International SportMed Journal
Heat adaptation: Guidelines for the optimisation of human performance

*Dr Nigel AS Taylor, PhD1 ,Dr James D Cotter, PhD2

1Department of Biomedical Science, University of Wollongong, Wollongong, NSW 2522, Australia.
2School of Physical Education, University of Otago, Dunedin, New Zealand.


Humans have an immense capacity to adapt anatomically, biochemically and physiologically to a broad range of environmental states, but they also possess the technological capacity to modify the local environment to support life. These characteristics have been critical to the survival and advancement of the human species. In this paper, the focus is on human adaptation to hot environments, and the integrated physiological responses that accompany such adaptation. The principal emphasis is on how athletic performance may be optimised through the development of these adaptation responses, although gender differences in the acute and adaptation responses are not discussed.

Physiological adaptation occurs in response to repeated stress application. Acute environmental stress, of either external (exogenous) or internal (endogenous) origin, disturbs the internal environment. Such stresses (forcing functions) displace physiological variables from one steady state towards another, typically in an exponential fashion. For example, the heart rate and ventilatory responses to an increase in exercise intensity display an exponential rise, to ensure oxygen supply matches elevations in metabolic demand 1.

Since all organisms are in a state of dynamic equilibrium with the environment, thermal energy can readily be gained or lost. Humans possess regulatory mechanisms that ensure the stability of the internal environment, with such stability being conducive to life and optimal physiological function. Exposure to exogenous and endogenous (metabolic) heat sources displaces body temperatures upwards. Homeostatic mechanisms, comprised of sensors, signal integrators, effector organs and a communication network, respond by modulating effector organ function to regulate body temperature within a narrow range. Repeated exposure to heat stress (an adaptation stimulus), either through exogenous sources or high-intensity exercise, elicits adaptations that result in a more effective defence of body temperature. These adaptations take the form of behavioural strategies or physiological adaptations, the latter of which are the principal focus of this paper.

Physiological heat adaptation can occur in response to naturally-occurring climatic changes (acclimatisation: 2, 3, 4), to artificial heat exposure (acclimation: 5, 6, 7) and to training-induced elevations in body temperatures 8, 9, 10. This paper’s second emphasis is on the adaptations that accompany acclimation and high-intensity, endurance exercise.

Adaptation theory

The capacity of any stress to induce adaptation is a function of its application intensity, duration, frequency and variability 11, and of the genetic, phenotypic and situational status of the individual. In a modification of the training impulse model 12, these variables may be used to quantify the cumulative adaptation impulse (stress volume). That is, the thermal impulse is the sum of the products of the changes in body temperature and the exposure duration to each adaptation stimulus. The adaptation impulse concept provides a very useful, albeit simplistic, way of comparing adaptation stimuli (see Appendix and section on Principles and practices of heat adaptation (Forcing function considerations).

Since humans contain many interdependent regulatory systems, with common and discrete effector organs, the nature of systemic and organ adaptations varies across stimuli, and even within an adaptation stimulus. Indeed, adaptation rarely affects one organ or system, but it is an integrated physiological response affecting many structures and mechanisms simultaneously, and at differentrates. The time course of adaptation may be described using six general characteristics 11, as illustrated in Figure 1.

Figure 1: Adaptation theory: A hypothetical illustration of physiological changes following the application and withdrawal of an adaptation stimulus (see text for discussion)

Adaptation requires the stimulus to exceed a critical threshold, which is a function of the regulatory system’s sensitivity.  For instance, if a stimulus fails to disturb homeostasis, then neither an acute corrective adjustment nor physiological adaptation will occur.

    • Whilst acute stresses evoke immediate physiological responses, there will always be a phase delay (latency) before adaptation becomes evident.
    • For each effector organ, there is a physiological maximum beyond which there is considerable adaptation resistance.
    • The speed at which tissues, organs or systems adapt varies widely 13.
    • Optimal adaptation results from some combination of the adaptation impulse size, its duration and frequency of application, and the number of stimulus applications (cumulative adaptation impulse).  It is well established that people respond different rates to an adaptation stimulus: high, moderate and low responders.  The higher the background adaptation, the lower the adaptation response.
    • There is the reversal (decay) of adaptation, once the adaptation stimulus is removed.

Why is heat adaptation necessary?

Environmental influences

Body tissues are thermal energy reservoirs, with heat loss facilitated through the transport of thermal energy in the blood, and exchanged with the environment via non-evaporative pathways (radiation, convection, conduction), and the conversion of sweat into vapour.  During exercise in the heat, non-evaporative heat dissipation is impeded, and even reversed, so humans become heavily reliant upon evaporative cooling.  The capacity to continue exercising without an excessive body temperature increase is now dictated by the presence of clothing and sweat evaporation.

The interaction of physiological and environmental characteristics determines thermal compensability 14, which identifies conditions where temperature regulation is challenged.  This is the ratio of the required evaporative heat loss (Ereq) to the maximal sustainable evaporative cooling (Emax; Appendix).  Thermal discomfort and physiological strain slowly increase as this ratio approaches unity.  However, when Ereq exceeds Emax, the conditions are uncompensable.  This occurs when air temperature or water vapour content (humidity) exceed critical thresholds.  At rest, these thresholds are much higher, but uncompensability may still eventuate (e.g. Turkish bath).  However, since exercise has a pronounced affect upon heat balance, then even cool conditions may become uncompensable for athletes.  This role of metabolic heat is often overlooked, with the environmental state invariably being considered the primary cause of heat stress 15.  Yet for athletes, the risk of heat-induced performance decrements and heat illness can have as much to do with heat production as they do with external heat loading.

Exercise affects
In hot-humid conditions, exercise can change a situation from a compensable to an uncompensable heat stress.  The speed of this transition is dictated by the interactions of temperature and water vapour gradients (air-skin), relative air velocity, solar radiation, exercise intensity, clothing, body composition, hydration state, endurance fitness and heat adaptation status 16.

For many athletes, this change in compensability is irrelevant.  In swimming, heat balance is minimally challenged, since pool temperatures generally ensure sufficient heat loss.  However, when an 80kg, 100m sprinter, wearing athletic clothing, runs at maximal speed, the metabolic heat production lowers the air temperature at which thermal compensability is lost, moving it from 31-32°C (rest) to ~10°C during a race, when external power averages ~900 Watts.  However, the race is so short that athletes store an insignificant quantity of heat.  For a fencer, the air temperature at which conditions become uncompensable during competition is ~12°C.  The proximity of these two air temperatures reflects the interaction of exercise intensity and clothing on heat balance.

Keeping a physiological perspective
During exercise, the cardiovascular system serves the metabolic demands of the active muscles and delivers blood to the skin for heat removal.  Athletes can easily satisfy these demands in the short term.  Indeed, in events lasting only a few minutes, thermal compensability becomes irrelevant.  However, during prolonged competition, thermal homeostasis is compromised.  If heat storage is sufficiently high, or the exposure long enough, then the capacity of the cardiovascular system to serve both the cutaneous and muscle blood flow demands will be compromised 17.  Blood pressure will fall due to a reduction in central blood volume and a failure of the cardiac output and visceral vasoconstriction to adequately compensate for the intramuscular and cutaneous vasodilation.  This results in a reduction in skin blood flow and heat loss.  Sweating remains functional, but there is acceleration in the rate of core temperature elevation.  This will lead to fatigue and impaired performance, due to reaching a critical core temperature 18, 19, 20, a reduction in neuromuscular drive 21 or a reduced metabolic function 22.

It is clear that, for a 100m sprinter, heat adaptation cannot provide a thermally meaningful physiological benefit.  Observation alone shows that, for marathon running, heat illness can be problematic.  Indeed, Pugh et al. 23 recorded core temperatures over 40°C for runners in comfortable conditions (22-23.5°C, relative humidity 52-58%).  Clearly exercise intensity drove core temperature upwards.  Others have reported core temperatures in the range 39.4-39.7°C during short training runs in late winter (4°C; 24) and even during a 5km run 25.  At these core temperatures, the safety margin is minimal, although much lower temperatures have also been observed following a marathon (26: 38.7°C (N=62); 27: 38.9°C (N=38)).

Conductive exchanges are negligible in many sports, since surface contacts are brief and localised.


Advantages and disadvantages of heat adaptation

When is heat adaptation appropriate?

Most athletes and coaches are familiar with altitude training, and many will be aware of the debate surrounding its possible benefits to performance at sea level 28.  However, there is no doubt that adaptation to altitude enhances performance at altitude.  This generalisation also applies to heat adaptation.  Using a first-principles thermodynamic model, several athletic events will be evaluated to illustrate the thermal impact of metabolic heat production, and then the possible benefits of heat adaptation will be assessed.

