INTRODUCTION

During muscular exercise, the magnitude of core temperature elevation is proportional to the metabolic rate and somewhat independent of the environmental condition (Nielsen, 1938). The elevation of the core temperature represents the storage of metabolic heat, which is a by-product of skeletal muscle contraction. At the initiation of exercise, the metabolic rate increases immediately; however, the thermoregulatory effector responses respond more slowly. The thermoregulatory effector responses, which enable dry and evaporative heat loss to occur, increase in proportion to the rate of heat production (Nielsen, 1966). Eventually, these heat loss mechanisms increase sufficiently to balance metabolic heat production, allowing a steady-state core temperature to be achieved.

An individual's aerobic fitness (Armstrong and Pandolf, 1988), acclimatization state (Wenger, 1988), and hydration level (Sawka, 1988) have been known to be the primary factors modifying the core temperature and thermoregulatory responses to muscular exercise. Aerobically fit people who are heat acclimated and fully hydrated optimize their ability to limit body heat storage and maintain performance during exercise-heat stress. Hydration level is particularly important because a body fluid deficit incurred before or during exercise in the heat neutralizes the thermoregulatory advantages conferred by high aerobic fitness (Cadarette et al., 1984) and heat acclimatization (Buskirk et al., 1958; Sawka et al., 1983).

BODY WATER LOSS

In hot environments, body fluid is lost primarily through eccrine sweat gland secretion, which results in evaporative cooling of the body. For a given person, the sweating rate is dependent on environmental conditions (ambient temperature, dew point temperature, radiant load, and air velocity), clothing (insulation and moisture permeability), and physical activity level (Adolph and Associates, 1947; Shapiro et al., 1982). Adolph and Associates (1947) reported that for 91 men studied during diverse military activities in the desert, the average sweating rate was 4.1 liters every 24 h, but values ranged from 1 to 11 liters every 24 h. During more intense physical exercise, much higher sweating rates can occur, and sweating rates of 1 liter/h are very common (Shapiro et al., 1982).

During physical exercise in the heat, the principal problem is that of precisely matching the volume of fluid intake to the volume of sweat output. This is a difficult problem to solve since thirst does not provide a good index of body water requirements (Adolph and Associates, 1947; Engell et al., 1987). Numerous investigators (Adolph and Associates, 1947; Bar-Or et al., 1980; Phillips et al., 1984) report that ad libitum water intake results in incomplete water replacement or voluntary dehydration during exercise and heat exposure. It is not uncommon for individuals to voluntarily dehydrate 2%-8% of their body weight during exercise-heat stress, despite the availability of adequate amounts of fluid for rehydration (Adolph and Associates, 1947; Buskirk and Beetham, 1960; Greenleaf et al., 1983).

Thirst is probably not perceived until an individual has incurred a water deficit of approximately 2% of body weight (Adolph and Associates, 1947). As a result, it is likely that unless forced hydration is practiced, some level of dehydration will occur during exercise in the heat. Neufer et al. (1988) recently found that hypohydration reduces the gastric emptying rate of ingested fluids during exercise in the heat. They found an approximate 20% reduction in gastric emptying rate during three successive 15-min bouts of exercise in a warm environment (35°C, 20% relative humidity) when subjects were hypohydrated as compared when they were euhydrated. The volume of ingested fluid emptied into the intestines was inversely correlated (Figure 7-1) with the subjects' core temperature (Neufer et al., 1988). In this paper it is shown that hypohydration mediates an increased core temperature during exercise. Therefore, forced hydration during the early stages of exercise-heat stress is important, not only to avoid voluntary dehydration but also to maximize the bioavailability of the ingested fluids.

FIGURE 7-1

Correlation of final rectal temperatures (°C) and the corresponding volume (ml) of original drink emptied during exercise (50% ) when euhydrated and hypohydrated by 5% of body weight. Source: Neufer et al. (1988).

