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1 Department of Physiology and 2 College of Medical Technology, Kyoto Prefectural University of Medicine, Kamigyo-ku, Kyoto 602 - 0841, Japan
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ABSTRACT |
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 TOP
 ABSTRACT
 INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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Heat acclimatization
improves thermoregulatory responses to heat stress and decreases sweat
sodium concentration ([Na+]sweat). The
reduced [Na+]sweat results in a larger
increase in plasma osmolality (Posmol) at a given amount of
sweat output. The increase in Posmol inhibits thermoregulatory responses to increased body core temperature. Therefore, we hypothesized that the inhibitory effect of plasma hyperosmolality on the thermoregulatory responses to heat stress should
be attenuated with the reduction of
[Na+]sweat due to heat acclimatization.
Eleven subjects (9 male and 2 female) were passively heated by
immersing their lower legs into water at 42°C (room temperature
28°C and relative humidity 30%) for 50 min following isotonic or
hypertonic saline infusion. We determined the increase in the
esophageal temperature (Tes) required to elicit sweating
and cutaneous vasodilation (CVD) (
Tes thresholds for
sweating and CVD, respectively) in each condition and calculated the
elevation of the Tes thresholds per unit increase in
Posmol as the osmotic inhibition of sweating and CVD. The
osmotic shift in the Tes thresholds for both sweating
and CVD correlated linearly with [Na+]sweat
(r = 0.858 and r = 0.628, respectively). Thus subjects with a lower
[Na+]sweat showed a smaller osmotic elevation
of the Tes thresholds for sweating and CVD. These
results suggest the possibility that heat acclimatization attenuates
osmotic inhibition of thermoregulatory responses as well as reducing
[Na+]sweat.
osmoregulation; sweating; cutaneous vasodilation; plasma osmolality; vasopressin
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INTRODUCTION |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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THE THERMOREGULATORY SYSTEM interacts strongly with the body fluid regulatory system. It has been reported that plasma hyperosmolality and hypovolemia both inhibit thermoregulatory responses to heat stress, such as sweating and cutaneous vasodilation (CVD; 7, 14). In addition to improving thermoregulatory function, heat acclimation expands the blood volume (BV) or plasma volume (PV) (2), increases sweat output at a given thermal drive, and reduces sweat sodium concentration ([Na+]sweat) (6, 15).
Increased BV or PV contributes to the production of a higher cutaneous blood flow and probably plays a role in the increase in sweating rate during heat stress because saline infusion (12), water immersion (10), a supine position (5), or negative pressure breathing (9) all increased maximal cutaneous blood flow during exercise by removing the leveling off of the cutaneous vasodilatory response to increased body core temperature, which usually occurs at an esophageal temperature (Tes) above 38.5°C during upright exercise (21).
Reduced [Na+]sweat results in a larger increase in plasma osmolality (Posmol) at a given sweat output, which is beneficial in minimizing the reduction of PV due to sweating, because a larger increase in Posmol withdraws more water from the intra- to extracellular space (13). In contrast, a larger increase in Posmol inhibits thermoregulation even more. Takamata et al. (19) recently reported that thermoregulatory CVD and sweating were attenuated linearly with the increase in Posmol by increasing the rise in body core temperature required to elicit these responses.
Taken together, we hypothesized that the inhibitory effect of plasma hyperosmolality on thermoregulatory responses to increased body core temperature should be attenuated in heat acclimated individuals and that this attenuation is one of the mechanisms that allows heat-acclimated individuals to maintain higher sweating rate and cutaneous blood flow during progressive dehydration induced by extensive sweating. To examine this hypothesis, we determined the relationship between osmotic inhibition of thermoregulatory responses to increased body core temperature and [Na+]sweat in 11 subjects.
