Encyclopedia of Sports Medicine and Science

Armstrong, L.E. (1998). Heat acclimatization. In: Encyclopedia of Sports Medicine and Science, T.D.Fahey (Editor). Internet Society for Sport Science: http://sportsci.org. 10 March 1998.

Physiological Responses
Heat Illness
Factors Affecting Acclimatization
Loss of Acclimatization
References

Subsequent to repeated bouts of exercise in a hot environment, there is a marked improvement in the physiologic responses of healthy humans. This improved tolerance to exercise in heat is known as heat acclimatization. When accomplished in an artificially controlled environmental chamber, this process is known as heat acclimation. The primary benefit of heat acclimatization is improved tolerance of exercise in the heat, evident as a reduction of the incidence or severity of symptoms of heat illness, and increased work output concurrent with reduced cardiovascular, thermal, and metabolic strain.

Physiological Responses

Heat acclimatization is specific to the stress imposed on the human body. For example, passive exposure to heat induces some responses, notably an improved ability to dissipate heat. In contrast, physical training in a cool-dry environment results in metabolic, biochemical, hematologic, and cardiovascular adaptations. Heat acclimatization via strenuous exercise induces responses attributed to both passive heat exposure and training in cool environments. Table 1 illustrates these relationships.

Complete heat acclimatization requires up to 14 days, but the systems of the body adapt to heat exposure at varying rates. The early adaptations (initial 1-5 days) involve an improved control of cardiovascular function, including expanded plasma volume, reduced heart rate, and autonomic nervous system habituation which redirects cardiac output to skin capillary beds and active muscle. Plasma volume expansion resulting from increased plasma proteins and increased sodium chloride retention, ranges from +3 to +27%, and is accompanied by a 15-25% decrease in heart rate. This reduction of cardiovascular strain reduces rating of perceived exertion, which is proportional to central cardiorespiratory stress, also decreases during the first five days of exercise-heat exposure. Plasma volume expansion is a temporary phenomenon, which decays during the 8th to 14th days of heat acclimatization (as do fluid-regulatory hormone responses, see below), and then is replaced by a longer-lasting reduction in skin blood flow that serves to increase central blood volume.

The regulation of body temperature during exercise in the heat is critical, because of the great potential for lethal hyperthermia. Thermoregulatory adaptations (i.e., increased sweat rate, earlier onset of sweat production), coupled with cardiovascular adjustments, result in a decreased central body temperature. This response is maximized after 5 to 8 days of heat acclimatization. However, the adaptations of eccrine sweat glands are different during humid and dry heat exposures. Heat acclimatization performed in a hot-humid condition stimulates a greater sweat rate than heat acclimatization in a hot-dry environment. Also, the absolute rate of sweating influences thermoregulation. If hourly sweat rate is small (<400-600 ml), a peripheral adaptation of whole body sweat rate may not occur.

Conservation of sodium chloride (NaCl) also occurs during heat acclimatization. The NaCl losses in sweat and urine decrease during days 3-9 of heat acclimatization, resulting in an expanded extracellular fluid volume. Subsequently, NaCl losses in sweat and urine increase toward pre-acclimatization levels, once physiologic strain (i.e., cardiovascular, thermal) moderates. Francesconi and colleagues (1993) recently demonstrated that NaCl losses, during a strenuous 10-day heat acclimatization protocol, were related to plasma renin (PR) and plasma aldosterone (A) concentrations. When subjects consumed a low salt diet (4g NaCl per day) and a moderate salt diet (8g NaCl per day), both PR and A increased during the first four days of heat acclimatization, but decreased during the remaining 6 days of heat acclimatization. The improved cardiovascular stability, which occurred on days 1-4 of heat acclimatization, allowed equivalent exercise performance with both diets and apparently reduced the stimulation and need for large elevations of PR and A. No change in plasma levels of arginine vasopressin (AVP) were observed across time, in either dietary group, possibly because hourly water intake matched the fluid lost in sweat. Usually, AVP synthesis is stimulated by an increase in plasma osmolarity or alterations in blood pressure, plasma volume, and renal or hepatic blood blow. Therefore, it is unlikely that the ability to successfully sustain exercise, during the latter days of the heat acclimatization process, is specifically related to the action of hormones that regulate fluid-electrolyte balance. This is particularly true when salt balance has been achieved.

Excess dietary water and electrolytes do not speed the process of heat acclimatization. When dehydration or salt deficits exist, however, cardiovascular and thermoregulatory responses may be negatively affected, and the theoretical risk of heat illness increases. Consistent daily monitoring of body weight will allow athletes to recognize water deficits which require consumption of fluid (-2 to -3% of body weight), reduction of training duration/intensity (-4 to -6%), or consultation with an experienced physician (in excess of -7%).

