Exercise in the Heat

Exercise in the heat: Fundamentals of Thermal Physiology, Performance Implications and Dehydration

By Douglas J. Casa, PhD, ATC, CSCS
From Journal of Athletic Training 1999;34(3):246-252
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Objective: To present the critical issue of exercise in the heat in a format that provides physiologic foundations (Part I) and then applies the established literature to substantial, usable guidelines that athletic trainers can implement on a daily basis when working with athletes who exercise in the heat (Part 11). Data Sources: The databases MEDLINE and SPORT Discus were searched from 1980 to 1999, with the terms "hydration," "heat," "dehydration," "cardiovascular," "thermoregulatory," "physiology," and "exercise," among others. The remaining citations are knowledge base. Data Synthesis: Part I introduces athletic trainers to some of the basic physiologic and performance responses to exercise in the heat. Conclusions/Recommendations: The medical supervision of athletes who exercise in hot environments requires an in-depth understanding of basic physiologic responses and performance considerations. Part I of this article aims to lay the scientific foundation for efficient implementation of the guidelines for monitoring athletic performance in the heat provided in Part II.

Key Words: cardiovascular, heat stress, thermoregulatory

Exercise in the heat, as compared with a neutral environment, causes many physiologic changes in the dynamics of the human body, including alterations in the circulatory, thermoregulatory, and endocrine systems. Many interrelated physiologic processes work together to sustain central blood pressure, cool the body, maintain muscular function, and regulate fluid volume. Attempting to sustain exercise (especially if it is intense) in a hot environment can overload the body's ability to properly respond to the imposed stress, resulting in hyperthermia, dehydration, deteriorated physical and mental performance, and a potentially serious (even fatal) exertional heat illness.

CIRCULATORY RESPONSES

The circulatory responses to exercise involve 3 important components: skin and muscle vasodilation, nonactive tissue vasoconstriction, and maintenance of blood pressure' (Figure 1). Skin vasodilation occurs in proportion to the degree of heat load (both exogenous and endogenous),2'3 and the amount of blood supplied to the muscles is dictated by the intensity of the exercise. Constriction of the splanchnic vascular system (supplying the kidneys, stomach, and other abdominal organs), in addition to an overall increase in the cardiac output, allows increased blood flow to the active tissues.

However, when intense exercise occurs in the heat, the cardiovascular (CV) system simply cannot meet the maximal demands of the skin (to decrease thermal load) and the muscle simultaneously.1 8 Ultimately, maintenance of blood pressure will take precedence over skin blood flow (ie, body cooling) and muscle blood flow (ie, performance capacity), but simultaneously increases the rate of hyperthermia and metabolic inefficiency.1' 10" This prioritizing can result in hyperthermia, especially in populations committed to maximal physical exertion (soldiers, athletes, etc). The metabolic changes are reflected in an increased lactate level, which results from decreased hepatic blood flow; muscle vasoconstriction (which influences waste removal, oxygen delivery, buffering capacity, etc); and an increase in muscle temperature. 1 Variations in the onset of these changes can alter the rate at which the athlete experiences fatigue.

Decreased venous return reduces the stimulation of pressuresensitive baroreceptors in the right heart and the pulmonary circulation.12 Messages are then sent to the medullary CV control centers, which can cause muscle or skin vasoconstriction, or both, thereby preserving blood pressure and CV function. 1,13 Minimal decreases in cardiac output have been found in subjects exercising at submaximal intensities in the heat."'3"14 An increase in heart rate compensates for the decreases in stroke volume, and CV capacity is not hindered, unless extreme sweat rates or lengthy exercise sessions, for example, induce significant dehydration. But when maximal exercise is attempted in the heat, the heart rate's finite limit does not compensate for the larger decreases in stroke volume, due mostly to shunting of blood to the skin and active muscle and to the progressive dehydration. 1"7"13 Rowell' concluded that the end result is decreases in both Vo2 and perfonnance capacity.

