Heat acclimation does not reduce the impact of hyperthermia on central fatigue.

Abstract

We tested the hypothesis that improved physiological symptoms of passively induced heat acclimation (HA) might impair the impact of hyperthermia on central fatigue and consequently cause greater peripheral fatigue. Subjects in the experimental group (7 males and 6 females) completed seven sessions of HA involving passive heating of the lower body by immersion up to the waist in a water bath at approximately 44 degrees C (air T 23 degrees C, rh 40%) for 45 min, repeated every other day for 2 weeks. During the first and the last HA sessions, participants performed a 2-min MVC of the knee extensors. A TT100 Hz was superimposed on the contraction at about 3, 14, 29, 44, 59, 74, 89, 104, and 119 s. At about 30, 60, 90, and 120 s, the knee extensors were relaxed for 2-3 s and a control TT100 Hz was delivered. The participants in the control group (6 males and 6 females) followed the same exercise protocol on days 1 and 14 in a thermoneutral condition. Peak torque and the muscle voluntary activation and half-relaxation time were assessed during the exercise. The attainment of HA was confirmed by significant decreases in the resting and final rectal temperatures (approximately 0.3 degrees C), heart rate, and physiological stress index, and increased sweating capacity. Lower-body heating resulted in greater central and peripheral fatigue when compared with the thermoneutral condition during the 2-min MVC. Following HA, central and peripheral fatigues were unchanged. We conclude that passively induced HA for 2 weeks improved the physiological symptoms, but did not change central or peripheral fatigue during exercise in hyperthermia.

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ORIGINAL ARTICLE
Heat acclimation does not reduce the impact
of hyperthermia on central fatigue
Marius Brazaitis•Albertas Skurvydas
Accepted: 25 February 2010/Published online: 11 March 2010
? Springer-Verlag 2010
Abstract
ological symptoms of passively induced heat acclimation
(HA) might impair the impact of hyperthermia on central
fatigue and consequently cause greater peripheral fatigue.
Subjects in the experimental group (7 males and 6 females)
completed seven sessions of HA involving passive heating
of the lower body by immersion up to the waist in a water
bath at *44?C (air T 23?C, rh 40%) for 45 min, repeated
every other day for 2 weeks. During the first and the last
HA sessions, participants performed a 2-min MVC of the
knee extensors. A TT100 Hz was superimposed on the
contraction at about 3, 14, 29, 44, 59, 74, 89, 104, and
119 s. At about 30, 60, 90, and 120 s, the knee extensors
were relaxed for 2–3 s and a control TT100 Hz was
delivered. The participants in the control group (6 males
and 6 females) followed the same exercise protocol on days
1 and 14 in a thermoneutral condition. Peak torque and the
muscle voluntary activation and half-relaxation time were
assessed during the exercise. The attainment of HA was
confirmed by significant decreases in the resting and final
rectal temperatures (*0.3?C), heart rate, and physiological
stress index, and increased sweating capacity. Lower-body
heating resulted in greater central and peripheral fatigue
when compared with the thermoneutral condition during
the 2-min MVC. Following HA, central and peripheral
fatigues were unchanged. We conclude that passively
We tested the hypothesis that improved physi-
induced HA for 2 weeks improved the physiological
symptoms, but did not change central or peripheral fatigue
during exercise in hyperthermia.
Keywords
Physiological stress index ? Rectal temperature ?
Voluntary activation
Heat stress ? Passive heating ?
Introduction
Heat acclimatization occurs after repeated exposure of
the body to heat stress during physical work under
stressful conditionsin
(Armstrong and Maresh 1991; Nielsen 1994). The main
physiologicaladaptationsto
include an increase in the sweating response and a
decrease in heart rate (HR), core temperature (Tco), skin
temperature, perceived exertion, and oxygen consumption
at a given work rate (Armstrong and Maresh 1991; Saat
et al. 2005; Kampmann et al. 2008). It has been shown
recently that the reduction in Tco at rest and Tco final
(i.e., at the end of exercise or at the end of passive
heating) can be achieved by either repeated exercise in
the heat (Kampmann et al. 2008) or passive exposure to
heat (Beaudin et al. 2009). The lower resting Tco may
allow an acclimated individual to exercise for a longer
time in the heat before a high Tcois reached (Saat et al.
