Diabetes Mellitus Aka: Diabetes Mellitus

1. See Also
1. Diabetes Mellitus Glucose Management
2. Type I Diabetes Mellitus
3. Type II Diabetes Mellitus
4. Insulin Resistance Syndrome
5. Diabetes Mellitus Education
2. Definition
1. Metabolic disorder of carbohydrate economy
2. Deficiency of pancreatic beta cell Insulin secretion
3. Resistance to Insulin effect peripherally
3. Epidemiology (U.S. statistics for 2004 per ADA)
1. Prevalence
1. Type I Diabetes Mellitus: 750,000
2. Type II Diabetes Mellitus: 13 million
3. Gestational Diabetes: 135,000
4. Undiagnosed with diabetes: 5.2 million
2. Incidence
1. Type 1: 30,000 new cases per year
2. Type 2: 850,000 new cases per year
3. Gestational Diabetes Mellitus: 4% of all pregnancies
4. Fastest growing groups
1. Ages 30 to 39 years
2. Type II Diabetes in children
4. Types
1. Type I Diabetes Mellitus
1. Juvenile Diabetes Mellitus
2. Insulin Dependent Diabetes Mellitus (IDDM)
2. Type II Diabetes Mellitus
1. Adult onset Diabetes Mellitus
2. Non-Insulin Dependent Diabetes Mellitus (NIDDM)
3. Pediatric Type II Diabetes Mellitus (Pediatric NIDDM)
4. Maturity onset Diabetes of youth (MODY)
5. Symptoms
1. Classic (75% of cases of Type I Diabetes Mellitus)
1. Polyuria or nocturia
2. Polydipsia
3. Unexplained Weight Loss
2. Other symptoms
1. Increased appetite
2. Blurred vision
3. Frequent Urinary Tract Infections
4. Frequent yeast infections
5. Fatigue
6. Dry or pruritic skin
 7. Numbness or tingling in the extremities
6. Diagnostic Criteria
1. Random Serum Glucose
1. Serum Glucose over 200 mg/dl with symptoms
2. Fasting Serum Glucose
1. Serum Glucose exceeds 126 mg/dl on 2 different days
3. Postprandial Glucose (2 hours post meal)
1. Serum Glucose over 200 mg/dl
2. Precedes fasting glucose increase
3. More predictive of Diabetes Mellitus Complications
4. Casual Plasma Glucose (random glucose)
1. Same criteria as postprandial glucose
5. Oral Glucose Tolerance Test (OGGT)
1. Two hour Glucose Tolerance Test (75 gram) >200 mg/dl
2. Consider in patients with Insulin Resistance
1. Patients with pre-diabetes to qualify for education
7. Other monitoring
1. Home Serum Glucose monitoring
1. Over 50% of values should fall in target range
8. Management: Severe Hyperglycemia at diagnosis
1. Start Insulin at onset if severe hyperglycemia
2. Criteria
1. Blood Glucose >300 mg/dl
2. Hemoglobin A1C >9.0
3. Protocol based on Urine Ketones
1. Urine Ketones positive
1. Evaluate for Diabetic Ketoacidosis
2. Check Metabolic panel and Serum Ketones
2. Urine Ketones negative
1. Type I vs Type II is not critical initially
1. Both get Insulin at this hyperglycemia level
2. Type II suspected
1. Consider adding Metformin
2. Insulin can likely be weaned later
1. Glucose toxicity causes low Insulin
level
2. Endogenous Insulin will later
normalize
2. Start LantusInsulin at 10 units SQ today
1. Low risk of Hypoglycemia
3. Teach glucose testing, Insulin injection today
1. Formal Diabetic Education within 1 week
2. Consider endocrinology consultation later
4. Give prescriptions today
1. Meter, strips, lancets, Insulin, syringes
9. Management: Initial Education
 1. Key Topics
1. See Diabetes Mellitus Glucose Management
2. See Diabetes Mellitus Education
2. Type specific Diabetes Information
1. See Type I Diabetes Mellitus
2. See Type II Diabetes Mellitus
3. Adjunctive Management
1. See Hypertension in Diabetes Mellitus
2. See Coronary Artery Disease Prevention in Diabetes
3. Tobacco Cessation
4. Weight loss
5. Aspirin in all diabetic patients
6. Consider ACE Inhibitor in all diabetic patients
1. Use low dose (2.5 to 5 mg) in normotensive patient
7. Lipid disorders
1. See Coronary Artery Disease Prevention in Diabetes
2. See Low Fat Diet
3. See AntiHyperlipidemic

