Vol. 86, Issue 3, 895-901, March 1999
The physiological strain index applied to heat-stressed rats
D. S.
Moran1,2,
M.
Horowitz3,
U.
Meiri3,
A.
Laor2, and
K. B.
Pandolf1
1 US Army Research Institute of
Environmental Medicine, Natick, Massachusetts 01760-5007;
2 Heller Institute of Medical
Research, Sheba Medical Center, The Institute of Military Physiology,
Tel Hashomer 52621; and
3 Department of Physiology,
Hadassa Schools of Medicine and Dental Medicine, The Hebrew University,
Jerusalem 91120, Israel
 |
ABSTRACT |
A physiological strain index (PSI) based on
heart rate (HR) and rectal temperature
(Tre) was recently suggested to
evaluate exercise-heat stress in humans. The purpose of
this study was to adjust PSI for rats and to evaluate this index at
different levels of heat acclimation and training. The corrections of
HR and Tre to modify the index for
rats are as follows: PSI = 5 (Tre t 
Tre 0) · (41.5 Tre 0)
1 + 5 (HRt HR0) · (550 HR0)1,
where HRt and
Tre t
are simultaneous measurements taken at any time during the exposure and
HR0 and
Tre 0 are the initial
measurements. The adjusted PSI was applied to five groups (n = 11-14 per group) of
acclimated rats (control and 2, 5, 10, and 30 days) exposed for 70 min
to a hot climate [40°C, 20% relative humidity (RH)]. A
separate database representing two groups of acclimated or trained rats
was also used and involved 20 min of low-intensity exercise
(O2 consumption ~50
ml · min1 · kg1)
at three different climates: normothermic (24°C, 40% RH), hot-wet (35°C, 70% RH), and hot-dry (40°C, 20% RH). In normothermia,
rats also performed moderate exercise (O2 consumption ~60
ml · min1 · kg1).
The adjusted PSI differentiated among acclimation levels and significantly discriminated among all exposures during low-intensity exercise (P < 0.05).
Furthermore, this index was able to assess the individual roles played
by heat acclimation and exercise training.
exercise; heart rate; heat acclimation; rectal temperature; rodent
| |
INTRODUCTION |
ANIMAL EXPERIMENTAL MODELS are very common in
investigations when one is trying to estimate human behavior and search
for new biological mechanisms to unlock some unresolved problems in humans. However, the animal model chosen must be
appropriate, and the characteristic details of the model should be
carefully identified (8). In some animal models, the physiology is
close to that in humans and is virtually identical biochemically (9). These models have a very important advantage when exertional
hyperthermia is investigated. A rat model is commonly used in
experiments studying heat stress where the focus is usually on
mechanisms and the dynamics of different systems (e.g., cardiovascular
and thermoregulatory; Refs. 4, 6, 11-15, 18).
Unfortunately, only a few investigations (3, 26) used heat-strain
indexes for evaluating animal (nonhuman) heat stress. Thus there is a
lack of heat-strain assessment in animals and a demand for a universal
index for different species.
Many heat-strain indexes for evaluating human physiological strain were
introduced during the last century (2, 16). These indexes are based
mainly on either environmental parameters or physiological variables
(7, 17, 27, 30). Attempts and efforts were also made to combine
environmental and physiological effectors in the development of a
unified heat-stress index (2). Although more than 20 heat-strain
indexes already exist, not one has been accepted as a universal
physiological strain index (PSI), with the main reason probably being
related to the number and complexity of the interactions among the
determining factors.
The cooling mechanisms to dissipate excessive heat from the body are
different between humans and rodents. Whereas the main mechanism for
humans is eccrine sweating, rats dissipate heat from their body by
salivation and vasodilatation in the tail. Despite these differences
between the two species, the rat's strain is similarly reflected in
the thermoregulatory and cardiovascular systems by elevation of core
temperature and heart rate (HR) (14, 20, 22).
Recently, Moran et al. (23) introduced a new PSI for humans based on
rectal temperature (Tre) and HR,
as representative of the combined strain reflected by the
thermoregulatory and cardiovascular systems. This simple-to-use index
scaled the strain to a range of 0-10 and can be used on-line or
during data analysis. It was shown that PSI can be applied at any time,
including rest or recovery periods, whenever
Tre and HR are measured (23).
Furthermore, this index successfully rated and correctly discriminated
among different clothing ensembles and climate conditions during heat stress and during different levels of hydration and exercise intensity (21).
