This chapter entends help the medical student to “get contact” with clinical control of IDDM and NIDDM patients and is diveded in four basical parts: (1) Normal Metabolism During Exercise (2) Utilization of glucose on diabetics that exercise themselves (3) Beneficts and risks of exercises for diabetics (4) Terapeutic estrategis.
Glucose Metabolism During Exercise
During exercise, muscle utilises metabolic fuels at an increased rate to provide the inergy required for contraction. In healthy individual, muscle glycogen is the predominant fuel used during very stenuous, short term exercise, whereas blood-borne glucose and free fatty acids (FFA) derived from adipose tissue triglycerides are used preferentially during prolonged exercise of low to moderate intensity. Glucose uptake by muscle increases 4 - to 5 - fold or more during exercises. Despite this, the level of glucose in the plasma is maintained as a result of enhanced glucose produciton by the liver.
At the onset of exercise and before increased oxygen transport by the circulatory system, the anaerobic breakdown of glycogen to form lactate provides an immediate source of adenosine triphosphate (ATP). Exercise that continues more than 30 minutes increases the dependence on blood borne energy sources. After 60 a 90 minutes of exercise, FFA are the principal energy source. The utilization of FFA continues to discrease as the duration of exercises increases. The “ability” to use glucose and to a greater extent FFA as an energy source is greatly influenced by endurance training. Trained subjects use a higher proportion of FFA than untramed subjects and are able to spare glycogen stores while minimizing lactate production: Occasionally singnificant hyperglycemia and clinically important hypoglycemia occur in normal individuals. Plasma glucose, nowever, remains within a narrow range when exercising at moderate intensities (30% a 60%) CO2 max.
Energy utilization at exercise is influenced by insulin and by counterregulatory hormones: glucagon, epinephrine and norepinephrine, cortisol, and growth hormone. The role of insulin in glucose transport to muscle is markedly reduce during exercise. The most significant effect of insulin during exercise involves inhibition of hepatic glycogenolysis / gluconeogenesis and lipolysis. Insulin secretion is also suppressed by the alpha-adrenergic inhibition of the pancreatic beta cell, allowing for mobilization of hepatic glucose and avoidance of hypoglycemia. Exercise also increases insulin sensitivity by enhancing the binding of insulin to receptor sites on the muscle cell. This allows for increased glucose uptake without changes in insulin concentration. Increased numbers of receptor sites area found in more fit individuals with increased insulin biding and insulin sensitivity lasting for up to 24 hours after exercise.
Greater use of hepatic glucose occurs to prevent hypoglicemia as glucose is used by exercising muscles. This increase in glucose production occurs throught hepatic glycogenolysis. Subsequently gliconeogenesis becomes increasingly important and is influenced by counterregulatory hormones.
In addition, adrenaline may act to maintain normoglycemia increasing muscle glicogenolysis adiposea tissue lipolysis, there by diminishing the need of blood born glucose.
Exercise in Type I Diabetes Mellitus
Changes in glucose homeostasis in the type I diabetic are variable and depend on the following factors: degree of insulin administration, prior metabolic control, the presence or absence of autonomic neuropathy, and caloric intake. Balanced energy supply and insulin availability can have significant effects on the exercising athlete with type I diabetes. Excessive insulin levels suppress hepatic glucose production, and lowred serum glucose levels may be met by deficient glucagon secretion, which is common after several years of disease.
The well-controlled diabetic may commonly work out for approximately 30 to 45 minutes of sustained intense aerobic exercise without problems. Type I patients may have decreased glycogen stores in the liver and to a lesser extent in skeletal muscle. Lack of adequate glycogen stores leads to impaired aerobic exercise endurance when compared with normals.
