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Athlete Health and Performance Research Centre, Aspetar Orthopaedic and Sports Medicine Hospital, Doha, QatarDepartment of Life Sciences, Centre for Sports Medicine and Human Performance, Division of Sport, Health and Exercise Sciences, Brunel University London, Uxbridge, UK
This review examines the cardiovascular adaptations along with total body water and plasma volume adjustments that occur in parallel with improved heat loss responses during exercise-heat acclimation. The cardiovascular system is well recognized as an important contributor to exercise-heat acclimation that acts to minimize physiological strain, reduce the risk of serious heat illness and better sustain exercise capacity. The upright posture adopted by humans during most physical activities and the large skin surface area contribute to the circulatory and blood pressure regulation challenge of simultaneously supporting skeletal muscle blood flow and dissipating heat via increased skin blood flow and sweat secretion during exercise-heat stress. Although it was traditionally held that cardiac output increased during exercise-heat stress to primarily support elevated skin blood flow requirements, recent evidence suggests that temperature-sensitive mechanisms may also mediate an elevation in skeletal muscle blood flow. The cardiovascular adaptations supporting this challenge include an increase in total body water, plasma volume expansion, better sustainment and/or elevation of stroke volume, reduction in heart rate, improvement in ventricular filling and myocardial efficiency, and enhanced skin blood flow and sweating responses. The magnitude of these adaptations is variable and dependent on several factors such as exercise intensity, duration of exposure, frequency and total number of exposures, as well as the environmental conditions (i.e. dry or humid heat) in which acclimation occurs.
) and that cardiovascular adaptations are important contributors to the improved exercise capacity and reduced risk of serious heat illness conferred by exercise-heat acclimation (
). Early physiologists recognized that a reduction in the elevated heart rate from heat stress likely was an important marker of adaptation to hot climates (
were among the first to appreciate that the cardiovascular system likely imposed a physiological limitation to exercise performance under heat stress by “drafting blood away from the brain and the muscles to the skin”. Subsequently,
demonstrated that improved evaporative cooling of the skin reduces cardiovascular strain and “keeps off fatigue” during exercise-heat stress. Perhaps the most important modern contributions regarding cardiovascular control with heat stress were made by
Integration of cardiovascular control systems in dynamic exercise.
in: LB Rowell JT Shepherd Handbook of Physiology: Exercise Regulation and Integration of Multiple Systems. American Physiological Society,
Bethesda, MD1996: 770-838
). This review examines the cardiovascular adaptations along with total body water and plasma volume adjustments that occur in parallel with improved heat loss responses during exercise-heat acclimation. These physiological adaptations/adjustments are critical to exercise-heat acclimation as upright posture, increased cutaneous vasodilation and greater sweat secretion provide severe challenges to blood pressure regulation, performance, and health during exercise hot conditions.
2. Adaptation to heat
When humans are repeatedly exposed to conditions that are sufficiently stressful to elicit profuse sweating and elevate skin and core temperature, adaptations develop that reduce the deleterious effects of heat stress: heat acclimation or acclimatization. Heat acclimation refers to repeated periods of heat exposure undertaken in artificial or laboratory settings, whereas heat acclimatization results from exposure to natural environments. Although both natural and artificial hot environments elicit similar physiological adaptations (
), heat acclimatization provides more specific responses due to exposure to the exact conditions that will be encountered during work or competition (i.e. exercise task, solar radiation and terrain/geography) (
). The phenotypic adaptations that develop during repeated exposure to hot conditions improve performance during submaximal exercise, increase maximal aerobic capacity (O2max) (
) in the heat. These benefits are achieved through plasma volume expansion, better maintenance of fluid balance, enhanced sweating and cutaneous blood flow responses, lowered exercising metabolic rate, and acquired thermal tolerance through the heat shock response, all of which contribute to improved cardiovascular stability and exercise performance during heat stress (
Physiological adaptations related to repeated heat exposure develop relatively quickly with 75–80% of the acclimation process occurring in the first 4–7 days (Fig. 1) (
argue that heat acclimation develops as a continuum of processes and have proposed a conceptual model characterized by a distinct biphasic pattern. The initial short-term phase is transient and manifested by a decreased effector organ output-to-autonomic signal ratio, such that accelerated efferent activity is required to override the suboptimal peripheral responsiveness and produce adequate effector output. The second long-term phase is stable and characterized by an increased effector organ output-to-autonomic signal ratio, as both central and peripheral adaptations enhance physiological efficiency and reduce the need for accelerated excitation.
