Heat Strain, Hydration Status, and Symptoms of Heat llness in

Surface Mine Workers, Andre Hunt, Queensland University of

Technology, 2011
Instead, the body responds by initiating sweating and increasing skin blood flow to facilitate heat loss.
Greater skin blood flow allows a faster rate of heat transfer from the core to the skin by convection. Secondly, the increased
skin perfusion raises skin temperature, which increases the gradient between the skin and ambient temperature, facilitating
heat loss by convection and radiation. In addition, increased skin temperature raises the skin water vapour pressure
relative to the ambient water vapour pressure, thus increasing the gradient for evaporative heat loss. With increased heat
loss, a new balance is attained to match heat gain, so that core temperature stabilizes at a higher level.
The magnitude of the increase in core body temperature is dependent on both the intensity of work and the
surrounding climate. In a cool climate exercise on a bicycle ergometer at 25, 50, and 70 % of maximal aerobic capacity
showed that core body temperature stabilised at higher levels corresponding to higher work rates. Exercising at a set
intensity in climates ranging between 13.3 26.5 C Corrected Effective Temperature (CET - a heat stress index
incorporating measures of wet-bulb temperature, globe temperature, and air velocity) resulted in a similar steady state core
body temperature after 30 40 minutes of treadmill walking (Lind, 1963). However, when performing the same intensity of
exercise in 29.5 31.5 C CET (increased climatic heat stress) core body temperature took longer to stabilise and did so at
progressively higher temperatures. This core body temperature response to variations in climate has also been observed
during coal mining activities (shovelling) (Lind, Humphreys, Collins, Foster, & Sweetland, 1970). Overall, research shows
that the core body temperature response to exercise heat stress is determined firstly by exercise intensity, and secondly by
climatic heat stress above a certain level. Interestingly, the climatic heat stress level, beyond which core body temperature
stabilises at a raised level, decreases when exercise intensity is increased.
Evaporation of sweat is the primary method for heat loss in hot environments and during physical activity.
Eccrine sweat glands are located in the dermis of the skin and can be found all over the body. The density of these glands
is greatest on the forehead, followed by the upper limbs, the trunk and lower limbs. The sweat secreted from these glands
predominantly consists of water, but small amounts of sodium chloride, urea, lactic acid, and potassium chloride can also
be found (Brooks et al., 2000).
As core body temperature increases during exercise, a temperature is reached at which sweating is
initiated. This is termed the threshold for the sweating response and has been found to occur at ~ 37.3 C (Buono &
Maupin, 2003; Shibasaki, Wilson, & Crandall, 2006). Variations in skin temperature can adjust the threshold core body
temperature to initiate sweating, such that higher skin temperatures lower the sweating threshold . After commencing,
sweat rate will increase linearly with increases in corebody temperature (Buono & Maupin, 2003; Nadel et al., 1971b). The
slope of this linear increase is termed the sensitivity of the sweating response.Sweat rates commonly range between 0.5
2.0 L/h during a variety of sports activities (Sawka et al., 2007). With each litre of sweat evaporated approximately 580 Kcal
of heat energy is removed from the body. The initial increase in sweat rate is due to both an increase in the number of
active sweat glands and increased output from sweat glands. As exercise continues, the number of active glands plateaus,
whilst sweat gland output continues to rise (Kondo et al., 2001).
This relationship is also seen at other body sites, including the forehead, chest, back, and thigh, however,
the contribution to sweat rate from the number of active glands and sweat output differs slightly between sites. The skin
blood flow response to exercise is also important for thermoregulation. At the onset of dynamic exercise, there is an initial
increase in cutaneous vasoconstriction which reduces skin blood flow in favour of diverting oxygenated blood to the
working muscles . As exercise continues, core body temperature rises and a threshold temperature to initiate vasodilation
of skin vasculature is attained, allowing increased skin blood flow. Skin blood flow will then continue to rise with core body
temperature until approximately 38 C, where a plateau is attained.
The threshold core temperature for vasodilation is influenced by skin temperature and exercise compared to
rest. If mean skin temperature is increased (in a hot environment or during exercise) the core body temperature at which
vasodilation is initiated will decrease, promoting skin blood flow for heat transfer. The opposite is the case in a cold
environment, where the core temperature threshold is raised to conserve body heat. The temperature threshold for
vasodilation has also been found to shift upward during exercise compared to rest in a hot environment. This results in a
lower skin blood flow, for a given core body temperature, during exercise compared to rest. For blood to be directed
towards the skin vasculature for cooling purposes indicates that a redistribution of blood is required.
The redistribution of blood during exercise heat stress raises cardiovascular strain.With all exercise there is
an increased demand for oxygen delivery to the working muscles. In the heat, an additional demand for increased blood
flow to the skin arises. These competing demands raise the cardiovascular strain experienced. Rowell and colleagues