At rest, heat production is ~1.5 15.  When exercising, additional heat is produced in proportion to the exercise intensity.  This is illustrated in Figure 2, using the predicted external power and total metabolic heat productions for world record performances in events from 100m through to the marathon, using the morphometric characteristics of each record holder.  In a worst-case scenario, without heat loss, the heat production curve in Figure 2 would also represent heat storage.  Since storing 3.47kJ of heat elevates 1kg of tissue 1°C, mean body temperature would rise ~2°C and ~4°C when racing the 1500m and 3000m races (respectively), at world record pace.  Therefore, unless body temperature was elevated substantially during the warm-up, athletes would theoretically not be expected to experience a clinically significant elevation in core temperature when running distances of 1500m or less, even when running at world record pace in an environment that prevented heat loss.

Figure 2: External work rate and total (metabolic) heat production during world record track performances over distances from 100m through to the marathon, using the morphometric characteristics of each record holder. If all of this heat is stored, core temperatures will rapidly rise, and two critical body temperature elevation lines have been added (2°C and 4°C: see text for discussion).

Since humans can actively dissipate heat, the scenarios in Figure 2 will rarely eventuate.  So the second stage of modelling included heat exchanges, typical athletic clothing (35% skin coverage), running speeds at record pace, and two climatic conditions: 22°C (50% relative humidity) and 33°C (50% relative humidity).  Heat exchanges, and the resultant heat storage, permitted computation of body temperature changes for the six races, with calculations performed to simulate athletes before and after heat adaptation.  In the latter instance, acclimation-induced changes in sweating, skin blood flow and skin temperatures (see text below), and the subsequent impact upon heat balance, were modelled.  These data are presented in Figure 3, but do not consider the significant impact of variations in solar radiation.  Events up to 1500m are not adversely affected by thermal strain.  At 23°C, this may extend to 5000m, and possibly 10 000m, with predicted body temperature changes.

Body temperature changes at 33°C, for distances >5000m are much higher than expected, and attributable to forcing the model to retain record pacing in uncompensable conditions, and to inherent model limitations.  Nevertheless, changes following adaptation provide a useful comparison.

being consistent with the literature 23, 24, 25.  However, under hot-humid conditions, people almost invariably modify pacing to facilitate task completion 29, 30.

Figure 3: Predicted changes in mean body temperature for heat-adapted and non-adapted athletes racing at world record pace over distances from 100m through to the marathon, under two environmental states.

A popular misconception with heat adaptation is that an elevated sweat secretion is accompanied by an equivalent rise in evaporative cooling.  Whilst increased sweating is advantageous for sedentary people with a low maximal sweat rate, this is rarely the case for endurance-trained athletes.  Evaporation is not determined by sweat rate, but the maximal evaporative cooling permitted by the environment and clothing.  To illustrate this, consider the predicted sweat rates necessary for heat balance at 33°C in the examples presented in Figure 3 (assuming complete evaporation): 1 960, 1 890 and 1 920 ml.h-1 (5000m to marathon).  These are not excessive sweat rates, and equate with an average required evaporation (Ereq) of 4200kJ (averaged over race durations and events).  However, the average maximal evaporation (Emax) was only 1100kJ.  Thus, only ~25% of the required sweat could be evaporated.  Indeed, sweat rates in excess of ~500 ml.h-1 represent wasteful fluid loss in these examples.

Heat adaptation can affect Emax.  Superior heat adaptation comes from long-term acclimatisation.  This is best observed in heat-adapted indigenes who display lower skin blood flows 31, 32 and higher skin temperatures during heat stress 32, 33, 34, relative to non-adapted controls.  However, such changes may not be evident in athletes following short-term adaptation.  Lower skin blood flows reduce cardiovascular strain, improve cardiovascular efficiency and result is less cardiovascular drift.  Higher skin temperatures reduce heat gain, and elevate cutaneous water vapour pressure, Emax and evaporation.  These effects are less apparent at high work rates (Figure 3).  However, significant reductions in body temperature may be evident, with respective increases in Emax at 22°C and 33°C averaging 8% and 12% across events.  The threshold for this effect occurs at some race distance beyond 1500m.

What about other sports?

From this analysis, it is clear that several factors affect the body temperature during competition, and these factors dictate thermal compensability (Ereq/Emax): exercise intensity, environmental conditions, clothing type and skin coverage, the work-to-rest ratio and the duration of competition.  Adaptation-induced optimisation of thermoregulatory efficiency is more important for longer events and sports, since dehydration is almost inevitable during competition in hot environments.  While it is impossible to address these issues for all sports, some generalisations are provided.

Firstly, consider team sports involving intermittent, high-intensity exercise.  Physiological strain, including core temperature, heart rate and sweat rates, is typically higher in intermittent than continuous exercise at the same average intensity.  Furthermore, team-sport athletes are generally larger and more heavily clothed, adversely affecting heat production and dissipation.  Indeed, sweat losses often exceed rehydration rates 35, with exercise impairing gastric emptying 36, 37, and progressive dehydration elevating intensity-specific core temperatures 38.

Field hockey provides a useful example.  Whilst the game is very fast, at any time, only a few players are working at high intensity, and only for a short duration.  International hockey is played on synthetic and watered surfaces.  Independently of the wider environmental humidity, evaporation elevates water vapour pressure immediately over the pitch.  Clothing typically covers 50-60% of the skin surface.  The exception being the goalkeeper, who is active for much of the game, albeit at a much lower intensity, but is heavily clad with protective and other clothing.  These factors reduce evaporation.  In Figure 3, this equates with an upward displacement of body temperature.  Heat adaptation must exert its influence by elevating skin temperature, since sweat rate increases have minimal impact.

Core temperatures in several field- and racquet sports appear to be similar to those for endurance exercise, presumably due to the factors described above.  Temperatures measured rectally and from gastro-intestinal thermometer pills at the completion of competition, have mostly been in the range 39-40°C for soccer 39, rugby 40, 41, squash (40-min game; 25), tennis (N=1; 20-min practice; Cotter: unpublished), and during golf played in the heat without rehydration 42.  However, as with endurance exercise, core temperatures may consistently exceed 40°C and even 41°C, bearing a stronger relationship with exercise intensity than fluid deficit 42.  A case exists for heat adaptation in those sports involving some combination of restricted water availability, prolonged play without player substitution, hot-humid environments, minimal air flow or the use of clothing, since there is minimal opportunity to implement behavioural strategies to combat core temperature elevations.  However, in sports such as golf, educational advice would suffice, since neither intensity nor speed should dictate behaviour.

Are there disadvantages of heat adaptation?
Cases where the benefits of heat adaptation are of minimal physiological consequence have been illustrated in this text.  While psychological and strategic advantages exist to undertaking heat adaptation, even if only to introduce the athlete to the heat, there are potential disadvantages.  These include impaired training quality, increased risk of overtraining during high-volume training periods, added time commitments, financial considerations and possibly athlete safety.

Throughout this paper, altitude training is referenced, since lessons should be learned from different adaptation practises.  For competition at altitude, athletes need to train and compete at altitude.  However, altitude training to improve sea level performance, whilst debated, is based on the premise that hypoxia stimulates red cell production and oxygen transport.  For adaptation to be initiated, the hypoxic stimulus must exceed a critical threshold (Figure 1), and this stimulus, by definition, must reduce performance.  One cannot occur without the other.  Therefore when athletes live at altitude, training quality is impaired.  Athletes can still work at maximal intensity, but this represents a sub-maximal performance.  The risk here is that one adaptation stimulus results in an intensity reduction of another.  This is the logic of the “live high and train low” approach.

This analogy transfers easily to heat adaptation.  Endurance training and heat adaptation serve quite different physiological and psychological outcomes, and require different training prescriptions.  There is no question that endurance exercise improves heat tolerance, but exercise-heat adaptation offers minimal benefit to the endurance fitness of highly trained athletes, but has some potential to even be detrimental.  If athletes are transported to hot-humid regions prior to competition, then training quality will suffer until the necessary adaptations become established.  The current authors offer the following recommendations (elaborated below) to optimise performance in the heat, whilst minimising negative outcomes: live in the heat, experience heat under competition, acclimate for a specific climate and do high-quality training in the cool.

First, hot-humid climates affect athletes during competition, but also have an immediate impact on arrival from abroad.  This is expressed in the form of lethargy, sleep disturbances, loss of appetite, mild dehydration, greater strain during training, and even a reduced training capacity.  The ideal way to become accustomed to these changes is to live for an extended time in the climate in which competition will occur (acclimatise).  This may require a moving into that climate at the end of winter so that physiological adaptations progress with seasonal changes: “live hot”.

