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This paper discusses human thermoregulation and how this relates to health problems during exposure to climatic stress. The heat exchange of the body with the environment is described in terms of the heat balance equation which determines whether the body heats up, remains at stable temperature, or cools. Inside the body the thermoregulatory control aims at creating the right conditions of heat loss to keep the body temperature stable. In the heat the main effector mechanism for this is sweating. The heat balance is affected by air temperature, radiant temperature, humidity and wind speed as climatic parameters and by activity rate, clothing insulation, and sweat capacity as personal parameters. Heat tolerance is discussed in the light of personal characteristics (age, gender, fitness, acclimatisation, morphology and fat) indicating age and fitness as most important predictors. Heat related mortality and morbidity are strongly linked to age.
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Extreme Weather Events and Public Health Responses
2005, Part 2, 69-80, DOI: 10.1007/3-540-28862-7_7
Chapter 7
Temperature Regulation, Heat Balance
and Climatic Stress
Human Thermal Environments Laboratory
Department of Human Sciences,
Loughborough University, LE11 3TU
Version 2004-March
Dr. George Havenith
Human Thermal Environments Laboratory
Department of Human Sciences,
Loughborough University,
Ashby Road
Loughborough, UK
LE11 3TU
Telephone: +44 1509 223031
Fax: +44 1509 223940
E mail:
Keywords: thermoregulation, heat, cold, comfort, vapour, age, stress, strain, mortality,
WHO, page 2
This paper discusses human thermoregulation and how this relates to health problems
during exposure to climatic stress. The heat exchange of the body with the environment is
described in terms of the heat balance equation which determines whether the body heats
up, remains at stable temperature, or cools. Inside the body the thermoregulatory control
aims at creating the right conditions of heat loss to keep the body temperature stable. In
the heat the main effector mechanism for this is sweating. The heat balance is affected by
air temperature, radiant temperature, humidity and wind speed as climatic parameters and
by activity rate, clothing insulation and sweat capacity as personal parameters. Heat
tolerance is discussed in the light of personal characteristics (age, gender, fitness,
acclimatisation, morphology and fat) indicating age and fitness as most important
predictors. Heat related mortality and morbidity are strongly linked to age.
1 Introduction
Recent extreme weather events have been linked to increased morbidity and mortality.
Longer periods of hot weather, especially when little relief is given at night have hit
mainly the older population. In order to understand the link between the climate, the
stress it poses for the human, and the way the physiological strain experienced by the
human is linked to age and other personal characteristics (e.g. a higher mortality was
observed in females than in males) this chapter will provide some background knowledge
on the parameters relevant to heat stress and strain.
In the evolutionary sense, man is considered a tropical animal. Our anatomy as well as
our physiology is geared towards life in moderate and warm environments. There, we can
maintain our bodily functions, especially thermoregulation, without artificial means. The
goal is to keep the body temperature within acceptable limits and the success of the
effector actions will very much depend on the climate conditions and the person’s
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clothing and work load. The interaction of the person with the climate is represented by
the heat balance equation, which will be discussed in detail. How the person reacts is
governed by the human thermoregulatory system. Finally, individual characteristics of
the person will affect his or her ability to thermoregulate and affect the risk of heat or
cold stress. Problems, in terms of morbidity and mortality, occur when thermoregulation
is impaired in conditions of high levels of heat or cold stress.
2 Temperature Regulation
In a neutral climate, at rest, the human body regulates its temperature around 37 °C. This
is by no means an exactly fixed temperature for all humans. Over a population, when
measured in the morning after bed-rest, the mean will be around 36.7°C, with a standard
deviation of 0.35°C (calculated from data of Wenzel and Piekarski (1984)). During the
day, the temperature will increase (typically by about 0.8°C), peaking in the late evening,
and declining again until early morning due to the circadian rhythm. Also, exercise will
cause an increase in body temperature; with temperatures around 38°C typical for
moderate work and values up to 39°C and occasionally above 40°C for heavy exercise
(e.g. marathon). Short term increases up to 39°C are seldom a problem to the body and
should be considered a normal phenomenon in thermoregulation of a healthy person.
In fever, an increase in body temperature is observed as well. This increase differs from that in
exercise in that the increase in temperature due to fever is defended by the body, whereas the
increase in temperature induced by exercise is not. Thus, when a fever of 38.5°C is present,
cooling the body will lead to activation of heat conservation mechanisms by the body (shivering,
vasoconstriction) to keep the temperature at that level. In exercise, the body would continue
sweating until the body temperature is back to neutral levels.
Figure 1
An example of how the body’s temperature regulation could be represented is given in Figure 1.
Here we have a body, which is represented by a body core temperature and by a skin temperature.
Afferent signals representing these body temperatures are relayed to the control centres in the
brain. There they are compared to a reference signal, which could be seen as a single thermostat
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setpoint, or as a number of thresholds for initiating effector responses. Based on the difference
between actual temperature and the reference value (the error signal), various effector responses
can be initiated. The main ones are sweating and vasodilation of skin vessels (if body
temperatures are higher than the reference, i.e. a positive error) and shivering and
vasoconstriction (negative error). Sweat evaporation will cool the skin, shivering will increase
heat production and heat the core, and vasodilation and constriction will regulate the heat
transport between core and skin.
Of course this is a simplified model, as many different thermosensitive regions of the body have
been identified, and many different and more complex models are possible.
When we think of clothing we can think of it as an additional, behavioural effector response. If
we can freely choose our clothing, which often is not the case due to cultural or work restraints,
we adjust our clothing levels to provide the right amount of insulation to allow the other effector
responses to stay within their utility range. The main effect of clothing will be its influence on the
heat exchange between the skin and the environment. To understand these effects we will need to
analyse the heat flows that exist between the body and its environment, in other words we have to
look at the body’s heat balance.
3 Heat Balance
Normally the body temperature is quite stable. This is achieved by balancing the amounts
of heat produced in the body with the amounts lost.