(1966) monitored several variables when walking for 15 minutes, at four different intensities, in both temperate (25.6 C dry
bulb and 16.8 C wet bulb) and heat stress (43.3 C dry bulb and 28.3 C wet bulb) conditions. The rate of oxygen
consumption was similar between climate conditions and increased with exercise intensity. Heart rate was elevated, and
stroke volume and central blood volume were reduced under heat stress for all intensities of exercise. Cardiac output was
lower for all intensities of exercise under heat stress; however it was only significantly lower statistically for the two highest
intensities. It was concluded that stroke volume and central blood volume are reduced due to a redistribution of blood to
the periphery (skin blood flow for heat transfer). In order to maintain sufficient blood flow to the muscles, heart rate is
elevated. Instead of increasing cardiac output during exercise heat stress, its distribution is altered to accommodate the
competing demands

Hydration Status
Water is a requirement for the human body to function effectively. Total body water accounts for
approximately 60 % of the bodys mass (Armstrong, 2005; Parsons, 2003), and can be separated into two compartments.
Intracellular water is found within the cells of the body and accounts for ~ 67 % of total body water. The remainder is found
in the extracellular compartment, comprised of water in blood plasma (~ 8 %) and that located between the cell
membranes and blood vessels (~ 25 %). Body water is continually being lost from the body through sweating, urination,
faeces, and respiration. To compensate for this continual loss, water must be ingested regularly through food and fluid
intake. In addition, the endocrine system helps to maintain water balance (Marieb, 2001). With body water loss there is a
reduction in plasma volume and an increase in plasma osmolality. Osmoreceptors detect this alteration and alert the
hypothalamus, which stimulates the posterior pituitary gland to release anti-diuretic hormone (ADH).
The result is an increase in water re-absorption from the kidneys, and the sensation of thirst to increase
water ingestion, both of which help to return plasma volume and osmolality to normal levels. The term euhydration is used
to describe the normal body water content. If water loss is insufficiently replaced, dehydration (or hypohydration) occurs,
where body water is reduced below the normal range. Such is commonly the case during exercise heat stress when large
amounts of body water are lost through sweating. Sweat rates range between 0.5 2.0 L/hr for a variety of sports settings
(Sawka et al., 2007) and similar values have been estimated in occupational settings (Brake & Bates, 2003; Kalkowsky &
Kampmann, 2006), with higher sweat rates when wearing protective clothing that dramatically limits evaporative heat loss
(Kenefick & Sawka, 2007).
Dehydration has significant consequences for the level of heat strain experienced by individuals performing
work in the heat. Exercise in the heat consistently results in higher core body temperatures when dehydrated compared to
when euhydrated. This was observed when comparing the core temperature response to exercise between commencing in
a euhydrated or dehydrated state and comparing progressive dehydration during exercise (due to insufficient fluid
replacement) with maintaining adequate hydration (through sufficient replacement of lost fluid. The rise in core body
temperature increases with the extent of dehydration. Sawka and colleagues (1985) reported core temperature to
increase 0.15 C for each 1 % decrease in body mass(due to sweat loss). This value is quite conservative compared to
other research which found core temperature to increase by 0.4 C for each 1 % decrease in body mass (Armstrong et
al., 1997b). Differences between these studies, and others, are likely the result of differing exercise intensities, climatic
conditions, and fluid replacement procedures. However, all reports show an increase in core temperature with dehydration,
and a recent review has suggested that core temperature increases between 0.10.25 C for each 1 % decrease in
body mass (Sawka, Montain, & Latzka, 2001). Since these studies required subjects to maintain a set exercise intensity
between trials of differing hydration status or fluid replacement, heat production must have remained the same, as shown
by Armstrong et al (1997b). As such, increased core body temperature when dehydrated must be the result of reduced
heat loss. Dehydration reduces both the sweating and skin blood flow responses to exercise heat stress. Mean body sweat
rate is commonly found to decrease with body mass loss. Sawka and colleagues (1985) proposed the magnitude of this
decline to be 29 g/m2/h for each 1 % decline in body mass.
Dehydration also affects the threshold and sensitivity of the sweating response. The threshold core body
temperature at which sweating is initiated is raised when dehydrated, allowing higher body temperatures before sweating
commences. The sensitivity of the sweating response is reduced when dehydrated during exercise heat stress with
insufficient fluid replacement, resulting in a smaller increase in sweat rate for a given increase in core temperature.
Dehydration also affects blood flow to the skin. Forearm and cutaneous blood flow are lower during exercise in the heat
when dehydrated .This is the result of increased cardiovascular strain. Gonzalez-Alonso and colleagues (1995; 1997)
report lower stroke volume during exercise in the heat when dehydrated. In turn, heart rate is increased in an attempt to
maintain cardiac output, however cardiac output tends to decline with dehydration. In order to maintain mean arterial
pressure, vascular resistance is increased which restricts blood flow through the skin vasculature and impairs heat transfer
to the skin. Other research has also reported an increased threshold and decreased sensitivity of the forearm blood flow
response to exercise heat stress when dehydrated (Fujii et al., 2008).