Second, athletes need to experience the discomforts of competing in hot-humid conditions.  This is necessary to more fully appreciate the physiological strain, to practice behavioural strategies, to counteract adverse physiological effects and to rehearse pacing strategies.  Whilst record pacing under 33°C (Figure 3) has been modelled in this paper, attempts to achieve this in longer events are certain to fail.  There is no better way to learn this than to attempt personal best pacing (with appropriate supervision) in hot-humid conditions: “experience heat”.

Third, if heat adaptation is essential, then it is supplementary training, and not a substitute for high-quality endurance training.  Use the acclimation procedures discussed below, and closely replicate the conditions of the target climate: “acclimation specificity”.

Fourth, athletes must sustain training quality.  Unlike the hypoxic stress of altitude, temperature and humidity fluctuate.  Well-prepared athletes will ensure that training quality has been maintained, so that optimal performance under more favourable conditions will also be assured.  To achieve this, the current authors recommend that athletes undertake high-intensity training under temperate conditions: “train cool”.

To continue with the altitude analogy, one may ask: does heat adaptation enhance performance in temperate environments?  To the best of the authors’ knowledge, there is no convincing evidence to support (or refute) this proposition, despite endurance-based competition being thermally stressful.  As discussed above, one may suggest that the reverse may hold, particularly if training quality is compromised.

Stages of heat adaptation
The hallmark of heat adaptation is a progressive reduction in physiological strain.  This is demonstrated by reductions in core temperature, cardiac frequency and effort sense, combined with a greater sweat (sudomotor) activity during stress exposure.  These adaptations increase heat tolerance and elevate the margin for safety during stress loading.

Adaptation responses are attributed to inherited (genotypic adaptation) and acquired variations (phenotypic adaptation).  The focus of this review is upon phenotypic adaptation, expressed through changes in morphological configuration (e.g. sweat gland size) and modification of effector organ control (e.g. sudomotor threshold or sensitivity).  Regulatory changes may be positive or negative 44, such that acute responses are either amplified or blunted (habituated).  The classical example of a negative adaptation is the blunted metabolic reaction of Australian Aborigines to cold 45, where shivering thermogenesis is less pronounced during an acute cold exposure, relative to that seen in non-adapted Europeans.  It is often thought that heat adaptation displays only positive phenotypic trends 46, 47. However, this is not correct 48.

The heat adaptation continuum
In the short term, only positive adaptations are observed.  With acclimatisation, and perhaps long-term acclimation, significantly lower sweating responses are observed for indigenes 31, 33, 34 and some Europeans 49.  This lower sudomotor sensitivity confers greater regulatory efficiency and conserves water.  Like most adaptation processes, heat adaptation is a continuum, with the position of an individual along that continuum dictating the magnitude, and perhaps direction, of subsequent adaptation responses.  This continuum may have at least six recognisable transitions.  These transitional states are not stages of heat adaptation.  Indeed, they represent separate physiological conditions that have arisen in response to variations in the nature and size of various stimuli.  However, they represent progressive increases in heat tolerance, and may therefore be viewed as falling along a common heat-adaptation continuum.

The least adapted state is typified by the sedentary and thermally non-adapted person, who lives and works in a temperate or air-conditioned environment.  In this state, there exists neither exercise- nor heat-induced adaptation traits.  However, such individuals typically respond favourably to both training and heat adaptation stimuli (high responders).

Regular exposure to passive heating (e.g. sauna or bath) induces cardiovascular and sweating changes 50: positive heat adaptation.  While advantageous at rest, these responses have traditionally been found not to confer an advantage during exercise, as passive heating typically induces only slight-moderate strain, and is therefore a less effective adaptation stimulus 51, 52.

If a sedentary person becomes physically active, further adaptation occurs.  Now effector systems that support both exercise and thermoregulation undergo adaptation 3, 8, 53.  The literature is replete with reports of 20-25% elevations in peak oxygen consumption, or sweating, in high responders following adaptation.  Nevertheless, such observations must not be over-interpreted or assumed to occur in more adapted, low-responding individuals.

The fourth transitional state eventuates when a physically active person experiences regular, exercise-heat adaptation stimuli.  At this stage, less powerful adaptations occur, but the person will now acquire the physiological characteristics accompanying heat adaptation.  Prior to adaptation, physically active people possess a thermal advantage over sedentary individuals during exercise in the heat.  However, this advantage is lost when both groups are exposed to exercise-heat acclimation 54.

The final two states are typified by the elite, non-adapted and the elite, heat-adapted athlete.  In this context, “elite” refers to endurance training state.  By definition, elite athletes are low responders to exercise and thermal adaptation stimuli, responding as if already heat adapted 55.  However, research with highly trained athletes shows that, despite a high basal adaptation, substantial shifts in the physiological-, psychophysical- and performance responses can be induced through acclimation 56, 57.  While there is evidence that physically active indigenes display a more efficient negative adaptation 31, these authors are unaware of corroborating data in athletes.

Physiological changes accompanying heat acclimation
During the first week of heat exposure, athletic performance is most affected, and the risk of heat illness is greatest.  This is the first of three phases of heat adaptation: the acute response 49.  Avoidance of heat illness depends upon cellular and systemic adaptations, as well as molecular and cellular modifications to increase heat tolerance 58, 59.  While modifications of skin blood flow and sweating are readily identified, a broad spectrum of physiological changes is apparent during the second (positive adaptation) and third (negative) adaptation phases 49.  Some of these changes are summarised below.

An early adaptative response is an expansion of the plasma volume.  This improves maintenance of the osmotic potential of the blood.  Either reduced plasma protein loss 60, 61, or greater extracellular electrolyte retention 62, mediate this expansion, which was thought to wane with repeated heat exposure 3, 63.  However, this trend is only evident when constant exercise intensities (forcing functions) are used during heat adaptation.  It has recently been established that, when physiological strain is maintained using progressive increments in exercise intensity (see Combined exercise-heat acclimation), this expansion can be sustained for at least three weeks 64.  Indeed, the entire extracellular fluid volume can be held in a significantly elevated state 64.

During exercise in the heat, protracted sweating contracts the interstitial and plasma volumes.  This reduces central blood volume and stroke volume, elevating cardiac frequency to sustain cardiac output and blood pressure.  Heat adapted people, with an expanded vascular volume and cardiovascular adaptations, more effectively regulate blood pressure in the face of this fluid loss.  Thus, for a given exercise intensity, the stroke volume is larger and the cardiac frequency lower 52, 54, 65.

The above changes permit an elevation in skin blood flow during heat exposure (positive adaptation), and often a lowering of the vasodilatory threshold 66, 67.  Both mechanisms facilitate a more rapid translocation of central heat for dissipation.  Accordingly, people report reduced effort sense and tolerate exercise better.  These skin blood flow changes represent a second-phase response, but are not always evident.  When indigenous people from hot regions are studied, skin blood flow is lower than in non-adapted controls 31, 32; the third (negative) phase of adaptation.  A reduced skin blood flow can elevate skin temperature, minimising heat gain and increasing evaporation.  Central blood volume and mean arterial pressure are better defended, and progressive cardiovascular drift, typically observed during endurance exercise in the heat 38, 68, is largely prevented.  The net result is increased cardiovascular efficiency.  The negative aspect of this change would be that heat flow from the core is reduced.  At this time, the net effect of a greater heat loss at the periphery and superior cardiovascular stability, relative to lower core-to-peripheral heat flow, has not been investigated in non-indigenous people exercising at greater intensities.

An elevated skin temperature buffers thermal energy influx, but sweating provides the most effective means of heat dissipation in hot environments.  While it is a wasteful process that takes a few days (7-14) to become established 13, the most generally observed heat adaptation response is a marked elevation in sweat secretion (positive adaptation), though this is not always present 69.  Such increases result from a rise in the steady state sweat rate 7, 70, 71, an increase in sudomotor sensitivity and a reduced threshold for sweating onset 6, 71.  Heat adaptation also produces glandular hyperthrophy 70, 72 and increased glandular secretion, but does not change the number of active sweat glands 73, 74, 75.  Sweat glands also reabsorb more sodium and chloride 76, and are less affected by water accumulation on the skin (hidromeiosis: 49).  As a result of these changes, the non-adapted sweat rate (1-1.5 l.h-1) can be doubled, with quite prolific sweating observed in some elite athletes 77.  However, Mitchell et al. 65 described much of this additional secretion as extravagant, finding that a 30% elevation in sweating only increased evaporation by 10%.  Many of these adaptations also accompany endurance training, even in cool-temperate climates 6, 78, 79, but are less than elicited through similar training in the heat.

