Temperature Regulation and Fluid and Electrolyte Balance
Chapter 15 Temperature Regulation and Fluid and Electrolyte Balance RONALD J. MAUGHAN AND ETHAN R. NADEL Introduction Temperature regulation in exercise Hard physical exercise poses a formidable challenge to the body’s ability to maintain its internal environment within the range that allows optimum function. In sport, however, both in training and competition, these homeostatic mechanisms are under constant threat, and fatigue is the result of a failure to stay within the zone of optimum functioning. It may be an excess acidosis resulting from lactic acid formation, a change in the extracellular potassium concentration causing a decrease in the muscle excitability or a rise in the temperature of the tissues as a result of a high rate of metabolic heat production. Some increase in body temperature is normally observed during exercise, and may even have beneﬁcial effects by increasing the rate of key chemical reactions and altering the elastic modulus of tissues, but high temperatures are detrimental to exercise performance and may be harmful to health. Sweating is the normal physiological response invoked to limit the rise in body temperature by increasing evaporative heat loss, but the loss of signiﬁcant amounts of sweat results in dehydration and electrolyte depletion if the losses are not replaced. Some understanding of the regulatory processes involved in the control of body temperature and of ﬂuid and electrolyte balance is therefore fundamental to the design of drinks intended for use during exercise and to an understanding of how and when these drinks should be used. The temperature of the skin can vary widely, depending on the environmental temperature, but the temperature of the deep tissues must be maintained within only a few degrees of the normal resting level of about 37°C. For this to be the case, the rate of heat gain by the body must be balanced by the rate of heat loss: any imbalance will result in a change in body temperature. All chemical reactions occurring in the body are relatively inefﬁcient, resulting in a large part of the chemical energy involved appearing as heat. The rate of heat production is therefore directly proportional to the metabolic rate. The resting metabolic rate for a healthy adult with a body mass of 70 kg is about 60 W. In a warm climate, this is sufﬁcient to balance the rate of heat loss, but in cold weather the insulative layer surrounding the body must be increased to reduce the rate of heat loss. In other words, more or thicker clothes are worn when it is cold. Alternative strategies are to raise the ambient temperature (by turning up the thermostat on the heating system if indoors) or to increase the metabolic rate, thus increasing the rate of heat production. The metabolic rate increases in proportion to the rate of energy turnover during exercise: in activities such as walking, running, swimming or cycling at a constant speed, the energy demand is a function of the rate of movement. In walking or running, where the body mass is moved against gravity at each step, body mass and speed will together determine the energy 203 204 nutrition and exercise cost. Air resistance becomes a factor at the higher speeds involved in cycling, and reducing the energy needed to overcome air resistance is a crucial factor in improving performance. In swimming, more so than in the other types of activity, technique is important in determining the energy cost of covering a ﬁxed distance or moving at a ﬁxed speed. In most sporting situations, as in most daily activities, the exercise intensity is not constant, but consists of intermittent activity of varying intensity and duration. Elite marathon runners can sustain speeds that result in rates of heat production in the order of 1200 W for a little over 2 h, which is the time it takes for the top performers to complete a marathon race (Maughan 1994a). In spite of this, however, the rise in body temperature that is observed seldom exceeds 2–3°C, indicating that the rate of heat loss from the body has been increased to match the increased rate of heat production. In general, the rise in body temperature during exercise is proportional to the exercise intensity, whether this is expressed in absolute terms as a power output or in relative terms as a proportion of each individual’s aerobic capacity. This observation indicates that the balance between heat production and heat loss is not perfect, but the relationship is none the less rather precise. Heat exchange between the body surface and the environment occurs by conduction, convection and radiation (Fig. 15.1), and each of these physical processes can result in either heat gain or heat loss: in addition, evaporation can cause heat to be lost from the body (Leithead & Lind 1964). Air has a low thermal conductivity, but the thermal conductivity of water is high, which is why an air temperature