Thermoregulation and Exercise: A Review
The concept of thermoregulation and the idea that the body controls and regulates body temperatures through different mechanisms has been discussed since the early work of Liebermeister in 1875 (Werner, 1979). Back in 1875, Liebermeister suggested that fever resulted from an imbalance between heat production and heat loss, which was ultimately controlled by brain centers (Werner, 1979). This early interest toward understanding the body’s ability to thermoregulate was greatly helped by the development of the mercury thermometer which enabled scientists to perform quantitative studies on thermoregulation (Cooper, 2002). The increase use of thermometers in clinical situations arose from a publication titled Manual of Medical Thermometry in 1871 by Wunderlich (Cooper, 2002). This publication aimed in defining the character of temperature changes associated with specific diseases and situations. Wunderlich described the body temperature ranges of mammals, birds, reptiles, insects and the effect of exercise on the body’s temperature (Cooper, 2002). The thermometer lead to the development of calorimetric techniques, allowing Lefevres to determine metabolic rates of human and animals (Werner, 1979) and Benzinger to investigate the central control of core temperatures (Benzinger, 1959). Today, thanks to analytical technology, neurophysiological and physiochemical techniques, we have a better understanding of the many mechanisms behind thermoregulation at both the whole human level and molecular level (Cooper, 2002). Knowledge about this topic has progressed from the rudimentary localisation of areas within the central nervous system involved in thermoregulation to a more complete, yet not totally complete, mapping of the neural circuitry involved in receiving and processing thermal inputs (Cooper, 2002). The regulatory aspect of thermoregulation was initially explored by Libermeister (Cooper, 2002), as mentioned earlier, but it was Ranson and Magoun that first located thermoregulatory structures within the hypothalamus using local heating and lesioning methods (Ranson and Magoun, 1939). The observations of hypothalamic tissue slices has shed light on the complex circuitry existing within the hypothalamus (Boulant, 1996) but the molecular mechanisms of transduction of temperature sensing into neural firing patterns leading to the initiation of vascular smooth muscle response and tissue heat production has not yet been fully understood (Cooper, 2002). Today, it is accepted that the body temperature is controlled around a predetermined physiological set-point but the mechanism by which this set-point is determined remains a mystery (Cooper, 2002)
Considering the fact that the central nervous system and many enzymes and bodily processes rely on an ideal body temperature to perform at full potential, it is of no surprise that the human thermoregulatory system has developed behavioural, autonomic and endocrine responses to maintain thermal homeostasis (Flouris, 2010). In a situation of exercise, due to the inefficiency of metabolic transfer, more than 75% of the generated energy through substrate oxidation taking place in skeletal muscle is liberated as heat (Wendt et al., 2007). In order to maintain thermal homeostasis of the body, physiological heat loss mechanisms must be activated to prevent an excessive and dangerous rise of body core temperatures (Wendt et al., 2007). The inability to dissipate this production of heat from the body into the environment can lead to serious performance decrements and increases the risks of developing heat illnesses (Wendt et al., 2007). The following review of the literature will examine the different physiologic responses that occur during exercise geared toward maintaining thermal homeostasis, the different factors influencing thermoregulation, the consequence of ineffective thermoregulation and the strategies for optimizing efficient thermoregulation.
Physiology of temperature regulation
When understanding that the integrity of the human body depends on the maintenance of the internal environment at a constant temperature, it is no surprise that the body has equipped itself with very efficient thermoregulatory mechanisms (Egan et al., 2004). The central nervous system integrates diverse neural inputs, such as afferent information about the skin and core temperatures, and initiates pathways responsible for generating heat, dissipating heat, and controlling the thermal exchange with the environment (Egan et al., 2004). More precisely, the hypothalamus and preoptic area of the hypothalamus play a crucial role in integrating and initiating autonomic thermoregulatory mechanisms such as sweating, skin vasomotor response and shivering (Zhang et al., 1997). It was the classic study by Magoun and al. conducted in 1938 that precisely defined the thermosensitive area’s of the hypothalamus (Boulant, 2000, Magoun et al., 1938) and paved the way for future research of thermoregulation and the role played by the hypothalamus.
Fundamental to the capacity of any organism to maintain thermal homeostasis is the ability to sense the temperature of its body components and its environment (Cooper, 2002). The ability to sense temperature has developed very early in evolution and both unicellular and multicellular organisms, such as humans, rely on various ion channels that respond to both heating and cooling (Cooper, 2002). These ion channels form the basis of thermosensitivity. These specialized ion channels can be found in keratinocytes, the predominant (95%) cell type of the epidermis located on the outermost layer of human skin, neurons of the hypothalamus and brain stem, and in the spinal cord (Yang et al., 2010, Cooper, 2002). Known as temperature-sensitive transient receptor potential channels or thermoTRPs, the channels convert thermal energy into protein conformational changes which leads to a channel opening (Yang et al., 2010) resulting in the generation of an action potential, the alteration of the neuron’s pattern of spike discharge (Hensel, 1981) or the release of messenger molecules that encode temperature information (Yang et al., 2010). Temperature-sensitive transient receptor potential channels are part of a larger group of channels, transient receptor potential channels, which serve many diverse functions throughout the body (Clapham, 2003). Among thermal sensing, this family of channels respond to touch, pain, osmolarity, pheromones, and taste (Clapham, 2003). ThermoTRPs include four heat activated channels, TRPV 1 to 4, and two cold-activated channels, TRPM8 and TRPA1 (Yang et al., 2010). These 6 types of ion channels share the responsibility of responding and activating to a certain physiological range of temperatures (Clapham, 2003). TRPV1 is a CA2+ permeable channel that activates in response to temperatures over 43 Celsius (Clapham, 2003). Almost identical to the TRPV1, TRPV2 is responsible for mediating high-threshold (over 52 Celsius) noxious heat sensation (Clapham, 2003). Highly expressed in skin, tongue and the nervous system, the TRPV3 channel activates from temperatures over 31 Celsius (Smith, 2002) while TRPV4 activates when temperature exceed 25 Celsius (Guler et al., 2002). As of the cold sensing TRPs, TRPM8 is a non selective channel that is activated by cold (8-28 celcius) and has enhanced activation when subject to cooling compounds such as menthol and icilin (Clapham, 2003). While the function and characteristic of the different channels mentioned above are well know, less is known about TRPA1 except that it is potentiated by cold temperatures (Clapham, 2003). These 6 types of ion channels form the basis of our thermal sensing and all posse 4 characteristics that must be present in order to be considered a temperature receptor (Hensel, 1970). These four characteristics consist of demonstrating a static sensitivity to a constant temperature, show a dynamic response to a change in temperature, show no excitation to mechanical stimuli and lastly, show activity within the range of non painful temperatures (Hensel, 1970). From these four characteristic, we see that TRPV2 is at the limit of these characteristic considering the fact that it is stimulated by high-threshold (over 52 Celsius) noxious heat sensations (Clapham, 2003).