Exercise in Diabetes MellitusAka: Exercise in Diabetes

Mellitus, Diabetes Mellitus and Exercise
1. See Also
1. Diabetes Mellitus
2. Exercise
2. Benefits of Exercise in Diabetes Mellitus
1. Exercise lowers Serum Glucose
1. Benefits Type I Diabetes Mellitus
2. Benefits Type II Diabetes most significantly
2. Exercise augments Insulin effect
1. Facilitates glucose transport across cell
3. Exercise reduces heart disease and stroke risk
1. Increases HDL
2. Lowers LDL
3. Lowers Total Cholesterol
4. Decreases SBP and DBP
4. Exercise improves general wellness
1. Increases self esteem
2. Improves socialization
3. Risks of Exercise in Diabetes Mellitus
1. Hypoglycemia
1. Use caution in Scuba Diving
2. Use caution in rock-climbing
 3. Use caution in long-distance swimming
2. Retinopathy
1. Avoid weight lifting
2. Avoid mountain climbing
3. Neuropathy
1. Avoid weight bearing Exercises
2. Choose stationary bike or water sports
4. Autonomic Dysfunction
1. Abnormal hemodynamic response to Exercise
1. Inappropriate Heart Rate response
2. Inappropriate Blood Pressure response
2. May not experience Anginal symptoms with Exercise
3. May not experience hypoglycemic symptoms
5. Diabetic Nephropathy
1. Avoid Resistance Training
6. Cardiovascular disease
1. Consider Stress Testing prior to Exercise program
4. Starting Exercise
1. Evaluate coronary, nephropathy, Neuropathy, retinopathy
1. Confirm no contraindications to starting Exercise
2. Goal energy expenditure (See METS)
1. No weight loss intended: 1000 KCal/week
2. Weight loss intended: 2000 KCal/week
3. Progressive Resistance Training
1. Low resistance (40-60% of 1 repetition maximum)
2. Low intensity
3. Gradually increase to 15-20 repetitions
5. General Exercise Tips in Diabetes Mellitus
1. Preparation for regular Exercise
1. Check feet for lesions related to Exercise
2. Pre-Exercise evaluation (consider Stress Test)
3. Medic-Alert tag
4. Exercising diabetics must use Glucometer
5. Pre-planned strategy for Hypoglycemia
6. Evaluate Exercise Energy Expenditure (METS)
2. Time Exercise appropriately
1. Avoid late-evening Exercise in Type I Diabetes
2. Aerobic Exercise recommended 6 to 7 days per week
1. Duration: 20 to 60 minutes
2. Level: 60-80% of maximum Heart Rate
3. Allow time for warm up and cool down
1. Reduces injury risk
2. Reduces post-Exercise arrhythmia risk
6. Blood Sugar Management
1. Check pre-Exercise blood sugar
1. Blood sugar <100 mg/dl
 1. Snack 15-20 grams carbohydrate before Exercise
2. Blood sugar 100 to 250 mg/dl
1. No snack needed
3. Blood sugar >250 with ketones (or >300 without)
1. Delay Exercise
2. Check Serum Ketones
3. Treat hyperglycemia and dehydration
2. Pre-ExerciseInsulin
1. Take Insulin more than 1 hour before Exercise
2. Inject Insulin into a non-exercising site
1. Absorption at abdomen is fastest and most reliable
3. Decrease short-acting Insulin before Exercise
1. Decrease 30% for Exercise less than 1 hour
2. Decrease 40% for Exercise 1-2 hours
3. Decrease 50% for Exercise over 3 hours
3. Decrease risk of Hypoglycemia
1. Avoid Exercise during times of peak Insulin activity
2. Consider HumalogInsulin
3. Insulin injection site may affect absorption rate
4. Avoid Sulfonylurea
4. Be aware of your own blood sugar response to Exercise
1. Pre-Exercise Food
1. Meals should be ingested 1-2 hours before Exercise
2. Strenuous or prolonged Exercise
1. Start increasing calorie intake 24 hours before
2. Supplement carbohydrates every 30 minutes during
2. Supplement during Exercise with glucose solutions
1. One bottle for each 30 minutes strenuous Exercise
3. Replenish glycogen stores after Exercise
1. Based on Exercise duration and intensity
2. Be aware of delayed Hypoglycemia
5. Carry an activity pack while exercising
1. Personal identification
2. Mobile phone
3. Adequate water and carbohydrate source
4. Blood Glucose monitor
7. Complications: Post-ExerciseHypoglycemia
1. Delayed Hypoglycemia
1. Occurs 6 to 28 hours after strenuous Exercise
2. Occurs despite normal blood sugars during Exercise
3. Occurs regardless of age or illness severity
4. Often occurs at night
2. Mechanism
1. Glycogen stores depleted and not replenished
2. Increased Insulin sensitivity post-Exercise
8. Resources
 1. Diabetes, Exercise and Sports Association
1.
2. Mountains for Active Diabetics (extreme sports)
1. http://www.mountain-mad.org
9. References
1. Whaley (2006) ACSM's Guidelines for Exercise
2. White (1997) Lecture: AAFP Sports Medicine, Dallas
3. Baraz (1994) Clin Diab 12(4):94-8
4. Fahey (1996) Am Fam Physician 53:1611-7
5. Landry (1992) Clin Sports Med 11:403-18