The purpose of this study was to examine the applicability of the PSI
concept for rats. We also aimed to modify the physiological parameters
used for PSI in rats and tested the ability of PSI as a tool to
evaluate and assess exercised-heat-stressed rats.
| |
MATERIALS AND METHODS |
The PSI was applied to two databases. The first served to modify and
evaluate PSI for HR and Tre of
rats at different levels of heat acclimation during sedentary exposure
to a hot climate. The second database, taken from an independent study,
examined the physiological responses [HR,
Tre, and blood pressure
(BP)] of acclimated or trained rats to exposures of exercise at
different climates (20).
Protocol 1.
Adjustment of PSI for a rat model was done by using five groups of 20 males each (Zabar strain, albino variation) with a 250- to 300-g body
wt. Experiments were performed on the anesthetized (60 mg/kg
pentobarbital Na+) animals
before or after different periods of heat acclimation. Nonacclimated
ambient temperature was 24 ± 1°C for the control (Con) group.
Heat acclimation was attained by continued exposure of the rats to 34 ± 1°C temperature, 40% relative humidity (RH) during 12:12-h
light-dark cycles for 2, 5, 10, and 30 days (groups 2A, 5A,
10A, and 30A,
respectively). Food and water were provided ad libitum. Heat stress was
attained by subjecting the rats to a hot-dry climate (40 ± 1°C,
20% RH) for 70 min. HR was measured by using electrocardiogram
electrodes, whereas Tre was
measured by using a rectal thermistor (YSI-402) inserted 6 cm beyond
the anal sphincter. Both measurements were taken continuously.
Protocol 2.
Evaluation of PSI for different treatments of heat acclimation or
exercise training during 20 min of heat stress was done with the use of
a database from Moran et al. (20). This database is within the range of
270-550 beats/min for HR, 37.5-41.5°C for Tre, and 100-150 mmHg for BP.
Four groups, each of 25 male Rattus
norvegicus rats (Zabar strain, albino variation)
weighing 300-350 g and fed on Amrod laboratory chow and water ad
libitum, were used. The animals were divided into groups according to
the treatment received before the experiment as follows: acclimated to
heat under sedentary conditions (A), nonacclimated (NA), exercise
trained (T), and nontrained (NT). Heat acclimation was achieved by
continuous exposure to 34 ± 1°C, 40% RH for 1 mo (11).
Exercise training entailed running the rats on a treadmill at a speed
of 25 m/min for 60 min, 5 days/wk, between 9:00 and 10:00 AM. The
intensity and duration of the exercise were gradually raised, starting
with 10 min/day at a speed of 15 m/min, up to 30 m/min for 60 min in
the third week of training (6).
Three days before experimentation, the rats were anesthetized with
pentobarbital sodium (60 mg/kg), and the carotid artery was cannulated.
On recovery, each rat was exercised on a treadmill (15 m/min) for 20 min. In all experimental groups, the rats were randomly subjected to a
low exercise intensity (O2 consumption ~50
ml · min1 · kg1;
Ref. 4) at various climatic conditions (normothermic: 24°C, 40%
RH; hot-wet: 35°C, 70% RH; and hot-dry: 40°C, 20% RH). In normothermia, rats were also exercised at a moderate intensity (25 m/min, O2 consumption ~60
ml · min1 · kg1).
All experiments were performed with rats on a treadmill equipped with
an electric shock grid and with a system for control of ambient temperature and RH. In the course of the exercise sessions, arterial BP
was continuously monitored on-line with a pressure transducer (Statham
23 dB) attached to the carotid cannula. Data were collected by using
Codas data-acquisition hardware and software (Dataq; Ref. 18). HR was
derived from the recordings, and the double product (DP) was
calculated. Tre was measured
before and after each exercise bout with the use of a rectal thermistor
(YSI-402) inserted 6 cm beyond the anal sphincter.
Calculations.
The PSI was calculated as suggested by Moran et al. (23), and
categorization of the strain was done according to Table
1, as shown in the original study (23).
However, corrections of HR and Tre
were assessed necessarily to modify the index for rats. Thus, assuming
that in rats the maximal acceptable HR during exposure to heat stress
is 550 beats/min and, similarly, the maximal acceptable Tre is 41.5°C, the following
normalized physiological stress index for rats is suggested
where
Tre t
and HRt are simultaneous
measurements taken at any time and
Tre 0 and
HR0 are the initial measurements.
