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The Diabetic Athlete

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The Diabetic Athlete
Chapter 34
The Diabetic Athlete
JØRGEN JENSEN AND BRENDAN LEIGHTON
Introduction
Diabetes mellitus is a disease of abnormal regulation of glucose metabolism, resulting in an
elevated blood glucose concentration which
may arise for different reasons. Consequently,
the treatments of the disease are varied. Exercise
training for people with diabetes mellitus must
also be viewed in the light of the aetiology of the
disease, as the physiological response to exercise
can differ. In one form of diabetes mellitus, training is regarded as a cornerstone in the treatment
of the disease, whereas training is a challenge in
the other form of diabetes.
Diabetes mellitus is classified into two distinct
types:
1 Insulin-dependent diabetes mellitus (IDDM,
or type I or juvenile diabetes), which requires
insulin replacement on a daily basis because
insulin secretion is almost totally lacking.
2 Non-insulin-dependent diabetes mellitus
(NIDDM, or type II), in which the early
pathological lesion is a decreased sensitivity of
skeletal muscle and liver to insulin (insulin resistance). The initial period of insulin resistance is
associated with increased circulating concentrations of insulin, but the blood glucose concentration remains normal. NIDDM develops when the
pancreatic b-cell is no longer able to secrete the
appropriate amount of insulin to maintain adequate blood glucose concentrations and hyperglycaemia is the direct consequence.
The incidence of diabetes mellitus has increased during recent decades. In particular, the
incidence of NIDDM has increased dramatically
and up to 10–20% of people over 65 years old
suffer from NIDDM in many countries. NIDDM
is associated with an increased risk for many diseases such as coronary heart disease, neuropathy,
renal failure, and blindness (Kahn 1998). In
NIDDM, the management of blood glucose concentration with prescribed pharmaceutical drugs
is poor and diet and regular physical exercise are
important therapeutic treatments for the disease.
Only a small portion of diabetics (about 10%)
are IDDM, but this group requires particularly
close monitoring because IDDM develops early
in life. Exercise training and physical activity
are natural things for children to do and the
opportunity to participate in sports is important
for social development. IDDM is treated with
insulin and the combination of exercise training
and insulin injection may cause too high a stimulation of peripheral glucose uptake, resulting in
hypoglycaemia. The requirement of insulin is
influenced by exercise and the dose of insulin
must therefore be varied with the intensity and
duration of exercise. Thus, in people with IDDM
physical exercise must be regarded as a challenge, but, with education and management,
people with IDDM can participate in exercise
training together with non-diabetics, and can
achieve the same health benefits.
Regulation of carbohydrate and
fat metabolism during exercise
In working skeletal muscle, the demand for for-
457
458
special considerations
mation of adenosine triphosphate, which fuels
muscle contraction, increases enormously (Newsholme & Leech 1983). The formation of adenosine triphosphate is driven by increased flux
through glycolysis and the tricarboxylic cycle.
Exercise mobilizes intramuscular fuels in the
form of glycogen and triacylglycerol to supply
glucose moieties and fatty acids, respectively.
Exogenous fuels, in the form of glucose and nonesterified fatty acids (NEFA), are also taken up
from the blood and oxidized together with intramuscular fuels.
The glucose concentration in the blood,
however, remains relatively stable because the
rate of peripheral glucose uptake is matched by
the rate of release of glucose into the circulation.
Regulation of blood glucose concentration is
complex and, in addition to exercise, several hormones participate in this regulation. Insulin is
the major hormone regulating the removal of
glucose from the blood. Glucose entering the
circulation may be absorbed from the intestine
(from food or glucose drinks) but most of the
time glucose is released from the liver as a result
of glycogen breakdown or glucose synthesized
via gluconeogenesis. During exercise, the concentrations of glucagon, catecholamines, cortisol
and growth hormone all increase and these
hormones stimulate glucose release from the
liver and ensure that blood glucose concentration remains relatively constant (Cryer & Gerich
1985). The hormones that stimulate glucose
release into the blood (and inhibit glucose
uptake) are often called counter-regulatory
hormones.
The rate of glucose uptake is elevated in skeletal muscle during exercise, although the insulin
concentration decreases during exercise. Several
studies have shown that glucose uptake is stimulated by exercise, even in the absence of insulin
(Richter 1996) and the reduction of insulin concentration during exercise may be important for
avoiding hypoglycaemia (Cryer & Gerich 1985).
