adrenalin (Dawson, 2005; Draznin, 2000). With exercise, glucose production by the liver is upregulated and muscles take up glucose from the blood stream and also use endogenous glycogen as a fuel source. Non-esterified fatty acids can be mobilized to provide extra substrate for working muscles. Insulin production is downregulated during exercise to prevent hypoglycemia because of increased muscle uptake of glucose from the bloodstream. When exercise is over, the body is relatively depleted of glucose and insulin counter-regulatory mechanisms stimulate gluconeogenesis by the liver. This leads to an increase in blood glucose, and therefore an increase in insulin production.
In Type 1 diabetics, there is no endogenous insulin production and so during exercise hypoglycemia or hyperglycemia
may occur (Dawson, 2005). If there is insulin excess, hypoglycemia may occur either during or after exercise because hepatic gluconeogenesis is inhibited and increased glucose uptake through the synergy of Glut-4 receptor stimulation by calcium released from muscles during exercise and by the insulin. If there is a shortage of insulin, ketosis may occur because of hyperglycemia and hyperlipidemia and this could lead to a comatose state. If there is a relative hyperglycemia and ketosis prior to commencing athletic activity, it may worsen during the exercise because of the increased production of cortisol, glucagon and non-esterified fatty acids.
As exercise intensity is increased, the normal feedback mechanism producing the symptoms of hypoglycemia may be masked (Dawson, 2005). Post exercise and delayed onset hypoglycemia can occur long after the athlete has stopped exercising. Hyperglycemia during exercise can cause excessive glycation of the tissues and increase the risk of multiple end organ disease. Blood sugar levels must therefore be well controlled in athletes.
Athletes with type 1 diabetes need to tailor their insulin, fluid...