Statistical calculations were performed by using SAS 6.04 software and
GLM with repeated measurement, and P
values of <0.05 were considered significant. The material and methods
of the second study are presented in greater details elsewhere (20).
| |
RESULTS |
Database 1.
HR and Tre dynamics of the five
different groups during 70-min exposures to the hot climate are
presented in Fig. 1. In general, HR
dynamics inversely correlated (r = 0.99) with the acclimation period (Fig. 1,
top). The Con group had the highest
values (P < 0.001), whereas the 10A
and 30A groups had the lowest HR values. However, no significant
differences in HR were found between 10A and 30A groups. Furthermore,
during the first 30 min of exposure, no significant differences
were found among the four different A groups.
View larger version (18K):
[in this window]
[in a new window]
|
Fig. 1.
Heart rate (HR; top), rectal
temperature (Tre;
middle), and physiological strain
index (PSI; bottom) dynamics during
70 min of rest in acclimated (accl.) rats at different levels (control
and 2, 5, 10, and 30 days) subjected to a hot-dry climate
[40°C, 20% relative humidity (RH)]. Each point
represents means ± SE for group (n = 11-14 rats).
|
|
Similar patterns of HR were found for
Tre, whereas significantly higher
(P < 0.001)
Tre values were observed in the
Con group. Furthermore, the lower
Tre values were observed in the
10A and 30A groups (Fig. 1, middle).
However, nonsignificant (P > 0.05) Tre values were observed between
the 10A and 30A groups and the 2A and 5A groups.
The modified PSI (Fig. 1, bottom)
was applied to the same data (HR and
Tre) obtained from the rats
exposed to the hot climate. In general, the strain increased linearly
with exposure time in all five groups of rats. However, PSI correctly
divided these five groups (including Con rats) into three categories as
follows: Con, 2A with 5A, and 10A with 30A. High physiological strain, rated as 7 after 70 min of exposure to hot climate, was observed for
Con rats; moderate strain, marked as 5.0-5.2 after 70 min of
exposure, for the 2A and 5A groups; and low strain, rated as 4.4, for
10A and 30A groups.
Database 2.
HR and Tre values after 20 min of
exercise in rats subjected to low or moderate (normothermia only)
exercise intensities and different climatic conditions are depicted in
Fig 2. In general, under normothermic
conditions, HR values of the NA group were lower than for the A group,
whereas under the hot climates (hot-dry and hot-wet), HR values were
lower for the A group than for NA. However, a significant difference
(P < 0.001) in HR was found only at
the low exercise intensity between hot-wet and normothermic conditions
(Fig. 2A). Further analysis of the
individual effects of hot-wet and hot-dry climates was also performed.
It was evident from our data that HR values of rats subjected to the
hot-wet climate were significantly higher than those of rats subjected to the hot-dry climate (P < 0.0001).
View larger version (21K):
[in this window]
[in a new window]
|
Fig. 2.
HR (A) and
Tre
(B) after 20 min of low exercise
intensity (means ± SE) in acclimated and nonacclimated rats
subjected to normothermic (24°C, 40% RH), hot-wet (35°C, 70%
RH), and hot-dry (40°C, 20% RH) climatic conditions. Normothermic
rats were also subjected to moderate-intensity exercise. bpm,
Beats/min. * Significant difference
(P < 0.05) between matched groups.
|
|
The Tre values obtained after 20 min for the same animals are shown in Fig
2B. In all experimental groups,
Tre increased more in the NA than
in the A group. However, significant differences (P < 0.001) were observed only at
the low exercise intensity between normothermic and hot-dry climate. No
significant differences were found in
Tre when
Tre values were compared between
hot-dry and hot-wet climates.
Cardiac work, expressed as the DP (DP = HR × BP), is presented in
Fig 3A.
Under normothermia, there was no significant difference between the A
and NA groups, whereas under conditions of heat stress, DP was lower in
the A rats than in the NA group. However, a significant difference
between A and NA rats was found only in the hot-wet climate
(P < 0.02), suggesting better
adaptation to heat stress. No significant differences were found for
climate effects on DP, although lower values were observed in
normothermia.
View larger version (20K):
[in this window]
[in a new window]
|
Fig. 3.
Double product (DP; A) and PSI
(B) after 20 min of low exercise
intensity (means ± SE) in acclimated and nonacclimated rats
subjected to normothermic (24°C, 40% RH), hot-wet (35°C, 70%
RH), and hot-dry (40°C, 20% RH) climatic conditions. Normothermic
rats were also subjected to moderate-intensity exercise.