Insulin is a strong inhibitor of lipolysis in fat cells
and of glucose release from the liver. A fall in the
insulin concentration is important to optimize
the supply of NEFA to the contracting muscles.
The decrease in basal insulin concentration
aids the release of NEFA from adipose tissue and
glucose from the liver.
During prolonged exercise, the concentration
of glycogen in skeletal muscles decreases and
glucose uptake from the blood becomes gradually more important. When skeletal muscles
are depleted of glycogen, glucose uptake may
account for nearly all carbohydrate oxidation
(Wahren et al. 1971). When the liver is depleted of
glycogen, glucose is released at much lower rates
and the blood glucose concentration decreases. A
decrease in blood glucose concentration is well
recognized as a major factor in the fatigue
that accompanies endurance exercise, and the
reduced supply of carbohydrate to the central
nervous system and to the muscle may both be
factors in the fatigue process (Costill & Hargreaves 1992).
The intensity of exercise is also an important
determinant of the rate of carbohydrate utilization. During exercise of an intensity of about 50%
.
of Vo2max., the energy comes equally from fat and
carbohydrate metabolism and, as the intensity
of the exercise increases, the percentage contribution from carbohydrates rises. At intensities
.
of exercise above 80% Vo2max., carbohydrates
become the major metabolic fuel. At this intensity of exercise, glucose uptake is also much
higher, and depletion of liver glycogen will occur
in 1–2 h followed by a decrease in concentration
of blood glucose. During exercise of short duration and high intensity, on the other hand, the
hepatic glucose output can exceed the rate of
glucose uptake and lead to hyperglycaemia.
Regulation of carbohydrate and
fat metabolism after exercise
The ability to convert chemical energy to fuel
skeletal muscle contraction is essential for
human movement. Skeletal muscles have,
however, also an important role for regulation of
the blood glucose concentration, as most of the
glucose disposal stimulated by insulin occurs in
skeletal muscle (Shulman et al. 1990).
After a carbohydrate-rich meal, the increased
the diabetic athlete
concentration of glucose in the blood causes a
release of insulin from the b-cells in the pancreas.
Insulin binds to its receptor and stimulates
glucose transport and metabolism, particularly
in heart, skeletal muscle and adipose tissue. The
signalling pathway for insulin has been studied
extensively and during the last decade the
mechanism of action of insulin has become much
clearer (Kahn 1998).
Glucose is transported into cells by proteins
called glucose transporters. There are different
isoforms of the glucose transporters and their
expression is tissue specific (Holman & Kasuga
1997). GLUT-4 is expressed in tissue where insulin stimulates glucose uptake (skeletal muscle,
heart and adipose tissue) and GLUT-4 is named
the insulin-regulated glucose transporter. Insulin
stimulates glucose uptake by recruitment of
GLUT-4 from intracellular sites to the sarcolemmal membrane (Fig. 34.1). GLUT-4 is normally
located in vesicles in the cells, but during insulin
stimulation, GLUT-4 is translocated to the cell
membrane by exocytosis (Holman & Kasuga
1997). When GLUT-4 transporter proteins are in
the sarcolemmal membrane, they will transport
glucose into the cells, and the amount of GLUT-4
in the sarcolemmal membrane is regarded as the
regulatory step for glucose uptake. GLUT-4 will
be internalized when the insulin stimulation is
459
removed and glucose transport will decrease to
basal level again.
Skeletal muscle makes up 30–40% of the body
weight and the 70–90% of the insulin-stimulated
glucose uptake occurs in this tissue (Shulman
et al. 1990). Therefore, it is evident that skeletal
muscles play a central role in regulation of
glucose metabolism. Glucose taken up in skeletal
muscle during insulin stimulation is incorporated into glycogen (Shulman et al. 1990), but
skeletal muscles are unable to release glucose
into the bloodstream to maintain blood glucose
concentration. Skeletal muscle glycogen can,
however, be broken down to lactate and released
from skeletal muscle for conversion to glucose in
the liver via gluconeogenesis. Skeletal muscle
glycogen is therefore indirectly a carbohydrate
source for maintaining blood glucose.