Sweat loss results in a reduction of total body water if an adequate amount of fluid is not consumed. The question arises as to how water loss is partitioned among the body fluid compartments. As a consequence of free fluid exchange, hypohydration affects each fluid compartment (Costill et al., 1976; Durkot et al., 1986; Nose et al., 1983). When body water loss is minimal, the water deficit comes primarily from the extracellular space. As more body water is lost, a proportionately greater percentage of the water deficit comes from the intracellular space (Costill et al., 1976; Durkot et al., 1986).

The plasma volume responses for heat-acclimated subjects when they were euhydrated and hypohydrated by 3%, 5%, and 7% of their body weight are presented on the bottom of Figure 7-2 (Sawka et al., 1985). Note that plasma volumes were generally smaller with increased hypohydration levels, although there was some evidence of a plasma volume defense during the 7% hypohydration experiment. The most important point from Figure 7-2 is the observation that the hypohydration-mediated plasma volume reduction that occurred at rest continued throughout the subsequent moderate-intensity exercise. In fact, the differences between the euhydration and hypohydration plasma volumes were greater during exercise than during rest because of the small exercise-induced hemodilution that occurred when subjects were euhydrated but not hypohydrated (Sawka et al., 1984a, 1985).

FIGURE 7-2

Plasma osmolality and plasma volume at rest and exercise when euhydrated and hypohydrated by 3%, 5%, and 7% of body weight. Source: Sawka et al. (1985).

It is known that exercise or heat-induced hypohydration increases the osmotic pressure in the plasma. Eccrine sweat is ordinarily hypotonic relative to plasma (Sawka, 1988); therefore, the plasma becomes hyperosmotic when hypohydration is induced primarily by sweat output (Sawka et al., 1985; Senay, 1979). For resting subjects, plasma osmolality increases from about 283 mosmol/kg when they are euhydrated to levels exceeding 300 mosmol/kg when hypohydrated (Figure 7-2). Sodium, potassium, and their anions (chloride) are primarily responsible for the elevated plasma osmolality during hypohydration (Senay, 1979).

EXERCISE PERFORMANCE AND PHYSIOLOGICAL RESPONSES

Several investigations have examined the effects of hypohydration on maximal aerobic power and physical work capacity. In the absence of heat stress, a relatively large water deficit (6%-7%) has a minimal effect on maximal aerobic power, but reduces physical work capacity by approximately 20% (Sawka et al., 1984b). In a hot environment, Craig and Cummings (1966) demonstrated that small (2%) to moderate (4%) water deficits reduce maximal aerobic power (10%-27%) and physical work capacity (22%-48%). In addition, these decrements increase dramatically with the magnitude of water deficit. Consistent with these findings, hypohydration combined with hyperthermia in a moderate environment reduces maximal aerobic power by 6% and exercise time by 12% from euhydration levels (Sawka et al., 1979b). These investigations demonstrate that maximal exercise performance is reduced when hypohydration is combined with thermal strain. Likewise, submaximal endurance exercise is also reduced by dehydration acting through the thermoregulatory and cardiovascular systems (Sawka et al., 1979a, 1980).

In comparison with euhydration, hypohydration increases core temperature during exercise in comfortable (Grande et al., 1959; Neufer et al., 1988; Sawka et al., 1980) as well as hot (Claremont et al., 1976; Pearcy et al., 1956; Pitts et al., 1944) environments. A water deficit of only 1% of body weight significantly elevates core temperature during exercise (Ekblom et al., 1970). It is believed that as the severity of hypohydration increases, there is a concomitant gradation in the elevation of core temperature during exercise. Two studies examined core temperature responses to exercise while hypohydration levels were varied during independent tests in the same subjects. Strydom and Holdsworth (1968) studied two miners at two hypohydration levels [low (3%-5%) and high (5%-8%) weight loss] and found higher core temperatures at the high hypohydration level. Sawka et al. (1985) reported that hypohydration linearly increased the core temperature response during exercise in the heat (0.15°C) for each percent decrease in body weight. Figure 7-3 provides an example of an individual's core temperature response to exercise in the heat while he was euhydrated and while he was at three separate hypohydration levels (Sawka et al., 1985). Clearly, the greater the water deficit, the greater the steady-state core temperature response during exercise.