* Significant difference (P < 0.05) between matched groups.
|
|
The PSI significantly (P < 0.05)
discriminated between A and NA groups at the different combinations of
exercise intensity and the environmental heat load (Fig.
3B). Categorization of the strain
was done according to Table 1, as shown in the original study (23). In
general, the A group had significantly
(P < 0.05) less strain than the NA
in all exposures. Furthermore, the strain in the hot climates (hot-wet
and hot-dry) for the same exercise intensity was significantly
(P < 0.05) higher than in
normothermia. In addition, exposures performed in the hot-wet climate
had higher strain (P < 0.05) than those in normothermia or the hot-dry climate. However, no
significant differences were found when comparing hot-dry and hot-wet
climates for the NA exposures.
The values of HR and Tre after 20 min of exercise in the T vs. NT group are depicted in Fig.
4. HR values were significantly (P < 0.05) lower in the T than in
the NT group, although the differences were not statistically
significant for the moderate exercise intensity (Fig.
4A). Significantly higher
(P < 0.05) HR values were found for
the hot-wet climate compared with the normothermic and hot-dry climates.
View larger version (27K):
[in this window]
[in a new window]
|
Fig. 4.
HR (A) and
Tre
(B) after 20 min of low exercise
intensity (means ± SE) in trained and nontrained rats subjected to
normothermic (24°C, 40% RH), hot-wet (35°C, 70% RH), and
hot-dry (40°C, 20% RH) climatic conditions. Normothermic rats were
also subjected to moderate-intensity exercise. * Significant
difference (P < 0.05) between
matched groups.
|
|
The Tre was not different between
the T and NT groups. However, at the moderate exercise intensity,
significantly higher Tre values
were found for the T group (Fig.
4B).
The T rats exhibited a lower DP at the end of the exposures than did
the NT rats (Fig.
5A).
However, this difference was statistically significant
(P < 0.003) only at the low exercise
intensity in normothermic and hot-wet climates.
View larger version (32K):
[in this window]
[in a new window]
|
Fig. 5.
DP (A) and PSI
(B) after 20 min of low exercise
intensity (means ± SE) in trained and nontrained rats subjected to
normothermic (24°C, 40% RH), hot-wet (35°C, 70% RH), and
hot-dry (40°C, 20% RH) climatic conditions. Normothermic rats were
also subjected to moderate-intensity exercise. * Significant
difference (P < 0.05) between
matched groups.
|
|
The PSI assessed the T groups as having less strain than the NT groups
for the same exposure, as depicted in Fig.
5B. However, significant
(P < 0.03) differences between the
two groups were found only at the low exercise intensity in
normothermic and hot-wet climates. Furthermore, the strain in the
hot-wet climate was higher than for normothermic or hot-dry climates
(P < 0.05).
| |
DISCUSSION |
The PSI, for the two different databases under investigation,
accurately described the heat strain of rats acclimated to five different levels during 70 min of sedentary heat exposure and the
strain accompanying a mild exercise intensity at three different climates for A or T rats. The PSI succeeded in rating each one of these
exposures on its universal scale of 0-10. The index, which is
based on only two physiological parameters, HR and
Tre, categorized these exposures
in the proper and expected order, whereas HR and
Tre during the different exposures
were limited in their individual ability to categorize each exposure
separately (Figs. 1, 2, and 4).
The PSI properly described the relationship between the strain in rats
during sedentary heat stress and the different levels of acclimation.
Thus, during heat exposure, the Con group was assessed with high
strain, the 2A and 5A groups were rated with moderate strain, and the
10A and 30A groups were categorized with low strain. These results
confirm other studies in rats and humans showing that 2-5 days of
heat exposure differ from long-term heat acclimation (13, 25). Horowitz
and Meiri (13) found that some differences between NA and A rats for
the cardiovascular system became significant after 14 days of
acclimation. These authors related their results to alterations in
excitability of the sympathetic and the parasympathetic pathways. At up
to 14 days of heat acclimation, bradycardia was achieved by tonic
parasympathetic acceleration and temporal sympathetic withdrawal, but,
after longer periods of acclimation, changes in the cardiac pacing
cells brought about changes in the intrinsic HR. In nonanesthetized
rats, this response pattern exhibits a clear biphasic process (12). In the anesthetized rats, temporal differences can be categorized into
short- and long-term phases. However, the change is gradual with a
uniform trend. These differences between the nonanesthetized and
anesthetized rats may stem from the barbiturate effects on the
autonomic outflow, which plays a major role in the initial phase of
heat acclimation.