Plasma cortisol concentration generally indicates the strain experienced by the body. Heat-acclimated, well-hydrated humans exhibit no change in plasma cortisol when exercise in a hot environment is mild. Under the same conditions, the lack of heat acclimatization and dehydration can result in large plasma cortisol increases. When exercise is intense and core body temperature rises markedly, the plasma cortisol concentration increases during the initial days of heat acclimatization, but returns to control levels after 8 days of heat acclimatization, reflecting the reduction in total body strain.

Physical training in a cool environment may or may not improve exercise economy. Metabolism can be affected by heat acclimatization, in that oxygen uptake during submaximal exercise is reduced. Large effects have been reported for stair stepping; treadmill and cycle-ergometer exercise produce smaller, but statistically significant, changes. The physiologic mechanism has not been defined exactly, but three theories exist: (a) blood flow to the skin increases, thus reducing central blood volume, venous return to the heart, and cardiac output; (b) the portion of cardiac output perfusing muscle decreases; and (c) the recruitment of muscle fibers shifts from predominantly oxidative to glycolytic fibers. Heat acclimatization reduces muscle glycogen utilization and post-exercise muscle lactate concentration.

Heat Illness

Heat acclimatization is of interest to physicians as well as athletes, because it reduces the incidence of heat illness and the intensity of symptoms. The most common heat illnesses among athletes are heat cramps, heat syncope, and heat exhaustion.

Heat cramps are usually unheralded and occur in the voluntary muscles of the legs, arms, and abdomen, after several hours of strenuous exercise in individuals who have lost a large volume of sweat, have drunk a large volume of hypotonic fluid, and who have excreted a small volume of urine. Sodium depletion probably causes heat cramps. Heat acclimatization decreases the risk of experiencing heat cramps.

Heat syncope (e.g., fainting) occurs most commonly during the first 3-5 days of heat exposure. This illness is related to the shunting of blood through dilated cutaneous vessels, postural pooling of blood, diminished venous return to the heart, reduction of cardiac output, and cerebral ischemia. Heat syncope typically occurs when the ambient temperature or humidity rises suddenly, or when a non-acclimatized individual performs exercise in a hot environment. Heat acclimatization reduces the incidence of heat syncope to nearly zero, after 3-5 days of exercise-heat exposure. This period corresponds with cardiovascular stabilization, early in the course of heat acclimatization (see above). Heat syncope is a syndrome distinct from heat exhaustion, because water and salt depletion do not always contribute to heat syncope.

Heat exhaustion is the most commonly diagnosed form of heat illness among athletes, despite the fact that its symptoms are often vague and differ greatly from one situation to another. Clinical descriptions include various combinations of headache, dizziness, fatigue, hyperirritability, tachycardia, hyperventilation, diarrhea, piloerection, hypotension, nausea, vomiting, syncope, heat cramps, as well as "heat sensations" in the head and upper torso. This explains why heat exhaustion is defined as the inability to continue exercise in a hot environment, and involves a diagnosis of exclusion. Heat acclimatization significantly reduces the signs and symptoms of heat exhaustion, after eight days of strenuous, intermittent running.

The three aforementioned heat illnesses all involve either fluid-electrolyte balance, extracellular volume and tonicity, or cardiovascular adaptation. This emphasizes the importance of (a) ample dietary intake of NaCl and fluids, and (b) fluid-electrolyte hormone regulation during heat acclimatization.

Factors Affecting Acclimatization

It is believed that host factors may influence the capacity to acclimatize to exercise in a hot environment. For example, older persons were previously thought to be less heat tolerant than their younger counterparts. Middle aged men (>45 yr) were shown to have higher heart rates, higher rectal temperatures, and lower sweat rates than young men, during exercise in the heat, both before and during exercise in the heat, both before and after heat acclimatization. Similarly, studies conducted in the late 1960s suggested that women were less tolerant of exercise in a hot environment than men. However, recent research has qualified and/or reversed these viewpoints. It is now recognized that few gender-related differences exist, when female and male subjects are matched for pertinent physical and morphological characteristics. It is also recognized that differences between older and younger subjects are not necessarily due to aging per se, but may be due to other factors such as decreased training volume and lower maximal aerobic power (VO2max)

Most experts agree that intense physical training in a cool environment improves physiologic responses and speeds the process of heat acclimatization. During training in cool conditions, optimal physiologic adaptations may be achieved if strenuous interval training or continuous exercise, at an intensity above 50% of VO2max, is performed for 8-12 weeks. Maintenance of an elevated core body temperature appears to be the most important physiologic stimulus.

