Vol. 276, Issue 4, R1095-R1101, April 1999
Core temperature and sweating onset in humans acclimated to
heat given at a fixed daily time
Osamu
Shido1,
Naotoshi
Sugimoto1,
Minoru
Tanabe2, and
Sotaro
Sakurada1
1 Department of Physiology,
School of Medicine, Kanazawa University, Kanazawa 920-8640; and
2 College of Medical Technology,
Hokkaido University, Sapporo 060-0812, Japan
 |
ABSTRACT |
The
thermoregulatory functions of rats acclimated to heat given daily at a
fixed time are altered, especially during the period in which they were
previously exposed to heat. In this study, we investigated the
existence of similar phenomena in humans. Volunteers were exposed to an
ambient temperature (Ta) of
46°C and a relative humidity of 20% for 4 h (1400-1800) for
9-10 consecutive days. In the first experiment, the rectal
temperatures (Tre) of six
subjects were measured over 24 h at a
Ta of 27°C with and without
heat acclimation. Heat acclimation significantly lowered Tre only between 1400 and 1800. In
the second experiment, six subjects rested in a chair at a
Ta of 28°C and a relative
humidity of 40% with both legs immersed in warm water (42°C) for
30 min. The Tre and sweating rates
at the forearm and chest were measured. Measurements were made in the
morning (0900-1100) and afternoon (1500-1700) on the same day
before and after heat acclimation. Heat acclimation shortened the
sweating latency and decreased the threshold
Tre for sweating. However, these
changes were significant only in the afternoon. The results suggest
that repeated heat exposure in humans, limited to a fixed time daily,
alters the core temperature level and thermoregulatory function,
especially during the period in which the subjects had previously been
exposed to heat.
human heat acclimation; sweating latency; heat stress; circadian
rhythm; metabolic hormone
| |
INTRODUCTION |
ACCLIMATION TO HEAT has repeatedly been shown to modify
various thermoregulatory functions in various species of animals, such
as the core temperature level (1, 6, 20), thermoeffector thresholds
(10), and magnitude of thermoregulatory responses to a given level of
central drive (10). Our previous studies (19, 21, 22) showed that when
rats were subjected to daily heat exposure, limited to ~5 h at a
fixed time of the day for more than 5 consecutive days, and then
transferred to a constant ambient temperature
(Ta) of 24°C, the pattern of
day-night variations in core temperature was altered so that the core
temperature of the rats fell in the same period during which they had
been previously exposed to heat. This drop in core temperature lasted
for several days after the termination of the daily heat exposure (19). In association with the drop in core temperature, threshold
temperatures for nonevaporative heat loss and cold-induced
thermogenesis shifted to low levels (23). Because the core temperature
may be preferably controlled within a range between thresholds for heat
loss and heat production, the drop in core temperature is considered to be a result of regulation by the thermoregulatory system. Based on
these observations, we postulated that a time memory for heat exposure
is established in heat-acclimated rats, and that their thermoregulatory
function changes to maintain their core temperature at a low level,
especially during the period in which they were previously exposed to heat.
Physiological changes in thermoregulation due to heat acclimation are
also well documented in humans, especially with respect to the sweating
response (5-7, 17, 18, 30). Acclimation to heat given for a few
hours per day for more than 9 days has been shown to lower the body
core temperature (1, 6, 7, 20), shorten the time lag of sweat onset
(13, 14), shift threshold temperatures for sweating (7, 17, 20) and
skin vasodilation (1) to low levels, and increase the sweating capacity (5, 14, 30). However, it is not known whether such thermoregulatory changes in heat-acclimated humans are consistent throughout a day or,
as observed in the heat-acclimated rats, seen clearly during the period
in which subjects were exposed to heat. The present study was therefore
conducted to determine how the core temperature level and sweating
response to a mild heat load differs between the period in which
subjects had previously been exposed to heat and during other parts of
the day in humans acclimated to heat given daily at a fixed time. It
was hypothesized that even in the human autonomic thermoregulatory
system, a memory for timed heat exposure could be formed and, according
to the time memory, the core temperature and sweating threshold might be lowered during the period in which subjects had been previously exposed to heat.
| |
METHODS |
Subjects.
Healthy male and female subjects volunteered for the present
experiments, giving informed consent. Before participating, they were
well familiarized with the test procedures and with the equipment to be
affixed to their bodies, but were not informed of the purpose of the study.