Diabetic EducationAka: Diabetic Education, Diabetes

Mellitus Education

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1. Approach: Employ a Pediatric Diabetes Team (Essential)

1. Physician
2. Nurse or Nurse Practitioner
3. Diabetes Educator
4. Nutritionist or Dietician
5. Social Worker
6. Psychologist
2. Approach: Initial Education
1. Describe Diabetes Mellitus pathophysiology
2. Management principles
1. Taking Insulin (when prescribed) is non-negotiable
2. Other issues are negotiable
3. Insulin action and use
4. Blood Glucose Monitoring
5. Urine Ketone testing
6. Hypoglycemia
7. Exercise in Diabetes Mellitus
8. Nutrition in Diabetes Mellitus
9. Psychological Issues
10. Home Treatment
3. Approach: Ongoing Education
1. Should occur at every visit
2. Must be age and education-level appropriate
1. Include children age 5 and older in discussion
 3. Include skill review
4. Prevention
1. Seasonal illness prevention
2. Immunizations: Influenza Vaccine
3. See Diabetic Foot Care
4. See Exercise in Diabetes Mellitus
5. See Nutrition in Diabetes Mellitus
5. Emergencies
1. Hypoglycemia
2. Type I Diabetes Mellitus Hyperglycemia
1. Diabetic Ketoacidosis (DKA)
3. Type II Diabetes Mellitus Hyperglycemia
1. Hyperosmolar Hyperglycemic Nonketotic Coma
6. Chronic Complications
1. Diabetic Retinopathy
2. Diabetic Nephropathy
3. Diabetic Neuropathy
4. Coronary Artery Disease

Sports Medicine
Mario Cesar Moreira de Araujo, MD & Marcelo Riccio Facio, MD
Medstudents' Homepage

Diabetes Mellitus and Exercise

Introduction

Nowadays the development of convinient and efficient ways of self monitoring blood
glucose, ande the admission of benefits of regular exercing permit and enconrage more
diabetics to engage into exercise programs. Consequenty, phisicians will have to be able
to prescribe arrangements in calorie ingestion and insulin dosage, as well imagine
possible hypoglycemia and unexpected prolonged exercise to permit a safe participation
on this activities.

Diabets Mellitus is a chronic discase characterized by relative or absolute absence of

insulin, with repercussion on glucose metabolism classified in Type I (Insulin Dependent
Diabetes), Type II (Non - Insulin Dependent Diabetes), Secondary Diabetes and Genetic
Defects of the Insulin Receptor. Diabetes Mellitus is a very common disoider, with an
estimated prevalence between 2 and 4 % in the Unitede States.

Type I Insulin - Dependent Diabetes Mellitus (IDDM) is better characterized by an auto-

imune disturbance in which panereatic b cells are distructed. Because off the marked
hupoinsulinemia patients usually presents hyperglycemia (with acute complications:
polymia, polydipsia and polyfagia) and the risk of developing ketoacidosis.

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