Thanks to these channels, neurons from the preoptic and anterior nuclei of the hypothalamus are able to monitor the blood flowing to the brain and detect changes in core temperatures (Cooper, 2002). Heat sensitive neurons represent about 20% to 30% of preoptic and anterior nuclei neurons, while cold sensitive neurons represent 5% to 10% and thermally insensitive neurons form 70% to 80% of the neurons found in that region of the brain (Hori, 1991). Thermosensitive neurons react to change in temperature by changing their rate of neural firing, which is translated by the hypothalamus as information about thermal change (Boulant, 2000). The understanding that these thermosensitive neurons play a central role in thermoregulation is based on the correlation existing between the activity of these thermosensitive neurons and the ensuing thermoregulatory responses (Hori, 1991). In a similar experiment than the one conducted in 1938 by Magoun and al., it was shown that localized warming of thermosensitive neurons found in the hypothalamus and spinal cord resulted in heat-defence responses (sweating, cutaneous vasodilatation and cooling behaviours) while local cooling of these neurons resulted in cold defense responses (shivering thermogenesis, non-shivering thermogenesis and heating behaviours) (Boulant, 1980, Magoun et al., 1938). It is also thanks to these channels that afferent thermal information coming from the skin, the spinal cord, the abdominal viscera and the greater veins can be sent to the thermoregulatory centers of the brain (Wendt et al., 2007). The neural pathway of skin thermoreceptors start from the thermosensitive fibers ascending from the skin and reaching the spinal cord via the dorsal root ganglion and terminates in the lamina of the dorsal horn (Schwark et al., 1997). From there, the afferent fibers are projected via the contralateral anterolateral spinothalamic tract and make their way to the thalamic relay nuclei and terminate in the hypothalamus where thermal information is managed (Schwark et al., 1997).
Role of the Hypothalamus
The hypothalamus, located below the thalamus and above the brainstem, is an indispensable portion of the brain possessing many functions. Although being the size of an almond, the hypothalamus is in charge many metabolic processes and an integral part of the autonomic nervous system controlling hunger, thirst, sleep, fatigue and as mentioned in earlier sections, body temperature (Cooper, 2002). Thermoregulation is controlled by the hypothalamus by coordinating and integrating afferent information from all over the body and directing efferent signals to the appropriate heat production or heat generating mechanisms of the human body (Cooper, 2002). Evidence that this portion of the brain is responsible for thermal homeostasis of the body comes from the pathological thermoregulatory responses witnessed in hypothalamic damaged patients (Bligh, 1973) and hypothalamic diseases (Fox et al., 1970). The control of body temperature is most probably a hierarchy of neural structures that includes the brainstem and the spinal cord, with the preoptic area of the hypothalamus acting as the highest coordinator (Boulant, 1996).
The thermoregulatory responsibility of this almond sized portion of the brain is achieved by comparing and integrating the central thermal information, provided by the neurosensitive neurons, and the peripheral temperature information provided by receptors found in the skin, within veins and the abdominal viscera (Wendt et al., 2007). The integration of this thermal afferent information coming from various sources enables the hypothalamus to initiate the appropriate thermoregulatory responses to any type of thermal stress (Boulant, 1996). Therefore, thermoregulation works as a classical negative feedback loop. The critical threshold at which thermoregulatory responses may be initiated is roughly 37 Celsius (98.6 Fahrenheit) in humans and all thermoregulatory mechanisms aim in bringing back the body’s temperature to this homeostatic set-point (Bezinger, 1969). This notion of a natural set point was investigated as early as the 1870’s by scientists such Currie, Liebermeister and Lefevre, but the advantage and the reason for this human set-point of 37 Celsius is still unknown today (Cooper, 2002).
Evidence pertaining to the neurotransmitters used in hypothalamic synapses was first found in the 1960’s and further research identified that cathecolamines, seretonine, dopamine, GABA, glutamate and acetylcholine were all used as thermoregulatory neurotransmitters (Bligh, 1973). More recent studies point to NO as an important neurotransmitter implicated in both the central nervous system thermoregulatory regions and in the adjustment of peripheral vascular tone involved in regulating temperature (Gerstberger, 1999). The exact chain of event surrounding the release of these neurotransmitters within the synapses and the individual role of these molecules is still under investigation (Cooper, 2002).
Cutaneous blood flow
Change in cutaneous blood flow is one of the main thermoregulatory mechanisms used by the body when attempting to restore thermal homeostasis (Charkoudian, 2003). Increase in skin blood flow increases radiation heat loss when the body faces excessive heat, such as in an exercise scenario, while decreased blood flow prevents heats of being dissipated during cold exposure (Charkoudian, 2010). Therefore, change in skin blood flow is a mechanism used in both heat stress and cold stress states.
As mentioned earlier, the inefficiency of mitochondria to oxidise substrates within skeletal muscle results in large production of thermal energy (Wendt et al., 2007). During exercise, heat production increases several fold as a result of the increased energy demand by muscle. This increased production of thermal energy results in an accumulation of heat within the body which poses a serious heat stress to many systems, disturbing homeostasis. In none-exercising or thermoneutral conditions, skin blood flow is around 250 mL/min which results in the dissipation of approximately 90 kcal/hour (Charkoudian, 2003). This amount of heat dissipation corresponds to the approximate amount of heat produced by the resting metabolic rate, thereby resulting in no net gain of body temperature (Charkoudian, 2003). As a result increased core temperatures triggered by exercise, cutaneous blood flow increases dramatically and can reach an impressive flow of 8L/min, which represents 60% of cardiac output (Charkoudian, 2010). This astonishing increase of flow is necessary to allow improved convective heat transfer from the body core to the surface of the skin, resulting in heat dissipation by radiation into the environment (Charkoudian, 2010). This type of heat dissipation, radiating from the skin, can be analogue to a radiator dissipating heat as a result of hot water flowing through the coils.