2005). However, the mechanism underlying this phe-
nomenon is not entirely clear. It is possible that repeated
high Tco is the main stimulus for lowering resting Tco
after HA and that HA may be achieved without repeated
physical exercise, which is less convenient for inducing
HA. This suggests that passively induced HA, which can
reduce Tcofinal significantly, can be used as a model for
thenaturalenvironment
heatacclimation(HA)
Communicated by George Havenith.
M. Brazaitis (&) ? A. Skurvydas
Department of Applied Physiology and Physiotherapy,
Lithuanian Academy of Physical Education, Sporto 6,
Kaunas, LT 44221, Lithuania
e-mail: kku712@yahoo.com
123
Eur J Appl Physiol (2010) 109:771–778
DOI 10.1007/s00421-010-1429-3

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analyzing the true changes in both the central nervous
system and the periphery in the absence of exercise-
induced adaptations (i.e., without a training effect).
It appears that exercise in the heat is associated with
central fatigue and hyperthermia may reduce the central
nervous systems ability to activate the skeletal muscles
(Nybo and Nielsen 2001; Todd et al. 2005). Exercise-
induced fatigue can be caused by limitations in the
skeletal muscles or in the nervous system, as in the case
of the so-called ‘‘central fatigue’’ (Bigland-Ritchie et al.
1986; Westerblad and Allen 2003; Bilodeau 2006). The
mechanisms that limit exercise performance in hyper-
thermia are not well understood. Accelerated fatigue
during repetitive isometric exercise could be associated
with metabolic inhibition of muscle contraction because
ATP turnover accelerates at high temperatures (Rall and
Woledge 1990). However, elevated Tco also plays an
important role (Nybo and Nielsen 2001). It is now clear
that the ability to activate skeletal muscles is sensitive to
changes in Tcobecause increasing Tcoby passive heating
inhibits voluntary activation in isometric contractions
(Todd et al. 2005). Interestingly, this inhibition remains
significant even when an increase in muscle temperature
is prevented by water cooling (Thomas et al. 2006),
indicating that hyperthermia causes impairment of the
nervous system.
It is, also possible that adaptations to passively
induced HA, especially diminished Tco, play a separate
role in central and peripheral fatigue during sustained
exercise in hyperthermia. This raises the question whether
passively induced HA affects voluntary and electrically
induced muscle performance. One might expect that
passively induced HA should reduce central fatigue
during maximal exercise in hyperthermia. We hypothe-
sized that HA impairs the impact of hyperthermia on
central fatigue,and consequently
peripheral fatigue because of the fuller voluntary acti-
vation of the exercising muscle during exercise. No clear
evidence exists to support this hypothesis, and we deci-
ded to examine it in greater detail.
causesagreater
Methods
Participants
We studied 13 healthy subjects (7 males and 6 females: age
22.8 ± 1.1 years, height 1.77 ± 0.24 m, mass 71.7 ±
4.7 kg) in experimental group and 12 healthy subjects
(6 males and 6 females: age 22.3 ± 0.3 years, height
1.73 ± 0.27 m, mass 71.1 ± 3.4 kg) in control group. The
subjects were physically active, but did not participate in
any formal physical exercise or sport program. They had
not been involved in any temperature-manipulation pro-
gram or procedure for at least 1 year. All female partici-
pants were tested during the follicular phase of the
menstrual cycle, when the Tco was at its lowest level
(Aoyagi et al. 1997). Each subject read and signed a written
informed consent form consistent with the principles out-
lined in the Declaration of Helsinki. The local ethics
committee approved this study.
Research design
The research design is presented in Fig. 1. Subjects in the
experimental group were required to attend the laboratory
on nine separate occasions and those in the control group
on three occasions. The initial visit for both groups
involved familiarization with the experimental procedures
and equipment. The subjects also undertook a progressive
incremental test of electrical stimulation until no increment
in single twitch torque could be detected by an additional
10% increase in current strength; 1 week later, the partic-
ipants from both groups returned to the laboratory for the
first experimental session. The subjects from the control
group exercised in a thermoneutral environment at 23?C
room temperature on day 1 (CON-1) and again 2 weeks
later on day 14 (CON-14) (see ‘‘Exercise protocol: 2-min
MVC’’). The first experimental session for the experi-
mental group, denoted as the control (CON), was per-
formed in a thermoneutral environment, as for the control
group. One week after this visit, the experimental group
Fig. 1 The research design.