From 2 wk before the start of measurements, the subjects' clock times
for waking up and going to bed were controlled (0700-0730 and
2300-2330, respectively), with the exact times left up to the
subjects. During this period, we instructed all subjects not to
participate in any strenuous exercise or to take a Japanese-style bath
(hot water immersion) to avoid a rise in core temperature. In addition,
the subjects were not allowed to stay in a
Ta above 28°C, except during
the heat exposure period.
For more than 3 days before the first measurements, we recorded all
food that the subjects consumed and the time of ingestion. The subjects
had the same food at the same time for the same period before and
during the second measurements. When the subjects consumed beverages
containing calories, the amount and the time of the ingestion were also
checked and repeated as with the food control. In addition, the
subjects were not allowed to have any food or beverage that contained
caffeine, alcohol, or a large amount of capsaicin for at least 1 wk
before the measurements. Water intake (without calories)
was not limited throughout the experiment. The food control was
performed to avoid the possible influence of calorie intake on
heat-loss responses (8).
Heat exposure.
The subjects wore T-shirts and shorts and stayed in a
temperature-controlled chamber (TBR-2HAG2A; Tabai Espec, Osaka, Japan) in which the air temperature was set at 46.0 ± 0.2°C and the
relative humidity was 20 ± 3% for 4 h (1400-1800). The
subjects could change their posture (e.g., lie down or sit in a chair),
read books, or study in the chamber. The heat exposure was repeated for
9-10 consecutive days in experiment
1 and 10 consecutive days in
experiment 2. Body mass was measured
before and after the heat exposure a few times in each subject. The
amount of decrease in body mass during the 4-h heat exposure was
~1.1-1.5 kg.
Experiment 1.
Four male subjects and two female subjects (mean age, height, and body
mass were 25 yr, 167 cm, and 64.9 kg, respectively) volunteered for
this experiment. On the day of the measurements, the subjects were
instructed to arrive at the laboratory by 0800 after having had
breakfast. Each subject wore a T-shirt and shorts and entered a
climatic chamber (A-X2; SHOWA, Tokyo, Japan) at a
Ta of 27.0 ± 0.5°C and a
relative humidity of 50 ± 5%. All devices for measurement were
then fitted on the subject. The subjects stayed in the chamber for the
following ~28 h. During this period, they were allowed to watch
television and videos and read books, but were encouraged to stay as
quiet as possible. The subjects' clock times for waking up and going
to bed were maintained, and lunch, supper, and breakfast of the next
morning were provided between 1200 and 1230, 1800 and 1830, and 0730 and 0800, respectively.
Each subject's rectal temperature
(Tre) was measured with a
thermistor probe introduced 15 cm into the rectum. Skin temperatures were recorded at the forehead and chest by skin thermistors held in
place with surgical tape. The heart rate (HR) was estimated by the
count of R wave in 1 min on an electrocardiogram. All data were sampled
every minute and stored with a portable four-channel memory
(VM4-064; VINE, Tokyo, Japan) for more than 24 h (at least between
1000 and 1000 of the next day).
The measurements were made twice in each subject. For three subjects,
we performed measurements in the control condition (CN) before
acclimation to heat, whereas for the other three subjects, we made the
measurements in the CN 3-4 wk after completing the 9- to 10-day
heat-exposure schedule. Measurements in the heat-acclimated condition
(HA) began on the next day after the heat-exposure schedule. For the
female subjects, we performed the measurements at the same stage of the
menstrual cycle.
In an additional study, we measured
Tre, temperatures of the forehead
and chest, and HR before and during the 4-h heat exposure (1300-1800) on the 4th day of the heat-exposure schedule using the
portable memory.
Experiment 2.
Six male subjects (mean age, height, and body mass were 24 yr, 174 cm,
and 70.9 kg, respectively) were used. All measurements were conducted
in a climatic chamber (TBL-6-S; Tabai Espec) at a
Ta of 28.0 ± 0.5°C and a
relative humidity of 40 ± 5%.
