Michael N. Sawka,1 C. Bruce Wenger, Andrew J. Young, and Kent B. Pandolf Show
IntroductionHumans often exercise strenuously in hot environments for reasons of recreation, vocation, and survival. The magnitude of physiological strain imposed by exercise-environmental stress depends on the individual's metabolic rate and capacity for heat exchange with the environment. Muscular exercise increases metabolism by 5 to 15 times the resting rate to provide energy for skeletal muscle contraction. Depending on the type of exercise, 70 to 100 percent of the metabolism is released as heat and needs to be dissipated in order to maintain body heat balance. The effectiveness of the thermoregulatory system in defending body temperature is influenced by the individual's acclimatization state (Wenger, 1988), aerobic fitness (Armstrong and Pandolf, 1988), and hydration level (Sawka and Pandolf, 1990). Aerobically fit persons who are heat acclimatized and fully hydrated have less body heat storage and perform optimally during exercise-heat stress. To regulate body temperature, heat gain and loss are controlled by the autonomic nervous system's alteration of (a) heat flow from the core to the skin via the blood and (b) sweating. Thermoreceptors in the skin and body core provide input into the hypothalamic thermoregulatory center where this information is processed, via a proportional control system, with a resultant signal for heat loss by the thermoregulatory effector responses of sweating and alterations in skin blood flow (Sawka and Wenger, 1988). This chapter reviews human temperature regulation and normal physiological responses to exercise-heat stress. In general, muscular exercise and heat stress interact synergistically and may push physiological systems to their limits in simultaneously supporting the competing metabolic and thermoregulatory demands. Core Temperature Responses to ExerciseDuring muscular exercise, core temperature initially increases rapidly and subsequently increases at a reduced rate until heat loss equals heat production, and essentially steady-state values are achieved. At the initiation of exercise, the metabolic rate increases immediately; however, the thermoregulatory effector responses for heat dissipation respond more slowly. The thermoregulatory effector responses, which enable sensible (radiative and convective) and insensible (evaporative) heat loss to occur, increase in proportion to the rise in core temperature. Eventually, these heat loss mechanisms increase sufficiently to balance metabolic heat production, allowing achievement of a steady-state core temperature. During muscular exercise, the magnitude of core temperature elevation is largely independent of the environmental condition and is proportional to the metabolic rate (Gonzalez et al., 1978; Nielsen, 1938, 1970). This concept was first presented by Nielsen (1938) who had three subjects perform exercise at several intensities (up to approximately 3.0 liters oxygen per minute) in a broad temperature range (5° to 36°C with low humidity). Figure 3-1 presents the heat exchange data for one subject during an hour of cycle exercise at a power output of 147 watts and at a metabolic rate of approximately 650 watts. The difference between metabolic rate and total heat loss represents the energy used for mechanical work and heat storage. The total heat loss and, therefore, the heat storage and elevation of core temperature were constant for each environment. The relative contributions of sensible and insensible heat exchange to total heat loss, however, varied with environmental conditions. In the 10°C environment, the large skin-to-ambient temperature gradient facilitated sensible heat exchange, which accounted for about 70 percent of the total heat loss. As ambient temperature increased, this gradient for sensible heat exchange diminished, and there was a greater reliance upon insensible heat exchange. When the ambient temperature was equal to skin temperature, insensible heat exchange accounted for almost all the heat loss. In addition, when the ambient temperature exceeded the skin temperature, there was a sensible heat gain to the body. Figure 3-1Heat exchange data averaged over 1 hour for one subject performing constant intensity exercise in a variety of ambient temperatures. The difference between metabolic rate and total heat loss is the sum of mechanical power (147 watts) and mean rate of (more...) Nielsen's finding that the magnitude of core temperature elevation is independent of environmental conditions is inconsistent with the personal experience of most athletes. For example, a runner will experience greater hyperthermia if he or she competes in a 35°C environment (Robinson, 1963). Lind (1963) showed that the magnitude of core temperature elevation during exercise is independent of the environment only within a certain range of conditions or a ''prescriptive zone.'' Figure 3-2 presents a subject's steady-state core temperature responses during exercise performed at three metabolic intensities in a broad range of environmental conditions. The environmental conditions are represented by the "old" effective temperature, which is an index that combines the effects of dry-bulb temperature, humidity, and air motion. Note that during exercise the greater the metabolic rate, the lower the upper limit of the prescriptive zone. In addition, Lind found that even within the prescriptive zone there was a small but significant positive relationship between the steady-state core temperature and the "old" effective temperature. It seems fair to conclude that throughout a wide range of environmental conditions, the magnitude of core temperature elevation during exercise is largely, but not entirely, independent of the environment. During exercise