Fig. 1The time course of adaptations to exercise-heat acclimation. Within a week of acclimation plasma volume expansion occurs and heart rate is reduced during exercise at a given work rate. Core and skin temperatures are also reduced when exercising at a given work rate, whereas sweat rate increases. Perceptually, the rating of thermal comfort is improved. As a result, aerobic exercise capacity is increased. Of note, the magnitude of these adaptations is dependent on the initial state of acclimation and the acclimation protocol (e.g. environmental conditions and exercise intensity). Adapted with permission from
). Accordingly, the magnitude of physiological adaptation induced by heat acclimation or acclimatization depends largely on the initial heat exposure status (i.e. recent heat exposure, season, fitness level), as well as the exercise intensity, duration, frequency, and number of heat exposures, along with the induction protocol (
Repeated exercise-heat exposure at a constant work rate (i.e. traditional occupational and military heat acclimation protocol) is not likely as effective in eliciting adaptation as maintaining hyperthermia at a given core temperature (e.g. 38.5 °C; controlled hyperthermia or isothermic heat acclimation) (
). Indeed, the traditional heat acclimation model offers a constant forcing function (i.e. fixed endogenous and exogenous thermal loads), which as adaptations progressively develop, results in decreased physiological strain and reduced further adaptations (
). In contrast, with controlled hyperthermia protocols the forcing function is increased in proportion to the adaptations by manipulating the endogenous and/or exogenous thermal loads (
). Therefore, it is suggested that greater physiological adaptations occur during a given period with controlled hyperthermia than traditional approaches. Interestingly, recent studies have not found greater adaptations with controlled hyperthermia and the explanation for those findings are unclear (
The similar adaptations between some traditional and controlled hyperthermia approaches may stem in part from different acclimation protocols inducing distinctive autonomic responses that result in comparable physiological adjustments. For example,
demonstrated in rats that both heat acclimation and exercise training improve cardiac efficiency (i.e. decreased rate pressure product: heart rate × systolic blood pressure) during exercise in the heat; however this was achieved via different pathways. Heat acclimation attenuated the increase in blood pressure, whereas exercise training had a more pronounced effect on heart rate during exercise in the heat (
). In humans, a controlled exercise intensity heat acclimation protocol has recently been suggested whereby maintaining a given level of cardiovascular strain during daily exercise-heat exposure may optimize adaptations (
). The level of strain achieved and sustained in this protocol would correspond to the heart rate associated with a specific relative exercise intensity (e.g. percent O2max, ventilatory or lactate threshold) in cool conditions. This heart rate would be sustained during exercise in the heat by increasing the power output accordingly as the individual adapted. Consequently, absolute work rate would increase as acclimation developed, thus providing a constant cardiovascular stimulus, based on the level of strain targeted.
The physiological adaptations associated with heat acclimation are transient and gradually disappear if consistent heat exposure is not maintained. The adaptations that develop most rapidly (e.g. improvements in heart rate) during acclimation are also those that are lost most quickly (
). Currently, there is no agreement concerning the rate of decay for heat acclimation. For example, it has been suggested that one day of exercise in the heat is required for every 5 days spent without heat exposure to maintain adaptation (
). Notwithstanding, there is support for the notion that aerobic fitness and regular exercise are critical during the decay period in providing stimulus for maintaining the achieved adaptations (
The fraction of mass represented by water in the human body is ~60%. This fraction varies in relation to body composition however, such that total body water estimations are generally calculated as a constant fraction of fat-free mass with a factor of ~0.737 (
Whole-body fluid distribution in humans during dehydration and recovery, before and after humid-heat acclimation induced using controlled hyperthermia.