Unfortunately, a more robust sudomotor system does not implicitly provide a physiological benefit for the clothed athlete.  Clothing is a semi-permeable barrier to water molecules, so the microclimate rapidly attains a water vapour pressure that prevents evaporation, and heavy sweating elevates thermal discomfort 80, leading to rapid dehydration and performance decrements 16, 81, 82.

Collectively, these physiological transformations enable a greater heat flow to the skin, they provide a greater potential for heat dissipation, and can result in reduced core temperatures 10, 65, 83.  Thus, the competing, heat-adapted and semi-clothed athlete can move from a state deemed to be uncompensable, into a state in which thermal compensation is attainable, but at a considerable fluid cost.

Before leaving this topic, the third phase of heat adaptation is revisited.  Elsewhere, the evidence has been reviewed and the case presented, that lower sweat rates in tropical indigenes represent thermoregulatory habituation (negative adaptation), and that this state is consistent with superior heat adaptation 48.  It is an energy- and water-efficient adaptation.  This phenomenon was first suggested by Glaser and Whittow 84, observed but not appreciated by Wyndham et al. 85, and then supported experimentally by Fox et al. 31, Hori et al. 86 and Candas 49.  The present authors are not aware of any evidence for its existence in highly trained athletes, though it is suspected to be present in endurance trained people who have lived for several years in hot climatic regions.

Though evidence is fragmentary, and often confounded by differences in diet and health, data do exist to show that indigenes from the hottest climates (South Asia, Africa, India and Australia) have larger surface area to body mass ratios 87.  This morphological configuration is well suited to the energy-efficient dry heat exchanges, and to a reduced reliance upon evaporation (at least when air temperature is <36°C in the shade, or <31°C in the sun).  This difference was recently discussed by Marino et al. 88, when comparing ethnic differences in elite distance runners.

Physiological versus psychological adaptation
Many athletes fail to prepare thoroughly for competition, and are ill-equipped to deal with circumstances outside their experience base.  This is seen when an exhausted athlete arrives at a drink station and fails to find a pre-prepared drink, which the athlete mistakenly believes to be vital to performance (see: 89).  Tunnel vision is a characteristic of some athletes, with such occurrences being catastrophic.  Preparation for elite performance must include the development of strategies to cope with the unexpected.

Consider a marathoner preparing for the Olympics.  Since 1984, only one Olympics was held in conditions for which the risk of heat illness was low, and for three Games, the risk was very high, as it will again be in Beijing, China.  Accordingly, a record attempt must not form part of the racing strategy.  But at which pace should the athlete race?  The development of a complete answer to this question is beyond the scope of this review, but some general guidelines may be noted.

  • The athlete must experience the discomforts of competing under hot-humid conditions.  From this, the athlete must learn that personal best pacing will fail.  
  • The athlete must experiment to find the fastest possible race speed.  The climatic conditions must approximate the worst case scenario, but must also include realistic air movement and solar radiation.  
  • Several strategies must be developed since races infrequently go according to plan.  Within these plans must appear fluid-replacement considerations: how much, how often and in what form?  
  • All strategies and scenarios must be rehearsed in the heat, so that the athlete becomes comfortable with each, and with switching strategies.  

Finally, the athlete needs to experience racing against others following different strategies. Consider a situation where one athlete decides that the ideal pace is 3 min 15 sec per km, while others decide that 3 min per km is the appropriate strategy.  How does the athlete deal with this?  Inappropriate choices can undo years of physiological preparation, so psychological adaptation is absolutely essential.

Principles and practices of heat adaptation

Natural acclimatisation
It is well recognised that the Sherpas possess superior adaptation to altitude than the sojourning lowlander.  In the same manner, the natural acclimatisation associated with long-term residence in a hot climate is a most effective means of increasing heat tolerance 90.  In regions experiencing marked changes in air temperature, people display seasonal adaptations 52, 91.  Subtle climatic changes, in combination with metabolic heat production, result in a progressive elevation in the thermal tolerance of all physically-active people.  The exception is those who through behavioural interventions modify the microclimate to minimise exposure.  Accordingly, long-term residents from hot regions often appear to be better adapted than do recent arrivals 4, 48.  However, extended acclimatisation is rarely possible, with athletes frequently expected to move from one season to another, so other forms of adaptation are sought.

Passive heat acclimation
Passive methods are those in which external (exogenous) heat is used to evoke adaptation, with minimal contribution from metabolism.  Just as acclimatisation induces adaptation in sedentary residents, passively raising body temperatures also results in adaptation.  Various methods have been used to apply heat, including water baths, saunas, climate chambers and vapour-barrier suits (50, 66, 91, 92, 93, 94, 95).  In the 1960s, Fox and co-workers developed a very effective method, with the body temperature first being rapidly elevated (exercise in heat), then clamped by controlling heat loss (vapour barrier) while resting in the heat 50.  While moderately effective, it is recognised that passive acclimation is less effective than techniques using exercise 51, 52.  For athletes, one might therefore consider passive methods to be techniques of last resort.

Exercise-induced heat adaptation
Muscle temperatures rise in proportion to exercise intensity 96, readily eliciting hyperthermia, even in cold conditions 24.  Sustained and repeated elevation of body temperature, in combination with its slow decay during recovery, induces adaptation.  This was first recognised by Bean and Eichna 53, Robinson et al. 5 and Bass et al. 3, with Greenleaf 55 and Piwonka et al. 8 reporting endurance trained subjects to respond to heat stress as if already adapted.

Endurance fitness increases cardiovascular stability 9, 97, resulting in more favourable fluid dynamics during exposure 60.  Furthermore, the repeated stimulation to remove heat improves heat tolerance. Indeed, endurance trained people have an earlier sweating onset 98 and show a more rapid increase in sweat secretion 97.

Not only does endurance training elicit heat adaptation, but it facilitates more rapid attainment of adaptation during subsequent heat acclimation 10, 99.  Indeed, Pandolf et al. 10 found subjects with a superior aerobic power (>65 would acclimate rapidly (~4 days).  Moreover, slower adaptation is seen in people with a low basal fitness 100; the high- but slowly-responding person.  For such people, the initial stages of acclimation elevate fitness more than acclimation state.

It is important to recognise that aerobic power per se does not enhance heat adaptation, but the physiological adaptations occurring during fitness acquisition are beneficial.  In particular, adaptations associated with an increasing thermal load are critical. This is evident from experiments on swimmers 79, and the sweatless training of Hessemer et al. 101.  These projects established that exercise without a sustained increase in body temperature is an insufficient stimulus for heat adaptation.

Many researchers have tried to determine the most effective method through which exercise may improve heat tolerance.  Unfortunately, such comparisons are limited by the absence of measures of the thermal load (core temperature change).  Consider the field-based studies of Edholm et al. 90 and Turk and Worsley 102.  These experiments evaluated the efficacy of exercise-induced heat adaptation accompanying military training regimens, but without quantifying or standardising thermal load.  Similarly, Cohen and Gisolfi 40 studied the influence of endurance-training intensity on heat tolerance, also without recording thermal strain.  Such reports often form a basis for developing heat adaptation strategies, but the current authors do not support this practise, because it is difficult to interpret observations from such experiments in the absence of thermal strain standardisation.  Exceptions include studies conducted by Shvartz et al. 103 and Regan et al. 104, where exercise adaptation was shown to be less effective than a combined exercise-heat acclimation, even with equivalent core temperatures.

Nevertheless, exercise under cool-temperate conditions can foster heat adaptation, and several generalisations are noteworthy.  First, adaptation depends upon the capacity of the exercise mode to elevate body temperature. Without this, adaptation is unlikely.  Second, since heat storage is proportional to exercise intensity, heavier workloads are essential for adaptation.  Third, the cumulative adaptation impulse appears more critical than workload intensity, once the critical adaptation threshold has been surpassed.  Fourth, continuous exercise under temperate conditions more readily supports an elevated core temperature than intermittent exercise.  Finally, one must consider the principles of adaptation specificity.  Since both systemic and local mechanisms are affected during adaptation, exercise-induced adaptation should occur using the exercise mode in which the athlete will compete.

In spite of the benefits of temperate endurance training, it does not provide an adequate stimulus for complete heat adaptation. For instance, Wyndham 51 has suggested that the thermoregulatory benefits during heat exposures are only beneficial in the first two hours.  Therefore, for activities that extend beyond this time, endurance training is not an adequate substitute for heat acclimation 105, 106.  Furthermore, once an adequate basal fitness is achieved, there is little additional thermoregulatory advantage accompanying continued training 53, 107.  Thus for the endurance athlete, heat exposure must form an integral component of preparation for competition in the heat.  Indeed, the elevation of both core and skin temperatures appears necessary for complete adaptation 104, 108.  A partial progression towards this state may be achieved by training under a solar load, or by adding clothing to retain heat and moisture.