: Heat Production = Heat Loss
In Figure 2, a graphical representation of all the heat inputs to and outputs from the body
is presented (Havenith, 1999):
Heat production is determined by metabolic activity. When at rest, this is the amount
needed for the body’s basic functions, e.g. respiration and heart function to provide body
cells with oxygen and nutrients. When working however, the need of the active muscles
for oxygen and nutrients increases as does the metabolic activity. When the muscles burn
these nutrients for mechanical activity, part of the energy they contain may be liberated
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outside the body as external work, but most of it is released in the muscle as heat. The
ratio between this external work and the energy consumed is called the efficiency with
which the body performs the work. This process is similar to what happens in a car
engine. The minor part of the fuel’s energy is actually effective in the car's propulsion,
and the major part is liberated as waste heat. The body, as the car engine, needs to get rid
of this heat; otherwise it will warm up to lethal levels. As an example: if no cooling
would be present, a person working at moderate levels (metabolic rate 450 Watt) would
show an increase in body temperature around 1°C every 10 minutes.
Figure 2
For most tasks, as e.g. walking on a level, the value for the external work (energy
released outside the body) is close to zero. Only the heat released by friction of shoes etc.
is released outside the body, whereas all other energy used by the muscles ends up as heat
within the body. In the cold, additional heat is produced by shivering: muscle activity
with zero efficiency. The basal metabolic rate and heat production can be increased up to
fourfold in this way.
For heat loss from the body, between skin and environment, several pathways are available. For
each pathway the amount of transferred heat is dependent on the driving force (e.g. temperature
or vapour pressure gradient), the body surface area involved and the resistance to that heat flow
(e.g. clothing insulation).
radient sur
ace area
Heat Loss resistance
A minor role is taken by conduction. Only for people working in water, in special gas
mixtures (prolonged deep-sea dives), handling cold products or in supine positions, does
conductivity becomes a relevant factor.
More important for heat loss is convection. When air flows along the skin, it is usually
cooler than the skin. Heat will therefore be transferred from the skin to the air around it.
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Heat transfer through electro-magnetic (mainly infra-red) radiation can be substantial.
When there is a difference between the body’s surface temperature and the temperature
of the surfaces in the environment, heat will be exchanged by radiation.
Finally, the body possesses another avenue for heat loss, which is heat loss by
evaporation. Any moisture present on the skin (usually sweat) can evaporate, with which
large amounts of heat can be dissipated from the body.
Apart from convective and evaporative heat loss from the skin, these types of heat loss
also take place from the lungs by respiration, as inspired air is usually cooler and dryer
than the lung’s internal surface. By warming and moisturising the inspired air, the body
loses an amount of heat with the expired air, which can be up to 10% of the total heat
For body temperature to be stable, heat losses need to balance heat production. If they do
not, the body heat content will change, causing body temperature to rise or fall. This
balance can be written as:
Store = Heat Production - Heat Loss
= (Metabolic Rate - External Work) -
(Conduction + Radiation + Convection + Evaporation + Respiration)
Thus if heat production by metabolic rate is higher than the sum of all heat losses, Store
will be positive, which means body heat content increases and body temperature rises. If
store is negative, more heat is lost than produced. The body cools.
It should be noted that several of the “heat loss” components might in special
circumstances (e.g. ambient temperature higher than skin temperature) actually cause a
heat gain, as discussed earlier.
4 Relevant parameters in heat exchange
The capacity of the body to retain heat or to lose heat to the environment is strongly
dependent on a number of external parameters (Havenith, 2004):
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4.1 Temperature
The higher the air temperature, the less heat the body can lose by convection, conduction
and radiation (assuming all objects surrounding the person are at air temperature). If the
temperature of the environment increases above skin temperature, the body will actually
gain heat from the environment instead of losing heat to it. There are three relevant
Air temperature. This determines the extent of convective heat loss (heating of
environmental air flowing along the skin or entering the lungs) from the skin to the
environment, or vice versa if the air temperature exceeds skin temperature.
Radiant temperature. This value, which one may interpret as the mean temperature of all
walls and objects in the space where one resides, determines the extent to which radiant
heat is exchanged between skin and environment. In areas with hot objects, as in steel
mills, or in work in the sun, the radiant temperature can easily exceed skin temperature
and results in radiant heat transfer from the environment to the skin.
Surface temperature. Apart from risks for skin burns or pain (surface temperature above
45°C), or in the cold of frostbite and pain, the temperature of objects in contact with the
body determines conductive heat exchange. Aside from its temperature, the object’s
properties, as e.g. conductivity, specific heat and heat capacity, are also relevant for
conductive heat exchange.
4.2 Air humidity
The amount of moisture present in the environment’s air (the moisture concentration)
determines whether moisture (sweat) in vapour form flows from the skin to the
environment or vice versa. In general the moisture concentration at the skin will be
higher than in the environment, making evaporative heat loss from the skin possible. As
mentioned earlier, in the heat, evaporation of sweat is the most important avenue for the
body to dissipate its surplus heat. Therefore situations where the gradient is reversed
(higher moisture concentration in environment than on skin) are extremely stressful
(condensation on skin) and allow only for short exposures. It should be noted that the
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moisture concentration, not the relative humidity, is the determining factor. The
definition of relative humidity is the ratio between the actual amount of moisture in the
air and the maximal amount of moisture air can contain at that temperature (i.e. before
condensation will occur). Air that has a relative humidity of 100% can thus contain
different amounts of moisture, depending on its temperature. The higher the temperature,
the higher the moisture content at equal relative humidities. Also: at the same relative
humidity, warm air will contain more moisture (and allow less sweat evaporation) than
cool air. The fact that relative humidity is not the determining factor in sweat loss can be
illustrated with two examples:
- In a 100% humid environment the body can still evaporate sweat, as long as the vapour
pressure is lower than that at the skin. So, at any temperature below skin temperature the
body can evaporate sweat, even if the environment is 100% humid.
- Sweat evaporation (at equal production) will be higher at 21 °C, 100% relative humidity
(vapour pressure is 2.5 kPa) than at 30 °C, with 70% relative humidity (vapour pressure =
3 kPa) as the vapour pressure gradient between wet skin (vapour pressure 5.6 kPa) and
environment at 21 °C is 5.6-2.5=3.1 kPa, whereas at 30 °C and, 70% relative humidity it
is only 5.6-3=2.6 kPa.
4.3 Wind speed
The magnitude of air movement effects both convective and evaporative heat losses. For
both avenues, heat exchange increases with increasing wind speed. Thus in a cool
environment the body cools faster in the presence of wind, in an extremely hot and humid
environment, it will heat up faster. In very hot, but dry environments the effects on dry
and evaporative heat loss may balance each other out.
