DPT-402.3- Exercise Prescription: Special Considerations – Diabetes Mellitus

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Diabetes is a chronic and currently incurable metabolic disorder, where the body is unable to produce or utilise insulin, and therefore cannot convert carbohydrates into energy (Albright, 1997). It is characterised by an abnormally high and persistent concentration of sugar in the bloodstream. Around 1.4 million people in the UK have been diagnosed with diabetes and that number is expected to double by 2010 (Diabetes UK, 2003). It is surmised that about the same number, if not more, are as yet undiagnosed.

The name diabetes mellitus derives from the Greek word ‘diabetes’ meaning siphon – to pass through, and ‘mellitus,’ the Latin for honeyed or sweet. It refers to a major symptom of diabetes, sugar in the urine, and is a far more acceptable name than that given in the 17th Century – the ‘pissing evil’.

Diabetes has been a recognised condition for over 3,500 years. About 2,000 years ago, it’s said that Arataeus of Cappadocia described diabetes as ‘a melting down of the flesh and limbs into urine.’ This reflected the weight loss and excess passing of urine that occurs in acute, undiagnosed diabetes.

The hallmarks of diabetes are characterised by three ‘polys’ (Tortora and Grabowski, 2002):

  • polyuria (excessive urine production due to an inability of the kidneys to reabsorb water)
  • polydipsia (excessive thirst)
  • polyphagia (excessive eating)

Pathophysiology

Carbohydrate metabolism:

In most people, carbohydrate (CHO) is broken down into glucose and other simple sugars in the small intestine through the process of digestion (breakdown of food into smaller molecules). Glucose is then absorbed from the small intestine into the body and carried firstly to the liver via the hepatic portal system (portal vein), then onto muscle and fat cells, to be stored or used as immediate energy. Glucose transport into cells is dependent on the hormone insulin. Insulin is manufactured and stored in the Islets of Langerhans by the beta-cells within the pancreas (a six inch long gland located behind the stomach). Under normal circumstances the hormone insulin carefully regulates how much glucose is in the blood. 

Insulin stimulates cells to absorb enough glucose from the blood for the energy that they need, with any excess being stored by the liver or in the adipose tissue. After a meal the amount of glucose in the blood rises, and this triggers the release of insulin. When blood glucose levels fall, during exercise for example, insulin levels fall too. A second hormone manufactured by the pancreas is called glucagon. It stimulates the liver to release glucose when it’s needed, and this raises the level of glucose in the blood.

With diabetics, the glucose has trouble getting from the blood into the cells where it can be used for metabolism. There are two identifiable problems (Tortora and Grabowski, 2002):

  • no insulin or not enough insulin being produced, called Type I diabetes
  • what is produced is not functioning properly, called Type II diabetes

The result of this is a ‘glucose glut’, where elevated levels of unused carbohydrates, or sugar, are trapped or ‘homeless’ in the bloodstream. Continued elevated blood glucose levels (hyperglycaemia), and glucose ‘escaping’ in the urine (glucosuria), are two signs of diabetes.

Types of Diabetes

Type I diabetes: Insulin Dependent Diabetes Mellitus (IDDM): 

Type 1 diabetes mellitus results from cellular-mediated autoimmune destruction of pancreatic islet beta-cells (Atkinson and MacLaren, 1994). It’s not clear why the body’s own immune system attacks and destroys apparently healthy cells, but a number of explanations and possible triggers for this reaction have been proposed (American Diabetes Association, 2003), including: 

  • infection with a specific virus or bacteria
  • exposure to food-borne chemical toxins
  • exposure as a very young infant to cow’s milk, where an as yet unidentified component, triggers the autoimmune reaction in the body

It is important to remember that these are only hypotheses and have yet to be proven.

The destruction of the beta cells that produce insulin causes a severe lack of this hormone. When approximately 80% of beta cells are destroyed, they no longer produce sufficient insulin to facilitate the uptake of ingested fuels. Type I diabetes is also called Insulin Dependent Diabetes Mellitus (IDDM) because sufferers depend on insulin injections to regulate sugar metabolism. 

More than 10% of adults with diabetes have Type I (Albright, 1997) and this is the most severe form of diabetes. It was also called juvenile onset diabetes mellitus because it was thought to only affect children and young adults. It is now known to develop at any age, although the majority of cases are below twenty years of age.

Type II diabetes: Non-insulin Dependent Diabetes Mellitus (NIDDM) :

Type II diabetics represent over 90% of all diabetic cases (Tortora and Grabowski, 2002). NIDDM was formerly known as adult, or maturity onset diabetes. This condition seldom develops before the age of forty but it can develop at any age. 