Interest in the latter procedure originated in the 1960s 9, 109, and it was thought to have significant practical advantages 110-113.  Unfortunately, there is little empirical evidence to support that possibility.  In fact, this method appears to have no greater benefit than endurance training alone.  Closer examination of the research shows a general failure to use appropriate experimental controls or to standardise dependent variables across conditions.  At this time, it is concluded that minimal physiological benefit can arise from using sweat clothing.

One might predict superior adaptation from training with a solar load, but few projects have focussed on this topic, and these are hard to interpret, due to difficulties controlling climatic conditions in the field.  However, such exposures most closely approximate the conditions that are obtained during acclimatisation and competition, and solar radiation readily elevates skin temperature.  In this regard, Jessen 114 established that the thermoregulatory responses for a fixed air temperature are significantly greater with solar radiation (goat model).  It is therefore reasonable to postulate that training with solar loading elicits a more specific adaptation, and one that is superior to that elicited within a climate chamber at the same temperature.  Evidence supporting this possibility was provided by Edholm et al. 90, who compared heat tolerance in soldiers living in different climates (desert versus cool).  Acclimatised soldiers displayed superior tolerance with fewer heat-related casualties.

Armstrong et al. 115 studied well-trained distance runners during spring and summer, finding equivalent heat tolerance.  Thus the solar loading of summer did not increase tolerance above that evident after spring.  This does not mean that these athletes were already optimally adapted.  It is more likely that summer training did not provide an adequate additional adaptation stimulus.  Two implications extend from this work.  First, well-trained endurance athletes do not need supplementary thermal preparation during seasonal changes in climate.  Second, when athletes travel from autumn-winter to compete in the opposite hemisphere, additional heat exposures will be required, due to the inability of the solar load during these months to elicit an adequate adaptation.

Combined exercise-heat acclimation
Whilst natural acclimatisation is a most effective means for heat adaptation, it is generally accepted that heat acclimation produces a reasonable approximation of those physiological benefits.  Artificial heat adaptation allows one to choose combinations of air temperature, humidity, wind speed and even radiant heat that most closely match the target conditions.  In addition, through the use of ergometers and training aids, the entire environment may be controlled.

Humid heat acclimation results in a greater elevation in sweating 69, 103.  Adaptation to dry conditions may not provide adequate protection for humid exposures 115.  While the experimental evidence relating to the transference of acclimation benefits between hot-dry and hot-humid conditions is sparse, it appears that adaptation specificity occurs 116.  For instance, Shvartz et al. 103 observed, when subjects were adapted to either hot-humid or hot-dry conditions, and subsequently exposed to hot-dry conditions, that less thermal strain was evident following hot-dry acclimation (see also: 2, 8, 9).

Conventional acclimation regimens involve moderate-to-heavy exercise in a temperature- and humidity-controlled chamber.  However, the cumulative adaptation impulse can be modified independently of climatic conditions, through changes in external power.  Three categories of exercise forcing function have been used: (a) constant work-rate regimens, (b) self-regulated exercise regimens, and (c) controlled-hyperthermia regimens 117.

(a)      Constant work-rate regimens
This is the most commonly reported heat acclimation method (see: 118, 119), and is the adaptation model used by researchers tasked with evaluating performance at fixed external work rates (10, 120).  For this procedure, subjects exercise at the same rate for the duration of every adaptation exposure.  Since heat storage is reduced as adaptation progresses, body temperatures are lower at the end of acclimation.

This method has wide application, but there are two major limitations regarding its effectiveness and interpretation.  First, since all subjects exercise at the same absolute intensity, their physiological strain may vary widely.  Second, since work rate is constant, thermal strain during sequential exposures progressively declines, constraining adaptation.  This point is further developed below.

(b)      Self-regulated exercise regimens
In this method, subjects follow prescribed work and rest intervals, but select and modify the work rate based on fitness or effort sense 122, 123.  Between-subject variability in adaptation is minimised, but the technique suffers in that it is difficult to control or standardise the endogenous thermal load.  This method has considerable practical utility in that it allows the athlete to adapt to and rehearse different pacing strategies under thermal loading.

(c)      Controlled hyperthermia regimens
The principle of the controlled hyperthermia (isothermal) method is to increase and clamp body temperatures above the sweating threshold, using intermittent exercise in the heat.  Fox et al. 124 first used this approach, with Turk and Worsley 102 adopting it to acclimate soldiers.  Havenith and van Middendorp 125 introduced a work-rest protocol, while the present authors have further developed the procedure to investigate acclimation-induced changes in sweating and body fluid balance 62, 64, 71, 104, 126.

From the present authors’ projects, two observations are important.  First, controlled hyperthermia in the heat invokes a superior adaptation, relative to that seen when the same method is used in temperate conditions, even though both stimuli elicited equivalent core temperature changes 104.  Thus exogenous heat seems necessary for adaptation.  Second, the present authors have established that the plasma volume expansion, considered once to be a transitory phenomenon, can be preserved for at least 21 days when the controlled hyperthermia method was used 64.

It is suggested that this regimen can induce a more complete adaptation than either of the other techniques.  But which regimen should the athlete adopt?  The controlled hyperthermia method targets thermal adaptation, and not athletic performance.  Its purpose is to clamp the thermal load.  For many athletes, particularly endurance runners, intermittent exercise is a training practise that does not mimic competition.  For such athletes, it is first recommended that intermittent exercise be used to stimulate adaptation, then continuous exercise to trial pacing strategies.  However, the use of a constant workload during acclimation is not recommended.

Forcing function considerations
Researchers evaluating the efficacy of acclimation regimens have typically compared adaptation responses elicited by different methods, and not differences in the exercise or thermal forcing functions.  Since it has been established that exercise without a core temperature elevation is not an adequate adaptation stimulus 79, 100, comparing heat acclimation methods without considering differences in thermal strain lacks validity.  It is more germane to compare the thermal potency of different methods, rather than physiological impact in isolation of the forcing function.  The apparent lack of recognition of this has made difficult the interpretation of many observations.

To illustrate the potential impact of differences in the thermal forcing function, the present authors compare two 12-day adaptation regimens, each of 90-min, each using exercise in the heat, and each aimed at initially elevating core temperature to 38.5°C.  The most common adaptation protocol uses a constant load function 10, 120.  Such regimens produce a gradual rise to the target core temperature (Figure 4A).  Since adaptation results in the physiological impact becoming progressively smaller, as reflected in core temperature, the adaptation impulse decreases over successive exposures.  The inset Figure shows this as a fall in cumulative core temperature.  Contrast this with the controlled-hyperthermia protocol, where the body temperature elevation is more rapid, and then held constant during successive exposures (Figure 4B).  The work rate must increase as adaptation progresses, resulting in the adaptation stimulus being higher and more stable (Figure 4A versus 4B inset).  Both regimens elicit acclimation.  One method targets a specific work rate, while the other targets a thermal load.  Both techniques have useful applications.  However, since physiological systems adapt to the specific nature of the adaptation stimulus, then both regimens invoke qualitatively similar, yet quantitatively different adaptations.

Figure 4: Core temperature changes on days 1, 4, 8 and 12 of two, 12-day heat acclimation regimens using either the constant work rate (A) and controlled hyperthermia methods (B). Insets show integrated core temperature for each day.

Hydration considerations
Rapid and effective adaptation occurs only through optimising the homeostatic disturbance.  This ultimately requires a thorough knowledge of the important elements and causal relations within and among stresses and the various strain responses.  Unfortunately, this knowledge is far from complete.  To illustrate this, current advice during heat acclimation 13, and during sustained exercise training in general 127, 128, is to attempt to maintain euhydration.  Yet, it is clear that fluid regulatory adaptations constitute an important facet of the heat adapted state 3, 63, 71, with dehydration being unavoidable in heat acclimation and most endurance training; albeit transient and relatively mild.  The present authors considered that thermal adaptation may actually be optimised by stressing fluid homeostasis. They tested this hypothesis during five days of heat acclimation using a cross-over (euhydration versus permissive dehydration) and controlled hyperthermia design.  Permissive dehydration resulted in greater gains in exercise capacity during a standardised, post-acclimation heat stress test 129.  It appears that mild, permissive dehydration (~2%) during acclimation may elicit favourable fluid regulatory responses.  This is equivalent to a 1.5kg mass change for an 80kg person.  This dehydration level will not be detrimental to health, training or performance (during or after acclimation).  Indeed, greater levels of dehydration are quite well tolerated, but can be detrimental to performance, and should generally be avoided.  For an evaluation of hydration practises, readers are directed to Noakes 37 (and the paper in this issue).