Exercise recruits GLUT-4 to the sarcolemmal
membrane in a manner similar to the effects of
insulin. Although both exercise and insulin stimulate glucose uptake by translocation of GLUT-4
to the sarcolemmal membrane, this process
seems to occur via different signalling pathways
(Richter 1996) and exercise stimulates glucose
uptake even in insulin resistant muscles (Etgen et
al. 1996). Another effect of exercise is that insulin
sensitivity increases in skeletal muscle after exercise (Richter 1996). This means that lower insulin
br
em
m
l
el
Insu
li
C
Glucose
transport
ane
Fusion
Fission
Vesicle
+
GLUT-4
Fig. 34.1 Schematic illustration showing regulation of glucose transport in skeletal muscle. When insulin binds to
the insulin receptor, GLUT-4-containing vesicles are translocated to the sarcolemmal membrane. GLUT-4
transports glucose into the cell when they are located in the sarcolemmal membrane. In insulin-resistant muscles,
translocation is reduced in response to insulin.
460
special considerations
concentrations are required to remove glucose,
and in line with this, highly trained people
have lower circulating insulin levels and a reduced insulin response to a glucose challenge.
However, the increased insulin sensitivity
during and after exercise increases the risk for
hypoglycaemia in insulin-treated diabetics.
Insulin-dependent diabetes mellitus
In people with IDDM, insulin secretion is lacking
or insufficient because of an almost total destruction of the insulin secreting b-cells in the pancreas. The b-cells are destroyed by the diabetic’s
own immune system (autoimmune destruction).
IDDM is treated with life-long insulin therapy by
insulin injection several times each day. Insulin is
produced as long-acting (elevates blood insulin
concentration for many hours) and rapid-acting
(elevates blood insulin for a much shorter period
of time) forms and most patients take a mixture
of both forms. In the evening (and some times
morning), long-acting insulin is injected to maintain the basal insulin concentration. Before each
meal, rapid-acting insulin is injected to stimulate
removal of the absorbed glucose. The insulin
dose required depends on the individual and it is
important to measure glucose concentration
often to establish the correct dose.
Exercise training for IDDM
IDDM normally develops at a young age and
exercise is a natural activity for children. It is particularly important for their social development
that they get the opportunity to participate in
group exercises with other children. Although
some children with IDDM develop fear of
participation in sports, exercise is regarded as
safe if children with IDDM are educated to adjust
their dose of insulin to the intensity of exercise.
Many people with IDDM participate in sport and
there are several examples of athletes at the top of
their sports.
These athletes clearly show that it is possible
for diabetic athletes to achieve a high performance level. In non-diabetics, exercise training
causes adaptations in skeletal muscle and circulatory system which is the background to the
increased performance (Holloszy & Booth 1976).
People with IDDM seem, however, to respond to
training in a similar way and there are therefore
no physiological reasons for not participating in
sport (Wallberg-Henriksson 1992).
Exercise training for people with IDDM is,
however, not without problems. The insulin concentration is important for control of the glucose
concentration and too high a concentration of
insulin in combination with exercise may cause
hypoglycaemia. Too low a concentration of insulin, on the other hand, may cause elevation in
blood glucose and ketoacidosis. The greatest
problem is the development of hypoglycaemia
because of the inability to regulate prevailing
blood insulin concentrations. In people with
IDDM the insulin concentration in blood will
depend on the amount of insulin administered
and the rate of release of insulin from the site of
injection. The normal decrease in insulin level
during exercise will therefore not occur in people
with IDDM and, as exercise increases insulin sensitivity, glucose uptake in skeletal muscles may
be too high. To mimic the reduction in concentration of insulin that occurs in normal subjects
during exercise, insulin injections have to be
avoided immediately prior to exercise in people
with IDDM.
Before exercise, it is important that the glucose
and insulin concentrations are neither too high
nor too low (Horton 1988). The concentration of
glucose should be measured to give information
about the insulin level. If the blood glucose concentration is below 5 mm, it may be a result of too
high a concentration of insulin and there is a high
risk for hypoglycaemia if exercise is performed.
It is therefore not advised to participate in exercise, and glucose should be taken to raise the
blood glucose concentration before exercise is
performed. Furthermore, it is important that
athletes with IDDM should be able to recognize
the symptoms of hypoglycaemia and respond
accordingly.
