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 con-
sumed 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). Labora-
tory 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 concentra-
tion 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 concentra-
tion 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
210 nutrition and exercise
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 main-
tained 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 anti-
diuretic hormone (ADH) which regulates water
reabsorption by increasing the permeability of
the distal tubule of the nephron and the collect-
ing duct to water. ADH is released from the pos-
terior lobe of the pituitary in response to signals
from the supraoptic nucleus of the hypothala-
mus: 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 reg-
ulated by the renal reabsorption of sodium from