The increased blood flow through the capillary system found within the skin can be measured using laser Doppler flowmetry, a technology based on the Doppler Effect (Johnson et al., 1984). Such a technique allows measurement to be recorded continuously, allowing great understanding of the variation of blood flow occurring during different situations, such as during an exercise bout (Charkoudian, 2003). The observed thermoregulatory response of skin in mainly due to a neural reflex of the sympathetic vasodilatator nerves found within skin (Charkoudian, 2003). Indeed, 80% to 90% of the increase blood flow in skin during hyperthermia is mediated by the sympathetic vasodilatator nerves in a skin (Rowell, 1983), which is one of the two division of the autonomic nervous system controlled by the hypothalamus. These nerves are not tonically active during ambient temperatures, becoming active only in response to an increase of internal temperatures. This contrasts with the other types of nerve found in skin, sympathetic vasoconstrictor nerves, which are tonically active during normothermic situations and become inactive during hyperthermic situations, contributing to the remaining 10% to 20% of the cutaneous vasodilatation seen in hyperthermia (Pergola et al., 1994). Older and more recent attempts have been made in order to identify the specific molecules responsible for the active vasodilatation in skin, triggered by the activation of the sympathetic vasodilatator nerves (Rowell, 1983), and results point out to many possible contributors which many are present in the vasodilatation mechanisms observed in skeletal muscle during exercise (Charkoudian, 2010). It was shown that nitric oxide (NO), a potent vasodilatator, constitutes a significant contributor of the active vasodilatation observed in skin (Charkoudian, 2010). Although variable among individuals, NO contributes on average for 30% of the active vasodilatation during hyperthermia (Kellogg et al., 1998). Another possible contributor to the active vasodilatation during heperthermic situations is substance P (Wong and Minson, 2006). Substance P, which binds to NK-1 receptors, has been localized in human skin and may be an important player in the active vasodilatation occurring during hyperthermia. When NK-1 receptor have been desensitised to substance P, via prior administration of that substance, the desensitized sites show a decrease of roughly 35% in vasodilatation. Such evidence strongly suggests that substance P plays a role in active cutaneous vasodilatation (Wong and Minson, 2006). Additional skin vasodilatators that have been identified during human active skin vasodilatation include histamine (Wong et al., 2004) and vasodilatator prostanoids (McCord et al., 2006). However, even if the sympathetic vasodilatator nerves in a skin are responsible for most of the cutaneous vasodilatation during a hyperthermic period, a local thermal control of skin blood flow exists and constitutes the initial response to local warming of the skin (Charkoudian, 2003). The initial rapid vasodilation during local warming of the skin predominantly relies on local activity of sensory nerves. This neural local mechanism is initiated by C-fibers afferents that when stimulated, causes local vasodilatation via release of calcitonin gene–related peptide (CGRP), substance P, and neurokinin A (Holzer, 1998).
This thermoregulatory response to hyperthermia is therefore initially triggered by local factors and followed by a reflex of the sympathetic nervous system. This increased blood flow to skin as a mechanism to restore thermal homeostasis has been shown to be very effective, but as discussed above, work still has to be done in order to unveil the exact and complex mechanism of control of skin blood flow during body hyperthermia (Charkoudian, 2010).
The dissipation of heat through the use of sweat constitutes the second important thermoregulatory mechanism that we possess. The autonomic response of sweat production in hyperthermic situations was first described in ancient Greece, where Aristotle described perspiration in human as:
‘’ The blood vessels get progressively smaller as they go on until their channel is too small for the blood to pass through. But although the blood cannot get through them, the residue of the fluid moisture, which we call sweat can do so, and this happens when the body is thoroughly heated and the blood vessels are open widely at their mouth.’’ (Shibasaki, 2006).
This understanding of sweat by Aristotle is erroneous, but the concept that this phenomenon occurs in situations of heat was correct. The basic description of human sweat glands in the 1600’s and the full acceptance by the scientific world of the existence of these glands in the 1800’s lead to a more complete understanding of this vital thermoregulatory mechanism (Shibasaki, 2006). The basic idea of sweat production relies in the heat dissipation that occurs when the sweat accumulated on skin is evaporated. This evaporation of this sweat on skin dissipates heat, and cools the body (Shibasaki, 2006). The heat dissipiating capacities of evaporation of sweat on skin proves to be very efficient as for every 1ml of evaporated sweat, 0.6kcal of heat is removed (Snellen et al., 1970)
Sweat glands are responsible for production of sweat, and in humans, can be divided into two types, the aporcrine sweat gland and the eccrine sweat gland (Shibasaki, 2006). Considering the fact that the eccrine sweat gland are in charge of sweat production for thermoregulatory purposes (Sato et al., 1989), this is the gland of most interest. Developing as early as the 16th fetal week, eccrine sweat glands cover nearly our entire body (Kuno, 1956). They are most numerous on our palms of the hands and the soles of our feet with 600 to 700 glands per cm2, and least numerous elsewhere with an average of 64 glands per cm2 (Cheshire and Freeman, 2003). The sum of all these sweat gland distributed over our body probably reaches an impressing range of 3 to 4 million (Kuno, 1956). As mentioned above, the distribution of these eccrine sweat glands varies accross the body, and this variation in distribution is associated with thermoregulatory needs of the various portion of the body (Kondo et al., 1998).
The exact neurological pathway behind sweat production is not completely known, considering the challenge in identifying precise neural tracts in human, but a certain consensus on the pathway is accepted (Shibasaki, 2006). Once the preoptic area of the hypothalamus has received and integrated thermal information through afferent signals, signalling that bodies thermal homeostasis of 37 Celsius has been disturbed, efferent signal from the region of the brain is sent via the tengmentum of the pons and the medullary raphe regions to the intermediolateral cell column of the spinal cord (Shibasaki, 2006). From the spinal cord, neurons emerge from the ventral horn and eventually synapse in to the sympathetic ganglia. From there, non-myelinated C fibers pass through the gray ramus communicans, combine with peripheral nerves and finally travel to the sweat glands (Shibasaki, 2006). These peripheral nerves are sympathetic cholinergic fibers and the cholinergic stimulation by acetylcholine, the main neurotransmitter involved in sweating, binds to the muscarinic receptors located on the eccrine sweat glands. When acetylcholine binds to muscarinic receptors, intracellular Ca2+ concentration increases, leading to an increased permeability of CI- and K+ ion channels and the release of a precursor fluid from the secretory cells (Sato et al., 1989). The composition of the precursor fluid resembles that of plasma, without the plasma proteins (Wendt et al., 2007). Therefore, the same minerals found in plasma are also found in sweat, consisting of mainly sodium chloride with potassium, calcium and magnesium found in smaller amounts (Wendt et al., 2007). As the precursor fluid flows through the duct portion of the sweat glands, leading to the skin, its composition is modified by active reabsorption of both sodium and chloride (Wendt et al., 2007). This active reabsorption results in sweat being hypotonic compared to plasma (Wendt et al., 2007). Other components found within sweat include lactate, urea, ammonia, amino acids, protein, histamine, prostaglandins and amphetamine-like compounds (Sato, 1977).