Type II diabetes exhibits a relative insulin deficiency. In this case, there is no need to inject insulin because, while insulin production may be reduced, enough is produced to control the blood sugar. However, while insulin is still produced it does not function normally in terms of enabling the passage of glucose into the cells, i.e. the cells have become ‘insulin resistant’. There is an often quoted link between Type II diabetes and obesity; in fact obesity is prevalent in 80% of people diagnosed with Type II diabetes (Kumar and Clark, 2001). Obesity has been shown to reduce the body’s sensitivity to insulin i.e. increase insulin resistance.

It should be pointed out that without proper management in terms of diet, medication and exercise, Type II diabetes can progress to a “Type I like” disorder. This is because the pancreas identifies the need for more insulin to be released due to high blood sugar levels, but additional insulin has no significant effect, owing to insulin resistance. Eventually, the insulin secreting cells in the pancreas may become exhausted and insulin production ceases (Albright, 1997).

Alternatively, with good management it is possible to reverse the disease process.

There are a few causative factors for Type II:

  • genetic predisposition
  • obesity (due to inactivity and diet)
  • age over 35 years

It is generally thought that a combination of excess weight and age triggers an existing predisposition (Souhami and Moxham, 1998).

Gestational diabetes:

Gestational diabetes occurs during pregnancy because of the contra-insulin effects of pregnancy (Albright, 1997). This follows a perfectly normal response to pregnancy in which the mother’s sensitivity to insulin decreases, in order to provide the foetus with sufficient glucose. Gestational diabetes does not describe those with diagnosed or undiagnosed diabetes, who then become pregnant. This type of diabetes is usually resolved in the postpartum period.  Albright (1997) lists the risk factors for gestational diabetes as including:

  • family history of gestational diabetes
  • previous delivery of a large weight baby
  • obesity

Short Term Complications of Diabetes

Hypoglycaemia:

Very low blood sugar levels (less than 3 mmol/L) are the more commonly encountered diabetic incident. It can be the result of missing a meal, too much exercise, injecting too much insulin or injecting it at the wrong time (i.e. too close to exercise) or a combination of all of these. The symptoms of hypoglycaemia include: 

  • shakiness 
  • dizziness 
  • sweating
  • hunger 
  • headache 
  • pale skin colour
  • sudden moodiness or behaviour changes, such as crying for no apparent reason 
  • clumsy or jerky movements 
  • seizure 
  • difficulty paying attention, or confusion
  • tingling sensations around the mouth 

(Barker, 1996, ADA, 2003)

Sometimes, a client may not demonstrate any of these symptoms prior to falling unconscious; this is called hypoglycaemia unawareness (ADA, 2003). Hypoglycaemia unawareness tends to happen to people who have had diabetes for many years. It is more likely in people who have neuropathy (nerve damage), people on tight glucose control, and people who take certain heart or high blood pressure medicines. It is therefore, critical to monitor a diabetic’s blood glucose levels.

It is important that the trainer learns to recognise the early warning signs of a hypoglycaemic incident. Clients should be encouraged to carry a quickly absorbed form of carbohydrate to relieve symptoms. If a client becomes unconscious then the emergency services should be sought or glucagon can be injected, in order to increase blood glucose levels. Glucagon is injected in the same fashion as insulin, and causes a release of stored carbohydrate from the liver into the blood, to elevate and stabilise blood glucose levels.

Additionally, if an individual passes out from hypoglycaemia, the following should be observed: 

  • do NOT inject insulin
  • do NOT give food or fluids 
  • do NOT put hands in their mouth 

Hyperglycaemia:

Elevated blood glucose levels will occur with every diabetic at some point, but continued elevation can be the result of poor management. It causes numerous long term complications (as explained later) and can also lead to coma and prove fatal in Type I diabetics. This is because of additional, underlying mechanisms occurring within the body. The main one is a condition called ketoacidosis, where excessive levels of ketones build up in the blood. When the glucose stays in the blood, and fails to get to the cells of the body, the cells must rely solely on fat for energy. The bi-products of breaking down fat, in the absence of carbohydrates, are ketone bodies. The body excretes these ketones in the urine, but when produced in excess they can accumulate in the bloodstream. This causes the pH of the blood to fall (ketoacidosis) and can be fatal if not treated. Initial symptoms include (ADA, 2003):

  • thirst or a very dry mouth
  • frequent urination
  • hyperglycaemia
  • ketones in the urine

Other symptoms may then appear:

  • shortness of breath (dyspnoea)
  • ‘fruity’ smelling breath
  • nausea, vomiting and abdominal pains
  • constantly feeling tired
  • dry or flushed skin
  • lack of concentration or confusion

Hunger and rapid weight loss may also be indicators of ketoacidosis (Howley and Franks, 1996). Exercise is contraindicated if ketones are present and blood glucose levels are elevated (250mg/dL). 