Irrespective of physical training, VO2max generally influences physiologic responses during the development of heat acclimatization. Individuals with a high VO2max (>60 ml.kg^-1.min^-1) exhibit superior heart rate and rectal temperature responses, and usually reach a stable heat acclimatization state faster, when compared to those with a low VO2max (<40 ml.kg^-1.min^-1). However, maximal aerobic power per se may not be as important in conferring heat tolerance as the underlying physiologic adaptations (i.e. altered blood volume, vasodilation/vasoconstriction, and muscle metabolism) which result in VO2max differences between individuals. A recent publication by Pandolf et al. (1988) demonstrates this concept well. They exposed nine young men (21 y) and nine middle-aged men (46 y) to a 10-day heat acclimatization protocol (100 min treadmill walking per day, 49°C air temperature). The results of testing on Day 1 indicated that middle-aged men were able to exercise longer, had lower heart rates and rectal temperatures, and exhibited greater whole-body sweat rates than young men. The differences persisted for the first few days of heat acclimatization, but were absent by day 10 of heat acclimatization. Both groups were closely matched for body mass, surface area, percent body fat, and maximal aerobic power (51 versus 53 ml.kg^-1.min^-1, respectively). The factor that distinguished these two groups was their level of regular weekly physical training: middle-aged men ran an average of 39 km per week, whereas young men averaged only 8 km per week.

The phrase "heat intolerance" has been used in a wide variety of contexts. Interestingly, heat intolerance has been defined by some experts as an inability to develop normal physiologic adaptations, during repeated days of exercise in a hot environment. Some humans do not show the classic decreases in heart rate and rectal temperature that exemplify successful heat acclimatization. This has been of particular concern among persons with cardiovascular disease and prior heat stroke patients. One recent publication (Armstrong et al., 1990), however, reported that 9 out of 10 prior heat stroke patients exhibited normal heat acclimatization responses (90 minutes treadmill walking per day, 7 days, 40°C air temperature), 61 days after experiencing heatstroke.

Loss of Acclimatization

The physiologic adaptations to exercise training in a cool environment are lost after several weeks or months of inactivity. In contrast, heat acclimatization adaptations may vanish after only a few days or weeks of inactivity (i.e., 18-28 days). The first adaptations to decay are those that develop first: heart rate and other cardiovascular variables. The rate of decay of adaptations is affected by the number of heat exposures per week, the number and format of training sessions, and the degree to which core body temperature is elevated. Athletes with high VO2max usually will lose heat acclimatization adaptations slower than individuals with low VO2max.

References

Armstrong, L E, J P De Luca, and R W Hubbard. Time course of recovery and heat acclimation ability of prior exertional heatstroke patients. Med. Sci. Sports Exerc. 22: 36-48, 1990.

Armstrong, L E and C M Maresh. The induction and decay of heat acclimatization in trained athletes. Sports Med. 12: 302-312, 1991.

Armstrong, L E and K B Pandolf. Physical training, cardiorespiratory physical fitness, and exercise - heat tolerance. In: Human Performance Physiology and Environmental Medicine at Terrestrial Extremes, K.B. Pandolf, M.N. Sawka, and R.R. Gonzalez (Eds.). Indianapolis: Benchmark Press, 1988, pp. 199-226

Francesconi, R P, L E Armstrong, N M Leva, R J Moore, P C Szlyk, W T Matthew, W C Curtis, R W Hubbard, and E W Askew. Endocrinological responses to dietary salt restriction during heat acclimation. In: Nutritional Needs in Hot Environments, B.M. Marriott (Ed.). Washington, D.C.: National Academy Press, 1993, pp. 259-276.

Greenleaf, J E and C J Greenleaf. Human acclimation and acclimatization to heat: A compendium of Research. Moffett Field, CA: Ames Research Center, Technical Memorandum no. TM X-62008, 1970, pp. 1-188.

Hubbard, R W and L E Armstrong. The heat illnesses: biochemical, ultrastructural, and fluid-electrolyte considerations. In: Human Performance Physiology and Environmental Medicine at Terrestrial Extremes, K.B. Pandolf, M.N. Sawka, and R.R. Gonzalez (Eds.). Indianapolis: Benchmark Press, 1988, pp. 305-359.

Pandolf, K B, B S Cadarette, M N Sawka, A J Young, R P Francesconi, and R R Gonzalez. Thermoregulatory responses of matched middle-aged and young men during dry-heat acclimation. J. Appl. Physiol. 65: 65-71, 1988.

Sawka, M N, C B Wenger, A J Young, and K B Pandolf. Physiological responses to exercise in the heat. In: Nutritional Needs in Hot Environments, B.M. Marriott (Ed.). Washington, D.C.: National Academy Press, 1993, pp. 55-74.

Sciaraffa, D, S C Fox, R Stockmann, and J E Greenleaf. Human acclimation and acclimatization to heat: a compendium of research, 1968-1978. Moffett Field, CA: Ames Research Center, National Aeronautics and Space Administration Technical Memorandum no. 81181, 1981, pp. 1-102..

Wenger, C B Human heat acclimatization. In: Human Performance Physiology and Environmental Medicine at Terrestrial Extremes, K.B. Pandolf, M.N. Sawka, and R.R. Gonzalez (Eds.). Indianapolis Benchmark Press, 1988, pp. 153-198.