). This increase is divided between extracellular (plasma and interstitial fluid) and intracellular fluid compartments. The division of the total body water increase between compartments is variable, with studies reporting that extracellular fluid accounts for greater, equal and smaller than its percentage increase in total body water after heat acclimation (
). Total body water, extracellular and intracellular fluid volumes and plasma volume were expanded either during or after exercise heat acclimation. The increase in total body water during heat acclimation was likely due to the large aldosterone and arginine vasopressin secretion occurring during exercise-heat stress (
). A further pathway modulating the increase in total body water lies with the conservation of sodium that occurs with heat acclimation, which also helps maintain the number of osmoles in the extracellular fluid, and thus to conserve or increase extracellular fluid volume during adaptation (
Fig. 2Resting total body water (TBW), plasma volume (PV), red cell volume (RCV), extracellular fluid (ECF), interstitial fluid (ISF) and intracellular fluid (ICF) prior to and during a three-week heat acclimation regimen. Upper panels n = 12, lower panels n = 8 (mean ± SEM). *Significantly different from Day 1 (P < 0.05). Reprinted with permission from
Whole-body fluid distribution in humans during dehydration and recovery, before and after humid-heat acclimation induced using controlled hyperthermia.
). Typically, the greatest expansion of plasma volume is observed on about the fifth day of exercise-heat acclimation in fully hydrated individuals. Previous studies have described the rapid increase in plasma volume as being a transient phenomenon, with a small contraction occurring from this expanded state after one week of acclimation (Fig. 1) (
). More recently however, it has been suggested that this phenomenon may have been an experimental artifact stemming from to the traditional constant work rate model of heat acclimation. It would appear that by using the controlled hyperthermia approach, which maintains a constant adaptation stimulus by clamping core temperature (e.g. 38.5 °C) throughout acclimation, plasma volume remains expanded (~14%) for a sustained period (8–22 days) of heat exposure (Fig. 2) (
Whole-body fluid distribution in humans during dehydration and recovery, before and after humid-heat acclimation induced using controlled hyperthermia.
The pathways via which the increase in plasma volume may be maintained include the oncotic effect of a net increase in total intravascular protein content during heat acclimation, which causes a movement of fluid from the interstitial to the intravascular space (
Movement of water, protein and crystalloids between vascular and extra-vascular compartments in heat-exposed men during dehydration and following limited relief of dehydration.
Changes in plasma volume and protein content during exposures of working men to various tem- peratures before and after acclimatization to heat: separation of the roles of cutaneous and skeletal muscle circulation.
); adaptations which in turn support plasma volume expansion. The maintenance of plasma volume expansion is also associated with an increase in extracellular fluid, mediated by the retention of crystalloids, primarily sodium chloride (
Whole-body fluid distribution in humans during dehydration and recovery, before and after humid-heat acclimation induced using controlled hyperthermia.
The retention of plasma volume expansion during chronic heat acclimation is in contrast to the acute effect of plasma volume expansion. Using a hyperoncotic 25% albumin solution or 0.9% saline,
demonstrated that plasma volume was acutely expanded for 9–12 h in both hot and temperate conditions, but by a greater magnitude under heat stress. The authors further demonstrated a return in plasma volume to near baseline values by 24 h post-infusion, which is suggestive of a circadian pattern of plasma volume expansion and contraction. Interestingly, it was noted that after albumin infusion, heat exposure significantly increased plasma volume compared with saline and appeared to extend the retention time of the infused albumin, resulting in a more prolonged increase in oncotic pressure (
). Although debate remains as to what level plasma volume can be expanded and whether or not this expansion is sustained during heat acclimation, an increase in plasma volume does provide two major physiological advantages: i) increasing vascular filling pressure to support cardiovascular stability (i.e. increased stroke volume and arterial blood pressure) (
Effects of changes in packed cell volume on the specific heat capacity of blood: implications for studies measuring heat exchange in extracorporeal circuits.