THERMOREGULATORY RESPONSES

The circulatory and thermoregulatory responses are interrelated, with each influencing and being influenced by the other. The degree of stress imposed by exercise in a hot environment is determined by the thermal load. Heat gain must be equaled (or closely matched) by heat dissipation if the athlete wishes to continue exercising at a consistent performance level. Exogenous factors that contribute to heat acquisition include ambient temperature, wind speed, humidity, solar radiation (direct and indirect), ground thermal radiation, and clothing.'5 Ambient temperature and humidity are the major contributors; lack of wind in the presence of high humidity and high ambient temperature can impose severe heat stress because copious sweating is not cooling the body (sweat is not evaporating from the skin), which exacerbates the hyperthermia.16 The predominant endogenous factor is the metabolic heat from contracting muscle (capable of increasing 15 to 20 times during exercise in healthy young adults), which is profoundly influenced by the intensity of the exercise. The body attempts to balance internal temperature by dissipating heat via conduction, convection, evaporation, and radiation. 15,17 Heat dissipation while exercising depends on the ambient temperature. As ambient temperature rises, radiation and convection decrease markedly; heat loss by conduction is insignificant at almost all times.15"8 Convection is compromised by a temperature gradient change between the peripheral blood vessels and the skin. Heat loss from evaporation thus becomes the predominant heat-dissipating mechanism for a subject exercising in a hot environment. In a hot, dry environment, evaporation can account for as much as 98% of cooling, whereas in a hot, wet environment, evaporation is still nearly 80% (the rest is largely convection and radiation).'8 The sweating response is critical to whole-body cooling during exercise in the heat; any disturbance in this mechanism (eg, high humidity, dehydration) can have profound effects on physiologic function and athletic performance. The reader is referred to Stitt'7 and Werner15 for in-depth analyses of the heat balance equations, but, in short, heat acquisition (from exogenous and endogenous sources) must be matched by the combined 4 heat-dissipation pathways to maintain thermal balance: heat storage = heat production minus heat dissipation or plus heat acquisition. This may be expressed as ±S = (M-W) ± C ± K ± R -E, where S is body heat storage, M is metabolic heat production, W is external work, and C, K, R, and E represent convection, conduction, radiation, and evaporation, respectively.17"19 When heat dissipation fails to equal heat acquisition, hyperthermia increases skin blood flow, and, depending on the environmental conditions, heat release via convection, radiation, and evaporation.19 Skin blood flow changes are regulated not just by body temperature, but also by blood pressure, brain blood flow temperature, skin-core temperature gradients, muscle metabolism, etc. As discussed previously, maintenance of blood pressure takes precedence over heat dissipation.

Kenney and Johnson2 and Sawka and Wenger7 reported on the integration of these regulatory processes, in addition to the important role of the efferent mechanisms controlling skin blood flow (ie, passive withdrawal of constrictor tone, reflex vasoconstriction, and active vasodilation). The inherent changes in sweating rate and body cooling associated with skin blood flow changes assist in controlling hyperthermia (the primary controller of sweating rate). Nadell' and Sato20 offer the best explanation of eccrine sweat secretion. Warmer air temperatures are associated with increased sweating.2' Since only evaporation is an efficient mode of heat dissipation in this situation, physiologic strain is exacerbated by the decreased extracellular fluid volume associated with copious sweating. In the short term, the body is being cooled, but increased dehydration alters CV functional capacity, which can lead to decreased skin blood flow and sweating rate as the body attempts to maintain the central circulation and blood pressure. In a cooler environment (with a larger temperature gradient between skin blood flow and skin temperature), the body can avoid hyperthermia while minimizing fluid losses via convection and radiation. In a warm, humid environment, all the critical variables work against the exercising individual: convection and radiation are nearly nonexistent,10 and evaporation is thwarted by a small water vapor pressure gradient.7 With no heat dissipation, dehydration occurs, and the core temperature rises at a potentially dangerous rate.22 The decreased physiologic function associated with hyperthermia is well documented, 23 and the rate of onset of hyperthermia can be influenced by fitness,15 acclimation,24 type of exercise,25 age,26 and numerous other factors.

PERFORMANCE IMPLICATIONS

The additive effect of the stresses imposed by exercise in the heat will ultimately compromise athletic performance. In addition, exercise in the heat often causes dehydration (since rates of sweating are rarely matched by rates of rehydration), which further exacerbates the situation.2728 It is extremely difficult to separate the effects of heat and dehydration, since they often occur in parallel during prolonged exercise, but some researchers have attempted to match sweat loss with fluid intake during exercise. Rowell et al29 found large reductions in stroke volume despite maintained central blood volume. Enhanced physical fitness and heat acclimatization increase heat tolerance independently but similarly and optimize heat tolerance when combined.30 Sawka et a13' reported a 7% decrease in maximal aerobic power in the heat as compared with euhydrated subjects in cool temperatures. Febbraio et a132 and Galloway and Maughan33 showed the effects of increasing temperature on the capacity to exercise to exhaustion. Febbraio et al32 found that subjects could exercise for 95 minutes at 37°F (2.78°C), 75 minutes at 68°F (20°C), and only 33 minutes at 104°F (400C), indicating an inverse linear relationship between ambient temperature and performance capacity. The 20-minute difference in the 2 cooler environments is an important reminder that extreme heat is not necessary for potential performance decrements. Galloway and Maughan33 concurred, reporting that subjects exercised for 92 minutes at 52°F (11.11°C), 83 minutes at 70°F (21.11°C), and 51 minutes at 86°F (300C). These studies supported the concept of Sawka et al34 that heat stress and dehydration can act independently to compromise physiologic function when the extreme demands for skin blood flow cause decreased cardiac output, which in turn limits the supply of oxygenated blood to the entire body. When heat stress and dehydration occur together (as they often do), this physiologic condition is exacerbated. In addition to performance decrements, the potential for an exertional heat illness increases as the environmental conditions worsen. The American College of Sports Medicine22 provided a concise analysis of how to determine when the environmental conditions preclude physical activity and what procedures should be followed to ensure safe participation in a hot environment (to be addressed in part II).

