Henriksson 1992). Too high a glucose concentra-
tion may be a result of a low concentration of
insulin. Exercise in under-insulinated diabetics
may result in a further increase in blood glucose
concentration as the normal inhibition of glucose
release from the liver is lacking (Wallberg-
Henriksson 1992). Low insulin concentration
will also cause elevated lipolysis and the high
concentration of NEFA may increase production
of ketone bodies, resulting in ketoacidosis (Wall-
berg-Henriksson 1992). In case of high glucose
concentration, it is recommended that ketone
body levels should be checked in urine (Horton
1988). However, if a large meal has been eaten
shortly before exercise and minimal rapid-acting
insulin is taken, exercise will decrease glucose
concentration to a normal level (Sane et al.1988).
Although exercise decreases blood glucose
concentration and increases insulin sensitivity in
skeletal muscle, exercise may not be regarded as
a treatment for IDDM (Kemmer & Berger 1986;
Horton 1988; Wallberg-Henriksson 1992). In
contrast to NIDDM, training does not seem to
improve glycaemic control in IDDM (Wallberg-
Henriksson et al. 1984; Wallberg-Henriksson
1992; Ebeling et al.1995). Elite athletes require
a higher amount of carbohydrates in the diet,
which makes the regulation of blood glucose
more difficult. Furthermore, participation in elite
sport is often accompanied with travelling and
other changes in their daily routine which also
make administration of insulin more difficult.
For elite athletes it is therefore important that the
blood glucose is monitored carefully and athletes
must learn to correct the insulin requirements to
the exercise performed. In learning this, it is
recommended that the athletes write down the
blood glucose concentration before and after
exercise of different type, intensity, and duration
and relate it to ingestion of carbohydrates and
injection of insulin.
Dietary considerations
An important part of treatment of IDDM is edu-
cation. Today it is normal to have a small blood
glucose analyser at home to monitor glucose
concentration on a regular basis. The dose of
insulin needed differs between individuals and
the requirement for insulin to handle a meal
varies even within the same individual since, for
example, exercise increases insulin sensitivity
and decreases the requirement for insulin.
Ideally, IDDM subjects will want to achieve a
normal pattern of food consumption. However,
some foods with a high glycaemic index will be
absorbed rapidly (e.g. glucose in a soft drink)
and this may cause some metabolic problems.
Importantly, the amount of insulin taken before a
meal should be matched with the anticipated
dietary glucose uptake. This means that if the
blood glucose concentration is high after a meal,
the insulin dose is increased and vice versa.
If postprandial exercise is planned, precau-
tions can be taken to improve glucose regulation.
To avoid hypoglycaemia, Horton (1988) suggests
eating a large meal 1–3 h before planned exercise
and to reduce insulin injection before this meal.
Although it is difficult to give a standard recom-
mendation, a reduction of 30–50% in rapid-
acting insulin may be a starting point for
adjustment of the dose to endurance exercise.
Reduction of the insulin dose before strength
training and ball games may be smaller.
However, it is important to measure blood
glucose concentration frequently, particularly
when a new type of exercise is performed or
when intensity or duration is changed. The dose
of insulin before meals must be optimized to the
new and unfamiliar exercises.
If the duration of the exercise is more than
30 min, extra glucose should be supplied.
This glucose ingestion has two effects in
IDDM; avoiding dangerous hypoglycaemia and
improvement of performance. As in non-diabet-
ics, glucose ingestion increases performance in
prolonged endurance sport. In IDDM, glucose
ingestion should also prevent hypoglycaemia.
Severe hypoglycaemia causes coma and hypo-
glycaemic coma is potentially fatal for the dia-
betic (Cryer & Gerich 1985). The only energy
substrate for the brain is glucose and severe brain
damage will occur within minutes at very low
glucose concentrations (Cryer & Gerich 1985). It