The relationship between sweat rate and change in internal temperatures has been examined and the conclusions point toward sweating being primarily controlled by central brain temperatures and secondarily affected by mean skin temperatures (Smiles et al., 1976). Internal body temperatures therefore initiate and modulate sweat production but this production of sweat can also be influenced by local temperature of the sweat glands via peripheral mechanisms (Van Beaumont & Bullard, 1965). Indeed, local heating of sweat glands increases sweat production (Bothorel et al., 1991). The suggested mechanism behind this modulation of sweat production via local heating of sweat glands consist in the observed increase in acetylcholine release in response to heat(and the opposite observation in response to decreased heat) or the sensitisation of sweat glands by heat (DiPasquale et al., 2003). It is unclear which of these two mechanisms, or whether both, are the cause of this increase sweat production by local heating (Shibasaki, 2006). The understanding that increased temperatures increases sweat production is well established, as mentioned above. This increase in sweat is the result of both the increase in the number of excited eccrine glands and the increase of sweet produced by each of these glands (Shibasaki, 2006). The increased sweat production in response to increased temperatures is initially increased via the increased number of activated eccrine cells, while further increase in sweat production results from increase in the production of sweat per gland (Kondo et al., 2001). The recruitment of sweat gland is very fast, achieving maximal recruitment of all glands within the first 8 minutes of exercise while the increase in sweat output occurs more gradually, slowly rising until the hyperthermic state cesses (Kondo et al., 2001).
Humans have a remarkable capacity of producing a high amount of sweat during prolonged exercise. The average maximum sweat rate is roughly 1.4 L/hour (Gerking & Robinson, 1946) but this high rate of sweat production cannot be maintained for long periods of time given the observation that sweat rates starts declining after 4 to 6 hours of hyperthermia (Gerkin & Robinson, 1946). Prolonged exercise, especially in hot environment, forces the thermoregulatory mechanisms of sweating to be very active. This profuse sweating may result in dehydration, which in turn lowers both intra and extra cellular volumes leading to plasma hyperosmolality and hypovolemia, which both impairs the mechanism of sweating (Shibasaki, 2006). This points out to the importance of hydration during exercise, a subject that will be discussed later, due to the fact that impaired sweating results in impaired thermoregulation capacities of the body.
Factors influencing thermoregulation
Many factors may impair or enhance the innate capacity of the body to thermoregulate. Factors influencing thermoregulation which are implicated during an exercise bout will be discussed in the following section.
With age, especially after 60 years of age, a considerable reduction of skin blood flow can be observed (Someran et al., 2002). For a given core temperature, there is a reduced cutaneous vasodilatory response in the elderly population, impairing heat radiation from skin, and therefore, impairing the control of thermal homeostasis (Kenney, 1988). Indeed, the maximal skin blood flow declines by a factor of three between the age of 5 to 85 and this considerable decrease in the capacity to provide blood to skin can only be partly attributable to changes in fitness level (Rooke et al., 1994).
The mechanism behind this decrease in skin blood flow observed during an elevated core temperature, such as during exercise, is argued to be associated with peripheral rather than central hypothalamic changes. A reduced sensitivity of the active vasodilatator system is most likely the main cause of this decline in skin blood flow capacities (Kenney et al., 1997). Remember from section 2.3 , it is this system that is in charge of the largest portion of the observed blood flow increase. In addition to the impaired sympathetic activation of vasodilatation in skin, structural changes in elderly skin may contribute to the impairment of this thermoregulatory mechanism. Structural changes in the cutaneous vasculature limits the wall expansion of these vessels, thereby limiting vasodilatation and flow of blood (Someran et al., 2002). These structural changes in the skin vasculature observed in the elderly population are also attributable to the flattened underside of the epidermis and a decrease in rete ridges (Kenney & Munce, 2003). These structural changes lead to a collapsing, disorganization and even total disappearance of the vessels found in the microvasculature of skin (Kenney & Munce, 2003).
As mentioned, the cutaneous vasodilatory mechanism observed in a hyperthermic situation is impaired with age but some argue that the sweating mechanism also becomes impaired. Indeed, the sweating response to a thermal stimulus observed in older adults is greatly decreased. This decreased response can be understood by a decreased sweating capacity and an increase in the thermal threshold initiating the thermoregulatory mechanism (Hensel, 1981). While some findings suggest a reduction of the capacity to sweat, other findings suggest that this decline in sweating is correlated to VO2 rather than age. The impaired sweating mechanism observed in the elderly would therefore not be due to age but to the decline in fitness levels usually associated with aging (Gonzales et al., 1980).
Although the uncontested evidence of higher mortality rates among older men and women from hyperthermia may lead to the conclusion that age is the root cause of an increased intolerance towards thermal stresses, there is general consensus that indeed some physiological changes due to age account for a greater intolerance, but not all of the blame must be put on such factors (Kenney & Munce, 2003). Confounding factors including change of fitness level associated with age and change in body mass composition must be taken into account when trying to understand the impaired thermoregulation observed in the elderly during exercise and other thermally stressing situations (Kenney & Munce, 2003).
Maintaining a thermal gradient and water vapour pressure gradient between the surrounding environment and the skin is crucial when attempting to dissipate heat from the body through the two mechanisms discussed earlier. Indeed, when air temperatures exceeds 36 Celsius, the gradient for heat exchange becomes reversed and the body starts gaining heat from the environment instead of radiating the heat traveling in blood into the environment (Wendt et al., 2007). Furthermore, sweat can only work as a thermoregulatory mechanism if it is able to evaporate. The potential for evaporative heat loss is dictated by the water vapour pressure gradient between skin and environment and by the movement of air over skin, further demonstrating the limit that the environment may pose on thermoregulatory processes (Wendt et al., 2007).
The driving force behind heat dissipation through radiation, the phenomena that takes place as heat is travelling in the microvasculature of skin, really resides in a large temperature gradient between skin and environment, as mentioned above (Cheuvront & Haymes, 2001). A very hot environment therefore diminishes this gradient between skin and environment, and as mentioned, heat begins to be gained when the external environments reaches 36 celcius (Wendt et al., 2007). In such a scenario, sweat becomes the main thermoregulatory mechanisms, but this mechanism also faces environmental limits. In a context of a very humid environment, air water vapour pressure approaches skin water vapour pressure and results in reduced evaporation and thereby, reduced heat dissipation (Cheuvront & Haymes, 2001). In a scenario of exertion in a hot and humid environment, both thermoregulatory mechanisms therefore face limits resulting in impaired thermoregulation and an accumulation of heat in the body that may lead to dangerous heat strains (Wyss et al., 1974). From such knowledge, the ideal external temperatures therefore seems to point to cool and dry conditions, where a high heat gradient will favour radiating heat loss through skin and the high water vapour gradient will favour heat loss through the evaporation of sweat.