Overall, dehydration results in a reduced capacity for heat dissipation through sweating and skin blood flow,
resulting in higher thermoregulatory strain during exercise.To avoid the deleterious effects of dehydration, it is
recommended that persons exercising in the heat aim to replace all sweat losses, or at least sufficient amounts to restrict
body mass loss to less than 2 % (Sawka et al., 2007). However, when the individual is allowed to consume fluid ad libatum,
it is common to observe only a 60 -70 % replacement rate. This phenomenon whereby individuals lose body mass during
exercise heat stress due to a lack of fluid consumption (when it is readily available) is termed voluntary dehydration (Adolf
1947 cited in). It has been attributed to the finding that thirst is not stimulated until a 2 % loss in body mass has been
incurred (Pitts, Johnson, & Consolazio, 1944). In support of this assertion, research where participants have commenced
exercise in a dehydrated state (34 % body massloss) has shown voluntary fluid consumption to be able to maintain this
level of hydration, or slightly improve it, compared to those who commenced euhydrated (Armstrong et al., 1997b; Maresh
et al., 2004).
Alternatively, some research has sought to determine the effects of hyper-hydration (greater than normal
body water content) on heat strain during exercise. Following two hours of treadmill exercise in the heat, core body
temperature, skin temperature, and whole body sweat rate did not differ between euhydration and hyper hydration trials. It
was concluded that hyper-hydration confers no thermoregulatory advantage over euhydration.

Age
Much of the research into the effects of aging onheat tolerance has been cross-sectional, comparing groups
of differing ages for their skin blood flow and sweating responses to heat stress. Skin blood flow in response to a relative
exercise intensity is lower in individuals over 55 years of age compared to those less than 30 years . Similar findings have
been found between these age groups when exposed to passive heat stress. Although earlier research suggested older
(~47 years) individuals had higher skin blood flow responses to an absolute intensity of exercise , these studies may not
have adequately controlled for individual differences, such as fitness, as evidenced by higher core temperatures in the
older subjects during this exercise. There are three possible explanations for an attenuation in the skin blood flow response
to heat stress including 1) a higher vasoconstrictor tone, 2) a lower sensitivity of active vasodilation, and 3) a reduced
response from the effector organs .
Comparing age groups of those < 30 and >60 years during cycling exercise at 50 60% VO 2max , a
pharmacological block to vasoconstrictor activity in one forearm did not result in a higher skin blood flow for a given core
temperature. These findings indicate that a higher vasoconstrictor activity during exercise heat stress for older individuals is
not responsible for the lower skin blood flow response. The majority of research supports the later two reasons (reduced
vasodilation sensitivity or effector organ response) for a reduced skin blood flow response in older individuals. The skin
blood flow response for a given core temperature (sensitivity of the response) is reduced in older subjects . Further
research has aimed to elucidate the reason for a reduced sensitivity of active vasodilation in older individuals. The
neurotransmitter responsible for the active vasodilation remains unknown; however, research has shown that nitric oxide
plays a contributing role to the active vasodilation seen during body heating . The inhibition of nitric oxide synthesis causes
a much greater reduction in the vasodilatory response to passive body heating in older men than young men, suggesting
that nitric oxide mediation of active vasodilation contributes more to the vasodilatory response of older individuals
(Holowatz et al., 2003).
This greater reliance on nitric oxide mediated mechanisms contributes to the lower blood flow response in
older individuals as nitric oxide synthesis is decreased with aging. An alteration to the effector organ response to heat
stress is another contributor to lower skin blood flow responses in older individuals. Maximal forearm vascular conductance
(FVC) has been found to progressively decrease with age, such that those over 55 years have significantly lower maximal
FVC compared to those less than 30 years . Maximal cutaneous vascular conductance is also lower in aged skin. Such
findings are thought to be due to changes in the structure of the vasculature including a breakdown of vessels in the
microcirculation, and a decrease in the number of capillary loops. Anotheraspect of effector organ responses is that of the
splanchnic and renal blood flows. With age there is a decrease in the magnitude of vasoconstriction to these organs during
exercise heat stress . As a consequence less blood is redirected to the skin from these regions compared to that seen in
younger
subjects.
The sweating response to exercise heat stress also differs between age groups. Older subjects (>52 years)
show lower sweating responses during exercise heat stress compared to young subjects (<30 years) for a given relative
intensity and absolute intensity . Passive heat exposure also produces lower sweating rates in older individuals , but not
always . This difference may be due to the level of heat stress subjects were exposed too.Finally, pharmacological
stimulation also produces lower sweating responses in the aged .The number of heat activated sweat glands remains
similar between age groups but the sweat gland output decreases with advancing age . This finding is thought to be due to
a decrease response to thermal stimuli or a reduced function of the sweat gland.