There may be no substitute for living and training under hot conditions to improve performance in the heat.  However, high intensity training is invariably hard to sustain in the heat.  With these points in mind, it is recommended that athletes live in the heat, experience heat under the pressure of competition, acclimate for a specific climate and then undertake high-quality training in the cool.  Athletes must not ignore the psychological aspects of preparing for competition in the heat, since inappropriate choices can undo years of physiological preparation.



Cumulative adaptation impulse: the sum of the products of the changes in mean body temperature and the exposure duration to each adaptation stimulus.

          Adaptation impulse = ((Tb-1-Tb-0)*t1) + ((Tb-2-Tb-0)*t2) + ((Tb-i-Tb-0)*ti)  [°C.min]
                      Tb-N = mean body temperature at time N [°C]
                      Tb-0 = initial (time zero) mean body temperature [°C]
                      tN = duration of each stimulus [min].

Thermal compensability: the ratio of required evaporative cooling to the maximal attainable evaporative cooling for a given environment and clothing configuration.

          Thermal compensability = Ereq / Emax       [dimensionless]
                      Ereq = required evaporative cooling [W]
                                  Emax = maximal attainable evaporative cooling [W].

          Ereq = H -Eresp ?R ?C          [W]
                      Ereq = required evaporative cooling [W]
                                              H = metabolic energy transformation; the algebraic sum of resting and exercising metabolism, and external work (M -(?W)) [W]
                                  Eresp = evaporation accompanying ventilation [W]
                                  R and C = heat exchanges via radiation and convection [W]

          R ?C = 6.45 * AD * (Tsk-Ta) / ITOT      [W]
                                  6.45 = constant
                                  AD = body surface area (Du Bois equation) [m2]
                                  Tsk = mean skin temperature [°C]
                                  Ta = air temperature [°C]
                                                                      ITOT = total insulation (1 clo = 0.155 m2.K.W-1), including trapped air and clothing insulation [m2.K.W-1].

          Emax = 6.45 * AD * im / ITOT * 2.2 * (Psk - (RHa* Pa))      [W]
                                  Emax = maximal attainable evaporative cooling [W]
                      AD = body surface area (Du Bois equation) [m2]
                      im = moisture permeability index (0.4 if unknown) [dimensionless]
                                              ITOT = total insulation (1 clo = 0.155 m2.K.W-1), including trapped air and clothing insulation [m2.K.W-1]
                      RHa = relative humidity of the air [%]
                      Pa = water vapour pressure of the air [kPa]
                      Psk = water vapour pressure at the skin surface [kPa]
                      6.45 and 2.2 = constants.

Address for correspondence:
Dr Nigel AS Taylor, Department of Biomedical Science, University of Wollongong, Wollongong, NSW 2522, Australia.
Tel.:+61 (2) 4221 3881
Fax:+61 (2) 4221 4094