4.4 Clothing insulation
Clothing functions as a resistance to heat and moisture transfer between skin and
environment. In this way it can protect against extreme heat and cold, but at the same
time it hampers the loss of superfluous heat during physical effort. For example, if one
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has to perform hard physical work in cold weather clothing, heat will accumulate quickly
in the body due to the high resistance of the clothing for both heat and vapour transport.
In cases where no freedom of choice of clothing is present, clothing may increase the risk
of cold or heat stress. Examples are cultural restrictions (long, thick black clothes for
older females in southern European countries) or work requirements (protective clothing;
dress codes).
The environmental range for comfort, assuming no clothing or activity changes are
allowed, is quite narrow. For light clothing with low activity levels it is around 3.5°C
wide (ISO7730, 1984). In order to widen this range, one has to allow for behavioural
adjustments in clothing and activity. An increase in activity level will move the comfort
range to lower temperatures, as will an increase in clothing insulation. E.g. an increase in
metabolic rate of 20 Watts (resting levels are 100-160 Watts) pushes the comfort range
down by approximately 1 °C, as does an increase in clothing insulation of 0.2 clo (clo is a
unit for clothing insulation. For reference, a three-piece business suit is 1 clo; long
trousers and short sleeved shirt around 0.6 clo). An increase in air speed will push the
comfort range up (1 °C for 0.2 m.s-1), i.e. allow for comfort at higher ambient
5 Heat Tolerance and Individual Differences
When a group of people is exposed to a heat challenge (e.g. heat wave, or working in the
heat), their body temperature will increase, but not to the same extent for all. Where some
may experience extreme heat strain, others may not show any sign of strain at all.
Knowledge of the mechanisms behind these differences is important for risk assessment
during climatic extremes, for health screening and for selection of workers for specific
stressful tasks. In order to get an insight into the relevant mechanisms, factors which may
influence the response of an individual to heat exposure are discussed here and include:
aerobic power, acclimation state, morphological differences, gender, use of drugs and age
(Havenith, 1985, 2001a,b,c, Havenith et al. 1995b).
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Aerobic power (fitness)
Body core temperature during work is related to the work load (metabolic rate), relative
to the individuals’ maximal aerobic power (usually expressed as the % of the maximal
oxygen uptake per minute; %V
O2max). In addition, a high aerobic power is typically
associated with improved heat loss mechanisms (higher sweat rate, increased skin blood
flow). The V
O2max of a subject is thus inversely related to the heat strain of a subject in the
heat, mainly through its beneficial effect on circulatory performance. The higher the
aerobic power, the higher the circulatory reserve (the capacity for additional increase in
cardiac output) when performing a certain task. Further, aerobic power is often
confounded with acclimatisation as training can result in an improvement of the
acclimatisation state. This is caused by the regular increase in body temperature, which
normally occurs with exercise. The result is a reduction of heat strain in warm climates.
This effect works both through circulation and through improved sweat response.
The only condition where a high V
O2max is not beneficial is for conditions where heat loss
is strongly limited (Hot, Humid), while work rate is related to the workers work capacity
(same percentage of V
O2max). In this case, the fitter person will work harder, thus
liberating more heat in his body than his unfit companion will. As he or she cannot get rid
of the heat, they thus will heat up faster than the slower working unfit person will.
Acclimatisation state
A subject's state of acclimatisation appears to be of great influence on his reaction to heat
stress. With increasing acclimatisation state, the heat strain of the body will be strongly
reduced, resulting in lower core temperature and heart rate during a given exercise in the
heat (Havenith, 2001c). This is related to improved sweat characteristics (setpoint lower
and gain higher), better distribution of sweating over the body and higher efficiency of
sweating (higher evaporated/produced ratio) and improved circulatory stability (better
fluid distribution, faster fluid recruitment from extra-cellular space, reduced blood
pressure decrease) during exercise in the heat. The individual state of acclimatisation can
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be changed by regular heat exposures, e.g. due to seasonal changes in the natural climate
or by heat acclimation due to regular artificial (e.g. climatic chamber) heat exposure.
Subjects living in the same climatic conditions can differ in acclimatisation status,
however, mainly due to the above-mentioned difference in regular training activity. The
combination of heat and exercise induces most optimal acclimatisation. Not all subjects
acclimatise equally well: some subjects do not show acclimatisation effects at all when
exposed to heat regularly.
Morphology and fat
Differences in body size and body composition between subjects affect thermoregulation
through their effect on the physical process of heat exchange (insulation, surface/mass
ratio) and through differences in the body weight subjects have to carry (Havenith, 1985,
2001). Body surface area determines the heat exchange area for both dry (convective and
radiative) and evaporative heat and thereby affects reactions to heat stress. A high surface
area is therefore usually beneficial. Body mass determines metabolic load when a subject
is involved in a weight-bearing task like walking. This implies that mass correlates
positively with heat production. Body mass also determines body heat storage capacity.
This is relevant with passive heat exposures, or when heat loss is limited and body
temperature increase is determined by storage capacity.
The effect of body fat content is somewhat confounded with that of body mass: Body fat
presents a passive body mass, which affects metabolic load during weight-bearing tasks.
I.e. a high fat content increases the metabolic load during activity.
In the cold, subcutaneous fat determines the physical insulation of the body (conductivity
of muscle=0.39, fat=0.20 Wm-1ºC -1). However, as the fat layer is well perfused by blood
flowing to the skin in warm conditions, it is not expected to hamper heat loss during heat
exposure. Further, as the specific heat of body fat is about half that of fat free body tissue,
people with equal mass but higher fat content will heat up faster at a certain storage rate.
With extreme obesity, cardiac function is reduced, which also leads to reduced heat
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When investigating the effects of subject’s gender on heat stress response, investigators
found that females had higher core temperatures, skin temperature, heart rates, blood
pressure, and setpoints for sweating, in comparison to males. Thus on a population level,
women appear to be less tolerant to heat than men, which seems to be reflected in
mortality numbers during heat waves. However, on a population level females differ also
in many physical characteristics from men, which may confound the gender issue in
thermoregulation research. A more precise evaluation of the gender effect was described
by authors, who compared gender groups which were matched in many other
characteristics (V
O2max, %fat, size; Havenith, 1985, Havenith et al. 1995b). They observed
in these matched groups that gender differences in thermoregulation are minimal, and
that some of these differences are climate specific (females perform better in warm,
humid; worse in hot dry climates). On a population basis however, females clearly
perform worse than men and, if exercising at the same level as men run a higher risk for
heat illness.