Long Term Damage Due to Hyperglycaemia

The continued effects of raised blood glucose levels can have detrimental effects on numerous structures of the body:

Coronary heart disease and circulatory damage:

Diabetes carries an increased risk of heart attack, stroke, and complications related to poor circulation, with 2 out of 3 people with diabetes dying from heart disease and stroke (ADA, 2003). This is because high or uncontrolled blood glucose affects small and large vessels causing:

  • thickening of the lining of the small blood vessels, making them leak or unable to supply nutrients to tissues
  • furring of the arteries (Souhami and Moxham, 1998)

Nerve damage (neuropathy):

One of the most common complications of diabetes is diabetic neuropathy (ADA, 2003). Neuropathy means damage to the nerves that run throughout the body, connecting the spinal cord to muscles, skin, blood vessels, and other organs. Peripheral nerves are particularly damaged, resulting in loss of sensation and numbness affecting the feet, legs, arms and hands.  As a result, injury is difficult to detect. This can lead to infection, gangrene and possible amputation (Souhami and Moxham, 1998).

Kidney damage and disease (nephropathy):

Diabetes can damage the renal blood vessels, and also cause the kidneys to be damaged through the excess excretion of glucose and ketones in the urine. As the kidneys fail, they lose their ability to filter out waste products, resulting in kidney disease (ADA, 2003; Souhami and Moxham, 1998).

Eye damage and disease (retinopathy):

High glucose levels lead to blockages in the small blood vessels in the retina.  To compensate for this, other vessels open and dilate and these enlarged vessels begin to leak blood (Souhami and Moxham, 1998). In clients with active diabetic retinopathy, strenuous activity may precipitate haemorrhage or retinal detachment (ADA/ACSM, 1997). The ADA/ACSM (1997), recommends these clients should avoid anaerobic exercise, and activities involving jarring, straining or Valsalva-like’ manoeuvres.

Foot complications:

People with diabetes can develop many different foot problems. Foot problems most often happen when there is nerve damage in the feet or when blood flow is poor. Diabetics need to learn how to protect their feet with good foot care.

Skin complications:

At some time in their lives as many as one third of people with diabetes will have a skin disorder caused or affected by diabetes. In fact, such problems are sometimes the first sign that a person has diabetes. Luckily, most skin conditions can be prevented or easily treated if caught early.

Exercise Recommendations

A diabetic’s exercise programme should address the following goals:

  • to help control blood sugar
  • to maintain ideal weight
  • to improve quality of life
  • to avoid developing diabetic complications 

The primary role of exercise is usually seen as aiding in glucose control by decreasing insulin resistance (by improving insulin sensitivity) and promoting glucose uptake.

Other points to consider:

  • the improvement in insulin sensitivity after exercise is short term and soon diminishes 
  • a well-trained athlete’s insulin sensitivity decreases after as little as three days of inactivity and is restored by a single bout of exercise 
  • exercise adherence is vital (De Araujo and Facio, 2002)
  • a decrease in body fat leads to a reduction in insulin resistance 
  • often weight loss is the only treatment Type IIs need (Albright, 1997)
  • exercise can decrease the risk of cardiovascular disease (De Araujo and Facio, 2002)
  • stress can disrupt diabetes control by increasing counter regulatory hormones, ketones, free fatty acids and urine output (Albright, 1997). So, implement stress management techniques
  • for prevention of Type II diabetes (Albright, 1997)  there is a theory that taking action to decrease blood sugar levels in the ‘pre-diabetic’ phase may well delay the onset and lessen the risks of later complications (Albright, 1997)

ACSM exercise recommendations for diabetics from Albright et al (2000):

Aerobic Exercise Recommendations
Frequencyat least 3 -5 sessions/ week 
Intensity40-70% vo2max RPE 11-13
Time20-40 minutes/main session
Type          predictable, aerobic physical activity, low impact, non-weight-bearing if at risk of orthopaedic injury
Resistance Training Exercise Recommendations
Frequency2-3 x/week
Intensityform failure – 15-20 repetitions
Time1-2 sets per exercise, 6-8 exercises
Type          all major muscle groups, following a circuit type training format. Select exercises that will not excessively raise blood pressure

Young clients with diabetes may use higher resistance exercises, but this is not advised for older clients, or those with long standing diabetes (ADA/ACSM, 1997).