). Fig. 3 provides the relation between the percent changes in heart rate at the end of exercise (4 h) to the percent change in plasma volume after 10 days of humid heat acclimation, relative to the first day of heat exposure (
). These data suggest that plasma volume expansion, and thus perhaps improved cardiac filling, contribute to the reduced heart rate response during heat acclimation. This is similar to the expansion of blood volume (i.e. plasma and erythrocyte) that occurs during aerobic training and which is considered an important contributor to improvements in endurance performance by allowing for greater ventricular filling and a consequent larger stroke volume (
Fig. 3Percent changes in heart rate relative to percent changes in plasma volume at the end of 4 h of exercise following 10 days of heat acclimation. Values from the first day of heat exposure were taken as control values. Redrawn with permission from
Thirst during exercise-heat stress has historically not been considered a good indicator of body water needs since ad libitum water consumption often resulted in incomplete fluid replacement, or voluntary dehydration (
). Drinking behavior and fluid replacement are processes influenced by physiological, psychological and environmental factors, as well as issues related to fluid palatability, food intake, and gastric distension/discomfort (
). The mechanisms via which drinking and fluid replacement are regulated during and following exercise include a sodium ion-osmotic-vasopressin pathway (
). Heat acclimation improves the relationship of thirst to body water needs by a reducing the time to first drink, increasing the number of drinks consumed per heat exposure, and increasing mean volume per drink (
). Note that after three days water deficits were reduced by 50%. Thus, heat acclimated individuals are better able to maintain hydration status during exercise-heat stress and minimize body water losses, provided access to fluids is not restricted.
Fig. 4Difference between ad libitum water intake and water loss in 15 men during work in humid heat over a 6-day period, compared with work in a cool environment (
Another important adaptation from heat acclimation to defend extracellular volume, and thus plasma volume, is improved sodium reabsorption in the eccrine sweat gland (
). Indeed, an unacclimated person may secrete sweat with a sodium concentration of 60 mEq/L or higher, and therefore if sweating profusely can lose large amounts of sodium (
). With heat acclimation, eccrine sweat glands increase sodium reabsorption along the duct, which can reduce sweat sodium concentrations to as low as 10 mEq/L. Fig. 5 demonstrates the relationship of sweat sodium concentration and sweating rate before and after heat acclimation (
Dehydration, or a reduction in total body water and plasma volume, is known to adversely increase cardiovascular strain and impair aerobic performance during exercise-heat stress (
). The deleterious cardiovascular effects of dehydration are characterized by difficulty to sustain blood pressure and cardiac output, and a potential reduction in skeletal muscle blood flow during exercise-heat stress (
). As shown in Fig. 6, combining dehydration with exercise-heat stress results in reduced cardiac output and skeletal muscle blood flow, compared to when euhydrated (
). Drinking sufficient fluids to minimize dehydration during heat acclimation should therefore help to sustain cardiac output and perhaps skeletal muscle blood flow, and thus optimize exercise capacity under heat stress.
Fig. 6Cardiac output and blood flows during dehydration and control trials. A: cardiac output, B: 2-legged blood flow, C: non-exercising tissue blood flow, D: forearm blood flow. Filled squares represent dehydration and open squares represent control. *Significantly lower than 20 min value (P < 0.05). †Significantly lower than control (P < 0.05). Reprinted with permission from
Adaptations in sweat rate were among the first described in response to heat acclimatization. Indeed, by the end of the 1940's it was widely accepted that heat acclimatization increases sweating capacity (
). Along with a shift in the onset threshold for sweating, which occurs earlier and at a lower core temperature, almost exact parallel improvements are noted in skin blood flow (
), which are depicted in Fig. 7. At the central level, heat acclimation decreases the body temperature at which thermoregulatory sweating and skin vasodilation are initiated. This adjustment in onset threshold is proposed to correspond to an absolute change in mean body temperature, rather than to the attainment of a predetermined mean body temperature (
). These adaptations include improved cholinergic sensitivity, and increased size and efficiency of eccrine glands in producing sweat per unit length of secretory coil (
). Peripheral factors contributing to improved sweating and skin blood flow responses likely include an increase in the number and sensitivity of muscarinic receptors, a decrease in cholinesterase activity that potentiates and prolongs acetylcholine concentration in the cholinergic neural junction, which improves the vascular response to a given acetylcholine level, or alterations to the pathway of vasodilation within smooth muscles or the endothelial cells (
Fig. 7Schematic representation of the central and peripheral adaptations that occur in response (Pre vs. Post) to heat acclimation (HA). The body core temperature threshold for the onset of sweating is reduced, while the rate and sensitivity (i.e. slope) are increased (
). Concomitantly, the body core temperature threshold for the onset of cutaneous vasodilation is reduced, whereas skin blood flow sensitivity is increased (
Fig. 8Improvements in sweating capacity on Days 1 and 6 of cycle ergometer exercise (25–30% O2max) in 40 °C air temperature and increasing humidity from a vapor pressure of 12 mmHg to 49 mmHg each day. Skin wettedness (w) is equal to skin evaporation (Esk)/maximum evaporative capacity (Emax). Adapted with permission from
The primary cardiovascular challenge during exercise in the heat is to provide sufficient cardiac output to adequately perfuse skeletal muscle to support metabolism, while simultaneously perfusing skin to support heat loss. The traditional belief was that skeletal muscle blood flow is not altered by heat stress and that increases in cardiac output support elevated skin blood flow requirements (
Local temperature-sensitive mechanisms are important mediators of limb tissue hyperemia in the heat-stressed human at rest and during small muscle mass exercise.
