and good shoes and attention to hygiene must be
stressed. In previously untrained NIDDM, the
training must start slowly, as with all sedentary
individuals who embark on an exercise pro-
gramme. However, although a larger percentage
of energy comes from fat at lower intensity
endurance training, it is important to achieve
a progressive increase in intensity to obtain
the largest improvement in glucose tolerance.
Endurance training at higher intensities is proba-
bly the most effective way to reduce body weight
and increase insulin sensitivity (Koivisto et al.
1986; Kang et al.1996).
In people with NIDDM, insulin-stimulated
glucose uptake is reduced in skeletal muscles
(Shulmanet al.1990). Much research is directed
at finding the reason for this reduced insulin
sensitivity. The amount of GLUT-4 is normal in
insulin-resistant muscle but insulin is unable to
translocate GLUT-4 to the cell membrane (Etgen
et al.1996). Exercise training, however, stimulates
glucose uptake in skeletal muscle and increases
insulin sensitivity in insulin-resistant muscles
(Koivistoet al.1986; Etgen et al.1997). Insulin
resistance in skeletal muscle develops prior
to NIDDM and endurance training seems to
prevent the development of insulin resistance.
Furthermore, endurance training increases
insulin sensitivity in people with NIDDM
and improves the regulation of blood glucose
concentration.
Strength training is normally not regarded to
be as effective as endurance training in increas-
ing insulin sensitivity (Koivisto et al. 1986).
However, most people with NIDDM are older,
untrained people and with increasing age the
skeletal muscle atrophies. Reduction in the mass
of muscle available to remove glucose from
the blood during insulin stimulation decreases
glucose tolerance. Strength training which
increases muscle mass in older, untrained people
with NIDDM may be more effective than
endurance training to increase glucose tolerance.
Strength training may, however, cause vascular
side-effects and precautions should be taken
(Wallberg-Henriksson 1992).
464 special considerations
Dietary considerations for NIDDM
NIDDM is often associated with obesity, hyper-
tension and hyperlipidaemia (Koivisto et al.
1986). Obesity is a risk factor for NIDDM and
weight reduction improves insulin sensitivity in
skeletal muscles. Weight reduction is therefore,
together with training, central in the treatment of
most people with NIDDM. For the reduction of
body mass, energy intake must be lower than
energy utilization and food intake must nor-
mally be reduced. Furthermore, a high-fat diet
causes insulin resistance in skeletal muscles.
People with NIDDM are therefore recommended
to reduce their fat intake. Furthermore, in con-
trast to IDDM, insulin treatment is unable to
stimulate glucose disposal after a large meal in
NIDDM. Large meals will therefore cause an ele-
vation in blood glucose. It is therefore advised
that people with NIDDM eat smaller meals and
that the content of complex carbohydrates is
high.
Hypoglycaemia during and after exercise is
not a major problem in NIDDM when the
therapy is changed diet and increased exercise
training. Pharmacological treatments of NIDDM
with insulin, sulphonylureas or metformin may
increase the risk of hypoglycaemia. However, the
risk for development of hypoglycaemia in phar-
macologically treated diabetics with NIDDM
is still much lower than in people with IDDM.
During exercise, carbohydrate supply is nor-
mally not necessary in people with NIDDM and
water should be drunk to replace fluid.
Replenishment of glycogen stores is important
for performance (Ivy 1991). However, in most
people with NIDDM, improved regulation of the
blood glucose concentration is more important
than improved performance. Most of the glucose
taken up during insulin stimulation is incor-
porated into glycogen and a high glycogen
concentration in skeletal muscle reduces insulin-
stimulated glucose uptake ( Jensen et al.1997).
Normal regulation of blood glucose metabolism
requires that glucose can be incorporated into
glycogen in skeletal muscles and a high glycogen