with a substantial metabolic requirement, the prescriptive zone might be exceeded, and there is a further elevation of steady-state core temperature. Figure 3–2Relationship of steady-state core temperature responses during exercise at three metabolic rates to the environmental conditions. Source: Sawka and Wenger (1988), used with permission. Redrawn from Lind (1963). As stated, within the prescriptive zone, the magnitude of core temperature elevation during exercise is proportional to the metabolic rate (Nielsen, 1938; Saltin and Hermansen, 1966; Stolwijk et al., 1968). Although the relationship between metabolic rate and core temperature is strong for a given individual, it does not always hold well for comparisons between different individuals. Åstrand (1960) first reported that the use of relative intensity (percentage of maximal oxygen uptake), rather than actual metabolic rate (absolute intensity), removes most of the intersubject variability for the core temperature elevation during exercise. MetabolismMetabolic RateThe effects of acute heat stress on a person's ability to achieve maximal aerobic metabolic rates during exercise have been thoroughly studied. Most investigators find that maximal oxygen uptake is reduced in hot compared to temperate environments (Klausen et al., 1967; Rowell et al., 1969; Saltin et al., 1972; Sen Gupta et al., 1977), but some investigators
report no differences (Rowell et al., 1965; Williams et al., 1962). For example, in one study (Sawka et al., 1985) maximal oxygen uptake Figure 3-3Maximal aerobic power values (liters per minute) for the pre-and postheat acclimatization tests in a moderate (21°C, 30 percent relative humidity) and a hot (49°C, 20 percent relative humidity) environment, r = Pearson product-moment correlation (more...) TABLE 3–1Papers Reporting the Effect of Heat on Metabolic Rate During Exercise* NC = No change. †LA = Plasma lactate. Acute heat stress increases resting metabolic rate (Consolazio et al., 1961, 1963; Dimri et al., 1980), but the effect of heat stress on an individual's metabolic rate for performing a given submaximal exercise task is not so clear (see Table 3-1). Such an effect would influence the calculation of the heat balance and might have implications for the nutritional requirements of individuals exposed to hot environments. Many investigators report that to perform a given submaximal exercise task, the metabolic rate is greater in a hot than temperate environment (Consolazio et al., 1961, 1963; Dimri et al., 1980; Fink et al., 1975). Some investigators, however, report lower metabolic rates in the heat (Brouha et al., 1960; Petersen and Vejby-Christensen, 1973; Williams et al., 1962; Young et al., 1985). Heat acclimation state does not account for whether individuals demonstrate an increased or decreased metabolic rate during submaximal exercise in the heat. However, other mechanisms can explain this discrepancy. Most investigators have only calculated the aerobic metabolic rate during submaximal exercise, ignoring the contribution of anaerobic metabolism to total metabolic rate. Dimri et al. (1980) had six subjects exercise at three intensities in each of three environments. Figure 3-4 presents their subjects' total metabolic rate (bottom) and the percentage of this metabolic rate that was contributed by aerobic and anaerobic metabolic pathways. The anaerobic metabolism was calculated by measuring the postexercise oxygen uptake that was in excess of resting baseline levels. Although there are limitations to this methodology, the study provides useful information. Note that to perform exercise at a given power output, the total metabolic rate increased with the elevated ambient temperature. More importantly, the percentage of the total metabolic rate contributed by anaerobic metabolism also increased with the ambient temperature. The increase in anaerobic metabolic rate exceeded the increase of total metabolic rate during exercise at the elevated ambient temperatures. Therefore, if only the aerobic metabolic rate had been quantified, Dimri et al. (1980) would probably have reported a decreased metabolic rate in the heat for performing exercise at a given power output. Investigations that report a lower metabolic rate during exercise in the heat also report increased plasma or muscle lactate levels (Petersen and Vejby-Christensen, 1973; Williams et al., 1962; Young et al., 1985) or an increased respiratory exchange ratio (Brouha et al., 1960), which also suggests an increased anaerobic metabolism. Likewise, other investigators report that plasma lactate levels are greater during submaximal exercise in a hot as compared to a comfortable environment (Dill et al., 1930/1931; Dimri et al., 1980; Fink et al., 1975; Nadel 1983; Robinson et al., 1941). Figure 3-4The total metabolic rate and percentage contribution of aerobic and anaerobic metabolism during exercise at different ambient temperatures. Source: Sawka and Wenger (1988), used with permission. Data from Dimri (1980). Interestingly, the oxygen uptake response to submaximal exercise does appear to be affected by
heat acclimatization (Sawka et al., 1983). Most reports indicate that oxygen uptake and aerobic metabolic rate during submaximal exercise are reduced by heat acclimatization, although a significant effect is not always observed (see Table 3-2). Large effects (14 to 17 percent reductions) have been reported for stair-stepping (Senay and
Kok, 1977; Shvartz et al., 1977; Strydom et al., 1966), but some of the reduction in
TABLE 3-2Papers Reporting the Effect Heat Acclimatization Has on Metabolic Rate During Exercise. Skeletal Muscle MetabolismSeveral investigations examined the effects of environmental heat stress on skeletal muscle metabolism during exercise. Fink et al.