PSI differs from other indexes that have been suggested in the past.
The DP, which is based on HR and BP, was also found to be a valid index
in establishing the heat stress of T rats during exposure to different
exercise intensities and climates (Fig. 5; Ref. 20). However, DP was
limited in estimating the strain of the A rats that exercised at
normothermia. The DP is thought to be limited for two main reasons.
First, this index directly represents the cardiovascular system, which
is not always a good indicator of the metabolic heat load and the
thermoregulatory system, particularly during heat stress. As a
consequence, the validity of DP has been limited to exposures with
either no heat stress or environmental effect (e.g., acclimation or hot
climate). Second, DP is based on either systolic BP or mean arterial
BP. This poses some difficulties in using DP, as it is not commonly used for measuring BP during heat stress in many species.
Furthermore, measuring BP invasively or noninvasively during exercise
is still considered to be a problematic procedure and associated with a few sources of error (19). Moreover, invasive BP measurement, which is
done by an arterial cannulation or catheterization (e.g., carotid
artery), involves a high risk of infection. In addition, as a result of
the cannulation, performance can be affected in some species. Thus
these limitations categorize the DP, like most of the strain indexes,
as one that applies to specific types of conditions and/or exposures.
Heat acclimation and exercise training improve physiological
performance in both normothermic and hot environments. This is manifested by decreased initial HR, increased cardiac reserve, and
greater peripheral blood flow and volume (5, 13, 24, 28). It is well
documented that both bradycardia and a larger blood volume can be
induced by exercise training or chronic exposure to heat (10, 24). Heat
acclimation leads to improved cardiovascular reserve in the face of a
decreased basal metabolic rate (15), whereas exercise training results
in improved cardiovascular reserve coinciding with increased metabolic
rate (24, 29). It is, therefore, difficult to resolve whether the
greater cardiovascular reserve obtained after the combined chronic
stress of heat acclimation and exercise training is attributable to
both or to either one of the individual stressors. In our
previous study (20), it was suggested that in humans training had a
more pronounced effect on HR than did heat acclimation during exercise
at different climates. Although both training and acclimation caused a
decrease in HR, the increments in HR with exercise progression were
smaller in those groups that underwent heat acclimation than in the T
rats. The latter was explained by the contribution of exercise training to the observed bradycardia rather than to the heat effect. As a
consequence, cardiac work, which is represented by DP, found the T
animals somewhat more capable of "coping" with exercise than
could the A group. Furthermore, that study (20) concluded that A rats
responded to exercise more sluggishly than did NA rats. This was
because of the unchanged vascular compliance in the T rats. The
Tre for the T rats was
unexpectedly higher than the values of the NT rats at the end of most
exposures (Fig. 4). However, PSI, which accounts for initial
physiological data (HR0 and
Tre 0), rated all the T
rats with lower strain than the NT rats.
The hot-wet and hot-dry climatic conditions were of a similar thermal
index according to the conventions defined for humans (e.g., discomfort
index and the wet bulb globe temperature; Refs. 27, 30). However, PSI
rated the exposures during the hot-wet climate with higher strain than
those for the hot-dry climate. The fact that the rat has a different
evaporative cooling system from that in humans may account for the
difference observed. It is noteworthy that DP was found to be limited
in assessing the different strain for the various climates (hot-wet and
hot-dry).
The ability of the adjusted PSI to assess our different groups of rats
and evaluate the individual roles played by heat acclimation and
exercise training is seen in this study. The individual effects of heat
acclimation and exercise training on rats have been studied in the past
(4, 20, 22). However, this is the first time that PSI succeeded in
correctly discriminating between these pretreatment groups exposed to
different combinations of climate and exercise intensity.
In 1970, Belding (1) suggested that the "rules of the game" for
index-making must be based on developing an easy-to-use index to
achieve universal validity. The PSI provides a meaningful assessment
that conveniently handled the physiological variables (HR and core
temperature) and is simple to calculate. Although PSI was initially
constructed and designed for humans, we believe the analogy for the rat
is also valid. In fact, this study presents the possibility of applying
the PSI, ranged from 0 to 10, for any species exposed to heat stress.