Am. J. Physiol. Heart Circ. Physiol.2015; 309: H369-H380
). The mechanisms mediating this increase may include an interaction of metabolic and thermal stimuli inducing the release of erythrocyte-derived ATP, a potent vasodilator (
). Thus, it may be postulated that in unacclimatized individuals higher body/tissue temperatures would induce greater skeletal muscle blood flow requirements, and that with heat acclimation these requirements might decline with lower body/tissue temperatures during exercise-heat stress.
These metabolic and thermoregulatory demands are generally viewed as competing, whereby cardiac function is altered, the distribution of cardiac output is modified, and/or the ability to sustain adequate blood pressure is compromised (
). Alternatively, the conflict between regulatory systems may be viewed as commensalism: an integrated balance of regulatory control where one circulation benefits without substantially affecting the other (
). Notwithstanding, heat acclimation improves the ability to sustain cardiac output during exercise-heat stress. Fig. 9 provides an example of this improvement with cardiac output, stroke volume and leg blood flow responses during exercise to exhaustion in a hot-dry environment before and after heat acclimation (
). Notably, heat acclimation improved the ability to perform endurance exercise in the heat. This was accompanied by lowered heart rate, increased stroke volume and sustained leg blood flow, and sustained or improved cardiac output responses.
Fig. 9Cardiac output (Q), stroke volume (SV) and leg blood flow (LBF) during exercise (10 and 40 min) and just before volitional exhaustion (Exh). Open hatching: before acclimation, Close hatching: after 9–12 days of acclimation. Before acclimation the 40 min values were those taken just before exhaustion (mean ± SEM). Number of measurements indicated. *Significantly different from final measurements before acclimation (P < 0.05). Reprinted with permission from
The effects of heat acclimation on stroke volume and cardiac output during exercise-heat stress depend largely on exercise intensity, as well as the type and severity of the heat stress. For example, two studies in which low to moderate work was conducted in the heat reported increases in stroke volume with little change in cardiac output as heart rate decreased with acclimation (
). Another study reported a decrease in cardiac output in association with a reduction in cutaneous blood flow, but little change in stroke volume as heart rate decreased, again during work performed in hot conditions (
). A separate study reported a mixed pattern, with two subjects showing a steady increase in stroke volume, one a transient increase reversing after the sixth day, and one showing no increase with heat acclimation (
). The reason for these differences is unclear, although differences in the methodology to assess these parameters may account for some variation, while another possibility might relate to exercise being performed in dry heat (
examined stroke volume responses during exercise (45–50%VO2max) before and after dry (40 °C, 10% relative humidity; RH) and humid (35 °C, 87% RH) heat acclimation. The authors reported that during exercise, dry heat acclimation increased stroke volume (~21 mL/beat) and cardiac output (~1.8 L/min) (
), despite both studies reporting a plasma volume expansion of 9–13%. Others have also shown that 10 days of dry heat acclimation improves maximal stroke volume and cardiac output during a O2max test in cool (13 °C), but not hot (38 °C) conditions, without influencing maximum heart rate (
). Moreover, short-term moderate intensity (70% O2max, 30 min/day) exercise-heat acclimation in 30 °C and 50% RH has been shown to increase plasma volume and stroke volume, and decrease heart rate (
). Taken together, these observations indicate that heat acclimation improves central hemodynamics, but that the magnitude of improvement may depend on the environmental condition (i.e. dry vs. humid heat), acclimation protocol (i.e. stimulus impulse), exercise intensity, and subject population. Hence, additional research is required to fully elucidate the impact of heat acclimation on central hemodynamic responses.