Exercise is not recommended when the blood
glucose concentration is above 16 mm (Wallberg-
the diabetic athlete
Henriksson 1992). Too high a glucose concentration 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 (WallbergHenriksson 1992). Low insulin concentration
will also cause elevated lipolysis and the high
concentration of NEFA may increase production
of ketone bodies, resulting in ketoacidosis (Wallberg-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 (WallbergHenriksson 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 education. Today it is normal to have a small blood
glucose analyser at home to monitor glucose
461
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, precautions 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 recommendation, a reduction of 30–50% in rapidacting 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-diabetics, glucose ingestion increases performance in
prolonged endurance sport. In IDDM, glucose
ingestion should also prevent hypoglycaemia.
Severe hypoglycaemia causes coma and hypoglycaemic coma is potentially fatal for the diabetic (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
462
special considerations
is therefore required that glucose, which can
be rapidly absorbed, is available when IDDM
athletes perform exercise training, to prevent
hypoglycaemia and to reduce the risk of coma
if hypoglycaemia occurs. This is particularly
important when running or cycling is performed
in conditions where it will be difficult to obtain
carbohydrates.
It seems that ingestion of 40 g carbohydrate ·
h–1 is sufficient to avoid hypoglycaemia (Sane et
al. 1988). Athletes with IDDM performed a 75-km
ski race and ingested glucose at an average rate
of 40 g · h–1 (more in the later part of the exercise);
ingestion of glucose at this rate prevented
hypoglycaemia when insulin injection also was
reduced (Fig. 34.2). The glucose concentration
was, however, in the lower range for many of the
IDDM athletes at the end and more glucose may
have improved performance. Horton (1988) suggested that glucose should be ingested at a rate of
24
Blood glucose (mmol.I–1)
20
16
70–80 g · h–1 during prolonged exercise. In normal
subjects, glucose ingestion at a rate of 60 g · h–1 is
recommended (Costill & Hargreaves 1992) and
glucose should be ingested at the same rate in
athletes with IDDM. Furthermore, in addition to
supply of carbohydrates, athletes with IDDM
must always be aware of the risk of hypoglycaemia and ingest glucose when symptoms of
hypoglycaemia come.
Exercise per se stimulates glycogen synthesis
after the training session when glucose is available. In diabetics, regulation of blood glucose
concentration is normally the focused subject
and glycogen synthesis in skeletal muscles is
regarded prerequisite for regulation of blood
glucose. In sport, on the other hand, the replenishment of muscle glycogen stores is normally
viewed from a performance perspective. Muscle
glycogen is the most important energy substrate
in most types of sport and for optimal performance, it is important that the glycogen stores
are replenished after each bout of exercise (Ivy
1991). Glycogen can be synthesized in people
with IDDM even in the absence of insulin injection after exercise (Mæhlum et al. 1978). In the
absence of insulin, however, only half of the
glycogen store seems to be replenished (Fig.
34.3). Injection of insulin is therefore necessary
for optimal glycogen synthesis, even though the
administration of insulin after exercise increases
the risk for hypoglycaemia.
12
Conclusion
8
4
0
10
33
Distance (km)
75
Fig. 34.2 Blood glucose concentration (individual and
mean) in athletes with IDDM during a 75-km ski race.
The shaded area shows healthy controls. The athletes
with IDDM reduced their daily insulin dose by about
35% and ingested about 270 g of carbohydrate during
the exercise (36 g · h–1). Adapted from Sane et al. (1988).
The nature and intensity of any exercise training
programme combined with the personal requirements of a person with IDDM make it difficult to
generalize about factors, such as dose of insulin
administered before exercise and amount of
dietary intake. Monitoring the concentration of
glucose prior to any exercise ensures that the performance is not undertaken in conditions which
may be adverse for the IDDM subject. If the
blood glucose level is low then the intensity of
exercise should be decreased or delayed until
ingested carbohydrate has time to boost the
blood glucose concentration. High blood glucose
the diabetic athlete
463
Recovery
Exercise
Fig. 34.3 Glycogen synthesis in
IDDM subjects after exercise in the
presence (䊉) or absence (䊊) of
insulin.
Subjects exercised at 75% of
.
Vo2max. until exhaustion and
received a carbohydrate-rich diet
and their normal insulin injection in
the control experiment. On the
other experimental day, insulin was
not injected. Adapted from
Mæhlum et al. (1978).