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METHODS |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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The experimental protocol was approved by the Review Board on
Human Experiments, Kyoto Prefectural University of Medicine. Nine male
and two female subjects gave their written informed consent prior to
participating in this study. Their age was 20.6 ± 0.4 yr, body wt
59.7 ± 2.0 kg, and height 168.3 ± 2.8 cm. Five subjects
engaged in regular "Kendo" (Japanese fencing) practice and were
supposed to be heat acclimated, whereas other subjects were active but
did not participate in any regular exercise program. To quantify the
osmotic inhibition of thermoregulation in each subject, we determined
the increase in body core temperature required to elicit sweating
(Tes threshold for sweating) and CVD (Tes threshold for CVD) twice during passive body heating hyperosmotic (HOSM) and normosmotic (NOSM) conditions. HOSM was induced by hypertonic saline infusion and NOSM by isotonic saline infusion prior
to passive body heating. Therefore, the conditions are hyperosmotic hypervolemia (HOSM) and normosmotic hypervolemia (NOSM). The
experiments were separated for a period of at least 1 wk, and the order
of the experiments was randomized. In the female subjects, the
experiments were conducted during the follicular phase. All of the
experiments were conducted during summer (August to September).
Protocol. Subjects reported to the laboratory at 9 AM. They had refrained from heavy exercise for 24 h and from salty food, alcohol, and caffeine for 17 h before arriving at the laboratory. They were instructed to eat a light breakfast and drink at least 200 ml of water. On reporting to the laboratory the subjects voided, drank 400 ml of water, and then were kept in the seated position for 1 h during a control period (ambient temperature 28°C, relative humidity 40%). During this period, subjects were inserted with a 20 G catheter (Insyte, Becton Dickinson Infusion Therapy Systems) for blood sampling and infusion into an antecubital vein. At the end of the control period a blood sample was drawn.
After the control period, the subjects were infused with either isotonic (0.9% NaCl) or hypertonic (3% NaCl) saline through the catheter for 90 min. The infusion rate was 0.2 ml · kg
1 · min1 for
isotonic saline infusion and 0.125 ml · kg1 · min1 for
hypertonic saline.
Thirty minutes after the end of the infusion period and preceded by a
10-min preheating control measurement, the subjects immersed their
lower legs in water at 42°C (ambient temperature 28°C, relative
humidity 40%) for 50 min. Blood samples were drawn just before heating
and at the end of the heating period.
Sweat collection for the measurement of
[Na+]sweat was conducted on separate days.
The subjects exercised twice, maintaining their heart rate at 120 beats/min for two 20-min periods, separated by a 10-min recovery period
at an ambient temperature of 36°C (relative humidity 40%). Forearm
and chest sweat was collected during the second exercise bout with a
plastic arm bag and a filter paper disk covered with a Plexiglas
capsule, respectively. The arm bag and capsule were set in place after
washing the skin with distilled water and wiping with a clean dry
towel. The collected filter paper disk was transferred immediately to a
plastic screw-capped bottle to prevent evaporation. After the filter
paper disk was weighed, 1 ml of distilled water was added, whereafter
it was soaked for at least 1 h. Thus the chest
[Na+]sweat was measured in a diluted state,
whereas forearm [Na+]sweat was measured
without dilution (18). We conducted this experiment
because the sweat output during passive body heating was too small to
collect enough sweat for the measurement of
[Na+]sweat.
Measurements. Tes as an index of body core temperature was measured with a copper-constantan thermocouple probe in the polyethylene tubing (PE-90, Clay Adams), placed at a distance one-fourth of the standing height from the external nares. Skin temperature (Tsk) was measured at the forehead, chest, upper arm, forearm, abdomen, thigh, and calf. Mean Tsk was calculated from the body surface area distribution and thermal sensitivity of each skin area (8). Heart rate and blood pressure were measured noninvasively every 1 min (Colin STBP-780, Komaki, Japan). The sweating rate on the chest (SRch) was measured by the capsule ventilation method. The capsule (12.56 cm2) was affixed on the chest skin with elastic surgical tape and ventilated with dry air at a flow rate of 2 l/min, and the relative humidity and temperature of the outlet air were measured continuously with a humidity and temperature sensor (Visala HMP233L, Helsinki). Measurement of both inlet and outlet air flow through the capsule with flowmeters demonstrated no air leakage during the experiments. Skin blood flow was measured with a laser-Doppler flowmeter on the forearm skin (Advance ALF21, Tokyo). Tes, Tsk, relative humidity, and temperature of the ventilated air, and output voltage of laser-Doppler flowmeter were measured every 1 s, and the average of every 30-s period was used for data analyses.