of, say, 28°C feels warm but water at the same temperature feels cool or even cold. The pool temperature is therefore of critical importance for swimmers. Convection and radiation are effective methods of heat loss when the temperature gradient between the skin and the environment is large and positive, i.e. when the skin temperature is much higher than the ambient temperature. Under such conditions, these two processes will account for a major part of the heat loss even during intense exercise. As ambient temperature rises, however, the gradient from skin to environment falls, and above about 35°C, the temperature gradient from skin to environment is reversed so that heat is gained by the body. In these conditions, evaporation is therefore the only means of heat loss. The heat balance equations are described by Kenney (1998) and are usually described by the following equation: S = M ± R ± K ± C – E ± Wk This indicates that the rate of body heat storage (S) is equal to the metabolic heat production (M) corrected for the net heat exchange by radiation (R), conduction (K), convection (C) and evaporation (E). A further correction must be applied to allow for work (Wk) done: this may be negative in the case of external work done, or positive when eccentric exercise is performed. A high rate of evaporative heat loss is clearly essential when the rate of metabolic heat production is high and when physical transfer is limited or actually results in a net heat gain by the body. Evaporation of water from the skin surface will result in the loss from the body of about 2.6 MJ (620 kcal) of heat energy for each litre of water evaporated. If we again use our marathon runner as an example, and again assume a rate of heat production of 1200 W, the effectiveness of evaporation is readily apparent. Assuming no other mechanisms of heat exchange, body temperature would rise rapidly and would reach an intolerable level within only about 20 min of exercise. Evaporation of sweat at a rate of 1 l · h–1 would result in heat loss by evaporation occurring at a rate of 2.6 MJ · h–1 (620 kcal · h–1), which is equivalent to 722 J · s–1 (172 cal · s–1), or 722 W. The entire metabolic heat load would therefore be balanced by the evaporation of about 1.7 l sweat · h–1, and this is well within the range of sweat rates normally observed in various sports during exercise (Rehrer & Burke 1997). Although the potential for heat loss by evaporation of water from the skin is high, this will only be the case if the skin surface is kept wet by constant replacement of the sweat that evapo- thermoregulation and fluid balance Air temperature Air humidity Sky thermal radiation 205 Solar radiation Respiratory Sweat Reflected solar radiation Skin blood flow Convection Convection Radiation low df loo e b ction scl e M u Conv Ground thermal radiation Work Conduction Ru nn ing Metabolic storage Contracting muscle spe ed Fig. 15.1 Main avenues of heat gain or heat loss in the exercising individual. rates or drips off the skin. Effective evaporation is also prevented if the vapour pressure gradient between the skin and the environment is low. This latter situation will arise if the skin temperature is low or if the ambient water vapour pressure is high: clothing that restricts air ﬂow will allow the air close to the skin to become saturated with water vapour and will therefore restrict the evaporation of water from the skin surface. A large body surface area and a high rate of air movement over the body surface are also factors that will have a major impact on evaporative heat loss, but these same factors may be a disadvantage in that they will promote heat gain from the environment by radiation and convection when the ambient temperature is higher than skin temperature (Leithead & Lind 1964). Smaller individuals will have a high surface area relative to their body mass, and may be at an advantage in hot conditions, but this will depend on the relative rates of evaporative heat loss and heat gain by physical transfer. 206 nutrition and exercise Fig. 15.2 Water may be less effective for dehydration but effective for cooling. Photo © Cor Vos. The ability of athletes to complete events such as the marathon, even in adverse climatic conditions, with relatively little change in body temperature, indicates that the thermoregulatory system is normally able to dissipate the associated heat load (Sutton 1990). Nielsen (1996) calculated that a marathon runner competing in a hot climate would be seriously disadvantaged: her calculations suggested that a marathon runner with a best time of 2 h 10 min, competing in conditions typical of the south-eastern United States at the time of the 1996 Summer Olympic Games, would not be able to run faster than about 3 h 20 min because of the limited heat loss that would be possible. The winner of the men’s race at those Games actually ﬁnished in a time of 2 h 12 min 36 s compared with his