FIGURE 7-3

Core temperature responses during exercise-heat stress when an individual was euhydrated and hypohydrated by 3%, 5%, and 7% of body weight. Source: Sawka et al. (1985).

The hypohydration-mediated increase in heat storage is the result of either an increase in metabolic heat production or a decrease in heat loss. Hypohydration does not influence the rate of aerobic or anaerobic metabolism during exercise (Greenleaf and Castle, 1971; Saltin, 1964; Sawka et al., 1979a, 1980, 1983, 1984a, 1985) and, as a result, does not cause greater metabolic heat production. Therefore, decreased heat dissipation must be responsible for the hypohydration-mediated heat storage during exercise. The relative contribution of evaporative and dry heat exchange during exercise depends on the specific environmental conditions, but both avenues of heat loss are adversely affected by hypohydration (Fortney et al., 1981a,b; Sawka et al., 1984b).

Hypohydration is associated with reduced or unchanged sweating rates at a given metabolic rate during exercise in the heat (Sawka et al., 1984b). Those investigators who report no change in sweating rate usually still observed an elevated core temperature. Therefore, during hypohydration the sweating rate is lower for a given core temperature, and the potential for heat dissipation through sweat evaporation is reduced. Figure 7-4 presents data (Sawka et al., 1989) showing that three hypohydrated subjects had an increased threshold temperature for thermoregulatory sweating during exercise. Since core temperature provides 90% of the drive for thermoregulatory sweating, Figure 7-4 indicates that the sweating rate is reduced for a given thermal drive. Likewise, a recent study has demonstrated a systematically reduced sweating rate with increased hypohydration levels during exercise in the heat (Sawka et al., 1985).

FIGURE 7-4

The local sweating rate (dew-point hygrometry) for a given core temperature during exercise-heat stress for three subjects when euhydrated and hypohydrated by 5% of body weight. Source: Sawka et al. (1989)

The physiological mechanisms mediating the reduced sweating rate response during hypohydration are not clearly defined. Both the singular and combined effects of plasma hyperosmolality (Candas et al., 1986; Fortney et al., 1984; Harrison et al., 1978; Sawka et al., 1985) and plasma hypovolemia (Fortney et al., 1981b; Hertzman and Ferguson, 1960; Sawka et.al., 1985) have have been suggested as mediating this reduced sweating response. Plasma hyperosmolality maintains a strong (r = −0.76) and consistent relationship with the reduced sweating rates during hypohydration. Consistent with these findings, Senay (1979) reported an inverse relationship between plasma osmolality and sweating rate (r = −0.62) when hypohydration occurs. Also, several investigators (Harrison et al., 1978; Nielsen, 1974; Nielsen et al., 1971) have reported that plasma hyperosmolality elevates core temperature responses during exercise-heat stress, despite the maintenance of euhydration. Hyperosmolality can decrease sweating by a direct central nervous system effect on the hypothalamic thermoregulatory centers (Doris, 1983; Senay, 1979; Silva and Boulant, 1984) or by a peripheral effect at the eccrine sweat gland (Greenleaf and Castle, 1971; Nielsen et al., 1971).

Hypovolemia can also mediate a decreased sweating rate during exercise in the heat (Fortney et al., 1981b; Sawka et al., 1985). The thermoregulatory disadvantages of hypohydration can also be partially reversed by the reestablishment of the normal blood volume during exercise in the heat (Stephenson et al., 1983). Fortney et al. (1981b) have provided strong evidence that an isosmotic hypovolemia causes a reduced sweating rate and elevated core temperature response during exercise. They theorized that hypovolemia may alter the activity of atrial baroreceptors that have afferent input to the hypothalamus. Therefore, a reduced atrial filling pressure might modify neural information to the hypothalamic thermoregulatory centers that control the sweating rate.