Two specific female processes do effect thermoregulation: the menstrual cycle and
menopause. The effect of the menstrual cycle at rest (a higher core temperature in the
postovulatory phase) is almost absent during exercise and or heat exposure, however.
Others found that existing male-female differences during exercise heat stress
disappeared with acclimation, or that they were completely absent from the beginning.
In addition, the effect of menopause on thermoregulation during heat exposure has been
studied. Postmenopausal hot flashes and night sweating provide anecdotal evidence that
thermoregulation is affected by oestrogen withdrawal. At equal stress levels higher core
temperatures were observed in postmenopausal women compared to young females with
equal aerobic power levels. Acute oestrogen replacement therapy reduces cardiovascular
and thermoregulatory strain in postmenopausal women.
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Studies of the role of hypertension in heat tolerance showed reduced circulatory
performance in hypertensives compared to normotensives. Though no differences
between groups were present in heart rate and core temperature response, reduced
forearm blood flows were observed in hypertensives as well as reduced stroke volumes
and cardiac output. This indicates a reduced heat transport capacity from body core to the
skin and thus an increased risk of overheating. Sweat rate was higher in the
hypertensives, however, which apparently compensated for the circulatory differences. It
is difficult to estimate whether this compensation will also be effective in other climatic
or work conditions. A certain increased risk seems present.
Use of drugs such as alcohol may predispose subjects to heat illness by changes in
physiological effector mechanisms and by changes in behaviour. Reviews list drugs that
are potentially harmful in heat exposure. The relevant drugs have mainly effects on the
body fluid balance, vasoconstrictor/dilator activity and on cardiac function. These
include: alcohol, diuretics, anti-cholinergic drugs, vasodilators, anti-histamines, muscle
relaxants, atropine, tranquillisers and sedatives, ß-blockers and amphetamines. Especially
anti-hypertensive drugs deserve attention because of their widespread use.
With advancing age our ability to thermoregulate tends to decrease (Havenith et al,
1995b; Inoue et al, 1999; Kenney and Havenith, 1993). This is a multi-factorial process
involving many of our physiological systems with an emphasis on the cardiovascular
system. The most important factor is that physical fitness tends to decrease with age
(Åstrand and Rodahl, 1970; Havenith et al, 1995b) mostly due to a reduced physical
activity level in the elderly (DTI, 1999). This implies that any activity performed
becomes relatively more stressful with advancing age. It will put more strain on the
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cardiovascular system, and leave less cardiovascular reserve. The cardiovascular reserve
is especially relevant to the capacity for thermoregulation as it determines the capacity to
move heat for dissipation from the body core to the skin by the skin blood flow. The
fitness reduction with age can work like a vicious circle as the increased strain
experienced with activity may in itself promote even further activity reduction. Due to a
reduced activity level, people also tend to expose themselves less to physical strain in the
form of heat or cold exposure. This leads to a loss of heat and cold acclimatisation
(Havenith, 1985), which will result in higher strain when the elderly are on occasion
exposed to extreme climates. Typically, on a population level these and other changes
lead to reduced muscle strength, reduced work capacity, a reduced sweating capacity, a
reduced ability to transport heat from the body core to the skin, and a lower
cardiovascular stability (blood pressure) in the elderly. These effects will put elderly
people at a higher risk in extreme conditions, leading to an increase in morbidity and
Apart from the physiological changes mentioned above, the percentage of people with
illnesses and disabilities increases with age as well. In the UK 41% of people aged 65-74
and 52% over 75 reported that their lifestyle was limited by an illness or disability,
compared to 22% of all age groups (DTI, 1998). This also has consequences for well
being in various thermal environments.
6 Mortality and morbidity with age
Of the individual characteristics age seems to be the best predictor of mortality increases
at high temperatures. As discussed above, this ageing effect is likely to be a combined
effect of changes in all physiological systems with age, many of which can be avoided by
staying fit. The main underlying factors with age are reducing fitness levels, which
reduce the spare capacity of the physiological systems to deal with the heat, the
increasing health problems in other areas (e.g. hypertension) and the concomitant
increase in use of drugs.
In order to provide an overview of the problems related to ageing and temperature
regulation, we will now discuss those aspects of mortality and morbidity that in the past
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have been associated with high or low temperatures. The main ones are heat stroke,
hypothermia, cardiovascular and cerebral stroke, and in-home accidents as falls.
Statistical evidence from heat waves in American and Japanese cities shows that
mortality increases dramatically with age when temperature increases. Figure 3 shows
data on the number of deaths due to heat stroke by age group for the period of 1968
through 1994 in Japan (Nakai et al., 1999). It is evident that there is a sharp increase in
deaths due to heat above the 6th decade. The peak daily temperatures when these heat
strokes occurred were typically above 38 °C, although a relatively increased heat related
mortality in the elderly compared to younger groups has also been observed at lower
temperatures. Data from the United States provide a similar picture, with typically above
60% of heat related deaths during heat waves above the 6th decade of age. While heat
stroke deaths among those aged below 64 years were typically exertion induced heat
strokes (outdoor sports or occupational hazards), this was not the case in the elderly. As
mentioned, they have a very limited cardiovascular reserve, have a reduced sweating
capacity, both putting them at higher risk to develop hyperthermia. Apart from heat
stroke, the high cardiovascular strain may also set them up for cardiovascular or cerebral
The analysis of mortality and morbidity data for cold exposure is more complex
(Jendritzky et al., 2000), as many cold related problems may not be attributed to the cold
in statistics. Only extreme hypothermia cases may be registered as such, but mild
hypothermia and in general excursions into the cold can have a severe impact on health
too. Suggested causes are the raised blood pressure and the induced haemoconcentration
(Donaldson, et al., 1997) which could put additional strain on the cardiovascular system
and which may set the elderly up once more for cardiovascular or cerebral stroke.
Figure 3
Figure 4
Another problem in the elderly is the incidence of falls. The number of falls increases
dramatically with age as can be seen in figure 4. At the age of 84, the number of falls is
over 60 percent higher than at the age of 65. At the same time the size of this age group is
much smaller than that of 65. There is no clear statistical evidence that these falls are
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related to temperature however. This lack of statistical significance is most likely due to
the large number of confounding factors involved in these falls. A relation with cold is
however likely. Cold reduces muscle force, and increases stiffness of joints and tendons
(Havenith et al., 1995a). Hence, in the elderly where fitness and muscle force are already
reduced, cold will aggravate these problems. Further, people will wear more clothing in
the cold, increasing the clothing stiffness and thus decreasing the freedom of movement
(Havenith, 1999).
