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 concen-
tration 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 reabsorp-
tion 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 nor-
mally 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 reabsorp-
tion occurs: of particular importance is the action
of aldosterone, which promotes sodium reab-
sorption 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 con-
centration or a rise in plasma potassium: aldos-
terone 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 reabsorp-
tion 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 pro-
longed 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 con-
centration 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 inten-
sity 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 excre-
tion of potassium, although the effect on potas-
sium 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