Hypoglycemia is a common ocurrence in type I diabetics while exercising. In normal subjects, plasma insulin levels decrease during exercise. Additionally, insulin counterrulatory hormones (glucagon an epinephrine) promote increased hepatic glucose production, which matches the amount of glucose used during exercise. In the type I diabetic, plasma insulin concentrations may not fall during exercise and may even increase if exercise occurs within 1 hour of insulin injection. These sustained insulin levels during exercise enhance peripheral glucose uptake and stimulate glucose oxidation by exercising muscle. More important, however, is tye inhibition of hepatic glucose production. Hight insulin levels inhibit both gluconeogenesis and glycolenolysis. Even thought adrenergic stimulation leads to excess production of counterregulatory hormones, hepatic glucose production fails to match the rate of peripheral utilization. During exercise of moderate duration, these effects may be considered beneficial; however, longe periods of exercise may result in hypoglycemia.
The type I diabetic is at greatest risk of developing severe hypoglycemia 6 to 14 hours after strenuous exercise. Muscle and hepatic glycogen must be restored during periods of rest. Combined wity increased insulin sensitivity in the postexercise period, depleted muscle glycogen stores along wity tye activation of glycogen synthetase in muscle contribute significantly to tye risk of hypoglycemia. Insulin and caloric intake must be adjusted after strenuous exercise to avoid severe nocturnal hypoglycemia. Hypoglycemia due to increased insulin absorption from injection sites of actively exercising extremities as been described. Consequently the abdomen has been recommended as the abdomen has been recommended as the primary injection site in the exercising diabetic. Absorption of insulin from the abdomen is generally faster and more reliable than using limb sities for injection and consequently does not prevent the occurrence of hypoglycemia.
Finally, the type I diabetic does not increase insulin secretion postexercise. Hyperglycemia after exertion can be profound and prolonged for days owing to insulin deficiency. In the presence of poor control and ketonuria, further exercise can lead to impaired glucose uptake and increased lipolysis, ketogenesis, and hepatic glucose production. The patient may rapidly unless exogenous insulin is given to the patient.
Exercise in Type II Diabetes Mellitus
Initial treatment of type II diabetes consists of weight reduction, dietary control, exercise, and oral hypoglycemic agents. Insulin replacement is seldom necessary but should be added to the treatment regimen when hyperglycemia remains unchecked by these methods. Exercise is a major contributor in controlling hyperglycemia through improved peripheral insulin sensitivity, enhanced insulin binding, and reduced obesity.
Exercise can aid glycemic control and in combination with proper diet help prevent type II diabetes from occurring in those persons at risk. Exercise does this by improving short-term insulin sensitivity and reducing insulin resistance, both of which begin to disappear a few days after exercise is discontinued. Althought the number of insulin receptors remains constant with exercise, the biding of insulin to adipocytes is increased with no increase noted in binding to myocytes. In both cell types, however, the number and activity of glucose transport proteins (particularly Glut-4-isoform) are increased with exercise. This results in an increase in insulin-stimulated glucose transport into these cells following exercise, which improves glycemic control.
With the onset of exercise, the type II patient, does not respont with a decrease in serum glucose concentration as in the nondiabetic. This is due to increased glucose uptake in the peripheral tissues. As a result, serum glucose is higher, and liver glucose production is halted to allow for normalization of the hyperglycemia by overall reduction in the glucose level. In constrast to the type I patient, type II diabetics do not usually suffer hypoglycemia because endogenous insulin levels can usually be maintained. Those athletes on oral hypoglycemic agents or insulin, however, may have problems with glucose homeostasis during exercise. The athlete may need to lower the medication dose or increase carbohydrate intake (or both) before exercise to prevent hypoglycemia. Severe hypoglycemia is unusual because individuals are still able to reduce endogenous insulin production as blood glucose levels decline.
Bibliography
1. Sports Medicine for Primary Care, Willian E. Moats
2. Goodman, The Pharmacological Basis of Therapheutics, Nineth Edition, Goodman & Gilman’s
3. The Medical Clinics of North America, Vol 78, Num 2 , Gray I. Wadler.
4. Cecil , Textbook of Medicine. twenth edition, Bennet & Plum
5. Exercise prescription fo Individuals with metabolic disorders (pratical considerations) John
C. Young. SPORTS MED. 19(1) PAG 43 - 54 1995
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