The
mix of fuel utilization during exercise in youth with T1DM appears to
be similar to that of nondiabetics, except that those with diabetes may
rely even more on fat and less on carbohydrates. In individuals with
T1DM, the pancreas does not regulate insulin levels in response to
exercise, making normal fuel regulation nearly impossible. Moreover,
there can be deficiencies in the release of epinephrine and glucagon
that would normally help facilitate glucose production and release by
the liver. As patients soon discover, they may have either increases
(hyperglycemia) or decreases (hypoglycemia) in blood glucose levels
during exercise. The following sections outline the typical problems of
over- and underinsulinization during exercise that can contribute to
the development of acute metabolic complications (Fig. 1B-D).
Intensive insulin therapy, over-insulinization, and hypoglycemia.
Many find that intensive insulin therapy helps with glucose management during exercise,
because
it allows for frequent changes in insulin dosages, particularly if they
use an insulin pump. Intensive insulin therapy (i.e., ‘tight’ control)
attempts to mimic the natural pattern of insulin secretion. Although
most believe it to include higher insulin dosages, it simply requires
closer blood monitoring and more frequent insulin injections or an
insulin infusion pump to prevent extreme glucose excursions. The move
toward more aggressive insulin therapy to prevent long-term
complications from diabetes increases the risk of exercise-associated
hypoglycemia for some active people with diabetes, especially young
patients. It has recently been stated that hypoglycemia is the most
severe acute complication of intensive insulin treatment, with exercise
being a frequent cause. For example, in a small cohort of youth with
diabetes, 45 min of moderate exercise performed 2 h after breakfast
caused asymptomatic nocturnal hypoglycemia in nine of 10 patients who
maintained their usual basal and bolus insulin pump infusion rates.
Even when basal insulin rates were omitted during exercise, six of 10
patients had nocturnal hypoglycemia . Nonetheless, such aggressive
insulin therapy should be considered because it helps to prevent
long-term complications from the disease and because physical
performance and aerobic capacity are related to the degree of metabolic
control (see above).
Most children and adolescents with type 1
diabetes who exercise for prolonged periods (i.e., >30 min)
experience a significant drop in blood glucose levels. Hypoglycemia is
not restricted to those individuals who begin exercise with lower
glycemic levels, as there appears to be a strong positive correlation
between the drop in glycemia and the pre-exercise value. In addition,
severe postexercise late-onset hypoglycemia (i.e., up to 36 h after
exercise) may be particularly prevalent in active children with T1DM,
possibly because proper insulin and nutritional strategies are not
adopted while muscle and liver glycogen stores are being replaced.
Patients and parents should be particularly cautious therefore if
exercise is performed before bedtime. Strategies to limit the
possibility of hypoglycemia caused by exercise are provided under the
Practical considerations section below.
In addition to intensive
insulin therapy, there are other factors that contribute to
over-insulinization and hypoglycemia during exercise:
(i) The
absorption of injected insulin increases withexercise. The increase
insubcutaneous tissue and skeletal muscle blood flow and rise in body
temperature is associated with a concurrent increase in insulin
absorption and acceleratedhypoglycemia .
(ii) Plasma
insulin levels do not decrease and may even increase during exercise
[see (i) above]. A failure in the ability to lower insulin levels
during exercise, as would normally occur in a non-diabetic individual,
causes a relative hyperinsulinemia that impairs hepatic glucose
production and initiates hypoglycemia, usually within 20-60 min after
the onset of exercise.
(iii) Exercise causes enhanced
muscle insulin sensitivity via increased activation of non-insulin
sensitive glucose transporters. During exercise, the dramatic increase
in non-insulin-mediated glucose disposal considerably reduces the need
for circulating insulin levels. Because the increase in insulin action
persists after the end of exercise in children with diabetes, probably
to help replenish muscle and liver glycogen stores, patients are at
increased risk of hypoglycemia after the completion of exercise.
Counterregulatory
failure. Hypoglycemia during exercise may also result from an impaired
release of counterregulatory hormones caused by previous exposure to
either exercise or hypoglycemia . The mechanisms for impaired
counterregulation are unclear, but repeated episodes of either
hypoglycemia or exercise appear to degrade the body’s ability to mount
a counterregulatory response to either stressor. This finding of a
blunted counterregulatory response to exercise is similar to the
scenario that occurs in intensively treated patients with diabetes who
develop defects in counterregulatory responses to hypoglycemia .
Under-insulinization
and hyperglycemia. Not all forms of exercise are associated with
hypoglycemia, and some patients frequently report hyperglycemia
immediately after heavy exercise, probably because of an inability to
secrete insulin to compensate for elevations in catecholamine levels .
Indeed, intermittent high-intensity exercise, which reflects field and
team sports, does not appear to increase the risk of hypoglycemia in
patients with T1DM, probably because of increases in catecholamine
levels.
In children with poor metabolic control, exercise can
cause an additional increase in blood glucose and ketoacidosis. The
rise in blood glucose is caused by exaggerated hepatic glucose
production and impairment in exercise-induced glucose utilization by
muscle (Fig. 1C). Increased ketone body production results from
elevated FFA release from adipocytes (i.e., lipolysis) and possibly
from an increase in intrahepatic ketogenic efficiency. Hyperglycemia
and ketosis during exercise is particularly undesirable because it
causes dehydration and may decrease blood pH, both of which impair
exercise performance. Heavy exercise (i.e., >60-70% VO2max or
>75-85% of maximal heart rate) may particularly aggravate this
condition, because increases in catecholamines and glucocorticoids will
further exaggerate the elevations in glucose concentrations and ketone
production.