The measurements in the CN, consisting of the morning and afternoon
tests, were made on the day before commencement of the 10-day
heat-exposure schedule. The subjects were instructed to arrive at the
laboratory by 0800 without breakfast. They wore only shorts. All
devices for measurement were fitted on the subjects. The subjects
rested in the chamber, seated in a chair in an upright position, for 60 min (0900-1000). A blood sample (~20 ml) was then taken from the
vein at the right cubital region. About 30 min after the blood
sampling, the subjects immersed their legs in a water bath (LTP-112;
Tabai Espec) in which the water temperature was controlled (42.0 ± 0.1°C) for 30 min (1030-1100). The same measurements were
repeated in the afternoon, i.e., the subjects rested between 1500 and
1600, a blood sample was taken at 1600, and the subjects' legs were
immersed in warm water between 1630 and 1700. Between the two tests,
the subjects were not allowed to have any food or beverage that
contained calories and all sensors except the skin thermistor probes
were kept in place.
Sweating rates
(
sw)
at the forearm and chest were measured by the ventilation method (26)
with 0.79-cm2 capsules (1.0-cm
diameter). The capsules were fixed to the skin of the left forearm and
to the center of the sternum with adhesive tape and highly ventilated
with dry air taken from a pressurized air tank at a constant flow of
500 ml/min. The outlet air was then sent into a capacitance hygrometer
(HMP23UT; Vaisala, Helsinki, Finland) and water content was computed
from the flow and relative humidity of the air. The left forearm skin
blood flow was measured by a laser-Doppler flowmeter (ALF-2100;
Advance, Tokyo, Japan). The probe was fixed to the skin surface and
held in place with adhesive tape. After the measurements were taken,
the subjects immersed their forearms in warm water (42°C) for 30 min to obtain maximal forearm skin blood flow (28).
Tre was measured with a thermistor
probe introduced 15 cm into the rectum. Skin temperatures were recorded
at seven body sites (forehead, trunk, forearm, hand, thigh, calf, and
foot) by skin thermistors held in place with surgical tape. The
accuracy of the thermistors (Techno Seven, Yokohama, Japan) was
estimated to be within ±0.05°C. Systolic and diastolic arterial
blood pressures (BP) and HR at the right arm were monitored every 5 min
with an electric sphygmomanometer (MPV-7101; Nihon Kohden, Tokyo, Japan).
All data except BP and HR were sampled every 30 s via a computer-based
logging system (PC9801VX; NEC, Tokyo, Japan). In addition, sw
values were continuously recorded with a potentiometer (INR-6041; TOA
Electronic, Tokyo, Japan) to determine the time of sweating onset. Mean
skin
(
sk)
and mean body
(b)
temperatures were then computed as follows
where
T1-7 are the temperatures of
the forehead, trunk, arm, hand, thigh, calf, and foot, respectively
(9).
Blood was collected into three different types of tubes, one containing
NaF for the glucose assay, one containing EDTA-2K for the arginine
vasopressin (AVP) and catecholamine assays, and the other empty. After
the hematocrit (Hct) was measured, the tubes were centrifuged at
4°C and 1,500 rpm. Plasma and serum samples were
frozen and stored at below 
20°C until assays. All of the
assays except Hct were performed by Sumitomo Metal Industry Bioscience
(Tokyo). Briefly, plasma osmolality
(Posmol) was determined by
freezing point depression and the plasma levels of Na, K, Cl, and
glucose (G) were measured by an ion-selective electrode
method. Total protein (TP) and albumin (Alb)
concentrations were measured by the Biuret and bromcresol green
methods, respectively, and triglyceride (TG) and nonesterified fatty
acid (NEFA) were measured by the enzyme method. Plasma
concentrations of
3,3',5-triiodo-L-thyronine (T3), free
T3
(FT3), thyroxine
(T4), free
T4
(FT4), AVP, and aldosterone (Ald) were determined by radioimmunoassay, and those of epinephrine (Epi) and norepinephrine (NE) were analyzed by HPLC.
The measurements in the HA were performed on the day after the 10-day
heat-exposure schedule. The procedure was repeated exactly the same way
as in the CN. The places where the sweating capsules were attached were
carefully marked after the control measurements, so that the sweating
rates were always measured at the same skin areas.
Data analysis and statistics.
In experiment 2, resting levels of
thermoregulatory and cardiovascular parameters were obtained as means
for 10 min before the 30-min leg water immersion. The forearm skin
blood flow is expressed as the percentage of maximal output of the
flowmeter (%Qsk) measured when
the arm was immersed in water at 42°C (28). The results are
presented as means ± SE. The effects of heat acclimation and time
of day on all parameters measured were evaluated by two-way ANOVA.