previous best time of 2 h 11 min 46 s. This apparently minor effect on performance was in part due to the environmental conditions being less severe than expected, but also indicated that the body is remarkably able to perform even in adverse environmental conditions. It is also worth noting that many of the spectacular collapses that have occurred in the history of marathon running have occurred in hot weather. Famous examples include those of Dorando Pietri at the 1908 Olympic marathon in London, Jim Peters at the Fig. 15.3 Even in cool conditions temperature regulation is a big factor in endurance events. Photo courtesy of Ron Maughan. thermoregulation and fluid balance 1954 Empire Games marathon in Vancouver, and Gabriella Andersen-Scheiss at the 1984 Los Angeles Olympics. Such problems are rarely encountered in cooler conditions. None the less, high rates of evaporation require high rates of sweat secretion onto the skin surface, and the price to be paid for the maintenance of core temperature is a progressive loss of water and electrolytes in sweat. If not corrected, this dehydration will impair exercise performance (Chapter 16) and may itself become life-threatening. Water balance The body’s hydration status is determined by the balance between water input and water losses from the body. As with all nutrients, a regular intake of water is required for the body to maintain health, and deﬁciency symptoms and overdosage symptoms can both be observed. Water is the largest single component of the normal human body, accounting for about 50–60% of the total body mass. Lean body tissues contain about 75% water by mass, whereas adipose tissue consists mostly of fat, with little water content. The body composition, and speciﬁcally the fat content, therefore largely determines the normal body water content. For a healthy lean young male with a body mass of 70 kg, total body water will be about 42 l. Losses of only a few per cent of total body water will result in an impaired exercise tolerance and an increased risk of heat illness, and yet the sweating rate can reach 2–3 l · h–1 in extreme situations. Sweat losses for various sporting and occupational activities are well categorized, but the variability is large because of the different factors that affect the sweating response (Rehrer & Burke 1996). Even at low ambient temperatures, high sweat rates are sometimes observed when the energy demand is high, as in marathon running, so it cannot be concluded that dehydration is a problem only when the ambient temperature and humidity are high: marathon runners competing in cool temperatures (10–12°C) typically lose between 1% and 5% of body mass during a 207 race (Maughan 1985). The sweat loss is, however, closely related to the environmental conditions, and large ﬂuid deﬁcits are much more common in the summer months and in tropical climates. Body mass losses of 6 l or more have been reported for marathon runners in warm weather competition (Costill 1977). This corresponds to a water deﬁcit of about 8% of body mass, or about 12–15% of total body water, and this is sufﬁcient to give cause for concern. It is well established that women tend to sweat less than men under standardized conditions, even after a period of acclimatization (Wyndham et al. 1965). It is likely, however, that a large part of the apparent sex difference can be accounted for by differences in training and acclimation status. There is a limited amount of information on the effects of age on the sweating response, and again levels of ﬁtness and acclimation are confounding factors, but the sweating response to a standardized challenge generally decreases with age (Kenney 1995). These observations should not, however, be interpreted as suggesting an inability of older people to exercise in the heat, nor should they be taken to indicate a decreased need for women or older individuals to pay attention to ﬂuid intake during exposure to heat stress. Rather, because of the reduced sensitivity of the thirst mechanism in older individuals (Kenney 1995), there is a need for a greater conscious effort to increase ﬂuid intake. There are some differences between children and adults in the sweating response to exercise and in sweat composition. The sweating capacity of children is low, when expressed per unit surface area, and the sweat electrolyte content is low relative to that of adults (Meyer et al. 1992), but the need for ﬂuid and electrolyte replacement is no less important than in adults. Indeed, in view of the evidence that core temperature increases to a greater extent in children than in adults at a given level of dehydration, the need for ﬂuid replacement may well be greater in children (Bar-Or 1989). There may also be a need to limit the duration of children’s sports events, or to provide for speciﬁed rest periods, when the temperature and humidity are high. 208 nutrition and exercise Water losses The turnover rate