An impaired capacity to dissipate heat from the body into the environment limits an athlete, or even a casual exerciser, to continue his exercise bout. A systematic review examined the effect of temperature on marathon times and revealed a correlation between lower environment temperatures and faster performance times (Cheuvront & Haymes, 2001). The idea than an impaired capacity to thermoregulate results in fatigue and impairs performances ties in with a theory of fatigue known as the thermoregulatory model of fatigue. Evidence from such a model of fatigue arises from a classic study performed by Nielson et al., where they found that well trained cyclists were forced to terminate their exercise bout when core temperatures approximately reached 39.5 Celcius (Abbiss & Laursen, 2005). Such an example puts even greater emphasis on the importance a thermal homeostasis, and how external factors such as the environment may accelerate heat accumulation and lead to precipitated fatigue during exercise.
As a result of prolonged sweating as a mean of regulating and maintaining thermal homeostasis, this mechanism results in a constant loss of body water, loss of salt and will typically lead to a state of hypohydration, known as dehydration, if inadequate fluid replenishment takes place (Merry et al., 2009). A state of dehydration during an exercise bout is characterized by a reduction of blood volume and an increased blood osmolality, both leading to an increased cardiovascular and metabolic strain while impairing thermoregulatory mechanisms (Hamilton et al., 1991). According to different model of fatigue, this increase strain on the cardiovascular system and the various thermoregulatory mechanisms may lead to impaired aerobic exercise performances and therefore understanding the repercussions of dehydration on the body and its effect on exercise performance is primordial.
In order to avoid dehydration, the principle is easy; water loss through sweat must be matched by water intake. But when considering that the stimulus to drink sent by the hypothalamus is only initiated after the body has lost 2% of its fluid, maintaining fluid balance becomes slightly more complex, especially during exercise (Wendt et al., 2007). It appears that thermoregulatory systems play a central role in the observed reduced exercise performance mediated by a water deficit (Wendt et al., 2007), indeed, it has been shown that dehydration reduces skin blood flow and the sweating response during exercise (Sawka & Montain, 2000). Although these observations have been made, the exact mechanism by which dehydration increases thermoregulatory strain has yet to be explained (Cheuvront & Haymes, 2001).
Pitts et al., were the first to systematically demonstrate that active dehydration, defined as progressive dehydration as a result of physical activity, resulted in a progressive and continued rise in internal temperatures during extended treadmill march (Cheuvront & Haymes, 2001). Further results from this classic study also demonstrated that partial or complete replacement of fluid loss attenuated the rise of internal temperatures precipitated by hypohydration (Cheuvront & Haymes, 2001). This study paved the way to further studies on dehydration and thermoregulation. One of these studies, performed by Gisolfi and Copping, compared the thermoregulatory responses of 6 men during 2 hours of treadmill running under 7 experimental conditions. Dehydration gradually elevated internal temperatures while regular fluid replacement dampened this effect, arriving to similar results as Pitts et al. in 1944. This duo also found strong correlations (r=0.76 to 0.87) between internal temperature rise and percentage of body fluid loss, predicting that for every 1% of fluid loss beyond an initial loss of 2% resulted in an internal temperature rise of 0.4 Celsius (Gisolfi & Copping, 1974). A similar relationship between fluid body loss and rise in internal temperature was achieved by Maron et al., two years later (Maron et al., 1976). More recent studies identified the relationship between body fluid loss and higher heart rate, lower stroke volume, lower cardiac output, as well as lower skin blood flow (Gonzales-Alonso et al., 1995, Montain & Coyle, 1992). Such studies demonstrate that competition for blood flow between active tissues(skeletal muscle, the heart, the brain) and cutaneous tissue exists even if internal temperatures rise, demonstrating that the need to maintain blood pressure overrides the need to dissipate heat through increased skin vasodilatation (Cheuvront & Haymes, 2001). As mentioned, loss of minerals through sweat results in increased blood osmolality (Hamilton et al., 1991), and it is proposed that this change in blood osmolality could trigger the impairment of thermoregulatory mechanisms observed during dehydration (Wendt et al., 2007). Indeed osmotic effects on thermoregulation could be mediated by a direct influence of extracellular fluid osmolality on thermosensitive neurons from the hypothalamus, which have been observed to decrease their firing rate in hypertonic medium (Silva & Boulant, 1984). In addition to affect the central nervous system, tonicity could also exert effects peripherally as high interstitial osmotic pressure may inhibit fluid availability to sweat glands (Sawka et al., 1985), explaining decrease sweating observed during dehydration.
Early studies on the subject of thermal homeostasis and gender concluded that women were more susceptible thermal stress and physical harm, but such findings were most likely shortcomings of early research methodology and strong bias toward female and their participation in sports, especially long distances such as marathons (Cheuvront & Haymes, 2001). Indeed women were not legally allowed to compete in marathons until 1972 (Kuscsik, 1977). The current 13 minutes separating the man and woman world marathon records (Association of Road Racing Statisticians, 2010) illustrates the capacity of women to perform, and gives evidence that they possess efficient thermoregulatory mechanism. As a matter of fact, it is even suggested that women may be advantaged in regards to some aspects of their thermoregulatory system (Cheuvront & Haymes, 2001).
In general, females tend to have smaller body mass and surface area when compared to their male counterparts, but possess larger surface area-to-mass ratios (SA/M) (Haymes, 1984). Understanding that heat production is proportional to body mass and heat loss is proportional to body surface area, female performing exercise will produce less heat while dissipating more heat than men, for the same relative intensity of exercise (Cheuvront & Haymes, 2001). From such a point of view, women possess a morphological advantage over men. Furthermore, considering the fact that women tend to have more subcutaneous fat than man, due to hormonal factors, it is suggested that they me put at an advantage in cold environments, as the extra fat may provide additional isolation to the cold (Cheuvront & Haymes, 2001). However, this logical conclusion does not usually translate in increase increased heat storage, possibly due to the increase heat dissipation observed in women caused by their larger surface area-to-mass ratios (Haymes, 1988).