    • Linnarsson D. Dynamics of pulmonary gas exchange and heart rates at the start and end of exercise. Acta Physiol. Scand. 1974; Suppl. 415: 1-68.
    • Eichna LW, Park CR, Nelson N, et al.  Thermal regulation during acclimatization in hot dry (desert type) environment. Am. J. Physiol. 1950; 163: 585-597.
    • Bass DE, Kleeman DR, Quinn M, et al. Mechanisms of acclimatization to heat in man. Medicine 1955; 34: 323-380.
    • Hellon RF, Jones RM, Macpherson RK, et al. Natural and artificial acclimatisation to hot environments. J. Physiol. 1956; 132: 559-576.
    • Robinson S, Turrell ES, Belding HS, et al. Rapid acclimatization to work in hot climates. Am. J. Physiol. 1943; 140: 168-176.
    • Nadel ER, Pandolf KB, Roberts MF, et al. Mechanisms of thermal acclimation to exercise and heat. J. Appl. Physiol. 1974; 37: 515-520.
    • Libert JP, Candas V, Vogt JJ. Modifications of sweating responses to thermal transients following heat acclimation.  Eur. J. Appl. Physiol. 1983; 50: 235-246.
    • Piwonka RW, Robinson S, Gay VL, et al. Acclimatization of men to heat by training. J. Appl. Physiol. 1965; 20: 379-384.
    • Gisolfi CV, Robinson S. Relations between physical training, acclimatisation, and heat tolerance. J. Appl. Physiol. 1969; 26: 530-534.
    • Pandolf KB, Burse RL, Goldman RF. Role of physical fitness in heat acclimatisation, decay, and reinduction. Ergonomics. 1977; 20: 399-408.
    • Adolph EF. Perspectives of adaptation: some general properties. In: Dill, D.B., and Adolph, E.F. Handbook of physiology. Section 4. Adaptation to the environment. American Physiological Society, Washington, D.C. 1964, pp. 27-35.
    • Banister EW, Calvert TW. Planning for future performance: implications for long term training. Can. J. Appl. Sport Sci. 1980; 5: 170-176.
    • Armstrong LE, Maresh CM. The induction and decay of heat acclimatisation in trained athletes. Sports Med. 1991; 12: 302-312.
    • Belding HS, Hatch TF. Index for evaluating heat stress in terms of resulting physiological strain. Heat Piping Air Cond. 1955; 27: 129-136.
    • Goldman RF. Introduction to heat-related problems in military operations. In: Pandolf, K.B., Burr, R.E., Wenger, C.B., and Pozos, R.S. (Eds). Medical aspects of harsh environments. Volume 1. In: Zajtchuk, R., and Bellamy, R.F. (Eds). Textbook of Military Medicine. Department of the Army, Office of the Surgeon General, and Borden Institute. Washington, DC. 2001, pp. 3-49.
    • Cheung SS, McLellan TM, Tenaglia S. The thermophysiology of uncompensable heat stress: physiological manipulations and individual characteristics. Sports Med. 2000; 29: 329-359.
    • Kenney LW, Johnson JM. Control of skin blood flow during exercise. Med. Sci. Sports Exerc. 1992; 24: 303-312.
    • Nielsen B, Hales JR, Strange S, et al. Human circulatory and thermoregulatory adaptations with heat acclimation and exercise in a hot, dry environment. J. Physiol. 1993; 460: 467-485.
    • Fuller A, Carter RN, Mitchell D. Brain and abdominal temperatures at fatigue in rats exercising in the heat. J. Appl. Physiol. 1998; 84: 877-883.
    • Gonzalez-Alonso J, Teller C, Andersen SL, et al. Influence of body temperature on the development of fatigue during prolonged exercise in the heat. J. Appl. Physiol. 1999; 86: 1032-1039.
    • Bruck K, Olschewski H. Body temperature related factors diminishing the drive to exercise. Can. J. Physiol. Pharmacol. 1987; 65: 1274-1280.
    • Mills PC, Smith NC, Casas I, et al. Effects of exercise intensity and environmental stress on indices of oxidative stress and iron homeostasis during exercise in the horse. Eur. J. Appl. Physiol. 1996; 74: 60-66.
    • Pugh LGCE, Corbett JL, Johnson RH. Rectal temperatures, weight losses, and sweat rates in marathon running. J. Appl. Physiol. 1967; 23: 347-352.
    • Gisolfi C, Wilson NC, Claxton B. Work-heat tolerance of distance runners. Annals NY Acad Sci. 1979; 301: 139-150.
    • Fuller A, Oosthuyse T, Maloney SK, et al. Evaluation of miniature data loggers for body temperature measurement during sporting activities. Eur. J. Appl. Physiol. 1999; 79: 341-346.
    • Maughan RJ, Leiper JB, Thompson J. Rectal temperature after marathon running. Br. J. Sports Med. 1985; 19: 192-195.
    • Noakes TD, Myburgh KH, du Plessis J, et al. Metabolic rate, not percent dehydration, predicts rectal temperature in marathon runners. Med. Sci. Sports Exerc. 1991; 23: 443-449.
    • Levine BD. Intermittent hypoxic training: fact and fancy. High Alt. Med. Biol. 2002; 3: 177-193.
    • Tatterson AJ, Hahn AG, Martin DT, et al. Effects of heat stress on physiological responses and exercise performance in elite cyclists. J. Sci. Med. Sport. 2000; 3: 186-193.
    • Tucker R, Rauch L, Harley YXR, et al. Impaired exercise performance in the heat is associated with an anticipatoiy reduction in skeletal muscle recruitment. Pflugers Arch. 2004; 448: 422-430.
    • Fox RH, Budd GM, Woodward PM, et al. A study of temperature regulation in New Guinea people. Phil. Trans. Royal Soc. London. Series B. 1974; 268: 375-391.
    • Katsuura T, Tachibana ME, Okada A, et al. Comparison of thermoregulatory responses of heat between Japanese Brazilians and Japanese. J. Therm. Biol. 1993; 18: 299-302.
    • Thompson ML. A comparison between the number and distribution of functioning eccrine glands in Europeans and Africans. J. Physiol. 1954; 123: 225-233.
    • Saat M, Tochihara Y, Hashiguchi N, et al. Effects of exercise in the heat on thermoregulation of Japanese and Malaysian males. J. Physiol. Anthropol. 2005; 24: 267-275.
    • Godek SF, Bartolozzi AR, Godek JJ, et al. Sweat rate and fluid turnover in American football players compared with runners in a hot and humid environment. Br. J. Sports Med. 2005; 39: 205-211.
    • Costill DL, Saltin B. Factors limiting gastric emptying during rest and exercise. J. Appl. Physiol. 1974; 37: 679-683.
    • Noakes TD. Overconsumption of fluids by athletes: advice to overdrink may cause fatal hyponatraemic encephalopathy. Brit. Med. J. 2003; 327: 113-114.
    • Montain SJ, Coyle EF. Influence of graded dehydration on hyperthermia and cardiovascular drift during exercise. J. Appl. Physiol. 1992; 73: 1340-1350.
    • Guerra I, Chaves R, Barros T, et al. The influence of fluid ingestion on performance of soccer players during a match. J. Sports Sci. Med. 2004; 3: 198-202.
    • Cohen I, Mitchell D, Seider R, et al. The effect of water deficit on body temperature during rugby. S. Afr. Med. J. 1981; 60: 11-14.
    • Goodman C, Cohen I, Walton J. The effect of water intake on body temperature during rugby matches. S. Afr. Med. J. 1985; 67: 542-544.
    • Kobayashi Y, Hosoi T, Takeuchi T, et al. Heat stress and fluid replacement in golfers. Jap. J. Phys. Fit. Sports Med. 1996; 45: 119-126.
    • Dancaster CP. Body temperatures after rugby. S. Afr. Med. J. 1972; 46: 1872-1874.
    • Mekjavic IB, Bligh J. The pathophysiology of hypothermia. Int. Rev. Ergon. 1987; 1: 201-218.
    • Hicks CS, Matters RF. The standard metabolism of the Australian Aborigines. Aust. J. Exp. Biol. Med. Sci. 1933; 11: 177-183.
    • Wyndham CH, Metz B, Munro A. Reactions to heat of Arabs and Caucasians. J. Appl. Physiol. 1964; 19: 1051-1054.
    • Duncan MT, Horvath SM. Physiological adaptations to thermal stress in tropical Asians. Eur. J. Appl. Physiol. 1988; 57: 540-544.
    • Taylor NAS. Ethnic differences in thermoregulation: genotypic versus phenotypic heat adaptation. J. Therm. Biol. 2005 [In press].
    • Candas V. Adaptation to extreme environments. Thermophysiological changes in man during humid heat acclimation. In: Dejours. Comparative physiology of environmental adaptations. Volume 2. Karger, Basel. 1987, pp. 76-93.
    • Fox RH, Goldsmith R, Hampton IFG, et al. Heat acclimatization by controlled hyperthermia in hot-dry and hot-wet climates. J. Appl. Physiol. 1967; 22: 39-46.
    • Wyndham CH. The physiology of exercise under heat stress. Ann. Rev. Physiol. 1973; 35: 193-220.
    • Shapiro Y, Hubbard RW, Kimbrough CM, et al. Physiological and hematologic responses to summer and winter dry-heat acclimation. J. Appl. Physiol. 1981; 50: 792-798.
    • Bean WB, Eichna LW. Performance in relation to environmental temperature. Fed. Proc. 1943; 2: 144-158.
    • Cadarette BS, Sawka MN, Toner MM, et al. Aerobic fitness and hypohydration response to exercise-heat stress. Aviat. Space & Environ. Med. 1984; 55: 507-512.
    • Greenleaf JE. Lack of artificial acclimatization to heat in physically fit subjects. Nature. 1964; 203: 1072.
    • Adams WC, Fox RH, Fry AJ, et al. Thermoregulation during marathon running in cool, moderate, and hot environments. J. Appl. Physiol. 1975; 38: 1030-1037.
    • Garrett AT, Creasy RH, Rehrer NJ, et al. Short-term heat acclimation is effective for highly trained athletes. In: The New Zealand Sports Medicine and Science Conference. Sports Medicine New Zealand Inc., Dunedin, New Zealand. 2003: 60.
    • Moseley PL. Heat shock proteins and heat adaptation of the whole organism. J. Appl. Physiol. 1997; 83: 1413-1417.
    • Kregel KC. Heat shock proteins: Modifying factors in physiological stress responses and acquired thermotolerance. J. Appl. Physiol. 2002; 92: 2177-2186.
    • Senay LC. Changes in plasma volume and protein content during exposures of working men to various temperatures before and after acclimatization to heat: Separation of the roles of cutaneous and skeletal muscle circulation. J. Physiol. 1972; 224: 61-81.
    • Harrison MH. Effects of thermal stress and exercise on blood volume in humans. Physiol. Rev. 1985; 65: 149-209.
    • Patterson MJ, Stocks JM, Taylor NAS. Heat acclimation-induced plasma volume expansion: The role of electrolyte retention. J. Physiol. 1999; 521: 102-.
    • Wyndham CH, Benade AJA, Williams CG, et al. Changes in central circulation and body fluid spaces during acclimatization to heat. J. Appl. Physiol. 1968; 25: 586-593.
    • Patterson MJ, Stocks JM, Taylor NAS. Sustained and generalised extracellular fluid expansion following heat acclimation. J. Physiol. 2004; 559: 327-334.
    • Mitchell D, Senay LC, Wyndham CH, et al. Acclimatisation in a hot, humid environment: energy exchange, body temperature, and sweating. J. Appl. Physiol. 1976; 40: 768-778.