of water exceeds that of most other body components: for the individual who lives in a temperate climate and takes no exercise, daily water losses are about 2–4 l, or 5–10% of the total body water content. Urine, faeces, sweat, expired air and through the skin are the major avenues of water loss, and the approximate size of these different routes of water loss are shown in Table 15.1. In spite of its relative abundance, however, there is a need to maintain the body water content within narrow limits, and the body is much less able to cope with restriction of water intake than with restriction of food intake. A few days of total fasting has relatively little impact on functional capacity, provided ﬂuids are allowed, and even longer periods of abstinence from food are well tolerated. In contrast, cessation of water intake results in serious debilitation after times ranging from as little as an hour or two to a few days at most. Environmental conditions will affect the basal water requirement by altering the losses that occur by the various routes. Water requirements for sedentary individuals living in a hot climate may be two- or threefold higher than the requirement when living in a temperate climate, even when this is not accompanied by obvious sweating (Adolph & Associates 1947). Transcutaneous and respiratory losses will be markedly inﬂuenced by the humidity of the ambient air, and Table 15.1 Avenues of water loss from the body for sedentary adult men and women. From Bender & Bender (1997). Water loss (ml · day-1) Men Women Urine Expired air Transcutaneous loss Sweat loss Faecal water 1400 320 530 650 100 1000 320 280 420 90 Total 3000 2100 this may be a more important factor than the ambient temperature. Respiratory water losses are incurred because of the humidiﬁcation of the inspired air. These losses are relatively small in the resting individual in a warm, moist environment (amounting to about 200 ml · day–1), but will be increased approximately twofold in regions of low humidity, and may be as high as 1500 ml · day–1 during periods of hard work in the cold, dry air at altitude (Ladell 1965). The nature of the diet has some effect on water requirements because of the requirement for excretion of excess electrolytes and the products of metabolism. An intake of electrolytes in excess of the amounts lost in sweat and faeces must be corrected by excretion in the urine, with a corresponding increase in the volume and osmolality of urine formed. The daily intake of electrolytes varies widely between individuals, and there are also regional variations. Daily dietary sodium chloride intakes for 95% of the young male UK population fall between 3.8 and 14.3 g, with a mean of 8.4 g; the corresponding values for young women are 2.8–9.4 g, with a mean value of 6.0 g (Gregory et al. 1990). A highprotein diet requires a greater urine output to allow excretion of water-soluble nitrogenous waste (LeMagnen & Tallon 1967). Although this effect is relatively small compared with other losses, it can become meaningful when water availability is limited, and may be a factor to be considered in some athletes who habitually consume diets with a very high protein content. When a high-protein diet is used in combination with ﬂuid restriction and dehydration practices as part of the making-weight process in weight category sports, there are real dangers. The water content of the food ingested will also be inﬂuenced greatly by the nature of the diet, and water associated with food will make some contribution to the total ﬂuid intake. Electrolyte losses in sweat The sweat which is secreted onto the skin contains a wide variety of organic and inorganic solutes, and signiﬁcant losses of some of these thermoregulation and fluid balance components will occur where large volumes of sweat are produced. The electrolyte composition of sweat is variable, and the concentration of individual electrolytes as well as the total sweat volume will inﬂuence the extent of losses. The normal concentration ranges for the main ionic components of sweat are shown in Table 15.2, along with their plasma and intracellular concentrations for comparison. A number of factors contribute to the variability in the composition of sweat: methodological problems in the collection procedure, including evaporative loss, incomplete collection and contamination with skin cells account for at least part of the variability, but there is also a large biological variability (Shirreffs & Maughan 1997). The sweat composition undoubtedly varies between individuals, but can also vary within the same individual depending on the rate of secretion, the state of training and the state of heat acclimation (Leithead & Lind 1964), and there seem also to be some differences between different sites on the body. In response to a standard heat stress, there is an earlier onset of sweating and an increased sweat rate with training and acclimation, but