DEHYDRATION AND EXERCISE

Each physiologic system in the human body is influenced by severe dehydration. The degree of dehydration will dictate how much these systems are compromised. Figure 2 describes similar terms used to describe water losses and gains. The work of Sawka and colleagues34-36 is definitive in the domain of hypohydration and its impact on performance and physiologic function. Their laboratory, located within the US Army Research Institute of Environmental Medicine in Natick, MA, is one of the preeminent locations in the world for investigating the human body's capacity to perform exercise in a variety of environments.

Physiologic Changes

Isolating which particular physiologic changes contribute to decrements in performance is difficult, if not impossible. The interrelation of the human body's systems means that any change in one system influences others. However, recent research has begun to uncover what occurs when an athlete becomes dehydrated during exercise. Dehydration induces changes in the thermoregulatory, cardiovascular, plasma, gastrointestinal, endocrine, muscular, and metabolic responses to exercise.37'38 As discussed earlier, the CV system of a ypohydrated, exercising subject attempts to maintain cardiac filling pressure while sacrificing peripheral circulation,' but hypohydration in combination with heat dissipation at the skin and increased muscle blood flow limits CV capacity, regardless of how much blood is shunted from the periphery to the central circulation. 1 39'40 Increased viscosity and decreased volume of blood returning to the heart decrease filling pressure, and in turn, stroke volume. 14.41,42 To counteract these changes, heart rate rises to its limit, but then cardiac output begins to fall, signaling CV system responses, which limit skin and muscle function.

3443 The end result is a diminished ability to dissipate heat, and thus, heat production exceeds heat loss. Excess heat in combination with decreased muscle perfusion limits performance and causes thermal strain.1 35 Exercising while dehydrated has some effects on the thermoregulatory system444-49 (Table) and may negate the physiologic advantages resulting from increased fitness24'50 and heat acclimatization. 24'51 Sawka et al36 noted decreased heat tolerance (by more than halt) in subjects dehydrated by 8% of body weight and found that soldiers became exhausted at lower core temperatures when hypohydrated. While 8% is an extreme amount of dehydration rarely encountered in sports, the study emphasizes the decreased heat tolerance associated with dehydration. The human body is composed of about 65% water, separated into extracellular (plasma and interstitial) and intracellular fluid.52 At rest with normal hydration, about 45% of body weight is intracellular fluid, 15% is interstitial fluid, and 5% is plasma.52 Exercise, heat stress, and dehydration all influence the redistribution of body fluids with changes in hydrostatic and osmotic pressure.52'53 For instance, because sweat is hypotonic to plasma, the dehydrated athlete experiences plasma hyperosmolality, which affects the distribution of fluids.35 Mild dehydration causes mostly extracellular space fluid losses, but, as dehydration worsens, proportionally more fluid is lost from the intracellular space.54'55 Nose et a156 reported that the loss of intracellular and extracellular fluid is largely from muscle and skin. This selective regulation of body fluids preserves the internal environment of the most essential organs: for instance, the brain and liver.35 Changes in the distribution of body fluids are associated with the ability to mobilize fluids from the intracellular space, which is intimately linked with sweat sodium concentrations.57 Thus, the de- creased sweat sodium concentrations noted after heat acclimatization may help to conserve plasma volume during dehydration. Ultimately, the fluid redistribution that results from dehydration causes a hypovolemic hyperosmolality,58 which stimulates the volume and fluid receptors in the body to conserve fluid and stimulate rehydration.

