Diabetes Mellitus (DM) is a group of disorders caused by the inability to produce or use insulin; resulting in either an increase in blood glucose (hyperglycemia) and a loss of glucose in urine (glucosuria) (Tatora & Grabowski, 2000).
According to Dr J.J Skelton (personal communication, March 16, 2005) the hallmarks of DM include:
- Polyuria- excessive urine production because of the inability of the kidneys to reabsorb water.
- Polydipsia- excessive thirst.
- Weight loss
HOW THE PANCREAS IS INVOLVED
The pancreas is responsible for releasing insulin and glucagon to lower blood glucose levels and to stimulate the release of glucose from the liver to the blood increasing blood glucose levels, respectively. The pancreas is made up of two tissues: The Acini from the Exocrine system; and Islets of langerhans from the Endocrine system. Islets of langerhans are made of Alpha cells (ά) and Beta cells (β) which secrete glucagon and insulin respectively (McArdle et al., 1991).
GLUCAGON AND INSULIN
When glucagon is released from alpha cells of islets of langerhans it results in increased glucose availability by stimulating glucogenolysis and gluconeogenisis in the liver. This results in glycogen being broken down into glucose, an important process needed during prolonged exercise where blood glucose and carbohydrate reserves are reduced (McArdle et al, 1991).
Insulin (from beta cells) on the other hand, is a mediator of ‘facilitated diffusion’. It allows glucose to combine with GLUT-4 (glucose carrier) form the cytosol. GLUT-4 inactivates cell membranes allowing an influx of glucose into the cell. This process occurs when there is an increased blood sugar levels (hypoglycemia).
TWO TYPES OF DIABETES MELLITUS
- Type 1:
Insulin dependent DM (IDDM) has a juvenile onset and persists through out life (“Diabetes Mellitus”, 2005). IDDM results in the immune system destroying pancreatic beta cells. Insulin is therefore not present to aid the entry of glucose into body cells. This causes the individual to become hyperglycaemic and cells begin using fatty acids to produce ATP having a detrimental effect on the individual. The by-products of fatty acid break down are ketones, which causes acidosis known as ketoacidosis. Ketoacidosis lowers the blood ph levels below normal values of 7.0 resulting eventually in either a diabetic coma and or death (“Diabetes Mellitus”, 2005).
- Type 1 complications:
Ketoacidosis is a result of abnormally low blood ph levels and occurs when a diabetic becomes seriously insulin deficient (Berman, 1999). Ketoacidosis is a result of either a neglecting medication or when the diabetic has been subject to severe physical stress. It usually develops over several days with a history of polyuria, polydipsia, nausea, vomiting, upper abdominal pain and a gradual decline in the level of consciousness (Berman, 1999). On examination patients are normally distressed, dehydrated, breathing is rapid and deep from metabolic acidosis and there is a sweet smell on the breath form the ketone body acetone (Berman, 1999).
- Type 2:
Non-dependent diabetes mellitus (NDDM) is more common than IDDM where lifestyle and age contribute to a more sedentary lifestyle resulting in weight gain. With IDDM the pancreas produces enough insulin, but the body does not use it in the right way and therefore blood glucose levels are not kept low enough resulting in hyperglycemia (“New Treatments for Diabetes, 1999).
- Type 2 complications:
Type 2 diabetics may develop non-ketotic hyperglycemia resulting in a hyperosmolar-coma. Blood sugar levels must therefore be monitored before and after exercise to prevent hyperglycemia.
TREATMENT FOR DIABETES MELLITUS
The goal of DM treatment is to keep blood sugar levels as close to normal as possible (80-120mg per 100ml). To achieve this, the first step would be to eat a healthy diet and exercise to control or even loose weight (“New Treatments for Diabetes, 1999). Sometimes healthy eating and exercise alone can not keep blood sugar levels normal and therefore other treatments may be required. Treatments can either be taken orally in the form of pills or by means of an insulin injection. Once on treatment the individual is advised to monitor blood sugar levels regularly through means of a diabetes monitor in the comfort of his/her home (“New Treatments for Diabetes, 1999).
Type 1 patients normally require treatment in the form of an insulin injection, and they should be advised to monitor blood sugar levels closely to see how much insulin is needed. With too much insulin the patient might experience hypoglycaemia, which in turn stimulates anti-insulin hormones such as epinephrine, glucagon and growth hormone (Tatora & Grabowski, 2000). With Hypoglycaemia a person may experience anxiety, sweating, tremor, increased heart rate, hunger and or weakness. Hypoglycaemia on the other hand can result in mental disorientation and because of lack of blood glucose to the brain; the person may experience convulsions, unconsciousness. In extreme cases death may be the result of an insulin shock if the blood glucose level is not raised (Tatora & Grabowski, 2000).
THE EFFECTS OF EXERCISE
With endurance training an individuals’ insulin and glucose in the blood is maintained closer to resting values (McArdle et al., 1991). Exercise is beneficial to diabetics as there is increased insulin sensitivity and therefore less insulin is required to regulate blood glucose after training than before (McArdle et al., 1991). During heavy exercise a trained individual can spare carbohydrates and use fats as a fuel. In essence, the trained state requires less insulin at any stage from rest through to light-moderate intensities of exercise resulting in enhanced insulin effectiveness (McArdle et al., 1991). It is important however for Type 1 diabetics to have their insulin injections near by when exercising, as exercise may trigger a dual response: an enhanced glucose uptake and greater insulin supply due to the rapid circulation that accompanies exercise. This response worsens the imbalance between glucose supply and utilization, which may lead to complications in terms of hypoglycaemia (McArdle et al., 1991).