the electrolyte content decreases although it would normally be expected to increase with increasing sweat rate, at least for sodium. These adaptations allow improved thermoregulation by increasing the evaporative capacity while conserving electrolytes. The con- Table 15.2 Normal concentration ranges of the major electrolytes in sweat, plasma and intracellular water. From Maughan (1994b). Sodium Potassium Calcium Magnesium Chloride Bicarbonate Phosphate Sulphate Sweat (mmol · l-1) Plasma (mmol · l-1) Intracellular water (mmol · l-1) 20–80 4–8 0–1 < 0.2 20–60 0–35 0.1–0.2 0.1–2.0 130–155 3.2–5.5 2.1–2.9 0.7–1.5 96–110 23–28 0.7–1.6 0.3–0.9 10 150 0 15 8 10 65 10 209 servation of sodium in particular may be important in maintaining the plasma volume and thus maintaining the cardiovascular capacity. The major electrolytes in sweat, as in the extracellular ﬂuid, are sodium and chloride (Table 15.2), although the sweat concentrations of these ions are invariably substantially lower than those in plasma, indicating a selective reabsorption process in the sweat duct. Contrary to what might be expected, Costill (1977) reported an increased sodium and chloride sweat content with increased ﬂow, but Verde et al. (1982) found that the sweat concentration of these ions was unrelated to the sweat ﬂow rate. Acclimation studies have shown that elevated sweating rates are accompanied by a decrease in the concentration of sodium and chloride in sweat (Allan & Wilson 1971). The potassium content of sweat appears to be relatively unaffected by the sweat rate, and the magnesium content is also unchanged or perhaps decreases slightly. These apparently conﬂicting results demonstrate some of the difﬁculties in interpreting the literature in this area. Differences between studies may be due to differences in the training status and degree of acclimation of the subjects used as well as difference in methodology: some studies have used whole-body washdown techniques to collect sweat, whereas others have examined local sweating responses using ventilated capsules or collection bags. Because sweat is hypotonic with respect to body ﬂuids, the effect of prolonged sweating is to increase the plasma osmolality, which may have a signiﬁcant effect on the ability to maintain body temperature. A direct relationship between plasma osmolality and body temperature has been demonstrated during exercise (Greenleaf et al. 1974; Harrison et al. 1978). Hyperosmolality of plasma, induced prior to exercise, has been shown to result in a decreased thermoregulatory effector response; the threshold for sweating is elevated and the cutaneous vasodilator response is reduced (Fortney et al. 1984). In short-term (30 min) exercise, however, the cardiovascular and thermoregulatory response appears to be independent of changes in osmolality induced 210 nutrition and exercise during the exercise period (Fortney et al. 1988). The changes in the concentration of individual electrolytes are more variable, but an increase in the plasma sodium and chloride concentrations is generally observed in response to both running and cycling exercise. Exceptions to this are rare and occur only when excessively large volumes of drinks low in electrolytes are consumed over long periods; these situations are discussed further below. The plasma potassium concentration has been reported to remain constant after marathon running (Meytes et al. 1969; Whiting et al. 1984), although others have reported small increases, irrespective of whether drinks containing large amounts of potassium (Kavanagh & Shephard 1975) or no electrolytes (Costill et al. 1976) were given. Much of the inconsistency in the literature relating to changes in the circulating potassium concentration can be explained by the variable time taken to obtain blood samples after exercise under ﬁeld conditions; the plasma potassium concentration rapidly returns to normal in the postexercise period (Stansbie et al. 1982). Laboratory studies where an indwelling catheter can be used to obtain blood samples during exercise commonly show an increase in the circulating potassium concentration in the later stages of prolonged exercise. The potassium concentration of extracellular ﬂuid (4–5 mmol · l–1) is small relative to the intracellular concentration (150–160 mmol · l–1), and release of potassium from liver, muscle and red blood cells will tend to elevate plasma potassium levels during exercise in spite of the losses in sweat. The plasma magnesium concentration is generally unchanged after moderate intensity exercise, and although a modest fall has been reported after extreme exercise, it seems likely that this reﬂects a redistribution of the available magnesium between body compartments rather than a net loss from the body (Maughan 1991). A larger fall in the serum magnesium concentration has, however, been observed during exercise in the heat than at neutral temperatures (Beller et