Although the subject of dehydration and thermoregulation has basically been unstudied in women, there is motive to suspect that gender may significantly affect dehydration and thermal homeostasis (Cheuvront & Haymes, 2001). Anatomically, women have a larger number of activated sweat glands per unit area but these eccrine sweat glands produce less sweat per gland when compared to males (Bar-or et al., 1968). Indeed, women produce less sweat in both absolute and relative terms. Therefore, in humid conditions when a low water vapour pressure gradient exists between skin and environment (recall section 3.2), excessive sweating may actually be counterproductive to heat dissipation (Cheuvront & Haymes, 2001). This fact combined with the larger SA/M, which encourages radiation of heat from the skin, may consequently position women in a thermoregulatory advantage over males in hot and humid exercise conditions (Cheuvront & Haymes, 2001).
Studying women and thermoregulation is distinctive due to the effect of the women’s reproductive cycle on internal temperatures and skin blood flow (Cheuvront & Haymes, 2001). The well known fact that women’s internal temperatures is approximetly 0.5 celcius higher during the luteal phase of the menstrual cycle produces a higher threshold for the initiation of sweating and cutaneous vasodilatation (Kolka & Stephenson, 1989), possibly putting women at a disadvantage if facing a hyperthermic situation during the luteal phase of their menstrual cycle. Consequently, this change may lead to increased heat accumulation, due to the delayed onset of thermoregulatory mechanisms, for the same work effort (Cheuvront & Haymes, 2001). As Cheuvront and Haymes eloquently phrase it “ What remains clear, however, is that menstrual cycle phase does affect thermoregulation and must, therefore, be considered in the assessment of gender-specific differences between male and female marathon runners.”
Heat illness in the context of exercise, referred as exertional heat illness, is a condition that ranges across a continuum of increasing severity (O’Brien et al., 2005) that if left untreated, may lead to a life-threatening disorder known as heat stroke (Lugo-Amador et al., 2004). These illnesses may be precipitated by the body’s thermoregulatory mechanisms themselves, or by the overall inability of the body to thermoregulate, resulting in high internal temperatures.
Minor heat illnesses
Albeit the evidence that mild heat illnesses namely heat edema, heat rash, heat cramps and heat syncope have not be shown to progress into severe heat illnesses if left unattended (Howe et al., 2007), an overview of these heat-related illness will nonetheless be described below.
Heat edema and heat rash are considered to be very mild forms of heat illnesses (Howe et al., 2007). Heat edema is the result of the cutaneous vasodilatation occurring during hyperthermic situations that leads in some individual to pooling of interstitial fluid in the distal extermeties (Howe et al., 2007). Heat rashes, or Miliaria Rurba, on the other hand results from profuse sweating saturating the surface of the skin, clogging the sweat ducts. This obstruction of sweat ducts results in the leakage of sweat into the epidermis, causing a rash (Howe et al., 2007). Heat syncope, where the person exercising will momentarily lose consciousness and in most case result in a fall, is the outcome of various factors. Indeed, heat syncope results from volume depletion due to sweating, peripheral vasodilatation and a decrease in the vasomotor tone, leading to acute hypotension (Lugo-Amador et al., 2004). As Lugo-Amador et al. phrase it: ‘’Prolonged standing after significant exertion and rapid change in body position after exertion, such as from sitting to standing, may lead to heat syncope.’’. Lastly, heat cramps can be characterized as painful muscle spasms mostly located in voluntary muscles of the calf, thighs, and shoulder (Lugo-Amador et al., 2004). Very common in athletic events, the exact cause of these cramps is unknown (Howe et al., 2007, Lugo-Amador et al., 2004, O’Brien et al., 2005), it is thought that they result from fluid and sodium depletion (Howe et al., 2007).
Serious heat illnesses
The more serious heat illnesses consist of heat exhaustion and ultimately, heat strokes. Contrary to minor heat illnesses, leaving heat exhaustion unattended will lead to a heat stroke, a life-threatening illness (Lugo-Amador et al., 2004). These illnesses are the result of the body’s inability to thermoregulate and maintain body temperate at the set-point of 37 Celsius, resulting in manifestation of symptoms and various body malfunctions.
Heat exhaustion is often precipitated by exercise, especially in hot environments, as heat energy starts building up within the body. The imbalance between heat storage and heat dissipation can be understood as the body’s inability to sustain the level of cardiac output needed to meet the increasing demand of skin blood flow for thermoregulation, the muscle exercising and the supply to vital organs (O’Brien et al., 2005). This condition is also associated in inadequate hydration, therefore resulting from dehydration (Wendt et al., 2007). The inability to support the increased cutaneous blood flow demand in addition to the negative effect of dehydration of thermoregulatory mechanisms discussed in section 3.3 leads to this accumulation of heat within the body. Heat exhaustion is the precursor to heat strokes (Lugo-Amador et al., 2004) and is symptomatically characterized by elevated core temperatures ranging from 37 to 40 Celsius, malaise, fatigue and dizziness (Howe et al., 2007). The stress put on the cardiovascular system often results in hypotension which can therefore make athletes collapse during the exercise bout (heat syncope), if they suffer from heat exhaustion (O’Brien et al., 2005). In a situation of heat exhaustion, it is therefore important to diminish cardiovascular and thermorulatory stresses by resting, cooling oneself, and rehydrating (O’Brien et al., 2005). The inability to decrease the stress that heat has placed on the body will lead to a much more serious heat illness known as heat stroke.
The life-threatening heat illness known as heat stroke is characterized by elevated core temperatures greater than 40 Celsius and CSN dysfunction ensuing in delirium, convulsions and coma (O’Brien et al., 2005). This medical emergency is often precipitated by exercising in hot environments, as the heat production of muscles combined with the inability to maintain the increase in heat dissipation requirements results in considerate heat accumulation (Wendt et al., 2007). Combining the redistributed blood flow to skin and the decreased blood volume due to loss of fluid through sweat, during exercise, results in a decline in central blood volume. This decreased central blood volume results in an unloading of baroreceptors which leads to diminished skin blood flow and sweating, increasing the risk of developing heat strokes (Hales, 1997). The decreased splanchic blood flow, a normal cardiovascular response in the effort to provide a greater portion of the cardiac output to skin, and the increased metabolic demand characterising exercise produces significant cellular hypoxia to the intestine and liver (O’Brien et al., 2005). This phenomenon, central to the development of a heatstroke, produces highly reactive oxygen and nitrogen species leading to mucosal damage in the intestines, creating intestinal hyperpermeability and leakage of endotoxins into the blood stream (Hall et al., 2001). Endotoxins are potent activator of proinflammatory cytokines which cause endothelial damage and inhibit heat shock proteins (Sona et al., 2004). Heat shock proteins found on the cellular membrane of various organs become expressed under thermal stress and increase thermotolerance via cellular protection of apoptosis, which is a gene activated cellular destruction (Sona et al., 2004). An inhibition of these heat shock proteins as a result of cytokine release into the blood stream therefore counteract thermotolerance and may result in multi-organ failure (Sonna et al., 2004), hence the life-threatening nature of a heat stroke.