When comparing age groups, it is important to take differences in aerobic fitness and body composition into
account. With advancing age aerobic fitness decreases approximately 10% for every decade. Early research indicated a
lower heat tolerance (higher core and skin temperatures) of older males (~47 years) during exercise heat stress for a given
absolute intensity of work . However, these studies do not report controlling for fitness and body composition between the
age groups. More recent research, matching differing age groups for these variables, revealed similar core body
temperature responses to exercise heat stress between age groups (< 30 and > 55 years). Some evidence suggests a
higher core temperature in older women, or greater change in core temperature during exercise . Skin temperature is also
similar for older individuals compared to younger. Thus when age groups are matched for fitness and body characteristics,
tolerance to heat stress appears to be similar. Interestingly, in an aerobic training program, subjects aged over 61 year s
were able to improve their skin blood flow and sweating responses to exercise heat stress), by lowering the core
temperature threshold for their initiation.
This finding further supports the assertion that reduced tolerance to heat stress in older individuals is more
aligned with fitness and body composition changes associated with aging rather than aging per se. Two final points to
consider in relation to the effects of age on heat strain include an altered thirst mechanism and psychological effects when
working with younger individuals. It has been concluded that older individuals have a reduced thirst response.This
indicates that older individuals are less likely to voluntarily replace fluid losses during exercise heat stress, and predisposes
them to raised heat strain, through dehydration. Secondly, in a military environment, it has been observed that older
individuals may feel the need to prove themselvesto younger troops and may work at a higher relative intensity as a
result, raising their heat strain levels (Goldman, 2001)

Gender
Heat strain can differ between men and women exposed to the same level of heat stress. It is not due to
gender per se, but is more closely related to differences in aerobic fitness and body characteristics. Women tend to have a
lower aerobic capacity compared to men, as well as a higher body fat content, lower total body mass, and lower surface
area. As discussed above, these factors are associated with lower tolerance and greater strain during heat stress.
However, when men and women who are similar for all of these characteristics are compared, little difference in
physiological strain is observed .
Even though men and women can be equally as tolerant to heat stress, some differences in
thermoregulation do exist. In terms of the capacity of the sweating response to heat stress, women appear to have a
greater density of active sweat glands. However, there is a smaller output per sweat gland than compared to men (Buono
& Sjoholm, 1988; Inoue et al., 2005). Even though sweat output tends to be less for women, a greater efficiency of
evaporation allows them to maintain similar core body temperatures as men (Kaciuba-Uscilko & Grucza, 2001).
The majority of research into physiological responses to heat stress primarily focuses on males. This is
because the hormonal state of males is constant compared to that of women, which varies with the menstrual cycle. The
follicular phase of the menstrual cycle involves an elevation in estrogen concentration whilst the luteal phase involves a rise
in progesterone concentration. Core body temperature and the temperature for the onset of sweating and cutaneous
vasodilation are similar between men and women in the follicular phase. However, during the luteal phase core body
temperature is raised and the thresholds for vasodilation and sweating are higher (Inoue et al., 2005). In spite of these
fluctuations in core temperature and thermoregulatory responses with changes in menstrual cycle, their effect on heat
tolerance in working situations appears to be minimal