Aliquots of blood sample for measurements of osmolality were centrifuged immediately and separated plasma was stored at
20°C until the measurements were performed. Blood for the assays of plasma
arginine vasopressin concentration ([AVP]p) and plasma aldosterone concentration was transferred into an ice-chilled EDTA tube
and centrifuged at 4°C, and the separated plasma was stored at
80°C until each assay was performed. The remaining blood was
immediately prepared for the hematocrit (Hct) and hemoglobin concentration ([Hb]) measurements.
Hct was determined by the microcapillary centrifugation method and
[Hb] by the cyanometohemoglobin method (Sigma Hemoglobin Kit), and
plasma protein concentration by refractometry (Atago Refractometer).
Posmol was measured by freezing point depression (Fiske
one-ten osmometer, Norwood, MA). The undiluted forearm [Na+]sweat and diluted chest
[Na+]sweat were measured with a
flamephotometer (Corning 480 Flamephotometer, Medfield, MA).
[AVP]p and plasma aldosterone concentration were
determined by radioimmunoassay (AVP RIA Kit and Aldosterone RIA Kit,
Mitsubishi Chemical). Intra- and interassay coefficients of variation
for 1.17 pg/ml AVP were 5.5 and 7.0%, respectively. The minimal
detection limit of the AVP assay was 0.21 pg/ml in this experiment
(0.063 pg/tube). Intra- and interassay coefficient of variation for
27.2 ng/dl aldosterone were 6.4 and 8.8%, respectively. All of the samples from a given subject were determined with the same assay kit.
Data analyses and statistics.
The percent change in PV was calculated from the change in Hct and
[Hb] according to the following equation (3)
![&Dgr;PV (%) = 100 ∗ ([Hb]<SUB>B</SUB>&cjs0823; [Hb]<SUB>A</SUB>) ∗](/content/vol280/issue3/fulltext/R623/img001.gif)
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![[ (1 − Hct<SUB>A</SUB>&cjs0823; 100)&cjs0823; (1 − Hct<SUB>B</SUB>&cjs0823; 100] − 100](/content/vol280/issue3/fulltext/R623/img002.gif)
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1 · cm2. Cutaneous
vascular conductance (CVC) was calculated from laser-Doppler flowmeter
output voltage and mean arterial pressure and presented as the percent
change from the mean of the preheating values.
To quantify the osmotic inhibition of the thermoregulatory responses,
we determined the increase in Tes required to elicit sweating and CVD (Tes thresholds for sweating and CVD,
respectively) for each subject in each condition. Tes
was presented as the difference from the mean of the 10-min preheating
values. We employed the Tes thresholds for these
responses instead of absolute Tes thresholds, because the
day-to-day variation of Tes was larger than the
Tes thresholds in NOSM and because the
Tes thresholds were linearly correlated with
Posmol in our previous data (19). Osmotic
inhibition of thermoregulatory sweating and CVD was quantified as the
increase in the Tes threshold per unit rise in
Posmol using the following equation
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![− (&Dgr;T<SUB>es</SUB> threshold)<SUB>NOSM</SUB>]&cjs0823; [(P<SUB>osmol</SUB>)<SUB>HOSM</SUB> − (P<SUB>osmol</SUB>)<SUB>NOSM</SUB>]](/content/vol280/issue3/fulltext/R623/img004.gif)
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Tes threshold)HOSM is the
change in Tes threshold determined during passive body
heating in HOSM and (Tes threshold)NOSM in
NOSM. (Posmol)HOSM is the Posmol
before passive body heating in HOSM and
(Posmol)NOSM, the Posmol before
passive body heating in NOSM. We also determined the thermal
responsiveness of sweating and CVD (the slope of the relationship
between these responses and Tes above the
Tes thresholds) for each subject in each condition.
Data were shown as the means ± SE of 11 subjects. Regression
analysis was performed using the standard least-squares method. Paired
t-test was performed to examine the difference between NOSM
and HOSM. P < 0.05 was considered significant.
