NOVEMBER 2001 • www.jap.org
2022 EEG AND EMG WITH OR WITHOUT HYPERTHERMIA
cycle trials with or without hyperthermia. In that
study, we used superimposed electrical stimulation of
the femoral nerve to differentiate between the central
and peripheral factors contributing to the development
of fatigue during prolonged, maximal voluntary iso-
metric contractions. The results revealed that hyper-
thermia did not affect the ability of the muscles to
generate force. Instead, central fatigue seemed to be
the cause of the attenuated performance during the
prolonged, maximal voluntary isometric contractions
(18). Increased difficulty to retain power output during
the hyperthermic cycle trial is reflected in the subjects’
RPE, and the identification of core temperature and F3
A␣/A␤ index as the best predictors of RPE may support
the idea that the EEG frequency shift reflects de-
creased arousal and impeded ability of the brain to
sustain motor activity (16). However, it is also possible
that the rise in the A␣/A␤ index simply reflects the
sensation of the increasing temperature or that it re-
sponds to other signals arising secondarily to the in-
crease in core temperature. At rest, hyperventilation-
induced reductions in cerebral blood velocity are
associated with a slowing of the EEG activity (13).
Considering the high association between MCA Vmean
and the A␣/A␤ indexes in all three electrode positions, it
seems plausible that, to some extent, the frequency
shift during the hyperthermic trial is a consequence of
the hyperventilation-induced reduction in the cerebral
blood flow (see Ref. 19 for further explanation). Fur-
thermore, this may be the reason why the frequency
shift was observed in all EEG positions (i.e., the fron-
tal, central, and occipital cortexes), and it could explain
why the electrical activity in all three cortical areas
was similarly affected by hyperthermia. However,
stepwise forward-regression analysis has limitations,
and although it provides a general description of the
impact that core temperature and A␣/A␤ indexes have
on RPE during exercise in the heat, it cannot identify
the source of the altered brain activity, and the causal
relationship between the altered cerebral circulation,
the changed electrical activity, and the development of
fatigue remains at present unsolved. Considering the
close association between RPE and the F3 A␣/A␤ index,
it is tempting to suggest that altered activity in the
prefrontal cortex might be a contributing mechanism
by which hyperthermia affects the ability to sustain
motor activity during prolonged exercise in the heat.
The prefrontal cortex is most likely involved in the
initiation of volitional movements (17, 21), and we have
recently demonstrated that hyperthermia reduces the
voluntary activation percentage during a sustained,
maximal isometric contraction (18). However, further
investigations are required to elucidate the relation-
ship among hyperthermia, altered cortical activity,
and central fatigue. The mechanism by which hyper-
thermia might act on brain activity could be far more
complex, involving afferent signals arising in the tem-
perature centers in hypothalamus (1, 2) or signals
sensing cardiovascular stressing, muscle and skin tem-
perature, etc. However, taken together with our previ-
ous demonstration of hyperthermia-induced central fa-
J Appl Physiol • VOL
tigue, the present results appear to support the
hypothesis that altered cerebral function rather than
muscular changes is associated with the development
of fatigue during prolonged exercise in the heat.
In conclusion, the present study demonstrates that
subjectively perceived exertion is highly associated
with increases in core temperature and frequency
changes of the EEG obtained over the prefrontal cor-
tex. In contrast, there were no correlations between
RPE and any of the measured EMG parameters. The
unaltered RMS, median frequency, and amplitude of
the smoothed EMG during both the control and hyper-
thermic exercise trial indicate that hyperthermia did
not result in fatigue-induced changes in motor unit
recruitment and/or discharge rates. The results appear
to support the idea that altered activity within the
central nervous system rather than changed muscular
activity is involved in the development of fatigue dur-
ing prolonged exercise in hot environments.
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