In summary the thermal strain of the body will be affected by climatic parameters such as
temperature, the air’s moisture content, wind speed, and radiation levels. In good health
the body can deal well with heat and cold stress, but when thermoregulation becomes
impaired, e.g. by inappropriate clothing and activity levels, or by a reduced efficiency of
the thermoregulatory system as typically occurs with ageing, the human is at risk, which
is reflected in increased mortality and morbidity numbers during extreme weather events.
The increased mortality with increasing age reflects a change in a number of
physiological systems that are observed with age. These changes lead to a reduced
capacity to deal with external stressors.
WHO, page 17
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16. Kenney WL, Havenith G (1993) Heat stress and age: skin blood flow and body temperature. J Therm Biol 18
17. Nakai S, Itoh T and Morimoto T (1999) Deaths from heat stroke in Japan: 1968-1994. Int.J. Biometeorol.
18. Wenzel HG and Piekarski C: Klima und Arbeit, Bayrisches Staatsministerium für Arbeit und Sozialordnung,
WHO, page 18
Figure 1, Schematic representation of the thermoregulatory control system. Tcore = body core temperature;
Tskin = mean skin temperature; brain controller graphs show reaction of effector (Y-axes) to error signal (x-
axes) (copyright G.Havenith, 2002).
Figure 2, Schematic representation of the pathways for heat loss from the body. M=metabolic heat
production (reproduced with permission, Havenith, 1999).
Figure 3, Deaths due to heat stroke by age group from 1968 to 1994 in Japan. Data from Nakai et al, 1999.
Figure 4, number of falls in selected UK area; 1=slip/trip/tumble; 2=stairs/steps; 3=level; 4=unspecified
(Data from DTI, 1999).
WHO, page 19
Skin Blood Flow
Brain Controllers
WHO, page 20
direct radiation
sweat evaporation
or other
WHO, page 21
WHO, page 22
60 70 80 90 100
Number of falls
... Vulnerability to heat-stress is highly driven by biologically adaptive, socio-economic, and physiological factors . Researchers have linked increased risk of heat-related illnesses to factors such as low socioeconomic status (Basu and Samet, 2002), lower levels of education (Michelozzi et al., 2005), age (Kenney and Munce, 2003), and gender (Havenith, 2005;D'Ippoliti et al., 2010). In Pakistan, studies have been conducted on the worsening impacts of open field jobs, longer working hours, and limited access to medical care on heat-stress among labourers (Bakhsh et al., 2016). ...
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According to the Global Climate Risk Index (2021), Pakistan is the eighth most vulnerable country in the world, and its southern province of Sindh is one of South Asia’s ‘hotspots’ for climate change (Mani, 2018). The 2015 heatwave in Karachi – Pakistan’s largest city – was a trigger for local action, with heatwaves becoming an object of climate governance for planners, policy makers and a large number of NGOs engaged in on-ground relief work. The resulting actions on overheating undertaken by urban governors and policy makers, remain top-down and challenged by unexamined assumptions about the vulnerabilities of poor groups. Such one-dimensional approaches to discrete climatic events led us to question whether current heat management strategies in cities like Karachi are, in fact, designed to fail in the protection of life. This scoping study draws on a review of key policy documents, plans, grey, academic, and scientific literature to outline the role of state and non-state actors in Karachi’s heat governance. It emphasizes the need to understand heat, microclimates, urban planning, infrastructural inequities, and vulnerability in a relational context. It also presents original climate data analysis for the last 60 years in Karachi, to quantify the rapid temperature change in the city: findings that underscore why it is important now, more than ever, to talk about heat in the context of an unequal city. This is even more pertinent in the context of a city like Karachi that lies in the ‘ultraviole(n)t’ zone of solar exposure (Kripa and Mueller, 2020). Fundamentally, this scoping study underscores that the experiences of heat must be understood as a slow onset disaster, particularly in terms of the effects of chronic heat exposure on daily life, worker productivity, health, and wellbeing, amongst other indicators (Opperman, et. al. 2019). In doing so, this Scoping Study proposes a way forward to think about Karachi’s changing weather and the onset of chronic heat exposure in terms of ‘zones of vulnerability’. Such zones are crucial to consider not only due to their higher vulnerability to detrimental effects of heat exposure, but also because risks associated with rising temperatures are likely to make them into nodes that reveal, deepen and sediment pre-existing socio-spatial inequalities within cities like Karachi. Finally, this scoping study serves as a resource base for those who are interested in studying the relationship between rising temperatures, chronic heat exposure, urban planning and vulnerability in other parts of the urban Global South.
... Non-optimal temperatures have a variety of effects on humans' physiological systems, as well as interact with pre-existing diseases and chronic disorders. Even when body temperature remains normal, thermoregulation strains the cardiovascular system [28]. The higher or lower the temperature and the longer the exposure, the more work is required of the cardiovascular system to maintain an optimal temperature. ...
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Objective: We examined whether seasonal and monthly variations exist in the subjective well-being of weather-sensitive patients with coronary artery disease (CAD) during cardiac rehabilitation. Methods: In this cross-sectional study, 865 patients (30% female, age 60 ± 9) were recruited within 2-3 weeks of treatment for acute coronary syndrome and during cardiac rehabilitation. The patients completed the Palanga self-assessment diary for weather sensitivity (PSAD-WS) daily, for an average of 15.5 days. PSAD-WS is an 11-item (general) three-factor (psychological, cardiac, and physical symptoms) questionnaire used to assess weather sensitivity in CAD patients. Weather data were recorded using the weather station "Vantage Pro2 Plus". Continuous data were recorded eight times each day for the weather parameters and the averages of the data were linked to the respondents' same-day diary results. Results: Weather-sensitive (WS) patients were found to be more sensitive to seasonal changes than patients who were not WS, and they were more likely to experience psychological symptoms. August (summer), December (winter), and March (spring) had the highest numbers of cardiac symptoms (all p < 0.001). In summary, peaks of symptoms appeared more frequently during the transition from one season to the next. Conclusion: This study extends the knowledge about the impact of atmospheric variables on the general well-being of weather-sensitive CAD patients during cardiac rehabilitation.