The hallmark cardiovascular adaptations induced during heat acclimation include a lowering of heart rate and an increase in stroke volume, which support the maintenance of cardiac output and the regulation of blood pressure during submaximal exercise (Table 1). The lowering of heart rate and increased stroke volume are likely supported by changes in myocardial autonomic tone. Autonomic adjustments during exercise are mediated by central command, cardiopulmonary and arterial baroreflexes, and carotid chemoreflexes (
). Therefore, the net affect on parasympathetic/sympathetic efferent activity and thus myocardial chronotropic, inotropic and lusitropic properties is likely specific to the exercise intensity, hydration status, fitness level, as well as heat acclimation status. With heat acclimation, it is anticipated that better tissue perfusion, reducing metaboreceptor stimulation; reduced metabolic lactate production, reducing carotid chemoreflex stimulation for respiratory compensation; improved cardiac filling and blood pressure regulation, reducing low and high pressure baroreceptor stimulation; and tissue (i.e. muscle and brain) temperatures, modifying central command; all contribute to alter cardiac autonomic regulation.
Table 1Adaptations in cardiovascular function associated with heat acclimation that lead to improved cardiovascular stability.
). This heat acclimation-induced bradycardia may further relate to a decrease in overall thermal (i.e. lower core and skin temperatures) and concomitantly cardiovascular strain, and to alterations in total blood volume (
), which as discussed earlier may reduce both skin and skeletal muscle blood flow requirements. The increase in plasma volume may serve to support greater venous return and cardiac preloading, leading to improved ventricular filling and increased stroke volume (
). A rightward shift in the diastolic pressure‐volume curve thus occurs, which allows for greater ventricular filling and augmented stroke volume without a change in pressure (
). Additionally, exercise-heat acclimated rats demonstrate increased left ventricular compliance and systolic pressure generation while myocardial O2 (i.e. the energetic cost of pumping) is lowered (Fig. 10) (
). Globally, the adaptations are suggested to stem from concerted adjustments induced by exercise-heat acclimation that alter the mechanisms associated with the excitation–contraction coupling cascade, Ca2+ regulation, contractile and metabolic responses (
). Although it remains to be determined whether such functional adaptations occur in humans, heat stress is known to reduce left ventricular pressure and increase left ventricular systolic function (
), such that following heat acclimation greater ventricular filling may occur at a lower ventricular pressures.
Fig. 10Relationship between oxygen consumption and cardiac work (expressed as the rate-pressure product) in hearts of sedentary unacclimated (C) and heat acclimated (AC) rats for 1 month. Marked shift to the right of the regression line of heat-acclimated hearts compared with that of unacclimated hearts implies significantly increased work efficiency of heat-acclimated hearts (P < 0.0007) (
Molecular adaptations at the level of the cardiac muscle also occur in response to the induction of heat shock proteins (Hsp), which were originally described for their role as molecular chaperones in maintaining cellular conformation and homeostasis (
). The heat shock response induced during exposure to heat stress confers transient thermotolerance and protection against subsequent exposure, as well as cardioprotection (
). Interestingly, exercise-heat acclimation appears to increase basal intracellular Hsp72 and Hsp90 levels, and blunt the acute response (i.e. inducibility) to exercise in the heat as adaptations develop (
demonstrated in peripheral blood mononuclear cells that individuals demonstrating the greatest physiological adaptations exhibit the greatest blunting in ex vivo Hsp72 and Hsp90 inducibility. At the extracellular level, increases in the basal expression of Hsp72 following exercise are less consistent. Indeed, whilst similar increases in intracellular (i.e. monocyte) and extracellular Hsp72 expression occur immediately following exhaustive exercise in the heat, the extracellular expression decreases below basal (i.e. pre-exercise) levels 24 h after exercise (
demonstrated that three cycling time trials (43 km) undertaken in hot outdoor conditions (~37 °C) were initiated at a similar power output to that of time trials conducted in cool conditions (~8 °C) (Fig. 11). However, a marked decrease in power output occurred in the heat following the onset of exercise, which was partly recovered after one week of training in the heat and almost fully restored after two weeks of training in the heat. As expected, heart rate was similar during all trials in the heat and slightly higher than in the cool, which supports the contention that a similar relative exercise intensity (i.e. % O2max) was maintained (
) and that with heat acclimation absolute intensity (i.e. power output) increased.
