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VOLUME 9 NUMBER 1 • MARCH 2012
33
SA JOURNAL OF DIABETES & VASCULAR DISEASE
REPORT
those individuals with the greatest fear of
physical activity had the poorest control of
their diabetes.
The literature suggests that type 1 dia-
betes patients are more lightly to develop
hypoglycaemia when participating in low-
intensity, long-duration events, due to the
fact that they circulate their insulin more
efficiently and they may have a blunted
counter-regulatory hormonal response.
In an interesting observation, Robitaille,
2007, found that type 1 diabetes patients in
the fed state used less liver and endogenous
glucose and significantly more muscle
glycogen when exercising for 30 to 60
minutes, in comparison to non-diabetic
controls. This may have implications for
post-exercise glycogen replenishment and
hypoglycaemia.
Tansey
et al.
6
explained that performing
low- or moderate-intensity endurance-type
exercise postprandially resulted in an 86%
chance of developing hypoglycaemia if
the patient’s blood glucose level was below
7.0 mmol/l before the exercise.
In McMahon’s euglycaemic clamp studies
in 2007, she found that patients perform-
ing endurance-type activities at 16:30 had
a biphasic need for glucose infusion. The
majority of glucose infusions were required
during the 45 minutes of exercise and for
45 minutes post exercise. Further glucose
infusion was required seven to 11 hours
post exercise, which equated to between
02:00 and 04:00.
Dealing with the glucose needs during
activity is not too difficult. However, dealing
with the late hypoglycaemia occurring in the
early morning has always been a challenge.
The literature suggests that hypoglycaemic
events can be reduced by exercising before
breakfast and using rapid-acting insulin, as
the patient will be slightly insulin-resistant
at this time.
According to Riddel, 2006, exercise late
in the day may lead to nocturnal hypogly-
caemia, which may be unnoticed during
sleep in the majority of individuals. The
incidence of hypoglycaemia may be as high
as 26% on the night of exercise in adoles-
cents and children. This may be due to a
child or adolesant’s low glycogen-carrying
capacity and blunted counter-regulatory
response, and the onset of sleep may also
be a factor.
The risk of hypoglycaemia can be man-
aged by increasing carbohydrate intake
before, during and after exercise. The rate
of intake is dependent on body mass and
the energy expenditure of the exercise.
Mr Heilbrunn recommends the article by
Grimm and colleagues.
7
This study indicates
that depending on the intensity and dura-
tion of exercise, patients should take in 15
to 100 g of carbohydrate per hour during
exercise, if exercise is performed at the peak
effect of insulin action. Furthermore, daily
insulin dosages should be decreased by 20
to 30% if exercising for one hour or more.
Hyperglycaemia may be common in exer-
cises such as squash, high-intensity spinning
or high-intensity resistance training, due to
an excessive counter-regulatory hormonal
response. In the non-diabetic, circulating
counter-regulatory hormones decrease rap-
idly post exercise and insulin levels increase,
allowing for rapid glycogen replenishment
and therefore a rapid decrease in glucose
levels.
Most type 1 diabetes patients choose to
exercise during the tail effect of their insu-
lin action, or they will decrease their insulin
dosage in order to avoid hypoglycaemia.
Therefore the post-exercise insulin levels
may be low. With high post-exercise circu-
lating counter-regulatory hormones and low
insulin levels in the type 1 diabetes patient,
the counter-regulatory response remains
high and the patient’s blood glucose levels
may remain high for a number of hours post
exercise. Competition days and extra carbo-
hydrates will exacerbate the problem. It is
suggested that one to two units of insulin
prior to exercise and/or after exercise may
counteract this hyperglycaemic effect.
Improvement of HbA
1c
level with exercise
has not been firmly established. The blood
glucose response to exercise is not always
predictable. Cardio-respiratory, metabolic
and perceptual effort may be altered in type
1 diabetes and this may impair exercise per-
formance.
In Herbst’s cross-sectional, multi-centre
analysis of 2006, the frequency of activity
had a significant influence on glycaemic
control without increasing the risk of severe
hypoglycaemia. Furthermore, patients who
exercised on a regular basis planned their
insulin and carbohydrate adjustments more
efficiently than patients exercising sporadi-
cally.
In Bernadini’s study in 2004, it was
observed that children participating in more
than 360 minutes of competitive sport a
week had significantly better glycaemic con-
trol than those children exercising less than
60 minutes per day.
Mr Heilbrunn felt that although there
are many guidelines and books to refer to,
our physiological understanding can help
guide individuals, but it cannot replace the
importance of individuals monitoring their
own blood glucose response to a particular
exercise.
He concluded by saying, ‘type 1 diabetes
patients who exercise regularly report that
they feel better, sleep better, have more
energy and are more self-disciplined’. Ide-
ally, patients should be exercising daily, or
on alternate days, to maximise insulin sensi-
tivity. Furthermore, ‘patients who exercised
on a regular basis planned their insulin and
carbohydrate adjustments more efficiently
than patients exercising sporadically. This
would aid the prevention and management
of hypoglycaemia.’
Review of 2001 type 2 diabetes
guidelines
SEMDSA is in the process of reviewing
guidelines for the management of type 2
diabetes. Dr Amod explained that this revi-
sion has been driven by two primary fac-
tors. He says, ‘Currently in South Africa,
many different guidelines are referred to…
there is a need for an integrative national
approach.’ Also, new data has emerged on
a number of considerations that affect the
management of the diabetic patient since
the 2008 primary-care guidelines were for-
mulated. These include diagnosis of type 2
diabetes, blood pressure and lipid targets,
hypoglycaemic risks, weight loss and bariat-
ric surgery, and the dismissal of some new
and some old therapeutic agents.
Dr Amod highlighted that many risk fac-
tors give rise to the widespread prevalence
of type 2 diabetes and that on the whole,
diabetes is a poorly managed disease with
fewer than half of patients achieving target
control levels. He emphasised that diabetes
is not a homogeneous disease. He argues
that the highly variable pathogenesis of type
2 diabetes and the varying degrees of dis-
ease manifestation are compounded by fur-
ther variability within the individual patient
dependant on duration and stage of his/
her disease. This implies that many patients
are inadequately managed at some point(s)
along the timeline of their disease, in both
public and private health systems.
A rigidly uniform therapeutic approach
with limited therapeutic options will have
limited success in managing the ever-in-
creasing diabetic population. The major-
ity of diabetic patients are treated at the
primary-care level and there is a need to
assess current therapeutic strategies, with
the goal of improving blood glucose con-
trol. It is thought that the earlier inclusion