Significant changes in thermoregulatory and cardiovascular parameters
during leg water immersion were also assessed by two-way ANOVA.
P < 0.05 was considered to be significant.
| |
RESULTS |
Experiment 1.
Figure 1 shows changes in
Tre and HR before and after the
4-h heat exposure. The heat exposure significantly increased the Tre (~0.75°C) and the
forehead and chest skin temperatures (data not shown). HR tended to
increase during the heat exposure, but because of the movement of the
subjects in the climatic chamber, the changes were not significant.
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Fig. 1.
Changes in rectal temperature
(Tre;
top) and heart rate (HR;
bottom) before and during 4-h heat
exposure (1400-1800). Data are means of 10-min periods ± SE
(vertical bars). Dotted lines on abscissae indicate period of heat
exposure. bpm, Beats/min.
|
|
There were clear nycthemeral variations in
Tre, skin temperatures, and HR in
all subjects. Figure 2 shows the mean
changes in Tre, forehead skin
temperature, and HR over 24 h in the CN and HA conditions. In the CN,
as is well known, Tre increased in
the morning and early afternoon and reached the maximal level around
the evening. It then fell gradually and started to rise just before
subjects woke up. Similar changes were seen in the forehead skin
temperature and HR. In the HA, however,
Tre did not increase in the
afternoon. The Tre levels in the
HA were significantly lower than those in the CN, especially between
1400 and 1800, when the subjects had been previously exposed to heat.
The Tre levels during sleep and in
the morning were the same between the CN and HA conditions. The skin
temperature and HR did not differ significantly between the two
conditions, regardless of the time of the day.
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Fig. 2.
Changes in Tre
(top), forehead skin temperature
(Tf;
middle), and HR
(bottom) during a 24-h period
(1000-1000 of next day) in control ( ) and heat-acclimated ( )
conditions. Data are means of 2-h periods ± SE (vertical bars).
Filled bars on abscissae indicate period of lights off. Spaces between
dotted lines indicate period of previous heat exposure
(1400-1800). * Significant difference between the 2 conditions.
|
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Experiment 2.
Table 1 shows the resting levels of the
thermoregulatory and cardiovascular parameters before the start of the
leg water immersion in the morning and afternoon tests in the CN and
HA. In the afternoon test,
Tre fell significantly after heat
acclimation, whereas in the morning test,
Tre fell in three subjects,
increased in two subjects, and did not change in one subject, resulting in an insignificant influence of heat acclimation on the
Tre level. b
appeared to be lowered by heat acclimation, but again, the change was
more evident in the afternoon test than in the morning test. There were
no significant differences in the resting
sk and
%Qsk between the periods of the
day and acclimation conditions. Similarly, the BP and HR values were
not significantly affected by heat acclimation or the time of day.
The 30-min leg water immersion increased the
Tre,
b,
sk,
%Qsk, and
sw
but did not affect BP or HR in all subjects tested. The onset of
thermal sweating was determined by a prompt increase of
sw
in each measurement (Fig. 3). The time at
the onset of thermal sweating after the commencement of the leg water
immersion and the Tre
corresponding to the sweating onset were defined as a sweating latency
and threshold Tre for sweating,
respectively.
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Fig. 3.
Example of changes in Tre and
sweating rate at forearm
(sw)
during 30-min leg water immersion.  , onset of sweating;
 , threshold Tre
for sweating.
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Figure 4 shows the sweating latency and
threshold Tre for sweating at the
forearm in each subject. In the morning test, heat acclimation elongated the sweating latency in two subjects, shortened it in three subjects, and had no effect in one subject. In the afternoon test, the sweating latency was shortened after heat acclimation in all subjects. Thus a significant effect on the latency
was seen only in the afternoon. The sweating latency in the afternoon
was significantly longer than that in the morning in the CN. However no
such difference was noted in the HA.
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Fig. 4.
Sweating latency and threshold Tre
for forearm sweating in each subject in control (CN) and
heat-acclimated (HA) conditions. Top,
values obtained in morning test;
bottom, values obtained in afternoon
test. * Significant effect of heat acclimation.
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In the morning test, the threshold
Tre for sweating shifted to higher
levels in two subjects and to lower levels in three subjects after heat
acclimation. In the afternoon test, the threshold was lowered by heat
acclimation in five of the six subjects. Again, the change was
significant only in the afternoon test. Similar effects of heat
acclimation on the sweating response were seen in the chest (Fig.