However, calculation of this index must be adjusted for maximum HR
(HRmax) and
Tre
(Tre max) for each animal
species as follows
In conclusion, the data obtained in the present investigation show that
both heat acclimation and exercise training lead to decreased PSI in
rats. This index provides the potential for a simple physiological
assessment of strain for any species, except possibly poikilotherms,
and, therefore, can be used universally.
| |
ACKNOWLEDGEMENTS |
This work was conducted at US Army Research Institute of
Environmental Medicine, Natick, in collaboration with the Department of
Physiology at the Hebrew University, Jerusalem. D. S. Moran was a
National Research Council Postdoctoral Associate.
| |
FOOTNOTES |
DISCLAIMER: The views, opinions, and/or findings contained in
this report are those of the authors and should not be construed as an
official Department of the Army position, policy, or decision unless so
designated by other official documentation. Approved for public
release; distribution is unlimited.
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: D. S. Moran, USARIEM, 42 Kansas St.,
Natick, MA 01760-5007 (E-mail: dmoran{at}natick-ccmail.army.mil).
Received 23 September 1998; accepted in final form 10 November
1998.
| |
REFERENCES |
1.
Belding, H. S.
The search for a universal heat stress index.
In: Physiological and Behavioral Temperature Regulation, edited by J. D. Hardy,
A. P. Gagge,
and J. J. Stolwijk. Chicago, IL: Thomas, 1970, p. 193-202.
2.
Belding, H. S.,
and
T. F. Hatch.
Index for evaluating heat stress in terms of resulting physiological strains.
Heat Pip. Air Condit.
27:
129-136,
1955.
3.
Bell, A. W.,
J. R. S. Hales,
R. B. Kink,
and
A. A Fawcett.
Influences of heat stress on exercise-induced changes in regional blood flow in sheep.
J. Appl. Physiol.
55:
1916-1923,
1983[Abstract/Free Full Text].
4.
Brooks, G. A.,
and
T. P. White.
Determination of metabolic and heart rate responses of rats to treadmill exercise.
J. Appl. Physiol.
45:
1009-1015,
1978[Free Full Text].
5.
Fox, R. H.,
R. Goldsmith,
D. J. Kidd,
and
H. E. Lewis.
Blood flow and other thermoregulatory changes with acclimatization to heat.
J. Physiol. (Lond.)
166:
548-562,
1963.
6.
Gleeson, T. T.,
W. J. Mullin,
and
K. M. Baldwin.
Cardiovascular responses to treadmill exercise in rats: effects of training.
J. Appl. Physiol.
54:
789-793,
1983[Free Full Text].
7.
Gonzalez, R. R.,
T. M. McLellan,
W. R. Withey,
S. K. Chang,
and
K. B. Pandolf.
Heat strain models applicable for protective clothing systems: comparison of core temperature response.
J. Appl. Physiol.
83:
1017-1032,
1997[Abstract/Free Full Text].
8.
Gross, D. R.
Animal models in cardiovascular research.
In: Quantitative Cardiovascular Studies of Engineering Principles, edited by N. H. C. Hwang,
D. R. Gross,
and D. J. Patel. Baltimore, MD: University Park, 1979, chapt. 1, p. 3-40.
9.
Hannon, J. P.,
C. A. Bossone,
and
C. E. Wade.
Normal physiological values for conscious pigs used in biomedical research.
Lab. Anim. Sci.
40:
293-298,
1990[Medline].
10.
Harrison, M. H.
Effects of thermal stress and exercise on blood volume in humans.
Physiol. Rev.
65:
149-205,
1985[Abstract/Free Full Text].
11.
Horowitz, M.
Acclimatization of rats to mild heat: body water distribution and adaptability of sub maxillary salivary gland.
Pflügers Arch.
336:
173-176,
1976.
12.
Horowitz, M.,
P. Kaspler,
Y. Marmary,
and
Y. Oron.
Evidence for contribution of effector organ cellular responses to the biphasic dynamics of heat acclimation.
J. Appl. Physiol.
80:
77-85,
1996[Abstract/Free Full Text].
13.
Horowitz, M.,
and
U. Meiri.
Central and peripheral contributions to control of heart rate during heat acclimation.
Pflügers Arch.
422:
386-392,
1993[Medline].
14.
Horowitz, M.,
and
S. Samueloff.
Circulation under extreme heat load.