... When walking, heat production increases with the muscle movements and the metabolism required for human locomotion. The efficiency of cooling by sweat is dependent on the sweat being able to evaporate (Kaynakli et al., 2014) and the heat conducted not exceeding the heat loss by evaporation (Havenith, 2005)-meaning that body temperature regulation while walking in an outdoor environment is dependent on a ratio of two values: Ereq, sol and Emax (Gonzalez et al., 2012). The first variable, Ereq, sol is the heat exchange between the skin surface and the radiant heat of a current location, and is measured in g/m 2 of body surface area per hour (Dozier & Frew, 1990;Ravanelli et al., 2019;Winslow et al., 1936). ...
U.S. public officials frequently argue that high temperatures are responsible for increasing mortality of undocumented border crossers (UBCs) in southern Arizona. In this article, we suggest that these kinds of assertions are not only empirically misleading, they also serve to naturalize UBC deaths in the region by helping to obscure their structural causes. Indeed, although heat exposure is a primary cause of death in the region, prior studies have also shown that migration patterns have shifted toward more remote and rugged terrain, characterized by higher elevations and greater shade cover. Using physiological modeling and a spatiotemporal forensic analysis, we assess whether the distribution of recovered human remains has shifted toward locations characterized by environments where the human body is more or less capable of regulating core temperature, and thus succumbing to heat stress. We find that the distribution of recovered UBC remains has consistently trended toward locations where the potential for heat stress is lower, rather than higher. This demonstrates that UBC mortality is not principally a function of ambient or regional temperature, but rather is a result of specific policy decisions that lead to cumulative stress and prolonged exposure due to factors like difficulty and distance of travel. To contextualize these findings, we discuss the evolution of the United States Border Patrol’s policy of Prevention Through Deterrence, and apply the concepts of structural and cultural violence to theorize its consistently deadly outcomes.
... 22 This process involves elevations in heart rate and blood pressure, vasodilatation to transfer heat to the skin, and respiration to lose heat with the expired air. [23][24][25] Physiological adaptation to higher temperatures takes time. If the temperature suddenly changes in a short period of time, people may have difficulty with internal thermoregulation, resulting in inflammatory responses and coagulation abnormalities induced by heat stress. ...
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Studies have investigated the effects of heat and temperature variability (TV) on mortality. However, few assessed whether TV modifies the heat-mortality association. Data on daily temperature and mortality in the warm season were collected from 717 locations across 36 countries. TV was calculated as the standard deviation of the average of the same and previous days’ minimum and maximum temperatures. We first used location-specific quasi-Poisson regression models with an interaction term between the cross-basis term for mean temperature and quartiles of TV to obtain heat-mortality associations under each quartile of TV, then pooled estimates at the country, regional, and global levels. Results show the increased risk in heat-related mortality with increments in TV, accounting for 0.70% (95% confidence interval [CI], -0.33–1.69), 1.34% (95% CI: -0.14–2.73), 1.99% (95% CI: 0.29–3.57), and 2.73% (95% CI: 0.76–4.50) of total deaths for Q1–Q4 (1st quartile–4th quartile) of TV. The modification effects of TV varied geographically. Central Europe had the highest attributable fractions (AFs), corresponding to 7.68% (95% CI: 5.25–9.89) of total deaths for Q4 of TV, while the lowest AFs were observed in North America, with the values for Q4 of 1.74% (95% CI: -0.09–3.39). TV had a significant modification effect on the heat-mortality association, causing a higher heat-related mortality burden with increments of TV. Implementing targeted strategies against heat exposure and fluctuant temperatures simultaneously would benefit public health.
... There are some potential biological explanations for the effects of temperature variability on AR outpatients. AR patients may feel uncomfortable with sudden changes in interday and intraday temperatures as they are not well prepared for temperature variability physiologically and behaviorally (Garrett et al. 2011;Havenith 2005;Martinez-Nicolas et al. 2015). Living in the weather conditions featured with greater intra-and interday temperature variation, the body's thermoregulator centers may work via vasodilation or vasoconstriction against the sharp increase or decrease in the unstable temperature (Sanchez-Gonzalez and Figueroa 2013), and the imbalance of the autonomic nerve system involved in regulation of vasomotor tone is expected to induce rhinitis symptoms via increasing the vascular permeability (Hoshino et al. 2015). ...
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Epidemiological studies have revealed associations between several temperature parameters and allergic rhinitis (AR). However, few studies have reported the association of AR with daily temperature variability, which indicates both short-term intra- and interday temperature changes. This study aimed to analyze associations between temperature variability and initial outpatient visits for AR. The analysis was conducted with an over-dispersed Poisson model using daily time-series data on temperature and the number of initial AR outpatients from 2013 to 2015 in Changchun, China. The composite index of temperature variability was derived by calculating the standard deviation of daily minimum temperature and maximum temperature over exposure days. Stratified analysis by season was also conducted. There were 23,344 AR outpatients during the study period. In the total period, per 1 °C increase in temperature variability at 0–2 days (TV0–2), 0–3 days (TV0–3), and 0–4 days (TV0–4) was associated with a 4.03% (95% CI: 0.91–7.25%), 4.40% (95% CI: 0.95–7.97%), and 4.12% (95% CI: 0.38–8.01%) increase in the number of AR outpatients, respectively. When stratified by season, the strongest effect was shown in spring. Our results suggested that temperature variability was associated with increased initial outpatient visits for AR, which may provide helpful implications for formulating public health policies to reduce adverse health impacts of unstable temperature.
... To maintain a stable body temperature, heat loss is needed to balance the heat production. If the body temperature is unstable, then the body core temperatures will change accordingly [20]. So the clothing and textile materials require the best thermal insulation properties accordingly for the cold and hot climates. ...