Muscle glycogen content
(mmol.kg–1 wet wt)
80
60
40
20
0
concentration should lead to the postponement
of exercise for the reasons given above. The dose
of insulin administered before any exercise
should be scaled down to reflect the degree of
intensity and duration of exercise. However,
individual IDDM subjects may have to reach the
optimum pre-exercise insulin dose by monitoring post-exercise glucose levels.
Non-insulin-dependent
diabetes mellitus
NIDDM is a world health problem and the
disease is often regarded as a disease of abnormal lifestyle. About 90% of all diabetics are
NIDDM and the disease develops gradually and
is normally associated with obesity and hypertension. Initially, the skeletal muscles and liver
becomes insulin resistant, but the body responds
by producing more insulin and glucose concentration remains normal. However, as the
insulin resistance increases, the pancreas
becomes unable to produce enough insulin to
regulate the metabolism of blood glucose concentration and hyperglycaemia occurs.
The pharmacological treatment of NIDDM is
poor. As the muscles are insulin resistant, insulin
therapy is not a satisfactory treatment of the
disease. There are some other drugs prescribed,
such as sulphonylureas and metformin. NIDDM
is in most case initially treated with dietary
manipulation and exercise. This treatment is
sufficient for many people with NIDDM if the
0
2
4
6
8
10
12
Time (h)
disease has not progressed too far. Exercise of
moderate intensity in people with NIDDM is
usually associated with a decrease in blood
glucose towards the normal range. A further
benefit of regular exercise is that it increases the
sensitivity of skeletal muscle to insulin, which
will have the beneficial effect of lowering the
requirement for circulating insulin concentration. It is important to recognize that exercise also
lowers the risk factors for cardiovascular disease
in people with NIDDM.
Exercise training for NIDDM
NIDDM is normally associated with obesity and
a low exercise capacity. NIDDM develops later in
life than IDDM and the majority of patients are
over 50 years old. The aims of exercise training
for people with NIDDM are therefore often different from those of young people with IDDM.
People with NIDDM are often untrained and an
improved level of physical fitness is normally the
main goal. As for untrained people in general,
there are large opportunities for improvement
and training studies have shown that endurance
training increases maximum oxygen uptake and
oxidative capacity in skeletal muscle (WallbergHenriksson 1992).
Obesity may hinder training and a high body
mass increases the risk of injury to joints and
tendons. In people with NIDDM, it is also important to be aware of the risk for foot problems, particularly in diabetics with peripheral neuropathy,
464
special considerations
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 programme. 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 probably 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
(Shulman et 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
(Koivisto et 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 increasing 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).
Dietary considerations for NIDDM
NIDDM is often associated with obesity, hypertension 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 normally 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 contrast to IDDM, insulin treatment is unable to
stimulate glucose disposal after a large meal in
NIDDM. Large meals will therefore cause an elevation 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 pharmacologically treated diabetics with NIDDM
is still much lower than in people with IDDM.
During exercise, carbohydrate supply is normally 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 incorporated into glycogen and a high glycogen
concentration in skeletal muscle reduces insulinstimulated 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
the diabetic athlete
content impedes this. The reduced glycogen concentration after exercise in people with NIDDM
is important for improved glucose metabolism
and reduced glycogen stores will aid the disposal
of blood glucose.
Conclusion
NIDDM is often associated with obesity and
reduction of body mass is important to improve
glucose metabolism. Exercise increases energy
consumption and has an important role is any
weight-loss programme. Exercise increases also
insulin sensitivity in skeletal muscle, leading to
an improved regulation of the blood glucose
concentration. Exercise therefore has a central
position in the management of most people
with NIDDM. However, as most of the people
with NIDDM are overweight, it is important to
find types of exercise that can be performed.
Endurance training such as running may cause
joint and tendon problems because of the high
body mass. Cycling or swimming may be good
alternatives. Furthermore, strength training may
be effective to increase glucose tolerance in older
people. Most of the glucose is taken up by skeletal muscles during insulin stimulation and an
increased muscle mass will improve removal of
glucose from the blood.
References
Costill, D.L. & Hargreaves, M. (1992) Carbohydrate
nutrition and fatigue. Sports Medicine 13, 86–92.
Cryer, P.E. & Gerich, J.E. (1985) Glucose counterregulation, hypoglycemia, and intensive insulin therapy in
diabetes mellitus. New England Journal of Medicine
313, 232–241.