In: Comparative Physiology of Environmental Adaptations. Part II. Adaptations to Extreme Environments, edited by P. Dejour. Basel: Karger, 1987, p. 94-106.
15.
Horowitz, M.,
and
S. Samueloff.
Cardiac output distribution in thermally dehydrated rodents.
Am. J. Physiol.
254 (Regulatory Integrative Comp. Physiol. 23):
R109-R116,
1988[Abstract/Free Full Text].
16.
Lee, D. H. K.
Seventy-five years of search for a heat index.
Environ. Res.
22:
331-356,
1980[Medline].
17.
McArdle, B.,
W. Dunham,
H. E. Holling,
W. S. S. Ladell,
J. W. Scott,
M. L. Thomson,
and
J. S. Weiner.
The Prediction of the Physiological Effects of Warm and Hot Environments: the P4SR Index. London: Medical Research Council, 1947. (Rep. R. N. P. 47/391)
18.
Meiri, U.,
M. Shochina,
and
M. Horowitz.
Heat acclimated hypohydrated rats: age dependent vasomotor and plasma volume responses to heat stress.
J. Therm. Biol.
16:
241-247,
1991.
19.
Moran, D.,
Y. Epstein,
G. Keren,
J. Sherez,
and
Y. Shapiro.
Calculation of mean arterial pressure during exercise as a function of heart rate.
Appl. Human Sci.
14:
293-295,
1995[Medline].
20.
Moran, D.,
Y. Shapiro,
A. Meiri,
A. Laor,
Y. Epstein,
and
M. Horowitz.
Exercise in the heat: individual impacts of heat acclimation and exercise training on cardiovascular performance.
J. Therm. Biol.
21:
171-181,
1996.
21.
Moran, D. S.,
S. J. Montain,
and
K. B. Pandolf.
Evaluation of different levels of hypohydration using a new physiological strain index.
Am. J. Physiol.
275 (Regulatory Integrative Comp. Physiol. 44):
R854-R860,
1998[Abstract/Free Full Text].
22.
Moran, D. S.,
Y. Shapiro,
U. Meiri,
A. Laor,
and
M. Horowitz.
Heat acclimation: cardiovascular response to hot/dry and hot/wet heat loads in rats.
J. Basic Clin. Physiol. Pharmacol.
7:
375-387,
1996[Medline].
23.
Moran, D. S.,
A. Shitzer,
and
K. B. Pandolf.
A physiological strain index (PSI) to evaluate heat stress.
Am. J. Physiol.
275 (Regulatory Integrative Comp. Physiol. 44):
R129-R134,
1998[Abstract/Free Full Text].
24.
Rowell, L. B.
Human Circulation Regulation During Physical Stress. New York: Oxford University Press, 1986, p. 363-406.
25.
Sawka, N. M.,
B. C. Wenger,
and
K. B. Pandolf.
Thermoregulatory responses to acute exercise-heat stress and heat acclimation.
In: Handbook of Physiology. Environmental Physiology. Bethesda, MD: Am. Physiol. Soc., 1996, sect. 4, vol. II, chapt. 9, p. 157-185.
26.
Schroter, R. C.,
and
D. J. Marlin.
An index of the environmental thermal load imposed on exercising horses and riders by hot weather conditions.
Equine Vet. J. Suppl.
20:
16-22,
1995.
27.
Sohar, E.,
J. Tennenbaum,
and
N. Robinson.
A comparison of the cumulative discomfort index (D.I.) and cumulative effective temperature (E.T.) as obtained by meteorological data.
In: Biometeorology, edited by S. W. Tromp. Oxford, UK: Pergamon, 1962, p. 395-420.
28.
Wyndham, C. H.,
A. J. A. Benade,
C. G. Williams,
N. B. Strydom,
A. Goldin,
and
A. J. A. Heynes.
Changes in central circulation and body fluids spaces during acclimatization to heat.
J. Appl. Physiol.
25:
586-593,
1968[Free Full Text].
29.
Wyndham, C. H.,
G. G. Rogers,
L. C. Senay,
and
D. Mitchell.
Acclimatization in a hot, humid environment: cardiovascular adjustment.
J. Appl. Physiol.
40:
779-785,
1976[Abstract/Free Full Text].
30.
Yaglou, C. P.,
and
D. Minard.
Control of heat casualties at military training centers.
Arch. Ind. Health
16:
302-316,
1957.
J APPL PHYSIOL 86(3):895-901
TOP
ABSTRACT
INTRODUCTION