The outcomes of heat injuries are positive if they are treated immediately (Lugo-Amador et al., 2004) and in the case of heat strokes, mortality rates are below 10% when adequate treatment and support is provided (Lugo-Amador et al., 2004). Adequate treatment for heatstrokes usually consist of in immediate reduction of internal temperatures, quick attention to the ABCs (Airway, Breathing, Circulation), cardiovascular support, control of seizures, and rapid transport to an emergency medical facility (Lugo-Amador et al., 2004). For the vast majority of heat stroke victims, long-term effects will be inexistent, and will recover without any sequels (Shibolet et al., 1967). Nevertheless, up to 33% of heat stroke survivors have reported residual neurological deficits which include paraplegia, paresis, dysarthia, memory loss, difficulty to concentrate and ataxia (Shibolet et al., 1967).
With a better comprehension thermoregulation and its implication on exercise performance and general health, it is understandable that different strategies have been developed in order to maximise human thermoregulatory capacities. The ability to keep cool during exercise becomes an evident advantage to any competitor, and may benefit from various strategies such as heat acclimatisation, whole-body pre-cooling, hyperhydration, and strategic clothing.
It is well established that regularly exposing the body to hot environments leads to a number of physiological adaptations that improve thermoregulation, especially in hot environments (Lorenzo & Minson, 2010). This plasticity in the thermoregulatory system allows for an increased ability of the cardiovascular system to provide blood to the microvasculature of skin, enhances evaporative cooling through increased sweat rates, and lowers core temperatures, all leading to better heat dissipation from the core to the environment (Lorenzo & Minson, 2010). It is also postulated that regular exposure to heat, known as heat acclimatisation, lowers the set-points in the hypothalamus at which sweating and vasodilatation are initiated (Yamasaki & Hamasaki, 2003). Such adaptation provide an obvious advantage in any exercise situation, as it improves the body’s ability to dissipate heat allowing for possible better athletic performance and decreasing the change of heat related illnesses.
The first report of heat acclimatisation on increased performance date as far back as the 1940’s, were soldiers and mine workers were studied (Lorenzo, 2010). Heat acclimatisation protocols vary, but general trend consist on a chronic exposure to high enough ambient temperatures to elevate core temperatures and initiate profuse whole body sweating (Lorenzo, 2010). The process of heat acclimatisation takes days, with full adaptation observed between 7 to 14 days for most individuals (Wendt et al., 2007). That various systems adapting from heat acclimatisation adapt at different rate, as seen in figure 7, with the cardiovascular adaptations occurring the earliest and the sweat and vasodilatation adaptations the latest (Wendt et al., 2007). As most adaptation that occur in the body, such as gain in muscular mass in response to strength training, heat acclimatisation is a transient process and will disappear if the chronic exposure to heat is not maintained (Wendt et al., 2007). There is varying agreement on the rate of decay heat acclimatisation related adaptations, but the general consensus is that the higher the level of fitness, the slower the decay (Wendt et al., 2007).
The specific mechanism by which heat acclimatisation increase skin blood flow is unclear (Lorenzo, 2010), but it is well documented that skin blood flow increase for a given core temperature after being subjected to heat acclimatisation (Nadel et al., 1974, Roberts et al., 1977). Some studies attribute this physiological adaptation to central factors, while other studies attribute this change to peripheral factors (Lorenzo, 2010). At the end of the day, the observed increased blood flow for a given core temperature that result from heat acclimatisation may be either due to an increased ability of the skin vessels to vasodilate or due to an improved vasodilatory response (increased sensitivity) for a specific stimulus (Lorenzo, 2010). Investigation on the exact mechanism should be considered for future research in the field of thermoregulation.
As of the increased sweat rate observed following heat acclimatisation, the current view is that this adaptation is a centrally mediated response (Lorenzo, 2010). Indeed, it was showed that a chronic exposure to heat increased sweat rates by lowering the internal temperature threshold for the initiation of sweating, and by increasing the slope of the sweat rate, that it, more sweat for a given core temperature (Robert et al., 1977). However, even if central factors seem to be responsible for this thermoregulatory adaptation, there is evidence that the increased sweat output may be due to an increased sweating capacity of the sweat glands, underlying adaptations that would be independent of central factors (Chen & Elizondo, 1974).
The concept behind body pre-cooling resides in cooling large tissue mass, mainly muscle, to create a ‘’heat sink’’ before exercise (White et al., 2002). Cooling large tissue masses therefore increases the heat storage capacity of the body which consequently delays the onset of heat dissipation mechanisms (Olshewski & Bruck, 1988). This delayed onset of heat dissipation mechanisms, namely sweating and skin vasodilatation, allows more work to be performed before a given increase in core temperature is reached resulting in less competition for blood flow between the skin and working muscles, hence decreasing cardiovascular stress (White et al., 2002). This strategy therefore does not directly affect the thermoregulatory system but rather indirectly plays a role in helping the thermoregulatory system.
As mentioned, the basis of precooling strategies is to increase the margin for metabolic heat production which consequently increases the time before the body reaches a critical thermal limit which forces a drop in exercise intensity (Nielson et al., 1993). Pre-cooling methods vary, but the most common practice consists of cold air cooling, cold water immersion and the use of water-cooled clothing (Wendt et al., 2007). Albeit the fact that the current literature shows evidence that these various cooling methods increase exercise capacity, the practicality of precooling method is limited (Wendt et al., 2007). Considering the time required to cool the body to cool enough temperature in order to improve performance, it is doubtful that athletes will want to put in use pre-cooling methods before any exercise bouts (Wendt et al., 2007).
Considering the negative impact of hypohydration on thermregulatory systems and performance, it is reasonable to suggest pre-exercise hyperhydration may delay or even prevent hypohydration during exercise. This technique has been suggested to enhance thermoregulation via expansion in blood volume (Freud et al., 1995, Lyons et al., 1990), and for such reasons, many studies have examined the potential of hyperhydration using water or water combined with electrolytes (Grucza et al., 1987, Moroff & Bass, 1965). Both methods lead to a transient increase of body fluid as the overload of fluid is promptly excreted by the kidneys (Magal et al., 2005). However, hyperhydration using glycerol leads to a higher retention of water, due to the osmotic properties of the metabolite (Magal et al., 2005).