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RESULTS |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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The mean forearm [Na+]sweat in 11 subjects was 36.3 ± 6.0 meq/l (range 16.5-87.0 meq/l) and
chest [Na+]sweat was 55.9 ± 9.3 meq/l
(range 25.8-124.5 meq/l). The chest [Na+]sweat was higher than the forearm
[Na+]sweat in all of the subjects, and the
chest and forearm [Na+]sweat were highly
correlated (chest [Na+]sweat = 1.52 *
forearm [Na+]sweat 0.55, r = 0.965). The [Na+]sweat was not
significantly correlated with plasma aldosterone concentration, ranging
from 48 to 115 ng/dl (r = 0.130).
Figure 1, top and
middle, shows PV and Posmol before infusion, and
before and during passive body heating. The increase in PV before
passive body heating was 8.8 ± 0.7% following isotonic saline
infusion and 13.1 ± 1.6% following hypertonic saline infusion, and PV remained unchanged during passive body heating.
Posmol increased by 10.4 ± 0.9 mosmol/kgH2O following hypertonic saline infusion and was
unchanged following isotonic saline infusion. Posmol in
NOSM remained constant during passive heating, whereas Posmol in HOSM decreased slightly during passive body
heating, but this change was relatively small. [AVP]p did
not change throughout the experiment in NOSM, whereas
[AVP]p increased in HOSM following infusion and increased
further during passive body heating (Fig. 1, bottom).
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Preheating Tes was 36.90 ± 0.07°C in HOSM and
36.78 ± 0.07°C in NOSM, demonstrating no significant difference
between the two conditions. The increase in Tes during
50-min passive body heating was much larger in HOSM (1.03 ± 0.06°C), compared with the increase in Tes in NOSM
(0.54 ± 0.05°C), even though the subjects received the same
heat load (Fig. 2, top). The
increase in SRch was delayed in HOSM compared with NOSM,
and the area under the curve of the SRch response in HOSM
was significantly lower than in NOSM (Fig. 2,
middle). The response of CVC during passive body heating was
similar to the SRch response in both conditions (Fig. 2,
bottom). Preheating mean Tsk was not different
between the two conditions (33.29 ± 0.10°C in NOSM and
33.39 ± 0.10°C in HOSM). The Tsk increased
immediately after the onset of immersion because of increased lower leg
temperature in both conditions (33.93 ± 0.10°C in NOSM and
33.98 ± 0.11°C in HOSM), and started to decrease during the
passive body heating in NOSM when sweating started, whereas
Tsk did not decrease significantly during the passive body
heating in HOSM. However, the difference of Tsk between the two conditions was <1°C.
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The mean Tes threshold for sweating of the 11 subjects was 0.17 ± 0.04°C in NOSM and 0.69 ± 0.06°C in HOSM (Fig. 3,
top), and the mean Tes threshold for CVD was
0.19 ± 0.04°C in NOSM and 0.63 ± 0.06°C in HOSM (Fig.
3, bottom). The Tes thresholds for
these responses in HOSM were significantly higher than in NOSM. A
comparison of HOSM and NOSM showed that the responsiveness of
SRch and CVC to increased Tes (the slope of
these relationships above the respective thresholds) were similar (Fig.
3).
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Figure 4, top, shows the
relationship between the osmotic elevation of the Tes
threshold for sweating and forearm
[Na+]sweat, showing a high correlation; i.e.,
the elevation of Tes threshold for sweating per unit
rise in Posmol was lower in those subjects with a lower
[Na+]sweat. The osmotic shift in the
Tes threshold for CVD was also correlated with
[Na+]sweat (Fig. 4, middle), but
the correlation coefficient was lower (r = 0.628)
compared with the relationship between the osmotic shift in
Tes threshold for sweating and
[Na+]sweat (r = 0.858). The
sensitivity of the osmotic AVP secretion (increase in
[AVP]p per unit rise in Posmol) was not
significantly correlated with [Na+]sweat
(Fig. 4, bottom).