    • Fox RH, Goldsmith R, Kidd DJ, et al. Blood flow and other thermoregulatory changes with acclimation to heat. J. Physiol. 1963; 166: 548-562.
    • Yamazaki F, Hamasaki K. Heat acclimation increases skin vasodilation and sweating but not cardiac baroreflexes in heat-stressed humans. J. Appl. Physiol. 2004; 95: 1567-1574.
    • Coyle EF, Gonzalez-Alonso J. Cardiovascular drift during prolonged exercise: new perspectives. Exerc. Sport Sci. Rev. 2001; 29: 88-92.
    • Henane R. Acclimatization to heat in man: giant or windmill, a critical appraisal. In: Szelenyi, M., and Szekely, M. Proc. 28th Int. Congress Physiol. Sci. 1980: 275-284.
    • Sato F, Owen M, Matthes R, et al. Functional and morphological changes in the eccrine sweat gland with heat acclimation. J. Appl. Physiol. 1990; 69: 232-236.
    • Patterson MJ, Stocks JM, and Taylor NAS. Humid heat acclimation does not elicit a preferential sweat redistribution towards the limbs. Am. J. Physiol. 2004; 286: R512-R518.
    • Sato K, Sato F. Individual variations in structure and function of human eccrine sweat gland. Am. J. Physiol. 1983; 245: R203-208.
    • Sargent F, Smith CR, and Batterton DL. Eccrine sweat gland activity in heat acclimation. Int. J. Biometeor. 1965; 9: 229-231.
    • Peter J, Wyndham CH. Activity of the human eccrine sweat gland during exercise in a hot humid environment before and after acclimatization. J. Physiol. 1966; 187: 583-594.
    • Inoue Y, Havenith G, Kenney WL, et al. Exercise- and methylcholine-induced sweating responses in older and younger men: effect of heat acclimation and aerobic fitness. Int. J. Biometeor. 1999; 42: 210-216.
    • Allan JR, Wilson CG. Influence of acclimatization on sweat sodium concentration. J. Appl. Physiol. 1971; 30: 708-712.
    • Armstrong LE, Hubbard RW, Jones BH, et al. Preparing Alberto Salazar for the heat of the 1984 Olympic Games. Physician & Sportsmed. 1986; 14: 73-81.
    • Avellini BA, Shapiro Y, Fortney SM, et al. Effects of heat tolerance on physical training in water and on land. J. Appl. Physiol. 1982; 53: 1291-1298.
    • Henane R, Flandrois R, Charbonnier JP. Increase in sweating sensitivity by endurance conditioning in man. J. Appl. Physiol. 1977; 43: 822-828.
    • Hensel H. Thermoreception and temperature regulation. In: Monographs of the Physiological Society. Number 38. Academic Press. London. 1981.
    • McLellan TM, Jacobs I, Bain JB. Influence of temperature and metabolic rate on work performance with Canadian Forces NBC clothing. Aviat. Space Environ. Med. 1993; 64: 587-594.
    • Goldman RF. Heat stress in industrial protective encapsulating garments. In: Martin WF and Levine SP. Protecting personnel at hazardous waste sites. Butterworth-Heinemann, Boston. 1994. pp. 258-315.
    • Houmard JA, Costill DL, Davis JA, et al. The influence of exercise intensity on heat acclimation in trained subjects. Med. Sci. Sports & Exerc. 1990; 22: 615-620.
    • Glaser EM, Whittow GC. Evidence for a non-specific mechanism of habituation. J. Physiol. 1953; 122: 3P-4P.
    • Wyndham CH, Bouwer WvdM, Devine MG, et al. Physiological responses of African labourers at various saturated air temperatures, wind velocities and rate of energy expenditure. J. Appl. Physiol. 1952; 5: 290-298.
    • Hori S, Ihzuka H, Nakamura M. Studies on physiological responses of residents in Okinawa to a hot environment. Jap. J. Physiol. 1976; 26: 235-244.
    • Roberts DF. Body weight, race and climate. Am. J. Phys. Anthrop. 1953; 11: 533-558.
    • Marino FE, Lambert MI, Noakes TD. Superior performance of African runners in warm humid but not in cool environmental conditions. J. Appl. Physiol. 2004; 96: 124-130.
    • Maughan RJ. Functional ingredients in sports drinks. In: Watson DH. Performance functional foods. CRC Press. Boca Raton. 2003, pp.119-139.
    • Edholm OG, Fox RH, Adam JM, et al. Comparison of artificial and natural acclimatization. Fed. Proc. 1963; 22: 709-715.
    • Inoue Y, Nakao M, Okudaira S, et al. Seasonal variation in sweating responses of elder and younger men. Eur. J. Appl. Physiol. 1995; 70: 6-12.
    • Fox RH, Goldsmith R, Hampton IFG, et al. The nature of the increase in sweating capacity produced by heat acclimatisation. J. Physiol. 1964; 171: 368-376.
    • Fox RH. A review of studies on the physiology of heat stress. Army Personnel Research Committee Report 68/A1. Ministry of Defence. U.K. 1968.
    • Sugenoya J, Ogawa T, Asayama M, et al. Involvement of the central sudomotor mechanism in an increased sweating capacity following heat acclimation. J. Aichi Med. Univ. Assoc. 1986; 14: 653-661.
    • Ogawa T, Ohnishi N, Yamashita Y, et al. Effect of facial cooling during heat acclimation process on adaptive changes in sweating activity. Jap. J. Physiol. 1988; 38: 479-490.
    • Saltin B, Hermansen L. Esophageal, rectal and muscle temperature during exercise. J. Appl. Physiol. 1966; 21: 1757-1762.
    • Wells CL, Constable SH, Haan AL. Training and acclimatisation: effects on responses to exercise in a desert environment. Aviat. Space & Environ. Med. 1980; 51: 105-112.
    • Nadel ER. Control of sweating rate while exercising in the heat. Med. Sci. Sports & Exerc. 1979; 1: 31-35.
    • Cohen JS, Gisolfi CV. Effects of interval training on work-heat tolerance of young women. Med. Sci. Sports Exerc. 1982; 14: 46-52.
    • Kok R. Heat tolerance of Bantu undergoing acclimatization. S Afr. Med. J. 1973; 47: 960.
    • Hessemer V, Zeh A, Bruck K. Effects of passive heat adaptation and moderate sweatless conditioning on responses to cold and heat. Eur. J. Appl. Physiol. 1986; 55: 281-289.
    • Turk J, Worsley DE. A technique for rapid acclimatization to heat for the army. Army Personnel Research Establishment Report 12/74. Ministry of Defence. Farnborough. U.K. 1974.
    • Shvartz E, Saar E, Meyerstein N, et al. A comparison of three methods of acclimatisation to dry heat. J. Appl. Physiol. 1973; 34: 214-219.
    • Regan JM, Macfarlane DJ, Taylor NAS. An evaluation of the role of skin temperature during heat adaptation. Acta. Physiol. Scand. 1996; 158: 365-375.
    • Pandolf KB. Effects of physical training and cardiorespiratory fitness on exercise-heat tolerance: recent observations. Med. Sci. Sports & Exerc. 1979; 11: 60-65.
    • Armstrong LE, Pandolf KB. Physical training, cardiorespiratory physical fitness and exercise-heat tolerance. In: Pandolf, K.B., Sawka, M.N., and Gonzales, R.R. Human performance physiology and environmental medicine at terrestrial extremes. Benchmark Press. Indianapolis. 1988, pp.199-226.
    • Eichna LW, Bean WB, Ashe WF, et al. Performance in relation to environmental temperature. Reactions of normal young men to hot, humid (simulated jungle) environment. Bull. Johns Hopkin's Hosp. 1945; 76: 25-58.
    • Chen WY, Elizondo RS. Peripheral modification of thermoregulatory function during heat acclimation. J. Appl. Physiol. 1974; 37: 367-373.
    • Bass DE. Thermoregulatory and circulatory adjustments during acclimatization to heat in man. In: Hardy, J.D. Temperature: its measurement and control in science and industry. Reinhold. New York. 1963, pp. 299-305.
    • Allan JR, Crowdy JP, Haisman MF. The use of a vapour-barrier suit from the practical induction of artificial acclimatization to heat: I. Winter experiment. Army Personnel Research Establishment. Report 4. Ministry of Defence. U.K. 1965.
    • Crowdy JP, Haisman MF. The use of a vapour-barrier suit from the practical induction of artificial acclimatization to heat: II. Summer experiment. Army Personnel Research Establishment. Report 4. Ministry of Defence. U.K. 1965.
    • Marcus P. Heat acclimatization by exercise-induced elevation of body temperature. J. Appl. Physiol. 1972; 33: 283-288.
    • Dawson B. Exercise training in sweat clothing in cool conditions to improve heat tolerance. Sports Med. 1994; 17: 233-244.
    • Jessen C. Thermal afferents in the control of body temperature. In: Schonbaum E and Lomax P. Thermoregulation, physiology and biochemistry. Pergamon Press. New York. 1990, pp.153-184.
    • Armstrong LE, Hubbard RW, DeLuca JP, et al. Heat acclimatization during summer running in the northern United States. Med. Sci. Sports & Exerc. 1987; 19: 131-136.
    • Goldman RF, Green EB, Iampietro PF. Tolerance of hot, wet environments by resting men. J. Appl. Physiol. 1965; 20: 271-277.
    • Taylor NAS. Principles and practices of heat adaptation. J. Human-Environ. Sys. 2000; 4: 11-22.
    • Greenleaf JE, Greenleaf CJ. Human acclimation and acclimatization to heat. A compendium of research. NASA Technical Memorandum. NASA TM X-62,008. Ames Research Center, Moffett Field. U.S.A. 1970.
    • Sciaraffa D, Fox SC, Stockmann R, et al. Human acclimation and acclimatization to heat: A compendium of research - 1968-1978. NASA Technical Memorandum. NASA 81181. Ames Research Center, Moffett Field. U.S.A. 1980.
    • Pandolf KB, Cadarette BS, Sawka MN, et al. Thermoregulatory responses of middle-aged and young men during dry-heat acclimation. J. Appl. Physiol. 1988; 65: 65-71.
    • Miller DA. Heat acclimation procedures developed for use by the U.S. Marine Corps aboard ship en route to hot weather operations. Naval Medical Research Institute Report number NMRI-CO1-DAM:rh-3902. Bethesda, U.S.A. 1984.
    • Armstrong LE, Hubbard RW, DeLuca JP, et al. Self-paced heat acclimation procedures. U.S. Army Research Institute of Environmental Medicine. Technical report number T8/86. Natick. U.S.A. 1986.
    • Fox RH, Goldsmith R, Kidd DJ, et al. Acclimatization of the sweating mechanism in man. J. Physiol. 1961; 157: 56-57.
    • Havenith G, van Middendorp H. Determination of the individual state of acclimatization. IZF report 1986-27. TNO Institute for Perception. Soesterberg, Netherlands. 1986.
    • Cotter JD, Patterson MJ, Taylor NAS. Short-term heat acclimation and its impact upon sudomotor function. Eur. J. Appl. Physiol. 1997; 76: 181-186.
    • American College of Sports Medicine. Position stand on exercise and fluid replacement. Med. Sci. Sports Exerc. 28:i-vii. 1996.
    • Casa DJ, Armstrong LE, Hillman SK, et al. National Athletic Trainers' Association Position Statement: Fluid Replacement for Athletes. J. Ath. Training. 2000; 35: 212-224.
    • Garrett AT, Goossens N, Rehrer NJ, et al. The role of dehydration in short-term heat acclimation. Med. Sci. Sports Exerc. 2004; 36: S83.