Plasma changes have been cited as the major cause for the thermoregulatory changes during hypohydration. Hyperosmolality59- 61 and hypovolemia'6 62 are likely responsible for the changes noted in skin blood flow and sweating rate and the resultant rises in core temperature.93540 Fortney et al"6 have argued that hypovolemia is primarily responsible for the thermoregulatory changes by reducing central blood volume, which may alter the feedback to the hypothalamus via the atrial baroreceptors. The hypothalamic thermoregulatory centers may then decrease the blood volume perfusing the skin in an attempt to reestablish a normal central blood volume. Some studies have provided support for this hypothesis,6364 but it is clearly not the only variable influencing thermoregulation during hypohydration. Two primary hypotheses have been proposed to explain the role of hyperosmolality on the thermoregulatory system. The first is a strong osmotic pressure influence of the interstitium, which may limit the available fluid sources for the eccrine sweat glands.65 While this pressure is likely to exert some influence, it seems more feasible that brain regulation, the second hypothesis, has the largest contribution. The neurons surrounding the thermoregulatory control centers in the hypothalamus are quite sensitive to osmolality.6'67 Thus, changes in the plasma perfusing the hypothalamus can affect body water regulation and the desire for fluid consumption.4043 The human body is well equipped to identify small changes in the internal environment and to respond with appropriate modifications. While research may someday identify a proportional contribution to the age-old question of hyperosmolality versus hypovolemia, it is most likely that both will always be considered major contributors to the mechanisms that perturbate body fluid regulation. Potential muscle changes associated with dehydration include an increased rate of glycogen synthesis,"'48 compromised buffering capacity of the muscle tissue,38 elevated muscle temperature,68 and decreased substrate exchange.",38

These factors are caused by a decrease in blood flow perfusing the muscle tissue, which may alter the dynamics during the recovery between contractions.69 These muscle changes seem to occur when exercise exceeds 30 seconds, which is reasonable from a metabolic perspective.70 These arguments would support the notion that strength during short-term activity is not affected until dehydration becomes more pronounced, largely due to the fact that the muscle energetics of very short-term activity are, for the most part, self-contained, and thus, not as influenced by changes in blood flow.38

Performance Implications

Research investigating the role of dehydration on muscle strength has yielded conflicting results. Some studies have shown performance decrements,7174 while others have shown no changes.'4'75 However, when strength decrements were found, they usually occurred when dehydration exceeded a 5% reduction in body weight.34'49 In addition, dehydration resulting from fluid restriction seems to be more harmful than that caused by exercise and heat stress; thus, the fluid restriction may be partially inducing a caloric deficit.34 The research on muscle endurance is a bit more conclusive. A sampling of the numerous studies14'7276-79 that have addressed the influence of dehydration on muscle endurance reveals, generally speaking, that 3% to 4% dehydration elicits a performance decrement but some studies investigating greater levels of dehydration did not find any differences in performance.34 Horswill38 concluded that, in wrestlers (who are frequently hypohydrated), combined hypohydration and maximal or near-maximal muscle activity exceeding 30 seconds may combine to decrease performance. Environmental conditions may also play an important role in muscle endurance, 34'68 and, since greater hypohydration often occurs in hot conditions, more studies should investigate this relationship. The research concerning maximal aerobic power and the physical work capacity for extended exercise is also relatively conclusive and consistent. Maximal aerobic power usually decreases when dehydration exceeds a 2% to 3% reduction in body weight, and, when performed in the heat, the decrements are exaggerated.34 Nearly every study that has examined physical work capacity has shown some degree of performance decrement.34 Even with only 1% to 2% hypohydration in a cool environment,8081 a decrement is noted. Pinchan et a182 and Walsh et a183 noted decreases in physical work capacity with less than 2% dehydration during intense exercise in the heat. As expected, when dehydration increased, physical work capacity decreased, sometimes by as much as 35% to 48%,84 and physical work capacity often decreased even when maximal aerobic power did not change.80'8"85 Buskirk and Puhl69 suggested that some of these decrements with low to moderate levels of hypohydration may be partly due to an increased perception of fatigue. The degree of change in physiologic function will be dependent on various exercise parameters, including intensity, duration, environmental stress, and individual factors.

CONCLUSION

Exercise in the heat triggers a disturbance of the internal environment of the human body. Understanding the responses requires an astute ability to focus on many independent physiologic processes that function cooperatively. The athlete wishes for these systems to rise to any challenge, but often excessive heat, dehydration, or both cause some degree of decrement in performance. The ensuing part of this 2-part series about exercise in the heat attempts to identify ways in which athletic trainers and athletes can work toward minimizing the decrement by maximizing heat dissipation and body fluid balance.

ACKNOWLEDGMENT

I would like to dedicate this paper to the memory of my former supervisor, Dean Leo W. Anglin, Jr, PhD. I would later learn that he took his final breaths as I wrote this article. He was a visionary in the field of education, and the passion that drove him was contagious. I shall strive in his memory.

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