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DISCUSSION |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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Body fluid status has a strong impact on thermoregulatory
function. It has been well demonstrated that both a reduction in PV and
an elevation of Posmol inhibit thermoregulatory responses to increased body temperature (1, 7). Furthermore, it has been reported that heat acclimation reduces
[Na+]sweat in addition to improving
thermoregulatory function (6, 11, 15). Reduced
[Na+]sweat and increased sweating rate at a
given thermal drive induced by heat acclimatization would result in a
larger elevation of Posmol at a given amount of sweat
output (13). A greater increase in Posmol will
withdraw more water from intra- to extracellular space and will
minimize the reduction of PV (13), which will be
advantageous to maintain body core temperature at a lower temperature during prolonged heat stress (13). In contrast, we have
shown that increased Posmol inhibits thermoregulatory
responses to increased body temperature (17, 19), and the
Tes thresholds for CVD and sweating elevated linearly
with the increase in Posmol, indicating that the
Tes thresholds for thermoregulatory responses are
osmosensitive (19). Thus we determined the relationship
between the osmotic inhibition of thermoregulatory responses to
increased Tes and [Na+]sweat. Our
hypothesis was that the elevation of the Tes thresholds for thermoregulation per unit rise in Posmol should be
attenuated in the subjects with lower
[Na+]sweat. We also determined the
relationship between osmosensitivity for AVP secretion
([AVP]p per unit rise in Posmol) and
[Na+]sweat to elucidate whether the
attenuated osmosensitivity with a lower
[Na+]sweat is specific for thermoregulation
or general in the osmoregulatory responses.
In the present study, we confirmed that elevated Posmol
inhibits both sweating and CVD by elevating the Tes
thresholds for these responses (Fig. 3). The responsiveness,
represented by the slope of the relationship between the responses
and Tes above the thresholds, for sweating and CVD were
similar between NOSM and HOSM. In addition, the increase in
Tes during passive body heating was highly correlated with
the Tes thresholds for sweating and CVD (Fig.
5). Therefore, the shifted
Tes thresholds for these responses must be the main
factor resulting in the excessive increase in Tes during
passive body heating in HOSM, and the shift in Tes threshold is likely to accurately represent the osmotic inhibition of
the thermoregulatory responses.
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The most significant finding of this study was that there exists a
highly significant correlation among osmotic shifts in the
Tes thresholds for sweating, the Tes
threshold for CVD, and [Na+]sweat,
respectively, i.e., the inhibitory effect of plasma hyperosmolality on
thermoregulatory responses was smaller in those subjects with a lower
[Na+]sweat. The data obtained in this study
suggest that the osmoregulatory inhibition of thermoregulatory
responses to increased body temperature would be attenuated in
heat-acclimated individuals as [Na+]sweat
decreases. In contrast to the significant correlation between the
osmotic shift in the Tes thresholds for thermoregulatory responses (increase in the Tes thresholds per unit rise in
Posmol) and [Na+]sweat, the
osmosensitivity for vasopressin secretion (increase in
[AVP]p per unit rise in Posmol) was not
correlated with [Na+]sweat, suggesting that
heat acclimation seems to modify the osmosensitivity for the inhibition
of thermoregulation selectively.
Although the osmotic shift in the thresholds for both sweating and CVD
correlated with [Na+]sweat, the correlation
coefficient of the relationship between Tes threshold
for CVD and [Na+]sweat was lower compared
with that Tes threshold for sweating and
[Na+]sweat. One possible reason for this is
that the control of cutaneous blood flow is influenced by more factors
than the control of sweating, and cutaneous blood flow is controlled by
the vasoconstrictor and vasodilator systems (4). Increased
Posmol may attenuate the thermoregulatory efferent system,
but it may not influence the nonthermal control of these responses. The
lower stability of the measurement of CVD by laser Doppler flowmetry
might be another factor involved in the lower correlation coefficient
of the relationship between Tes threshold for CVD and
[Na+]sweat.