Testing assessment of muscle
function was performed in the
experimental group [week
before (CON), on day 1 (HA-1)
and day 14 (HA-14) of heat
acclimation] and control group
[on day 1 (CON-1) and day 14
(CON-14) in a thermoneutral
environment]
772Eur J Appl Physiol (2010) 109:771–778
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started the HA protocol (see ‘‘Heat acclimation protocol’’).
The experimental sessions were performed by the experi-
mental group on day 1 (HA-1) and day 14 (HA-14) of HA.
Initially, body mass, rectal temperature (Tre), and HR was
measured. Subjects in experimental group performed
10 min of treadmill running and then an MVC with the
superimposed 250-ms test train of stimuli at 100 Hz
(TT100 Hz), and the same TT100 Hz was repeated 1–2 s
after the MVC, as for the control group. After the MVC
test, the subjects left the dynamometer chair and sat for
45 min immersed up to the waist in a water bath at *44?C.
Immediately after this procedure, each volunteer was towel
dried and the Tremeasurement was repeated again. Within
*3 min after leaving the bath, the volunteer dressed in
light sportswear and returned to the chair of the isokinetic
dynamometer. The stimulating electrodes were placed on
the right leg and the subject performed a 2-min MVC with
application of the TT100 Hz, as for the control group.
Nude body mass was recorded within 30 min after exit
from the water bath.
Exercise protocol: 2-min MVC
The warm-up for the assessment of muscle function com-
prised 10 min of treadmill running at an intensity eliciting
an HR of 120–130 beats min-1. After the warm-up, each
volunteer was positioned in the dynamometer chair, and the
stimulating electrodes were placed on the right leg. After a
5-min rest, three 5-s MVCs were obtained with a 2-min rest
between each. At *3 s of the MVC, the TT100 Hz was
superimposed on the voluntary contraction. The same
TT100 Hz was repeated 1–2 s after the MVC. These
TT100 Hz contractions were used to assess the voluntary
activation of the quadriceps muscle. The subjects rested for
5 min, and the final 2-min MVC was performed. The
TT100 Hz was superimposed on the contraction at about 3,
14, 29, 44, 59, 74, 89, 104, and 119 s. At about 30, 60, 90,
and 120 s, the knee extensors were relaxed for 2–3 s and
the control TT100 Hz was delivered.
The amplitude of the superimposed tetani was calculated
from the baseline, estimated as the average torque over 1 s,
just before the stimulation. The superimposed TT100 Hz
produced measurable torque increments in all subjects.
The central activation ratio index was calculated as the
ratio of the maximal voluntary torque to the peak torque
generated with the additional TT100 Hz superimposed on
an MVC (Behm et al. 2001; Bilodeau 2006; Streckis et al.
2007). The half-relaxation time was also calculated for the
TT100 Hz contractions as the time taken for the torque to
decline from the peak value to half of the value at the end
of the TT100 Hz contraction.
Heat acclimation protocol
The HA protocol comprises seven sessions of passive low-
body heating, which were repeated every other day for
2 weeks.TestingwasconductedfromDecembertoMarchto
limit the effects of HA through casual exposure to high-
ambient temperatures. Passive heating was conducted
indoors at the same time of day (10:00 a.m. to 12:00 p.m.).
The subjects refrained from consuming any food for at least
12 h before the experiment. To standardize the state of
hydration and the feeling of thirst, subjects were allowed to
drink still water as desired until 60 min before the first body
mass measurement. The experiments were performed at
23?C room temperature and 40% relative humidity (rh). On
arrival at the laboratory, each subject was weighed in the
nude and then attired in sportswear (T-shirt, shorts and
socks) and asked to rest in a chair for 30 min. Treand HR
stabilization was assessed, and the control measurements of
TreandHRweremade.HRwasmonitoredbyanHRmonitor
(S-625X, Polar Electro, Kempele, Finland). The volunteer
thensatfor45 minimmerseduptothewaistinthewaterbath
at *44?C as described previously by Sargeant (1987).
Before the subject left the bath, HR was measured again.
Within *1 min after leaving the bath, the volunteer was
towel dried and the Tremeasurement was repeated. The
subject dressed in light sportswear and was asked to rest in
the chair. Nude body mass was recorded within 30 min after
exiting from the water bath, when body sweating had ended.
The same experimental procedure was repeated every other
day for 2 weeks.
Core body temperature
Rectal temperature was measured using a thermocouple
(Rectal Probe, Ellab, Hvidovre, Denmark) inserted to a
depth of 12 cm past the anal sphincter before and at the end
of passive heating.