(1975) had six subjects perform 45 minutes of cycle exercise (70 to 85 percent of Young et al. (1985) had 13 subjects perform 30 minutes of cycle exercise (70 percent of Data from Dimri et al. (1980) and Young et al. (1985) support the concept of increased anaerobic metabolism during submaximal exercise in the heat. Much of the other support for this concept is based on the findings that, during submaximal exercise, the plasma lactate accumulation is greater in a hot than in a comfortable environment. However, any inference about metabolic effects within the skeletal muscle from changes in plasma lactate is open to debate. Plasma lactate concentration reflects the balance between muscular production, efflux into the blood, and removal from the blood. Rowell et al. (1968) have shown that during exercise in the heat the splanchnic vasoconstriction reduced hepatic removal of plasma lactate. Therefore, the greater blood lactate accumulation during submaximal exercise in the heat can be attributed, at least in part, to a redistribution of blood flow away from the splanchnic tissues. Lactate accumulation in blood and muscle during submaximal exercise is generally found to be reduced following heat acclimatization (Young, 1990). Figure 3-5 shows that heat acclimatization resulted in lower postexercise muscle lactate concentrations. Muscle lactate concentrations were still higher in the heat than in the cool, and changes in blood lactate concentrations followed exactly the same patterns (Young et al., 1985). King et al. (1985) and Kirwan et al. (1987) observed that heat acclimatization reduced muscle glycogen utilization during exercise in the heat by 40 to 50 percent compared to before acclimatization. Young et al. (1985) also observed a statistically significant glycogen sparing effect due to heat acclimatization, but the reduction in glycogen utilization was small and apparent only during exercise in the cool conditions. Glycogen utilization during exercise in the heat was negligibly affected. The mechanism(s) for the reduction in lactate accumulation during exercise associated with heat acclimatization remains unidentified. Figure 3-5Effects of heat acclimatization on pre-and postexercise muscle lactate concentration (mean ± standard error) in cool (24°C) and hot (49°C) environments. Source: Young et al. (1985), used with permission. Evaporative Heat LossFigure 3-1 illustrates that when ambient temperature increases, there is a greater dependence on insensible (evaporative) heat loss to defend core temperature during exercise. In contrast to most animals, respiratory evaporative cooling is small in humans when compared to total skin evaporative cooling. The use of skin provides the advantage of having a greater surface area available for evaporation. The eccrine glands secrete sweat on the skin surface, which is cooled when the sweat evaporates. The rate of evaporation depends on the wetted area, air movement, and the water vapor pressure gradient between the skin and the surrounding air; the wider the gradient, the greater the rate of evaporation. For a given person, sweating rate is highly variable and depends on environmental conditions (ambient temperature, dew point temperature, radiant load, and air velocity); clothing (insulation and moisture permeability); and physical activity level (Shapiro et al., 1982). Adolph et al. (1947) reported that for 91 men studied during diverse military activities in the desert, the average sweating rate was 4.1 liters every 24 hours, but values ranged from 1 to 11 liters every 24 hours. The water requirements of soldiers on the modern battlefield may be even greater. The threat of chemical warfare may require military personnel to wear nuclear-biological-chemical (NBC) protective clothing, which prevents noxious agents from reaching the skin. Characterized by low moisture permeability and high insulating properties, NBC clothing prevents the normal dissipation of body heat. As a result, both core and skin temperatures can rise excessively and result in high levels of sweat output, which cannot evaporate within the garments. For example, during light-to moderate-intensity (about 150 to 400 watts) exercise in hot environments, soldiers wearing NBC clothing routinely have sweating rates of 1 to 2 liters per hour (Muza et al., 1988; Pimental et al., 1987). For athletes, the highest sweating rates occur during prolonged highintensity exercise in the heat. Figure 3-6 (Sawka and Pandolf, 1990) provides an approximation of hourly sweating rates and, therefore, water requirements for runners based on metabolic rate data from several laboratories. The sweating rates were predicted by the equation developed by Shapiro et al. (1982). The amount of body fluid lost as sweat can vary greatly, and sweating rates of 1 liter per hour are very common. The highest sweating rate reported in the literature is 3.7 liters per hour, measured for Alberto Salazar during the 1984 Olympic Marathon (Armstrong et al., 1986). Figure 3-6An approximation of the hourly sweating rates (liters per hour) for runners. Running speed is indicated in meters per minute. Source: Sawka and Pandolf (1990), used with permission. If sweat loss is not fully replaced, the individual's total body water will be decreased (dehydration). Because sweat is more dilute than plasma, dehydration from sweat loss results in an increased plasma tonicity and decreased blood volume, both of which will act to reduce sweat output and skin blood flow (Sawka and Pandolf, 1990). As a result, the body's ability to dissipate heat will be decreased, and dehydration will result in a greater rise in core temperature during exercise-heat stress. In addition, the combination of an elevated core temperature and a reduced blood volume will increase the circulatory strain. Skin Blood Flow and Circulatory ResponsesBlood flow from the deep body tissues to the skin transfers heat by convection. When core and skin temperatures are low enough that sweating does not occur, raising skin blood flow brings skin temperature nearer to blood temperature, and lowering skin blood flow brings skin temperature nearer to ambient temperature. This phenomenon allows the body to control sensible (convective and radiative) heat loss by varying skin blood flow and thus skin temperature. In conditions in which sweating occurs, the tendency of skin blood flow to warm the skin is approximately balanced by the tendency of sweating to cool the skin. Therefore, there is usually little change in skin temperature and sensible heat exchange after sweating has begun, and skin blood flow serves primarily to deliver to the skin the heat that is being removed by sweat evaporation. Skin blood flow and sweating thus work in tandem to dissipate heat under such conditions. During exercise-heat stress, thermoregulatory skin blood flow, although not precisely known, may be as high as 7 liters per minute (Rowell, 1986). The higher skin blood flow will generally, but not always, result in a higher cardiac output, and one might expect the increased work of the heart in pumping this blood to be the major source of cardiovascular strain associated with heat stress. The work of the heart in providing the skin blood flow necessary for thermoregulation in the heat imposes a substantial cardiac strain on patients with severe cardiac disease (Burch and DePasquale, 1962). In healthy subjects, however, the cardiovascular strain associated with stress results mostly from reduced cardiac filling and stroke volume (Figure 3-7), which necessitate a higher heart rate to maintain cardiac output (Nadel et al., 1979; Sawka and Wenger, 1988). This change occurs because the venous bed of the skin is large and compliant and dilates reflexively during heat stress. Therefore, as skin blood flow increases, the blood vessels of the skin become engorged and blood pools in the skin, thus reducing central blood volume and cardiac filling. Figure 3-7Thermal and circulatory responses of one subject during cycle exercise at 70 percent Several reflex adjustments compensate for peripheral pooling of blood and decreases in blood volume to help maintain cardiac filling, cardiac output, and arterial pressure during exercise-heat stress.
Splanchnic and renal blood flows are reduced during exercise in proportion to relative exercise intensity (that is, as a percentage of During exercise in the heat, the primary cardiovascular challenge is simultaneously to provide sufficient blood flow to exercising skeletal muscle to support metabolism and to provide sufficient blood flow to the skin to dissipate heat. In hot environments, the core-to-skin temperature gradient is less than in cool environments, so that skin blood flow must be relatively high to achieve sufficient heat transfer to maintain thermal balance (Rowell, 1986; Sawka and Wenger, 1988). This high skin blood flow causes pooling of blood in the compliant skin veins, especially below heart level. In addition, as discussed, sweat secretion can result in a net loss of body water, and thereby a reduction in blood volume (Sawka and Pandolf, 1990). Heat stress can reduce cardiac filling through pooling of blood in the skin and through reduced blood volume. Compensatory responses include reductions in splanchnic and renal blood flow; increased cardiac contractility, which helps to defend stroke volume in the face of impaired cardiac filling; and increased heart rate to compensate for decreased stroke volume. If these compensatory responses are insufficient, skin and muscle blood flow will be impaired, possibly leading to dangerous hyperthermia and reduced exercise performance. Summary
References
1 Michael N. Sawka, Ph.D., Thermal Physiology and Medicine Division, U.S. Army Research Institute of Environmental Medicine, Kansas Street, Natick, MA 01760-5007 How long does it take your body to adapt to heat?Pushing to the point of heat exhaustion will hurt, not help, your heat tolerance. Typically, acclimatization requires at least two hours of heat exposure per day (which can be broken into two, 1-hour periods). The body will acclimatize to the level of work demanded of it. Simply being in a hot place is not sufficient.
How does body adapt to exercising in heat?Training in the heat increases body (core and skin) temperature, induces profuse sweating and increases skin blood flow. All of these responses stimulate physiological adaptations, which improves the athlete's tolerance to exercise in the heat and reduces the risk of heat illness.
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