5).
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Fig. 5.
Sweating latency and threshold Tre
for chest sweating in each subject in CN and HA conditions.
Top, values obtained in morning test;
bottom, values obtained in afternoon
test. * Significant effect of heat acclimation.
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Because %Qsk varied greatly and
the onset of the rise in %Qsk was
not reliably identified, we could not assess the effects of heat
acclimation on the onset for skin vasomotor response.
Tables 2 and
3 summarize the data for Hct,
Posmol, plasma levels of
electrolytes, energy substrates, and various hormones in the CN and HA
in the morning and afternoon tests. Although Hct in the
HA appeared to be lower than that in the CN in the afternoon test, heat
acclimation and the time of day had no significant influence on Hct.
Posmol in the afternoon test was
significantly lower than that in the morning test regardless of the
acclimation conditions. However, heat acclimation did not affect
Posmol in the two periods of the
day. The plasma G level slightly decreased and the plasma TG and NEFA
levels significantly increased in the afternoon test compared with the
morning test in both the CN and HA, which may have been attributable to
fasting. Again, heat acclimation had no significant effect on the
levels of plasma energy substrates. The plasma levels of Na, K, Cl, TP,
and Alb, and the concentrations of all plasma hormones tested, were not
affected by heat acclimation in either the morning or the afternoon
test.
| |
DISCUSSION |
Heat acclimation brought about by daily heat exposure for a short
duration has been shown to lower the core temperature level in humans
(1, 6, 20), e.g., heat exposure for 0.5-3 h daily for more than 12 days decreased oral temperature by 0.19°C (6), and repeated
exercise under heat for 1.5-2.0 h daily for 9 days reduced
Tre by ~0.3°C (1). The
present results are comparable with these observations, i.e., after
subjects were acclimated to heat given for 4 h daily at a fixed time
for 9-10 consecutive days, their
Tre was significantly decreased
(0.19-0.24°C) (Fig. 2 and Table 1). However, the fall in core
temperature was not consistent throughout the day. The
Tre in the HA were kept at lower
levels than those in the non-acclimated condition in the afternoon,
especially around the period when the subjects had been previously
exposed to heat, whereas heat acclimation had no significant influence
on the Tre levels in the morning,
at night, or during sleep (Fig. 2). Thus, similar to the observations of rats (19, 21-23, 25), our data suggest that even in humans, daily heat exposure for several hours limited to a fixed time alters
the pattern of nycthemeral variations in core temperature so that the
core temperature falls during the period in which the subjects were
previously exposed to heat.
It is also well documented that in humans with short-term heat
acclimation, the latency for thermal sweating is shortened (6, 14) and
threshold core temperatures for heat-loss responses are shifted to low
levels (1, 17, 30). Such thermoregulatory changes, especially the
downward shift of the thermoeffector threshold, may contribute to
keeping core temperature at a low level (23). The present study
confirmed these observations (i.e., in the HA, the sweating latency was
significantly shortened and the threshold Tre for thermal sweating was
significantly lowered). However, the changes in evaporative heat-loss
response were evident only when measurements were made in the afternoon
(between 1500 and 1700), the period when the subjects had previously
been exposed to heat. Again, in agreement with results in the
heat-acclimated rats (23, 25), heat exposure of several hours limited
to a fixed time daily may modify thermoregulatory function, especially during the period corresponding to the previous heat-exposure time in humans.
There are several possible explanations for the early onset of thermal
sweating in the HA. The onset of local thermal sweating is known to be
regulated by both central thermoregulatory drive and local skin
temperature (14, 15). The central thermoregulatory drive to the
effectors is a function of the total thermal input from a whole body
and an excitability or a sensitivity of the central nervous system to
the thermal stimuli. In addition, the responsiveness of sweat glands is
likely to be modified with heat acclimation (3, 5). Thus the shortening
of the sweating latency occurring with heat acclimation could be
attributed to an increase in thermal input, an enhanced sensitivity of
the central nervous system, a rise in the skin temperature of the area
where sw
was measured, and/or an increased sweat gland sensitivity to a given
level of central drive. In the present observations, b, an
indicator of total thermal input, did not increase at the onset of
thermal sweating, but rather decreased after heat acclimation. Local
skin temperatures at the forearm and chest were not higher in the HA
than in the CN. It therefore appears that the sensitivity of the
central thermoregulatory system to thermal stimuli or a responsiveness
of local sweat glands increases in the HA, especially during the period
in which the subjects were exposed to heat.