Physiological stress index
To evaluate heat stress on universal scale of 0–10 and to
overcomethelimitationsofcontinuallygettinghighervalues
during rest or recovery periods, we have used an index that
enabled us to calculate the physiological strain online at any
time. The index was based on the same maximal rise values
for Tre and HR (according to the Human Use Review
Committee Limits). Thus, the following normalized
physiological stress index is suggested (Moran et al. 1998):
PSI ¼ 5 Tret? Tre0
? 180 ? HR0
ðÞ ? 39:5 ? Tre0
Þ:
ðÞ?1þ HRt? HR0
ðÞ
ð
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The measurements for PSI were taken before (Tre0and
HR0) and at the end (45 min) of passive heating (Tretand
HRt), respectively. Treand HR were assigned with the same
weight using a constant of 5. Thus, the index was scaled to
a range of 0–10 within the limits of the following values:
36.5 B TreB 39.5?C and 60 B HR B 180 beats min-1.
State of hydration
The body mass of each subject was determined by taking
their nude mass before and 30 min after the passive heating
(TBF-300, Tanita, UK Ltd. Philpots Close, UK). The state
of hydration was calculated by the formula: loss of body
mass (%) = (body mass before passive heating - body
mass after passive heating)/body mass before passive
heating 9 100%.
Isometric torque and electrical stimulation
The isometric torque of the knee extensor muscles was
measured using an isokinetic dynamometer (System 3;
Biodex Medical Systems, Shiley, New York). The subjects
sat upright in the dynamometer chair with the knee joint
positioned at an angle of 120? (180? - full knee exten-
sion). The equipment and procedure for electrical stimu-
lation were essentially the same as described previously
(Skurvydas et al. 2006, 2008). Direct muscle stimulation
was applied using two carbonized rubber electrodes,
covered with a thin layer of electrode gel (ECG-EEG
Gel; Medigel, Modi’in, Israel). One of the electrodes
(6 9 11 cm) was placed transversely across the width of
the proximal portion of the quadriceps femoris. Another
electrode (6 9 20 cm) covered the distal portion of the
muscle above the patella. A standard electrical stimulator
(MG 440; Medicor, Budapest, Hungary) was used. The
electrical stimulation was delivered in square-wave pulses,
each 0.5 ms in duration. The tolerance of volunteers to
electrical stimulation was assessed on a separate occasion,
and only participants who showed good compliance with
the procedure were recruited for the study. The intensity of
electrical stimulation was selected individually by applying
single stimuli to the muscles tested. During this procedure,
the current was increased until no increment in single
twitch torque could be detected by an additional 10%
increase in current strength.
Statistical analysis
The data were tested for normal distribution using the
Kolmogorov–Smirnov test, and all data were normally
distributed. Two-way analysis of variance (ANOVA) for
repeated measures was used to determine the effects of
hyperthermia (CON vs. HA-1) and time (2-min MVC), the
effects of heat-acclimation (HA-1 vs. HA-14) and exercise
(CON-1 vs. CON-14), and the effects of heat-acclimation
(HA-1 vs. HA-14) and time (2-min MVC) on central and
peripheral fatigue of the quadriceps femoris muscle. If
significant effects were found, post hoc testing was per-
formed using the paired tests with Bonferroni correction
for multiple comparisons. Significance of all tests was set
at P\0.05. Descriptive data are presented as mean and
standard error (SE).
Results
Physiological symptoms of passively induced heat
acclimation
The effect of HA on Treand HR before and after passive
muscle heating, the data on PSI and the ratio of loss in
body mass are presented in Table 1. Treand HR increased
significantly after passive low-body heating in both the
HA-1 and the HA-14 experimental sessions (P\0.05). Tre
measured before and after passive heating decreased by
*0.3?C after passively induced heat acclimation (HA-14
compared with HA-1) (P\0.05). In contrast, Tre did
not change significantly from CON-1 (37.4 ± 0.1?C) to
Table 1 The effect of heat acclimation (HA) on rectal temperature (T) and heart rate (HR) before and after passive muscle heating and the
physiological stress index (PSI) and ratio of loss in body mass (LBM) in the HA day 1 (HA-1) and HA day 14 (HA-14) experiments
HA-1 experiment HA-14 experiment
Before heatingAfter heatingBefore heatingAfter heating
Rectal T (?C)
HR (beats min-1)
37.5 ± 0.139.5 ± 0.1*37.2 ± 0.1?
39.2 ± 0.1*,?
127.3 ± 5.1*,?
1.4 ± 0.2?
