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Temperature Regulation and Fluid and Electrolyte Balance

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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.
Exercise normally results in a decrease in the
renal excretion of sodium and an increased 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. 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
214
nutrition and exercise
electrolyte losses in most exercise situations is
small.
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