Ebeling, P., Tuominen, J.A., Bourey, R., Koranyi, L. &
Koivisto, V.A. (1995) Athletes with IDDM exhibit
impaired metabolic control and increased lipid
utilization with no increase in insulin sensitivity.
Diabetes 44, 471–477.
Etgen, G.J., Wilson, C.M., Jensen, J., Cushman, S.W. &
Ivy, J.L. (1996) Glucose transport and cell surface
GLUT-4 protein in skeletal muscle of the obese
Zucker rat. American Journal of Physiology 271,
E294–E301.
465
Etgen, G.J., Jensen, J., Wilson, C.M., Hunt, D.G.,
Cushman, S.W. & Ivy, J.L. (1997) Exercise training
reverses insulin resistance in muscle by enhanced
recruitment of GLUT-4 to the cell surface. American
Journal of Physiology 272, E864–E869.
Holloszy, J.O. & Booth, F.W. (1976) Biochemical adaptations to endurance exercise in muscle. Annual Review
of Physiology 38, 273–291.
Holman, G.D. & Kasuga, M. (1997) From receptor to
transporter: insulin signalling to glucose transport.
Diabetologia 40, 991–1003.
Horton, E.D. (1988) Role and management of exercise
in diabetes mellitus. Diabetes Care 11, 201–211.
Ivy, J.L. (1991) Muscle glycogen synthesis before and
after exercise. Sports Medicine 11, 6–19.
Jensen, J., Aslesen, R., Ivy, J.L. & Brørs, O. (1997) Role of
glycogen concentration and epinephrine on glucose
uptake in rat epitrochlearis muscle. American Journal
of Physiology 272, E649–E655.
Kahn, B.B. (1998) Type 2 diabetes: when insulin secretion fails to compensate for insulin resistance. Cell 92,
593–596.
Kang, J., Robertson, R.J., Hagberg, J.M. et al. (1996)
Effect of exercise intensity on glucose and insulin
metabolism in obese individuals and obese NIDDM
patients. Diabetes Care 19, 341–349.
Kemmer, F.W. & Berger, M. (1986) Therapy and better
quality of life: the dichotomous role of exercise
in diabetes mellitus. Diabetes/Metabolism Reviews 2,
53–68.
Koivisto, V.A., Yki-Järvinen, H. & DeFronzo, R.A.
(1986) Physical training and insulin sensitivity.
Diabetes/Metabolism Reviews 1, 445–481.
Mæhlum, S., Høstmark, A.T. & Hermansen, L. (1978)
Synthesis of muscle glycogen during recovery after
prolonged severe exercise in diabetic subjects. Effect
of insulin deprivation. Scandinavian Journal of Clinical
and Laboratory Investigations 38, 35–39.
Newsholme, E.A. & Leech, A.R. (1983) Biochemistry for
the Medical Sciences. John Wiley & Sons, Chichester.
Richter, E.A. (1996) Glucose utilization. In Handbook of
Physiology. Section 12. Exercise: Regulation and Integration of Multiple Systems (ed. L.B. Rowell & J.T.
Shepherd), pp. 912–951. Oxford University Press,
Oxford.
Sane, T., Helve, E., Pelkonen, R. & Koivisto, V.A. (1988)
The adjustment of diet and insulin dose during
long-term endurance exercise in type 1 (insulindependent) diabetic men. Diabetologia 31, 35–40.
Shulman, G.I., Rothman, D.L., Jue, T., Stein, P.,
DeFronzo, R.A. & Shulman, R.G. (1990) Quantification of muscle glycogen synthesis in normal subjects
and subjects with non-insulin-dependent diabetes
by 13C nuclear magnetic resonance spectroscopy.
New England Journal of Medicine 322, 223–228.
466
special considerations
Wahren, J., Felig, P., Ahlborg, G. & Jorfeldt, L. (1971)
Glucose metabolism during leg exercise in man.
Journal of Clinical Investigation 50, 2715–2725.
Wallberg-Henriksson, H. (1992)) Exercise and diabetes
mellitus. Exercise and Sport Sciences Reviews 20,
339–368.
Wallberg-Henriksson, H., Gunnarsson, R., Henriksson,
J., Östman, J. & Wahren, J. (1984) Influence of physical training on formation of muscle capillaries in
type I diabetes. Diabetes 33, 351–357.
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