7.2 ± 0.3?
77.7 ± 2.6139.2 ± 5.3* 73.0 ± 2.9
LBM (%)1.0 ± 0.1
PSI8.2 ± 0.3
Data are mean ± SE
* Significant difference from the values before heating P\0.05
?Significant difference between HA-1 and HA-14 experiments, P\0.05
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CON-14 (37.5 ± 0.2?C) (P[0.05). The HR at min 45
of passive heating decreased significantly by 11.9 ±
2.3 beats min-1following HA (P\0.05), but it had no
effect on preheating values (i.e., HR before passive heating
did not differ significantly between HA-1 and HA-14). PSI
decreased significantly by *1 point after HA (P\0.05).
The relative loss of body mass from before to after passive
heating was significantly larger after HA [0.4 ± 0.2%
(P\0.05)].
Central and peripheral fatigue during the 2-min MVC
The effect of HA on knee extension peak torque, the
central activation ratio index, half-relaxation time and
changes in the control TT100 Hz torque during the 2-min
MVC are presented in Fig. 2. Peak torque (Fig. 2a) and the
centralactivationratio index
(P\0.05) during the 2-min MVC in the CON, HA-1, and
HA-14 experiments. These decreases were significantly
greater in HA-1 and HA-14, than in CON (P\0.05),
although the differences between the HA-1 and HA-14
sessions were not significant. As shown in Fig. 2c, the
TT100 Hz torque decrease (P\0.05) during the 2-min
MVC was significantly greater in both the HA-1 and the
HA-14 than in the CON sessions, although the torque did
not differ significantly between the two HA sessions. The
half-relaxation time increased (P\0.001) during the
(Fig. 2b)decreased
2-min MVC (Fig. 2d). Half-relaxation time was longer in
the CON experiment than in the HA-1 and HA-14 exper-
iments (P\0.05). The peak torque, central activation ratio
index, half-relaxation time and superimposed TT100 Hz
values in the control group did not change significantly
after the 2 weeks (P[0.05) (Fig. 3).
Discussion
The present study demonstrates that the seven-session
passively induced HA protocol, repeated every other day
for 2 weeks, was successful in inducing adaptations, such
as a significant decrease in Tre, decreased PSI, and
increased sweat rate and HR from before to after passive
heating. However, the HA protocol did not change indi-
cators of central or peripheral fatigue significantly during
the 2-min MVC performed in hyperthermia.
The effect of passively induced heat acclimation
on physiological symptoms
The lowering of resting Tcoindicated positive adaptations
after HA (Buono et al. 1998; Saat et al. 2005; Kampmann
et al. 2008). The significant *0.3?C decrease in resting
and final Trefollowing acclimation is consistent with other
findings (Buono et al. 1998; Patterson et al. 2004). The
Fig. 2 Maximal voluntary
contraction torque (a), central
activation ratio (b), control
TT-100 Hz torque (c) and
half-relaxation time (d) during
the 2-min MVC in the control
(CON) experiment and
experiments with body heating
on the first and seventh sessions
on day 1 (HA-1) and day 14
(HA-14), respectively. The
values for time 0 are taken from
the initial measurements in
these experiments. *P\0.05
compared with time 0. The data
are expressed as mean ± SE
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reported reduction in resting and final Tcois 0.2–0.8?C, and
this difference might reflect the use of different exercise
(Saat et al. 2005, Kampmann et al. 2008) or passive
(Beaudin et al. 2009) HA protocols and climatic condi-
tions. Repeated high-level passive heat stress can reduce
resting Treto the same extent as that reported for exercise-
induced heat exposure (Armstrong and Kenney 1993;
Cheung and McLellan 1998; Saat et al. 2005; Kampmann
et al. 2008). Our study used a passive method to induce
HA, which included a 1-day rest, whereas others used daily
heat exposure. However, a passively induced heat stress
stimulus is reliable for inducing adaptations even with 48-h
rest between heating sessions. The effect of a decrease in
Treat rest after HA, would be to reduce Treat any given
point during exercise in the heat, if the same amount of
heat is generated (Saat et al. 2005).
In our study, HR decreased significantly by 12 beats
min-1at min 45 of passive heating following HA.