al. 1972), supporting the idea that losses in sweat are responsible, and further studies with more reliable methodologies are required to clarify this issue. Although the concentration of potassium and magnesium in sweat is high relative to that in the plasma, the plasma content of these ions represents only a small fraction of the whole body stores; Costill and Miller (1980) estimated that only about 1% of the body stores of these electrolytes was lost when individuals were dehydrated by 5.8% of body weight. Control of water intake and water loss The excretion of some of the waste products of metabolism and the regulation of the body’s water and electrolyte balance are the primary functions of the kidneys. Excess water or solute is excreted, and where there is a deﬁciency of water or electrolytes, these are conserved until the balance is restored. Under normal conditions, the osmolality of the extracellular ﬂuid is maintained within narrow limits; since this is strongly inﬂuenced by the sodium concentration, sodium and water balance are closely linked. At rest, approximately 15–20% of the renal plasma ﬂow is continuously ﬁltered out by the glomeruli, resulting in the production of about 170 l ﬁltrate · day–1. Most (99% or more) of this is reabsorbed in the tubular system, leaving about 1–1.5 l to appear as urine. The volume of urine produced is determined primarily by the action of antidiuretic hormone (ADH) which regulates water reabsorption by increasing the permeability of the distal tubule of the nephron and the collecting duct to water. ADH is released from the posterior lobe of the pituitary in response to signals from the supraoptic nucleus of the hypothalamus: the main stimuli for release of ADH, which is normally present only in low concentrations, are an increased signal from the osmoreceptors located within the hypothalamus, a decrease in blood volume, which is detected by low-pressure receptors in the atria, and by high-pressure baroreceptors in the aortic arch and carotid sinus. An increased plasma angiotensin concentration will also stimulate ADH output. The sodium concentration of the plasma is regulated by the renal reabsorption of sodium from thermoregulation and fluid balance the glomerular ﬁltrate. Most of the reabsorption occurs in the proximal tubule, but active absorption also occurs in the distal tubules and collecting ducts. A number of factors inﬂuence the extent to which reabsorption occurs, and among these is the action of aldosterone, which promotes sodium reabsorption in the distal tubules and enhances the excretion of potassium and hydrogen ions. Aldosterone is released from the kidney in response to a fall in the circulating sodium concentration or a rise in plasma potassium: aldosterone release is also stimulated by angiotensin which is produced by the reninangiotensin system in response to a decrease in the plasma sodium concentration. Angiotensin thus has a two-fold action, on the release of aldosterone as well as ADH. Atrial natriuretic factor (ANF) is a peptide synthesized in and released from the atria of the heart in response to atrial distension. It increases the glomerular ﬁltration rate and decreases sodium and water reabsorption leading to an increased loss: this may be important in the regulation of extracellular volume, but it seems unlikely that ANF plays a signiﬁcant role during exercise. Regulation of the body’s sodium balance has profound implications for ﬂuid balance, as sodium salts account for more than 90% of the osmotic pressure of the extracellular ﬂuid. Loss of hypotonic ﬂuid as sweat during prolonged exercise usually results in a fall in blood volume and an increased plasma osmolality: both these changes act as stimuli for the release of ADH (Castenfors 1977). The plasma ADH concentration during exercise has been reported to increase as a function of the exercise intensity (Wade & Claybaugh 1980). Renal blood ﬂow is also reduced in proportion to the exercise intensity and may be as low as 25% of the resting level during strenuous exercise (Poortmans 1984). These factors combine to result in a decreased urine ﬂow during, and usually for some time after, exercise (Poortmans 1984). It has been pointed out, however, that the volume of water conserved by this decreased urine ﬂow during exercise is small, probably amounting to no more than 12–45 ml · h–1 (Zambraski 1990). 