In the present study, we determined the relationship between the
osmotic shift in the thresholds for thermoregulatory responses to heat
stress and [Na+]sweat using the data obtained
from 11 subjects (cross-sectional study). It would of course be better
to determine the changes in the Tes thresholds for
thermoregulatory responses and [Na+]sweat
before and after a heat acclimation program (longitudinal study). We
determined the relationship twice (in NOSM and in HOSM), and the
experiments were separated by at least 1 wk with the order of
experiments randomized. Thus it was impossible to examine the effect of
a short-term acclimation program on the
[Na+]sweat and osmotic inhibition of the
thermoregulation, because acclimation status should be changed between
the two experiments (15, 20). It is expected that studies
will be performed to examine the effect of long-term acclimation.
The forearm [Na+]sweat in the present study was relatively low (36.3 ± 6.0 meq/l). In a different series of experiments in our laboratory, the mean forearm [Na+]sweat measured with the same experimental procedure in different subjects during winter was 62.7 ± 5.7 meq/l (39.4-83.8 meq/l, n = 9). In the present study, we performed the experiments at the end of summer, and five subjects participated in regular "Kendo" practice in which they wore heavy protectors in a hot environment. Thus we speculate that the relatively low forearm [Na+]sweat in the present study was not due to measurement error, but rather due to a higher acclimation status of these subjects. In the present study, plasma aldosterone concentration was not correlated with [Na+]sweat, thus the increased responsiveness of the sweat gland may be augmented in the subjects with a lower [Na+]sweat (6). We found a regional difference of [Na+]sweat between the forearm and chest. All of the subjects showed higher [Na+]sweat in the chest than in the forearm, and forearm [Na+]sweat and chest [Na+]sweat were strongly correlated (r = 0.965), suggesting that there is extremely low inter-individual variation in the regional [Na+]sweat difference. The regional difference in [Na+]sweat might be due to the difference in sweat collection methods. However, a strong correlation between osmotic inhibition of thermoregulatory responses and [Na+]sweat was not influenced by the method for sweat collection or collection site.
In summary, we confirmed that increased Posmol inhibits
both thermoregulatory sweating and CVD by elevating Tes
thresholds for these responses. The osmotic inhibition of
thermoregulation, represented by the elevation of the
Tes thresholds per unit rise in Posmol, and
[Na+]sweat were highly correlated, and the
inhibitory effect of plasma hyperosmolality was smaller in those
subjects with a lower [Na+]sweat. The results
of this study suggest the possibility that heat acclimation attenuates
the osmotic inhibition of thermoregulatory responses in addition to
reducing [Na+]sweat, which would be
beneficial in maintaining thermoregulatory sweating and CVD during
prolonged heat stress accompanying a large amount of sweating.
Perspectives
It has been reported that the thermoregulatory system interacts with other functional systems, including the body fluid regulatory system (16). Heat acclimation status might be acquired as a result of integrated adaptation of several functional systems. In the present study, we demonstrated that osmoregulatory adaptation, i.e., attenuated osmosensitivity for the inhibition of thermoregulation, may be involved in the acquisition of heat-acclimation status by which heat-acclimated individuals can maintain lower body core temperature by sweating and CVD during prolonged heat stress, even though their [Na+]sweat is lower than unacclimated individuals. Although we demonstrated the strong correlation between the osmotic inhibition of thermoregulation and [Na+]sweat, the present study was a cross-sectional study. A longitudinal study that examines the effect of heat acclimation on osmotic inhibition and [Na+]sweat would provide further information on the acquisition mechanism of heat acclimation.| |
ACKNOWLEDGEMENTS |
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We thank Yoshiko Kawaguchi, Mikako Matoba, and Yoko Fujiwara for technical assistance.
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FOOTNOTES |
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This work was supported in part by the Ministry of Education, Science, Sports and Culture of Japan and the Descente and Ishimoto Memorial Foundation for the Promotion of Sports Science to A. Takamata.
Address for reprint requests and other correspondence: A. Takamata, Dept. of Physiology, Kyoto Prefectural Univ. of Medicine, Kawaramachi Hirokoji, Kamigyo-ku, Kyoto 602-0841, Japan (E-mail: akira{at}basic.kpu-m.ac.jp).
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.
Received 26 May 2000; accepted in final form 12 October 2000.
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REFERENCES |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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, subjects
supposed to be acclimated; 
, other subjects.