Hypoglycemia is the result of there being an increase insulin absorption during exercise or because of high initial plasma insulin concentrations from previous injection. High plasma insulin concentrations result in a smaller increase in hepatic glucose production and glucose clearance being more than normal causing plasma glucose concentrations to fall. Hypoglycemia occurs several hours after exercise because A) glucose concentrations decrease and B) there is an increased sensitivity to insulin (Richer and Galbo, 1986).
Single exercise may decrease glycaemia, but the magnitude of response is variable within and between individuals and it depends on the timing of exercise to the insulin injection, intensity, duration and meals (Richer and Galbo, 1986). Sometimes shifting the injection site from an exercising muscle to a non-exercising muscle is little help in preventing hypoglycemia during or after exercise. Therefore, one must consider decreasing the insulin dose and/or increasing the intake of carbohydrates. Decreasing the insulin dosage is preferable in the case of an obese diabetic. Again, individual approaches must be taken (Richer and Galbo, 1986).
GUIDELINES FOR THE EXERCISING DIABETIC
To use exercise safely diabetics should follow a regular daily schedule; meaning that exercise should be done at a certain time of day at a fixed intensity and duration (Richer and Galbo, 1986).
The main guideline when exercising is to prevent hypoglycaemia. This can be done by:
- Exercising 30-60 minutes after a meal
- Keeping the body hydrated during exercise
- Keeping sweets nearby in case sugar levels drop
- Avoid injecting the limbs required for exercise, as it will result in an increased glucose uptake by the active muscles, which will cause hypoglycaemia.
- Avoid exercising between 60-90 minutes after insulin injection because this is the time of peak insulin action.
Insulin deficiency (Type 1):
Hyperglycemia is likely to worsen during exercise in insulin deficient states because insulin deficiency is accompanied by an exaggerated exercise-induced increase in counter-regulatory hormones which cause glucose output from the liver while at the same time muscular glucose uptake is impaired (Richer and Galbo, 1986). This impaired glucose uptake is due to high concentrations of free fatty acids (FFA), ketone bodies and catecholamines that accompany insulin deficiency. The dramatic changes in plasma hormone levels during exercise in an insulin deficient state also enhances lipolysis, which supplies FFA to the liver and enhances ketone production (Richer and Galbo, 1986). Diabetics are recommended to abstain from exercise if ketonuria is present or ketoacidosis will result.
Exercise for type 2:
Hyperglycemia in IDDM is primarily the result of an absolute insulin deficiency, whereas, hyperglycemia in the NDDM patient is in part because of insulin resistance. Many of NDDM patients are hyperinsulinemia and most of them are obese. The role of exercise in the treatment of these diabetics is therefore primarily to lessen the insulin resistance (Richer and Galbo, 1986). Also exercise may diminish the load on the beta cells by diminishing the average plasma glucose level. This may result in the prevention of the development of type 2 diabetes in the genetically disposed individual as well as diminishing mean insulin levels and other cardiovascular diseases (Richer and Galbo, 1986).
Type 2 diabetics are recommended to regular exercise using large muscle groups for 4-7 days a week. Majority of type 2 diabetics are obese and therefore emphasis should be placed on losing weight. Low intensity high compliance exercise should therefore be prescribed to reduce body fat and minimize the risk of any injury. Weightlifting and other high intensity activities that raise blood pressure should be avoided (William, Sherman and Albright, 1992).
Exercise planning
Uncomplicated diabetics do not need any activity restriction, but they should be attentive to hypoglycaemia. In uncomplicated diabetics the effect of exercise is all the more favourable if the activity is carried out on a regular basis, several times a week. Diabetics who are 40 years and older or those who have had diabetes for more than 10 years should have medical examinations including a exercise stress test before they start exercising.
When planning an exercise program for type 1 diabetics’ there should be a restriction to sports, which require short explosive bursts of muscular activity, such as weight training (Vitug, Schneider and Ruderman, 1988). Exercise should entail predominantly aerobic work progressively spread out over several hours such as brisk walking, swimming and cycling. These exercises help lower blood glucose and risks of cardiovascular disease. Exercise intensity for younger diabetics should be between 50-80% of maximal oxygen consumption (V02 max) and for older diabetics between 50-65% V02 max. Duration of exercise should be restricted between 20-40 minutes.
Sports that are dangerous to non-diabetics such as sky diving, scuba diving, hang-gliding and mountaineering can provoke eventual hypoglycaemia and should therefore be avoided by diabetics. Physically active diabetics should always be in the company of someone who is aware of diabetic complications and who knows how to go about treatment if any problems arise during the activity.
Avoiding exercise related problems
As mentioned earlier glycaemia response to exercise is highly variable even in the same subject due to variations in exercise intensity, duration, the timing of exercise to insulin injections, meals and time of day (Richer and Galbo, 1986). Therefore, self-monitoring of blood glucose is important. During conditions of insulin deficiency, hyperglycemia and ketosis exercise should be discouraged until metabolic control is regained with insulin therapy (Richer and Galbo, 1986).
Any diabetics who takes part in running programs should consult a podiatrist so that adequate footwear is provided so that sensory loss in the feet due to neuropathy is avoided (Richer and Galbo, 1986).