The effects of hypohydration on cardiovascular responses to submaximal exercise have been investigated (Allen et al., 1977; Nadel et al., 1981; Saltin, 1964; Sawka et al., 1979a; Sproles et al., 1976). During the submaximal exercise with little thermal strain, hypohydration elicits an increase in heart rate and a decrease in stroke volume, with no change in cardiac output relative to euhydration levels (Allen et al., 1977; Saltin, 1964; Sproles et al., 1976). During hypohydration, a decreased blood volume apparently reduces the end-diastolic ventricular volume and stroke volume, requiring a compensatory increase in heart rate to maintain cardiac output. During submaximal exercise with moderate (Nadel et al., 1981) or severe (Sawka et al., 1979a) thermal strain, hypohydration (3%-4%) increases heart rate, decreases stroke volume, and decreases cardiac output relative to euhydration levels. Likewise, Sproles et al. (1976) demonstrated that a severe water deficit (7% of body weight) in the absence of thermal strain, can also reduce cardiac output during submaximal exercise.

The combination of exercise and heat strain results in competition between the central and peripheral circulations for a limited blood volume (Rowell, 1983). As the body temperature increases during exercise, cutaneous vasodilation occurs, thus decreasing venous resistance and pressure. As a result of decreased blood volume and increased blood displacement to cutaneous vascular beds, venous return and thus cardiac output are decreased below euhydration levels (Nadel et al., 1981; Sawka et al., 1979a). Nadel et al. (1981) report that these conditions also reduce cutaneous blood flow for a given core temperature and therefore the potential for sensible heat exchange. Likewise, hyperosmolality, in the absence of hypovolemia, can also reduce the cutaneous blood flow response during exercise-heat stress (Fortney et al., 1984).

Another physiological mechanism by which hypohydration might limit submaximal endurance exercise is by altering skeletal muscle metabolism. In preliminary work (Neufer et al., 1989b), we found higher plasma glucose, lactate, and glycerol responses during 1 h of cycling exercise (50% 18°C, 30% relative humidity) when subjects were hypohydrated (−5% body weight) than when they were euhydrated (Figure 7-5). However, no significant differences were observed in the respiratory exchange ratio, muscle glycogen use, or plasma free fatty acid concentrations between experiments. In the absence of any apparent differences in lipolysis and muscle substrate use, we interpreted these findings as probably indicating a reduced hepatic blood flow, as evidenced by the higher plasma glucose, lactate, and glycerol levels observed during the hypohydration experiment. Since 3 to 4 g of water is bound to each 1 g of glycogen, we hypothesized that hypohydration might also reduce glycogen resynthesis, despite the intake of an adequate carbohydrate diet. Preliminary findings (Neufer et al., 1989a) indicate that despite reduced muscle and body water availability muscle glycogen resynthesis is not altered by hypohydration during the first 15 h after heavy exercise.

FIGURE 7-5

Skeletal muscle glycogen resynthesis after exercise when euhydrated and when hypohydrated by 5% of body weight (d.w. indicates dry weight). The asterisks indicate values significantly different (P < 0.05) from those at zero. Source: Neufer et (more...)

In summary, it is of optimal importance that individuals rapidly replace their sweat losses while performing exercise. The fluid replacement is necessary to minimize plasma hyperosmolality and to restore the blood volume in hypohydrated individuals. The plasma hyperosmolality and hypovolemia, which result from body water loss, act singularly and together to reduce the efficiency of the thermoregulatory system.

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Footnotes

1

Michael N. Sawka, U.S. Army Research Institute of Environmental Medicine, Natick, MA 01760