211 The effect of exercise is normally to decrease the renal excretion of sodium and to increase the excretion of potassium, although the effect on potassium excretion is rather variable (Zambraski 1990). These effects appear to be largely due to an increased rate of aldosterone production during exercise (Poortmans 1984). Although the concentrations of sodium and more especially of potassium in the urine are generally high relative to the concentrations in extracellular ﬂuid, the extent of total urinary losses in most exercise situations is small. The daily water intake in the form of food and drink is usually in excess of obligatory water loss, with the kidneys being responsible for excretion of any excess and the regulation of body water content. The kidneys can only function effectively, however, if the ﬂuid intake is in excess of the requirement. Drinking is a complex behaviour which is inﬂuenced by a number of physiological, psychological and social events. The sensation of thirst is only one of the factors involved, and short-term studies suggest that it is a poor indicator of acute hydration status in man (Adolph et al. 1947). The overall stability of the total body water content, however, indicates that the desire to drink is a powerful regulatory factor over the long term (Ramsay 1989). The urge to drink, which is perceived as thirst, may not be directly involved with a physiological need for water intake, but can be initiated by habit, ritual, taste or desire for nutrients, stimulants, or a warm or cooling effect. A number of the sensations associated with thirst are learned, with signals such as dryness of the mouth or throat inducing drinking, while distension of the stomach can stop ingestion before a ﬂuid deﬁcit has been restored. There are clearly changes in the sensitivity of the thirst mechanism associated with the ageing process, with older individuals showing a reduced response to mild levels of dehydration (Kenney 1995). Notwithstanding the various factors that modulate the subjective perception of thirst, there is an underlying physiological basis involving both chemical and pressure sensors. The sensation of thirst is controlled separately by 212 nutrition and exercise both the osmotic pressure of the body ﬂuids and the central venous volume. The same mechanisms are involved in water and solute reabsorption in the kidneys and in the control of blood pressure. The thirst control centres are located in the hypothalamus and forebrain, and appear to play a key role in the regulation of both thirst and diuresis. Receptors in the thirst control centres respond directly to changes in osmolality, volaemia and blood pressure, while others are stimulated by the ﬂuid balance hormones which also regulate renal excretion (Phillips et al. 1985). These regions of the brain also receive afferent input from systemic receptors monitoring osmolality and circulating sodium concentration, and from alterations in blood volume and pressure. There may also be a direct neural link from the thirst control centres to the kidneys which would allow a greater degree of integration between the control of ﬂuid intake and excretion. Changes in the balance of neural activity in the thirst control centres regulated by the different monitoring inputs determine the relative sensations of thirst and satiety, and inﬂuence the degree of diuresis. Input from the higher centres of the brain, however, can override the basic biological need for water to some extent and cause inappropriate drinking responses. A rise of between 2% and 3% in plasma osmolality is sufﬁcient to evoke a profound sensation of thirst coupled with an increase in the circulating concentration of ADH (Hubbard et al. 1990). The mechanisms that respond to changes in intravascular volume and pressure appear to be less sensitive than those that monitor plasma osmolality, with hypovolaemic thirst being evident only following a 10% decrease in blood volume (Fitzsimons 1990). As fairly large variations in blood volume and pressure occur during normal daily activity, this lack of sensitivity presumably prevents excessive activity of the volaemic control mechanisms. Prolonged exercise, especially in the heat, is associated with a decrease in plasma volume and a tendency for an increase in plasma osmolality, but ﬂuid intake during and immediately following exercise is often less than that required to restore normal hydration status (Ramsay 1989). This appears not to be due to a lack of initiation of the drinking response but rather to a premature termination of the drinking response (Rolls et al. 1980). When a water deﬁcit is present and volunteers are allowed free access to ﬂuids, the normal drinking response involves an initial period of avid drinking during which more than 50% of the total volume is consumed; this is followed by a longer period of intermittent consumption of relatively small volumes (Verbalis 1990). The initial alleviation of thirst occurs before signiﬁcant amounts of the beverage have been absorbed and entered the body pools. Therefore, although decreasing osmolality and increasing extracellular volume promote a reduction in the perception of thirst, other preabsorptive factors also affect the volume of ﬂuid ingested. Receptors in the mouth, oesophagus and stomach are thought to meter the volume of ﬂuid ingested, while distension of the stomach tends to reduce the perception of thirst. These preabsorptive signals appear to be behavioural, learned responses