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This study, mainly focused on the effect of core-sheath ratio, twist and stitch length on the thermal comfort properties of single jersey knitted fabrics produced from various ratios (100:0, 80:20 and 60:40) of cotton/ polyester core spun yarns. The Box-Behnken design tool was used to study core-sheath ratio, twist and stitch length on the thermal comfort properties of single jersey knitted fabrics and response surface equations were derived and design variables were optimized. From this study, the findings reveal that the decrease in cotton ratio among the fabrics made from core spun yarns decreases the fabric thickness and hence a more porous structure that results in higher thermal conductivity, air permeability, water-vapour transmission and less thermal resistance. It is also evidenced that, increase in the yarn twist (high) and the stitch length (tight) in the fabric structure makes thicker and less porous fabric which results in higher thermal resistance and lesser thermal conductivity, air permeability and water-vapour transmission. ARTICLE HISTORY
... Consequently, the speed, volume, and direction of airflow are also affected (Cauna 1982), as well as the efficiency of air conditioning processes (Churchill et al. 2004;Naftali et al. 2005;Zhao and Jiang 2014;Ma et al. 2018). Indeed, the nasal airway is the place where air conditioning takes place, which is necessary to optimize gas exchanges in the pulmonary alveoli and thus participate in global homeostatic thermoregulation (Havenith 2005;White 2006) while protecting the lungs from thermal damage, desiccation, and infection (Proetz 1951(Proetz , 1953Walker and Wells 1961;Cole 1982b;Proctor 1982;Keyhani et al. 1995;Williams 1998;Keck et al. 2000;Eccles 2002;Wolf et al. 2004;Yokley 2006;Doorly et al. 2008;Elad et al. 2008;Yokley 2009;Hildebrandt et al. 2013). A large mucosal surface and a narrow channel generally facilitate heat and moisture exchange (Schmidt-Nielsen et al. 1970;Collins et al. 1971;Hanna and Scherer 1986;Schroter and Watkins 1989;Lindemann et al. 2009). ...
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The development of the human craniofacial skeleton results from the complex interaction of genetic, physiological, biomechanical, and environmental influences. Among environmental influences, air temperature has been identified as a factor impacting craniofacial morphology, particularly the upper airway. According to whether they live in warm or cold environments, humans tend to display different morphological features in this anatomical region: in cold environments, the nasal cavity is, for example, reduced mediolaterally and increased anteroposteriorly and superoinferiorly. The purpose of this chapter is to provide an overview of the current knowledge of temperature-related morphological variation of nasal and paranasal structures and to explore the temperature-sensitive developmental pathways that might have a role in this variation. We begin with the knowledge that temperature both directly and indirectly affects bone formation. Directly, by altering the activity of preosteoblast cells, bone-forming osteoblasts, and bone-resorbing osteoclasts. Indirectly, by inducing proteins or hormones (e.g. heat shock proteins, clock genes, thyroid hormones, leptin) involved in the’ activity of bone cells. Here, we provide a review of the literature that could inspire novel approaches to improve our understanding of the role of these mechanisms in human evolution.
The thermo-physiological human simulator has been used in many regions for estimating thermal behavior of the locals. The applicability of the human simulator to populations from different regions is, however, questioned due to its lack of consideration for the ethnic diversities in thermoregulation. This study checked the potential of improving the applicability of the Newton human simulator, one of the most popular simulators, by correcting its local set point skin temperatures according to the target population (Chinese as an example). First, new set point skin temperatures were obtained by conducting tests with 101 Chinese under a thermal neutral condition. Then, simulator tests using the original and new set point skin temperatures were conducted separately for evaluating thermal responses of the Chinese under non-neutral conditions. The evaluated skin and core temperatures by the simulators were compared with those measured from the real human tests. It demonstrated that the evaluated skin temperatures are positively related with the set point skin temperatures of the simulator. Adjusting set point skin temperatures according to the Chinese improved the prediction performance of the local skin temperatures, with the root-mean-square-deviation being reduced for over 50% of the body segments. The proposed idea of correcting local set point skin temperatures would contribute to evaluating the thermal interaction between human body and its surroundings with a higher accuracy.
Os males associados aos extremos de calor são uma realidade, embora pouca importância seja dada ao assunto. Em parte, a falta de atenção é decorrente do desconhecimento. Outro motivo é a negligência do poder público, no que diz respeito à fiscalização, especialmente das condições laborais. Neste trabalho, os índices HUMIDEX e WBGT foram calculados para a Região Metropolitana de Sorocaba, interior paulista, com um conjunto de dados de 14 anos. Apesar de estar próximo ao leste paulista, Sorocaba não é influenciada pela brisa marítima, que poderia contribuir para amenizar o calor, pois o clima da região é caracterizado por temperaturas elevadas em vários meses do ano. A mensuração de índices bioclimáticos pode contribuir para as políticas de saúde pública de forma a reduzir a insalubridade de trabalhadores expostos ao calor excessivo e consequentemente promovendo melhora da qualidade de vida e até mesmo da produtividade, como indicam as pesquisas.
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Myocardial infarctions (MI) are a major cause of death worldwide, and temperature extremes, e.g., during heat waves and cold winters, may increase the risk of MI. The relationship between health impacts and climate is complex and is influenced by a multitude of climatic, environmental, socio-demographic, and behavioral factors. Here, we present a Machine Learning (ML) approach for predicting MI events based on multiple environmental and demographic variables. We derived data on MI events from the KORA MI registry dataset for Augsburg, Germany between 1998 and 2015. Multivariable predictors include weather and climate, air pollution (PM10, NO, NO2, SO2, and O3), surrounding vegetation, as well as demographic data. We tested the following ML regression algorithms: Decision Tree, Random Forest, Multi-layer Perceptron, Gradient Boosting and Ridge Regression. The models are able to predict the total annual number of MI reasonably well (adjusted R2 = 0.59 − 0.71). Inter-annual variations and long-term trends are captured. Across models the most important predictors are air pollution and daily temperatures. Variables not related to environmental conditions, such as demographics need to be considered as well. This ML approach provides a promising basis to model future MI under changing environmental conditions, as projected by scenarios for climate and other environmental changes.
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ABSTRACT Humans show a marked variation in their thermoregulatory behaviour. In this review, an attempt was made to determine in how far this variation is caused by differences in sex, age, anthropometric measures, hydration state and circadian rhythm and to which underlying parameters their effect can be ascribed. For the following factors (in approximate ranking order of significance), such parameters have been found: - State of acclimatization The state of acclimatization is defined by the sweat characteristics (high state of acclimatization implies high maximal sweat rate, high gain and/or low setpoint for sweat rate-Tcore relation. improved sweat distribution) and by the circulatory capacity (high state of acclimatization: more constant blood pressure and blood volume; lower heart frequency; high stroke volume). -Physical fitness The effect of physical fitness on thermoregulation is mainly determined by circulatory capacity. As this is also a parameter for the state of acclimatization, it is obvious that fitness and acclimatization are strongly related. - Hydration state The influence of the state of hydration on thermoregulatory function is determined by two parameters: 1 Plasma osmolality: the plasma osmolality affects either the thermoregulatory centres in the brain or directly the function of the sweat gland. These effects may be ion specific ( Na+ , Ca++). 2 Plasma volume: changes in plasma volume and consequently blood viscosity influence cardiac efficiency and through this the strain of the body during heat stress. - Anthropometric measures These will have a physical influence through: heat exchange surface area (body surface), insulation (fat) and weight load (inactive body mass). - Time of day The influence of the time of day on thermoregulation is determined by the related variations in sweat characteristics, skin blood flow and body temperature. In how far this also influences body heat strain and heat tolerance is yet unknown. The factors sex and age are supposed to be of little importance for the reactions to heat stress, as effects ascribed to these factors can be described by the above mentioned factors with their parameters. At the end of this report, the findings will be expressed in propositions for the determination of the selected factors and parameters.
