Influence of Aerobic Fitness on Thermoregulation During Exercise in the Heat

Ricardo Mora-Rodriguez, Ph.D.

Disclosures

Exerc Sport Sci Rev. 2012;40(2):79-87. 

In This Article

Effects of Aerobic Fitness Level on Exercise Core Temperature

Core temperature originally was believed to be determined by the absolute workload being performed by the subject.[16] However, in 1966, Saltin and Hermansen reported the core temperature response of seven subjects with a wide range of aerobic fitness levels (V̇O2max = 38–76 mL O2·kg−1·min−1) when cycling in a thermoneutral environment (20-C and 55% relative humidity;[28]). For a given absolute workload, there was a scatter of rectal temperature responses. However, when rectal temperature was presented for a given percentage of V̇O2max, the interindividual variation was reduced by 65% (reference;[28] Fig. 1). These data put forward the longtime held notion that core temperature is set according to the relative load to the maximal aerobic capacity of the individual and not to the absolute workload performed as it was contended previously.[16] However, the concept that core temperature is set according to the exercise intensity relative to V̇O2max was challenged from its inception by the proposing investigators[10] and others.[27] In these studies, the investigators acutely reduced the subjects' blood oxygen saturation, thereby lowering their V̇O2max. The subjects then exercised at the same absolute workload, which then represented a higher percent of their transitorily reduced V̇O2max. However, neither hypoxia[27] nor simulated altitude[10] had an effect on exercising core temperature. Therefore, exercise core temperature, although related to percent V̇O2max, does not seem to be linked directly to oxygen uptake, transport, or consumption.

Figure 1.

A. Rectal temperature responses during treadmill walking at three intensities while varying the environmental heat load (expressed as wet bulb globe temperature (WBGT)). The prescriptive zone (thermal equilibrium) remains to the left of the dotted line. [Adapted from [16]. Copyright © 1963 The American Physiological Society. Used with permission.] B. Rectal temperature response in aerobically trained subjects after 45 min of exercise at different relative intensities (%V̇O2max) under environments with different WBGT.

In addition to improving V̇O2max, aerobic training results in enhanced heat dissipation by lowering the core temperature threshold for skin vasodilation and sweating.[13,24] The dual effect of aerobic training on improving V̇O2max and heat dissipation may explain why percentage of V̇O2max is associated tightly with exercise core temperature. When exercising at a similar percent of V̇O2max, endurance-trained subjects will be exercising at a higher absolute workload than untrained individuals, thereby generating more metabolic heat (MNET). This higher workload also will result in increased cutaneous blood flow[7] and sweat rate (15,24) in the aerobically trained subjects than in the untrained subjects during exercise at a given percentage of V̇O2max. Therefore, the higher metabolic heat production is compensated by the higher heat dissipation resulting in heat balance in trained subjects exercising at moderate intensities in a thermoneutral environment (19°C–24°C db;).[28] However, when exercising in a hot environment, metabolic heat production can exceed the capacity of the environment to accept heat (EMAX). Because aerobically trained subjects produce more heat at a given percentage of V̇O2max, higher heat accumulation values could be seen in those subjects as well (Fig. 2;[21]).

Figure 2.

Rectal temperature response to exercise in a hot environment (36°C dry bulb; 26°C WBGT) at three relative intensities (i.e., 40%–60%–80% V̇O2max) in aerobically trained and untrained subjects (V̇O2max = 60 vs 44 mL O2·kg−1·min−1). *Statistical differences between groups (P < 0.05). [Adapted from [21]. Copyright © 2010 Springer. Used with permission.]

There are data to support higher sweat rates[15] in trained subjects compared with untrained subjects, when exercising at a given percentage V̇O2max (i.e., 50% V̇O2max). We have found that even at a high relative exercise intensity (i.e., 80% V̇O2max), sweat rate is higher in trained individuals. The higher sweat rate in conjunction with an increased skin blood flow resulted in lower skin temperature than in the untrained subjects during high-intensity exercise. So, the larger hyperthermia reached by the trained subject during intense exercise at 80% V̇O2max occurred despite an enhanced functioning of all measured indexes of heat dissipation as is shown in Figure 3.

Figure 3.

Sweat rate, mean skin temperature, and forearm skin blood flow during exercise at 80% VO2max in trained and untrained subjects.

The enhanced heat dissipation likely allowed the trained subjects to achieve similar rectal temperatures as the untrained despite producing more heat during exercising at 40% and 60% of V̇O2max (Fig. 2). However, the rate of heat production exceeded the heat dissipation adaptations during exercise at 80% of V̇O2max (i.e., by 555 W·m−2). Of note, the trained individuals started all trials at a lower basal level of rectal temperature in comparison to the untrained individuals. Thus, the gain in rectal temperature was larger for the trained individuals compared with the untrained individuals to result in similar end rectal temperature during 40% and 60% V̇O2max intensities. If the differences in rectal temperature gain were to be maintained, it could be extrapolated that trained subjects will end up reaching higher rectal temperature during very prolonged exercise even at moderate intensities.