Therefore, understanding the properties of hyperhydration using glycerol and the concept behind the negative effects on thermoregulatory processes precipitated by hypohydration, it is logical expect an thermoregulatory advantages from such a technique. While many studies demonstrate lower core temperatures and higher sweat rates associated with hyperhydration with glycerol (Gisolfi & Copping, 1974, Grucza et al., 1987), many studies also demonstrate no thermoregulatory-related advantaged to the technique(Hitchins et al., 1999, Latzka et al., 1997), leading to the conclusion that hyperhydration provides no clear thermoregulatory advantage (Magal et al., 2005). However, hyperhydration may delay the body-water deficit, and thereby helping thermoregulatory processes by delaying hypohydration and its negative effects (Magal et al., 2005).
The use of clothing during exercise creates a layer of thermal insulation creating a barrier for heat transfer and evaporation from the skin to the environment (Gavin, 2003). This thermal barrier between skin and the environment may therefore becomes an advantage during exercise in colder environments, or create an addition thermal stress when exercising in warmer settings.
In hot environments, clothing represents a layer of insulation imposing a barrier to heat transfer from skin to environment, and a barrier to sweat evaporation from skin to the environment (Gavin, 2003). As mentioned in section 2.4, the rate of sweat evaporation from skin to environment is dependent on the skin to air water vapour pressure gradient and air velocity. Considering the fact that clothing affects both of these variables, reducing air flow on skin and diminishing the water vapour gradient, the body’s cooling efficiency is inevitably reduced, due to impairment in the body’s main thermoregulatory mechanism known as sweating (Pascoe et al., 1994). From such knowledge, clothing that provides the least amount of interference to sweating would prove to be advantageous for any individual trying to help his thermoregulatory mechanisms, and would consist of minimal clothing such as short sleeve t-shirts and mid-thighs shorts (Gavin, 2003). Such type of clothing would also result in greater airflow on skin, and when understanding that thermal stress is greater under condition of no air-flow (Brown & Banister, 1985), it would prove to be beneficial for the body’s task of maintaining thermal homeostasis. On the other hand, albeit the fact that clothing in warm environments can impair thermoregulatory mechanisms and lead to faster increase of core and skin temperatures (Gavin, 2003), clothing can also serve as protection from radiant heat gains from the sun (Pascoe et al., 1994). The colour of clothing should not be based on aesthetics, as white clothing reduces radiative heat gain from the sun, reducing thermal stress, when compared with black clothing (Nielson, 1990). As of the fabric type, Zhang et al. demonstrated that fabrics with fewer air space provided lower air-permeability, leading to an impaired sweating capacity and consequently thermal homeostasis (Zhang et al., 2002). Indeed, they found that that exercising in high air permeability fabrics resulted in significantly lower rises of core temperatures, compared to low air permeability fabrics (Zhang et al., 2002).
In contrast to exercise in warm temperatures, where minimal clothing becomes advantageous, exercising in cold temperatures requires the selection of clothing that promotes thermal insulation (Gavin, 2003). The ideal role of clothing is to maintain a thermal balance between the exerciser and the environment, and exercising in cold becomes tricky due to the possibility of either over or under insulation due to clothing choices (Gavin, 2003). While too little clothing may lead to hypothermia, excessive clothing may lead to discomfort due to increase in body temperature, excessive sweating and skin wetness (Gavin, 2003). Wet skin leading to wet clothing is associated with discomfort but also a reduced thermal insulation provided by clothing (Bakkevig & Nielsen, 1994), counteracting the core function of wearing cloth in cold environments. Reducing sweat accumulation is also important in order to decrease the probability of post-exercise chill and discomfort (Bakkevig & Nielsen, 1995). Ideal clothing for cold weather therefore seems to consist in clothing that blocks air movement, but allows for water vapour to escape through the clothing as sweating occurs (Gavin, 2003).
Reviewing the more dated and current literature, we can appreciate thermoregulation and its implication during exercise as a fascinating and complex field of study. The interest from the scientific community toward human thermoregulation is not new, as seen from the early work by Liebermeister and Wunderlich in the 1870’s. These pioneers paved the way for future research permitting important discoveries ranging from localizing brain centers controlling thermoregulation to identifying the specific ion channels in charge of sensing skin and internal temperatures.
Responsible for integrating afferent thermal information and initiating adequate thermoregulatory mechanisms, the hypothalamus plays a vital role during exercise since such a situation thermally stresses the body as a consequence of heat production from working muscles. This heat production from working muscles results from the inefficiency of metabolic transfer. Indeed more than 75% of the generated energy through substrate oxidation taking place in skeletal muscle is liberated as heat. This accumulation of heat disrupts the thermal set point of 37 Celsius, triggering thermoregulatory mechanisms that aim in dissipating heat from the body into the environment. These thermoregulatory mechanisms consist of skin vasodilatation and sweating. Increasing cutaneous blood flow allows heat to be dissipated into the environment by radiation, while evaporation of sweat from skin results in dissipating 0.6 kcal of heat per 1ml of evaporated sweat.
However, even if the human body is equipped with efficient thermoregulatory mechanisms, particular situations may interfere with our innate capacity to thermoregulate and lead to an accumulation of heat, known as hyperthermia. Indeed age, the environments and dehydration have been shown to impair various aspects of thermoregulation. On the other hand, recent studies seem to point out that women may be advantaged compared to man in regards of thermoregulation during exercise, but further investigation needs to be completed since the literature on women and thermoregulation is limited.
In a circumstance where core temperatures increase due to the inability to maintain thermal homeostasis via thermoregulatory mechanisms, various forms of heat illness may ensue. These various heat illnesses ranging from minor heat rashes to a life-threatening condition known as heat stroke are often precipitated by strenuous exercise since such a situation thermally stresses the body.
Considering the importance of thermoregulation and its effect on exercise and performance, various techniques have been developed to optimize thermoregulatory systems. The most efficient method seems to be heat acclimatisation which results in a collection of physiological adaptations including increased skin blood flow and increased sweat output. Other techniques have been investigated, and rightly so, due to their theoretically correct basis. These techniques, namely body pre-cooling and hyperhydration, have shown mixed results and may not be very practical. Exerciser should rather concentrate on adequate clothing, as inadequate clothing choices has been shown to affect thermoregulation.
Thermal homeostasis is part of an assortment of variables controlled by the central nervous system during exercise, and should not be overlooked. Reviewing the literature allows the understanding that maintaining thermal homeostasis is as vital as other variables monitored during exercise such as blood glucose levels, blood pressure and pH. The body’s ability to control and monitor temperature with such precision and efficiency should leave anyone in awe, and respect must be paid to the greatest and most complex machine ever created, the human body.
Antoine Del Bello
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