Flexibility Recommendations
Frequencyminimum of 2-3 x/week
Intensityto a position of mild discomfort
Time          10-15 seconds per hold for maintenance10-15 seconds repeated with 6-8 second contractions for development3-4 repetitions for each stretch
Type all major muscle groups used in the sessions

Precautions for exercise:

  • a thorough medical examination prior to beginning an exercise programme (Morris and Sadler, 2001)
  • wear identification at all times (Morris and Sadler, 2001)
  • do not inject into the limbs about to be exercised.  Increased circulation in the area may speed up the absorption of insulin and therefore, may bring on a hypoglycaemic incident (abdominal sites may be safer) (De Araujo and Facio, 2002)
  • avoid exercising at the peak of insulin action (Diabetes Care, 2003)
  • adjust carbohydrate intake or insulin dosage before exercise. Eat more carbohydrate or have a smaller dose of insulin pre-exercise 
  • any adjustments to dosages are for the client to discuss and monitor with their GP
  • consume adequate fluids before, during and after exercise (ADA/ACSM, 1997)
  • avoid extremes of temperature (Morris and Sadler, 2001)
  • practice good foot care (Morris and Sadler, 2001)

Clients can avoid problems if they:

  • inspect and wash feet daily, blot dry both thoroughly, especially between the toes
  • wear comfortable shoes or trainers and change socks at least once a day
  • avoid any position or garments that restrict circulation to the legs e.g. crossing  legs
  • avoid extreme heat around the feet like heat lamps and hot water bottles

Dietary Recommendations

Nutritional considerations should be part of the initial screening and management of the diabetic. The main consideration is the type of carbohydrates consumed, and this relates to something called the Glycaemic Index (GI). The GI is a ranking system to show how quickly certain foods get broken down, and thus how quickly blood glucose levels will rise. Low scoring GI foods will take longer to break down, and will thus cause a smaller, more gradual rise in blood glucose. High GI foods will break down quickly, and will therefore, cause a greater, faster increase in blood glucose. The higher the blood glucose levels rise, the more insulin is required. Low or moderate GI foods would therefore be recommended, or ensuring a combination of high GI foods with low ones to make a ‘moderate GI meal’.

Other general points:

  • high fibre foods are important to lower cholesterol levels and to reduce the rise in blood glucose after meals
  • high fat consumption inhibits insulin action (Barker, 1996)
  • a carbohydrate to protein ration of 2:1 allows for optimal secretion of insulin
  • low or moderate GI foods should be favoured
  • small, regular meals are preferable (ACSM, 1997)

Specific dietary recommendations:

  • several hours before exercise have a high carbohydrate, low fat and protein meal
  • one hour of exercise generally requires an additional 15g of carbohydrate (CHO) before exercise (Diabetes Care, 2000) 
  • 10g CHO every 15-20 minutes during sustained exercise e.g. ½ cup of a sugary drink
  • if vigorous or long duration, additional 15-30g every hour (Diabetes Care, 2000)
  • client should be encouraged to check blood sugar before, after and if possible,    during exercise
  • easily digestible/fast acting carbohydrate e.g. juice, candy on hand, in the event of a hypoglycaemic incident (Barker, 1996)

References

Albright, A. L. (1997). Diabetes. In ACSM’s Exercise Management for Persons with Chronic Diseases and Disabilities(J. L. Durstine, ed.). pp. 94-100, Human Kinetics.

Albright, A., Franz, M., Hornsby, G., Kriska, A., Marrero, D., Ullrich, I. and Verity, L. S. (2000). American College of Sports Medicine position stand. Exercise and type 2 diabetes. Med. Sci. Sports Exerc., 32, 1345-60.

American Diabetes Association (2003). Diabetes. http://www.diabetes.org.

Atkinson, M. and MacLaren, N. (1994). The pathogenesis of insulin dependent diabetes. N Engl J Med, 331, 1428-1436.

Barker, H. M. (1996). Nutrition and Dietetics for Health Care. Churchill Livingstone.

Diabetes Care (2000). Diabetes. http://www.findarticles.com

Diabetes UK (2003). Diabetes. http://www.diabetes.org.uk.

Expert Committee on the Diagnosis and classification of diabetes mellitus (1997). A report of the Expert Committee on the Diagnosis and classification of diabetes mellitus. Diabetes Care, 20,1183-1197.

Howley, E. T. and Franks, B. D. (1996) Health and Fitness Instructors Handbook. Human Kinetics.

Kumar, P. and Clark, M. (2001) Clinical Medicine Fourth Edition. W.B. Saunders.

Morris, P. and Sadler, C. (1999). The Diabetic Client. http://www.ptonthenet.com/articles /special_populations /diabetes.htm

NHSDirect(2003).Diabetes.http://www.psychiatry.ox.ac.uk/diabetes/patient/diagnosis/symptoms

Souhami, R. L. and Moxham, J. (1998). Textbook of Medicine. Churchill Livingstone.

Tortora, G. J. and Grabobowski, S. (2002). Principles of Anatomy and Physiology. 10th Edition. John Wiley and Sons.

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