and may be subject to disruption in situations which are essentially novel to the individual. This may partly explain the inappropriate voluntary ﬂuid intake in individuals exposed to an acute increase in environmental temperature or to exercise-induced dehydration. In addition to the water consumed in the form of drinks, some water is obtained from solid foods, and water is also available as a result of the oxidation of nutrients. The amount of water available from these sources will depend on the amount and type of food eaten and on the total metabolic rate. Oxidation of the components of a mixed diet, with an energy content of 12.6 MJ (3000 kcal) per day, will give about 400 ml water · day–1. The contribution of this water of oxidation to water requirements is appreciable when water turnover is low, but becomes rather insigniﬁcant when water losses are high. Role of the kidney The excretion of some of the waste products of metabolism and the regulation of the body’s thermoregulation and fluid balance water and electrolyte balance are the primary functions of the kidneys. Excess water or solute is excreted, and where there is a deﬁciency of water or electrolytes an attempt is made to conserve these until the balance is restored. Blood volume, plasma osmolality and plasma sodium concentration seem to be the primary factors regulated. Under normal conditions, the osmolality of the extracellular ﬂuid is maintained within narrow limits. As the major ion of the extracellular space is sodium, which accounts for about 50% of the total osmolality, maintenance of osmotic balance requires that both sodium and water intake and loss are closely coupled. At rest, about 20% of the cardiac output goes to the two kidneys, and approximately 15–20% of the renal plasma ﬂow is continuously ﬁltered out by the glomeruli, resulting in the production of about 170 l ﬁltrate · day–1. Most (99% or more) of this is reabsorbed in the tubular system, leaving about 1–1.5 l to appear as urine. The volume of urine produced is determined primarily by the action of ADH which regulates water reabsorption by increasing the permeability of the distal tubule of the nephron and the collecting duct to water. ADH is released from the posterior lobe of the pituitary in response to signals from the supraoptic nucleus of the hypothalamus: the main stimuli for release of ADH, which is normally present only in low concentrations, are an increased signal from the osmoreceptors located within the hypothalamus, a decrease in blood volume, which is detected by low-pressure receptors in the atria, and by high-pressure baroreceptors in the aortic arch and carotid sinus. An increased plasma angiotensin concentration will also stimulate ADH output. The sodium concentration of the plasma is regulated by the reabsorption of sodium from the glomerular ﬁltrate, with most of the reabsorption occurring in the proximal renal tubule. Several factors inﬂuence the extent to which reabsorption occurs: of particular importance is the action of aldosterone, which promotes sodium reabsorption in the distal tubules and enhances the excretion of potassium and hydrogen ions. Aldosterone is released from the kidney in 213 response to a fall in the circulating sodium concentration or a rise in plasma potassium: aldosterone release is also stimulated by angiotensin which is produced by the renin–angiotensin system in response to a decrease in the plasma sodium concentration. Angiotensin thus has a twofold action, on the release of aldosterone as well as ADH. ANF is a peptide synthesized in and released from the heart in response to atrial distension. It increases the glomerular ﬁltration rate and decreases sodium and water reabsorption leading to an increased loss: this may be important in the regulation of extracellular volume, but probably does not play a signiﬁcant role during exercise. Regulation of the body’s sodium balance has profound implications for ﬂuid balance, as sodium salts account for more than 90% of the osmotic pressure of the extracellular ﬂuid. Loss of hypotonic ﬂuid as sweat during prolonged exercise usually results in a fall in blood volume and an increased plasma osmolality: these changes in turn act as stimuli for the release of ADH (Castenfors 1977). The plasma ADH concentration during exercise has been reported to increase as a function of the exercise intensity (Wade & Claybaugh 1980). Renal blood ﬂow is also reduced in proportion to the exercise intensity and may be as low as 25% of the resting level during strenuous exercise (Poortmans 1984). These factors combine to result in a decreased urine ﬂow during, and usually for some time after, exercise. The volume of water conserved by this decreased urine ﬂow during exercise is small, probably amounting to no more than 12–45 ml · h–1 (Zambraski 1990): compared with water losses in sweat, this volume is trivial. 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