According to Wyndham et al. (1976), the causes of the
changes in HR during heat acclimation are complex. The
major advantages attributed to a lower HR following HA
are a higher aerobic fitness level and the ability to tolerate a
higher Tcothroughout exercise and at exhaustion (Selkirk
and McLellan 2001). It is well established that HA leads to
earlier onset of sweating and a faster increase in sweat rate
(Nielsen et al. 1993; Cheung and McLellan 1998; Saat
et al. 2005). Although we did not measure the sweating
sensitivity, we did measure whole-body sweat loss
(Table 1) after the passive heating procedure, and as
expected, the sweating capacity improved following HA.
The adjusted PSI was measured throughout the seven-
session HA protocol, during which the subjects were
immersed up to the waist in a warm water bath. Our study
did not include exercise-induced heat exposure. To our
knowledge, ours is the first study to show that HA induced
by repeated passive heating decreases the PSI in humans.
Only one study in animals has shown a decreased PSI in
rats after exercise-induced HA (Moran et al. 1999). We
also found that the PSI ranged between moderate and high
strain. A similar range in PSI strain rating was reported by
Moran et al. (1998) in humans performing exercise
(treadmill running) in the heat (air T 40?C, rh 40%,
1.34 m s-1at a 2? grade) for 120 min. The similar PSI
ratings indicate that physiological strain can be induced to
a similar extent by exercise-induced and passively induced
heat exposure.
The effect of passively induced heat acclimation
on central and peripheral fatigue
The low-body heating procedure increased not only muscle
temperature (Sargeant 1987), but it had also raised Tre
(Table 1). However, Morrison et al. (2004) showed that a
similar increase in Tcoimpairs voluntary activation of the
Fig. 3 Maximal voluntary
contraction torque (a), central
activation ratio (b), control
TT-100 Hz torque (c) and
half-relaxation time (d) during
the 2-min MVC in the control
experiment on day 1 (CON-1)
and day 14 (CON-14). The
values for time 0 are taken from
the initial measurements in
these experiments. *P\0.05
compared with time 0. The data
are expressed as mean ± SE
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quadriceps muscle even during a brief MVC. Thus, we
expected to find impairment of voluntary activation and
exercise performance during the 2-min MVC after low-
body heating. This is consistent with the data of Nybo and
Nielsen (2001) who concluded that hyperthermia attenu-
ates the ability to generate force during a prolonged MVC
(2 min) and that the impaired performance is associated
with a reduction in the voluntary activation percentage.
Thornley et al. (2003) noted out that local tissue temper-
ature does not impair peak force production, but may
change isometric muscular endurance at submaximal
intensity. Inhibition of the nervous system might have
played a major role in central fatigue (Todd et al. 2005;
Thomas et al. 2006), although an additional mechanism
might also operate under these conditions. The muscle
relaxation rate increases at high temperatures and this
change might depress force generation because the increase
in fusion frequency requires higher motor unit firing fre-
quency to produce the same force (Todd et al. 2005). We
did not assess the muscle half-relaxation time after low-
body heating before the 2-min MVC, but it tended to be
shorter in the heated muscles than in the thermoneutral
experimental conditions even when assessed after 30 s of
MVC.
Discriminating between the central and peripheral
mechanisms that limit voluntary activation is often com-
plicated by the fact that both muscle temperature and Tco
increase at high environmental temperatures and after body
heating. However, the main aim of our study was to
investigate if improved physiological symptoms of HA can
affect central and peripheral fatigue during exercise in the
hyperthermia. Surprisingly, we found no significant chan-
ges in the indicators of central and peripheral fatigue,
during a 2-min MVC performed in hyperthermia from
before and after the 2 weeks of HA. Moderately fit indi-
viduals reach the point of voluntary exhaustion at a con-
sistent Treof *38.7?C, whereas highly fit individuals reach
exhaustion at a Treof *39.2?C (Cheung and McLellan
1998). In our study, the Tre(i.e., after low-body passive
heating) at which subjects started exercising (2-min MVC)
before and after HA was higher or similar to those reported
for physically fit persons. Our subjects were physically
active, but not highly fit individuals. It is possible that the
Tre at which the exercise was started was too high to
enhance voluntary activation of the exercising muscles
following HA. The seven-session protocol, with a rest day
in between sessions, adopted in the passively induced HA
protocol may have been insufficient to induce changes in
central and peripheral fatigue. Future studies should
include an HA protocol involving heat exposure on con-
secutive days and more sessions to produce greater effects.
In conclusion, our results indicate that passively induced
heat acclimation for 2 weeks was successful and improved
physiological symptoms of acclimation, but did not change
central or peripheral fatigue during a 2-min MVC in
hyperthermia.
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