Fig. 11Power output during 43.4 km cycling time trials performed in Cool (~8 °C; average of trials performed before and after heat acclimatization) and Hot (~37 °C) conditions after one (Hot 1), six (Hot 2) and fourteen (Hot 3) days of training in the heat. *§†Cool time trial significantly higher than TTH-1, TTH-2, and TTH-3, respectively (P < 0.05). Redrawn with permission from
noting increases of 8–10% (38 °C). Despite these improvements, acute heat stress mediates a reduction in O2max relative to values recorded in temperate conditions that cannot be compensated for by heat acclimation (i.e. O2max in the heat remains lower than in cool conditions). Notwithstanding, heat acclimation has been shown to increase cycle exercise time trial performance in the heat in conjunction with an increase in cardiac output and lactate threshold, plasma volume expansion, lower skin temperatures, and a larger core-to-skin gradient after heat acclimation (
Observations of enhanced self-paced exercise performance have also been noted in cool conditions in proportion to improvements in O2max under the same conditions (
). It also supports findings of team-sport athletes improving endurance performance (i.e. Yo-Yo Intermittent Recovery test) in temperate conditions (~22 °C) following training camps in the heat (~34 °C) (
). The pathways via which a transfer of adaptation between hot and cool conditions would increase performance might be linked to a variety of ergogenic responses, including cardiovascular, thermoregulatory and cellular adaptations (
) were utilized, did not demonstrate an improvement in O2max or time trial performance in cool conditions in trained cyclists. Clearly, this will become a controversial area and merit additional research with well-designed protocols to elucidate the mechanisms and possible transfer of ergogenic benefits from heat acclimation towards improving aerobic performance in cooler conditions.
There are several additional potential benefits that may be conferred by heat acclimation that could contribute to improved exercise capabilities. Heat acclimation can decrease the oxygen uptake response to submaximal exercise (
). This glycogen-sparing effect of heat acclimation has also been shown to be quite small however, and apparent only during exercise in cool conditions (
). The mechanisms mediating these adaptations remain unclear, but could stem from the increase in total body water enhancing lactate removal through increased splanchnic circulation (
Acute heat stress impairs aerobic exercise capacity and elevated cardiovascular strain has long been considered an important contributor. Repeated heat exposure however, induces adaptations that abate cardiovascular strain and likely contribute to attenuate the exercise performance impairment, and reduce the risk of serious heat illness. The cardiovascular adaptations supporting this include an increase in total body water, plasma volume expansion, better sustainment and/or elevation of stroke volume, reduction in heart rate, improvement in ventricular filling and myocardial efficiency, and enhanced skin blood flow and sweating responses. The magnitude of these adaptations is dependent on several factors such as exercise intensity, duration, frequency and number of exposures to the heat, as well as to the environmental conditions (e.g. dry vs. humid heat) and protocol in which acclimation occurs.
Acknowledgments
The authors report no conflict of interest. No funding was received for this review.
Effects of changes in packed cell volume on the specific heat capacity of blood: implications for studies measuring heat exchange in extracorporeal circuits.
Local temperature-sensitive mechanisms are important mediators of limb tissue hyperemia in the heat-stressed human at rest and during small muscle mass exercise.
Am. J. Physiol. Heart Circ. Physiol.2015; 309: H369-H380
Whole-body fluid distribution in humans during dehydration and recovery, before and after humid-heat acclimation induced using controlled hyperthermia.
Integration of cardiovascular control systems in dynamic exercise.
in: LB Rowell JT Shepherd Handbook of Physiology: Exercise Regulation and Integration of Multiple Systems. American Physiological Society,
Bethesda, MD1996: 770-838
Movement of water, protein and crystalloids between vascular and extra-vascular compartments in heat-exposed men during dehydration and following limited relief of dehydration.
Changes in plasma volume and protein content during exposures of working men to various tem- peratures before and after acclimatization to heat: separation of the roles of cutaneous and skeletal muscle circulation.
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