It is our hypothesis that absolute heat production will have a greater influence on core body temperature during exercise of longer duration and/or higher intensities. Thus, in an environment with reduced heat acceptance (i.e., 26°C WBGT), absolute heat production is the better predictor of core temperature compared with percentage of V̇O2max. Figure 4 is an extrapolation of Mora-Rodriguez et al., data[21] to show higher and lower exercise intensities. It can be seen that relative intensity is a good predictor of core temperature in situations of compensable heat load (EREQ < EMAX); however, absolute intensity is a better predictor in an uncompensable heat stress situation (EREQ > EMAX). Uncompensable heat stress can be achieved by increasing exercise intensity (i.e., raising EREQ) and/or by reducing environmental air flow or increasing relative humidity (i.e., reducing EMAX).

Figure 4.

Exercise intensity factor (relative or absolute) that determines core temperature during exercise in the heat (~26°C wet bulb globe temperature) when EREQ < EMAX and when EREQ > EMAX.

The practical message from the high-intensity condition from Figure 2 is that when exercising at a high relative intensity in a hot environment, aerobically trained individuals are at a higher (not lower) risk of developing hyperthermia. The enhanced heat dissipatory adaptations associated with a greater aerobic fitness level do not prevent athletes from reaching high core body temperatures during intense exercise in the heat. Hyperthermia could lead to heat exhaustion and exertional heat stroke. Thus, caution should be taken when recommending exercise intensity in the trained population solely based on percentage of V̇O2max when exercising under heat stress.

When a group of individuals exercise at a fixed pace in a hot environment, the less aerobically fit person will be working at a higher percentage of his/her V̇O2max, reaching higher levels of hyperthermia and having a higher risk of heat-related injuries. This fixed pace exercise for individuals of different aerobic fitness level is a situation common during team sports practice. In contrast, when individuals can self-pace exercise (e.g., running a 10-km race), trained and untrained individuals default into an intensity that demands a similar percentage of their maximal aerobic capacity (i.e., similar %V̇O2max). In this situation, the more fit individuals will be producing more heat and may fall into the higher risk category for heat-related injuries.

Heat Exhaustion in Aerobically Trained and Untrained Subjects

A high core temperature has been proposed as the cause of heat exhaustion.[9] It could be argued that the 0.3°C greater hyperthermia found in the Mora-Rodriguez et al. study (Fig. 2) during intense exercise (i.e., 80% V̇O2max) is tolerated easily by adaptations that permit trained individuals to store more heat than the untrained before incurring fatigue. It is debatable whether absolute temperature or the rate of heat storage is the signal evoking the fatigue associated to the central nervous system that develops during prolonged exercise in the heat. In 1993, Nielsen and co-workers[25] observed with progressive heat acclimatization that subjects were able to exercise longer in a hot environment, yet they still fatigued at the same core temperature (~39.7 ± 0.15-C). Gonzalez-Alonso et al.,[9] confirmed this finding with observations that aerobically trained individuals fatigued at rectal temperatures of ~40-C, despite different starting core temperatures. Contrary to what often is believed, aerobically trained individuals do not withstand higher core temperatures before fatiguing than untrained individuals,[30] although this finding has been questioned.[33] Thus, the improved performance (i.e., time to exhaustion) in trained subjects when exercising in the heat, in comparison to untrained counterparts, unlikely is due to an increased tolerance to hyperthermia.

An emerging body of literature suggests that fatigue may be triggered from an elevated rate of heat storage rather than from an absolute level of core temperature. It is hypothesized that either a voluntary behavioral or an involuntary reduction in motor unit recruitment (afferent feedback) regulates the workload to a rate of heat accumulation that allows the exercise to proceed without reaching heat exhaustion. One of the most commonly seen adaptations to heat acclimatization[25] and to training[21] is a lowering of resting core temperature by 0.2°C–0.3°C in comparison to unacclimatized or untrained individuals. The lower resting core temperature permits aerobically trained individuals to have greater increases in core body temperature during exercise, likely contributing to the longer time to exhaustion. Trained individuals exercising at the same relative intensity as untrained have a higher rate of heat storage[21] but fatigue at the same level of core temperature.[30] Therefore, it is possible that one of the adaptations to training and heat acclimatization is to allow a higher rate of heat accumulation without a behavioral or an involuntary reduction in work output.