In addition to thermoregulatory factors, the onset of the evaporative
heat-loss response is shown to be strongly influenced by the body
hydration state and Posmol (4, 11,
12, 16, 27). For instance, hyperosmolality delayed a sweating onset (4)
and enlarged the amount of rise in core temperature required to elicit
thermal sweating (27). In the present study, the plasma Posmol was significantly lower in
the afternoon test than in the morning test. However, heat acclimation
had no significant effect on the
Posmol. The Hct in the afternoon
test appeared to be lower in the HA than in the CN, suggesting an
occurrence of plasma expansion due to heat acclimation. Again, the
change in Hct was not significant. Thus changes in plasma volume or
Posmol may not have a close
association with the shortening of sweating latency and the downward
shift of sweating threshold observed in the afternoon test in the HA.
Short-term heat acclimation has been shown to increase the magnitude or
capacity of evaporative and nonevaporative heat-loss responses in
humans (1, 13, 30). In rats acclimated to heat given daily at a fixed
time, their thermoregulatory responses to acute heat load were
facilitated only during the period in which the animals had been
exposed to heat (25). Thus, in the present study, we expected that the
magnitude of sweating and blood flow responses to heat would differ
between the periods of the day in the HA. The heat stress
(leg water immersion) applied in this study was rather mild because we
had to repeat the same heat stress within several hours. Therefore, the
amount of increase in
sw
and skin blood flow was not sufficient to assess their responsiveness
and capacities. Whether the magnitude of thermoregulatory responses to
heat load is enhanced during the previous heat-exposure time remains to
be investigated.
Acclimation to heat has also been shown to bring about several
adjustments in endocrine functions related to thermogenic activity and
body water balance, e.g., heat acclimation altered the patterns of
nycthemeral variations in plasma thyroid hormones (24) and Ald (2)
concentrations in animals. We have reported that in rats acclimated to
heat given daily at a fixed time, plasma levels of
T3,
FT3,
T4, and
FT4, which are known to decline in
heat-acclimated subjects, paradoxically increased during the period
corresponding to the previous heat-exposure time (24). However, in the
present heat-acclimated human subjects, we observed no significant
changes in plasma thyroid hormone levels during the specific period.
The plasma concentrations of energy substrates, catecholamines, AVP, and Ald were also not modified by heat acclimation.
In experiment 1, the control
measurements were performed 3-4 wk after the termination of the
heat exposure in three subjects. Short-term heat acclimation is known
to be transient and to disappear gradually. Although there are great
variations in the rate of decay for heat acclimation among the reports
(29), the major physiological changes associated with heat acclimation
could be lost within 2-3 wk. Thus the residual effect of heat
acclimation in those measurements might be minimal. Indeed, we could
observe clear differences in the pattern of nycthemeral variations of Tre between the CN and HA.
In summary, after humans were subjected to daily heat exposure given
for 4 h at a fixed time for more than 9 consecutive days, the pattern
of day-night variations in core temperature was modified so that the
core temperature fell during the period when the subjects had been
previously exposed to heat. Additionally, the latency for thermal
sweating was shortened and the threshold temperature for sweating was
lowered by heat acclimation, especially during the period corresponding
to the previous heat exposure. As in heat-acclimated rats, a time
memory for heat exposure could be formed in the human thermoregulatory
system and, according to the memory, autonomic thermoregulatory
function could change during the period of previous heat exposure time
without actual temperature stimuli.
| |
ACKNOWLEDGEMENTS |
This study was supported in part by Grants-in-Aid for Science
Research 07670079 and 06404018 from the Ministry of Education, Science
and Culture of Japan.
| |
FOOTNOTES |
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. §1734 solely to indicate this fact.
Address for reprint requests and other correspondence: O. Shido, Dept.
of Physiology, School of Medicine, Kanazawa Univ., 13-1 Takara-machi,
Kanazawa 920-8640, Japan (E-mail:
o-shido{at}med.kanazawa-u.ac.jp).
Received 21 September 1998; accepted in final form 16 December
1998.
| |
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