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The ability to thermoregulate typically decreases with age. This is strongly related to decreases in physical fitness and increases in the incidence of disabilities with ageing. The reduced thermoregulatory capacity leads to increased mortality and morbidity. Heat stroke, hypothermia, increased number of falls, and in home drowning are some of the problems that are identified to be associated with this reduced thermoregulatory capacity. As solution, using advanced technology in terms of full climate control is suggested as a short-term solution for the ill or infirm only. For longer-term solutions, limited climate control (taking away peak loads), improved housing design and proper use of modern clothing are proposed to alleviate the problems. For the clothing, better education of the elderly in the possible advantages of high tech clothing materials is proposed, as well as education to their proper way of use. Manufacturers should consider adjusting their marketing policies to include the elderly in their targeted groups.
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The effects of morphological factors (body surface area (AD), body mass and surface to mass ratio (AD/M)) on exercise heat stress responses in a hot wet (HW) (35°C 80% rh) and hot dry (HD) climate (45°C, 20% rh) of equal WBGT (≃31.6°C) were studied in 30 and 25 subjects respectively. In both climates there were positive correlations of Tre with AD/M, negative with AD and mass, giving the bigger subjects an “advantage” that remained (AD/M) when data were corrected for differences in , which accounted for a substantial part of the variance in Tre. The observed AD/M effect contradicts earlier studies but is consistent with model calculations.
Individualized model of human thermoregulation for the simulation of heat stress response. J Appl Physiol 90: 1943-1954, 2001. - A population-based dynamic model of human thermoregulation was expanded with control equations incorporating the individual person's characteristics (body surface area, mass, fat%, maximal O2 uptake, acclimation). These affect both the passive (heat capacity, insulation) and active systems (sweating and skin blood flow function). Model parameters were estimated from literature data. Other data, collected for the study of individual differences {working at relative or absolute workloads in hot-dry [45°C, 20% relative humidity (rh)], warm-humid [35°C, 80% rh], and cool [21°C, 50% rh] environments}, were used for validation. The individualized model provides an improved prediction [mean core temperature error, -0.21 → -0.07°C (P < 0.001); mean squared error, 0.40 → 0.16°C, (P < 0.001)]. The magnitude of improvement varies substantially with the climate and work type. Relative to an empirical multiple-regression model derived from these specific data sets, the analytical simulation model has between 54 and 89% of its predictive power, except for the cool climate, in which this ratio is zero. In conclusion, individualization of the model allows improved prediction of heat strain, although a substantial error remains.
1. 1. The ability to increase skin blood flow is an important mechanism for transferring heat from the body core to the skin for dissipation. 2. 2. During exercise, skin blood flow is typically 20-40% lower in men and women aged 55 and over (compared with 20-30 years old) at a given body core temperature. Yet criterion measures of heat tolerance (changes in core temperature, heat storage) often show minimal or no age-related alterations. From a series of studies conducted in our laboratory over the past 5 years, the following conclusions can be drawn. 3. 3. When fit healthy older subjects are matched with younger subjects of the same gender, size and body composition, VO2max, acclimation state, and hydration level, age-related differences in skin blood flow are evident. However, these differences often do not translate into "poorer" heat tolerance or higher core temperatures. 4. 4. The larger core-to-skin thermal gradient maintained by the older individuals allows for effective heat transfer at lower skin blood flows. 5. 5. Furthermore, there is an increased coefficient of variation for thermoregulatory response variables with increasing age. 6. 6. Despite differences in the mechanisms underlying thermoregulation, true thermal tolerance is less a function of chronological age than of functional capacity and physiological health status. 7. 7. While this conclusion is based primarily on cross-sectional studies, it is supported by the results of more recent studies using multiple regression analyses. 8. 8. Implicit in this conclusion is the notion that thermal tolerance, at any age, is a modifiable individual characteristic.
Cross-section comparisons of the effect of age on physiological responses to heat stress have yielded conflicting results, in part because of the inability to separate chronological age from factors which change in concert with the biological aging process. The present study was designed to examine the relative influence of age on cardiovascular and thermoregulatory responses to low intensity cycle exercise (60 W for 1 h) in a warm humid environment (35°C, 80% relative humidity). Specifically, the relative importance of age compared to other individual characteristics [maximal oxygen uptake (V̇O(2max)), physical activity level, anthropometry, and adiposity] was determined by multiple regression analysis in a heterogeneous sample of 56 subjects in which age (20-73 years) and V̇O(2max) (1.86-4.44 l·min-1) were not interrelated. Dependent variables (with ranges) included final values of thermoregulatory responses [rectal temperature (T(re), 37.8-39.2°C), calculated heat storage (S, 3.4-8.1 J·g-1), sweat loss (238-847 g·m-2)] and cardiovascular responses [heart rate (HR, 94-176 beats·min-1), forearm blood flow (FBF, 5.3-31.3 ml·100 ml-1·min-1), mean arterial blood pressure (MAP, 68-122 mmHg), and forearm vascular conductance (FVC = FBF·MAP-1, 0.06-0.44 ml·100 ml-1·min-1·mmHg-1). Age had no significant influence on T(re), S, or sweat loss, all of which were closely related to V̇O(2max). On the other hand, HR, MAP, FBF, and FVC were related to both age and V̇O(2max). Anthropometric variables and adiposity had secondary, but statistically significant, effects on MAP, FBF, FVC, and sweat loss. With respect to exercise in a warm humid environment, it was concluded that the effect of age on body temperature and sweating was negligible compared to effects related to V̇O(2max), but that chronological age had an independent effect on cardiovascular effector responses.