Thermoregulatory Benefits of Aerobic Training versus Heat Acclimatization

The thermoregulatory adaptations that emerge from exercise in a hot environment (i.e., heat acclimatization) are similar to but extend beyond the adaptations obtained as a result of aerobic training. Heat acclimatization expands plasma volume, improves cardiac function and sweating pattern and acts to conserve sweat sodium. Aerobic training increases sweat rate for a given core temperature, but subsequent heat acclimatization leads to further increases in sweat rate and earlier onset of sweating.[24] The rate at which heat acclimatization occurs is related to the initial V̇O2max level[26] with untrained subjects requiring more sessions to obtain full adaptation than the trained. Although many thermoregulatory adaptations occur with aerobic training, training in the heat will enhance those adaptations. That likely is why well-trained cyclists can enhance local sweat rate and skin vasodilation upon acclimatization without improvements in V̇O2max.

The thermoregulatory adaptations that improve heat dissipation (i.e., increased in cutaneous blood flow and sweat rate) during exercise training or heat acclimatization are directed to prevent excessive hyperthermia during exercise. End exercise rectal temperature gives information of the heat dissipation improvements as heat acclimatization progresses. In addition, the effect of aerobic fitness level on thermoregulation can be seen by plotting the individual V̇O2max levels against the end exercise rectal temperatures. Several authors have found negative correlations when plotting those variables and calculated that aerobic fitness level accounts for around 40% of the variability in the rectal temperature response.[34] Nevertheless, these plots are a good tool to compare the thermoregulatory benefits of aerobic training versus the benefits derived from heat acclimatization.

The length of the arrows in Figure 5 suggests that untrained subjects obtain more benefits from heat acclimatization compared with trained subjects because training provides similar thermoregulatory adaptations to those associated with heat acclimatization. Although smaller in magnitude, the reduction in rectal temperature of the trained subjects with acclimatization requires enhancement in the functioning of the heat dissipatory mechanisms.[24]

Figure 5.

Regression lines of subjects' maximal oxygen uptake versus rectal temperature after 140 min of intermittent treadmill walking at 4.8 km·h−1 in a hot environment (49°C dry bulb, 20% relative humidity) while normally hydrated. Acclimatization consisted on a 10-d exercise program in the heat. [Adapted from [4]. Copyright © 1984 Aerospace Medical Association. Used with permission.]

One of the most important adaptations seen with heat acclimatization is the attenuated reduction in plasma volume for a given body water deficit compared with unacclimatized persons.[32] By having more dilute sweat, heat-acclimated persons conserve more solutes to defend plasma volume. Sweat sodium concentration collected during exercise varies (range, 35–81 mEq·L−1) depending on sweating rate, heat acclimatization, salt in diet, and genetic factors. In fact, during exercise in a hot environment, individuals with a genetically induced high sweat sodium concentration (91 mEqILj1) reduce their plasma volume more than individuals with normal sweat sodium (44 mEqILj1) at the same level of dehydration.[2] Sweat rate increases linearly with exercise intensity, leading to linear increases in sweat sodium concentration as well. This occurs because most functional sweat glands are recruited at the onset of exercise, and further increases in sweat rate must arise from augmenting the velocity that sweat travels through each individual sweat gland duct. This increase in sweat velocity reduces the possibility for the duct to reabsorb electrolytes resulting in higher secretion of sodium.[3] Thus, when studying sweat sodium losses among subjects with different aerobic fitness or acclimatization level, it is important to compare them at similar sweat rates. It will be inappropriate to compare sweat sodium concentration at a given percentage of V̇O2max because sweat rates typically will be higher in the trained subjects resulting in greater sweat sodium concentration.

When sweat sodium ion concentration is compared at similar local sweat rates before and after 10 d of heat acclimatization, a reduction of approximately 30% is reported (Fig. 6;).[3] Surprisingly, we have not been able to find reductions in sweat sodium concentrations when comparing aerobically trained and untrained individuals using a crosssectional experimental design (Fig. 6;).[11] We alternatively propose that the sodium conservation response observed in some acclimatization studies may be influenced by a dietary sodium deficit. In fact, when the sodium losses induced by 100 min of walking at 45-C are replaced carefully in the diet, sweat sodium concentration is maintained during 7 d of exercise.[35]

Figure 6.

Sweat sodium concentration versus local sweat rate relationship with 10 d of heat acclimatization [Adapted from [3]. Copyright © 2007 The American Physiological Society. Used with permission.] or between aerobically trained and untrained subjects [Adapted from [11]. Copyright © 2011 Springer. Used with permission.].

The difference in local sweat rates between studies along the x axis in Figure 6 likely is due to the different exercise intensities used in the two studies plotted. This figure suggests that training and heat acclimatization do not share all adaptations with regard to sweat electrolyte conservation. Reductions of sodium secretion in sweat seem to be induced specifically by heat acclimatization. Likely, the long exposures to heat during heat acclimatization are needed to elicit large body fluid deficits initiating the endocrine responses (e.g., release of aldosterone) that signal the sweat gland to conserve sodium.

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