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DSI Newsletters, Issue 17:
Diabetes and Physical Therapy —
Implications for Physical Therapy in the Treatment of Patients with Diabetes Mellitus




Why should physical therapists be concerned about diabetes?
 In 1994, it was estimated that 12 million Americans have diabetes and this number has been rapidly increasing since we redefined diabetes as beginning with a fasting glucose level of 126. As a result, it is very likely that physical therapists will be treating patients who have diabetes as a coexisting medical condition or who are being treated for conditions, such as stroke or amputation, secondary to diabetes. For this reason, it is important for physical therapists to understand the effects of diabetes upon their patients and the special considerations which must be made when treating such patients. This paper will focus on the physical therapy treatment considerations surrounding the use of exercise and physical modalities in the diabetic population along with the basic pathophysiology of diabetes. In addition, diabetic foot care will be discussed.
Diabetes in the elderly
 While diabetes can affect children, adolescents, and young adults, it is primarily seen in those over the age of 65. Diabetes is ten times as likely in people over 65 than in those between the ages of 20 and 44 years.2 The Departments of Labor and Health and Human Services estimates that one in five 65-year-olds have diabetes and that elders with diabetes are hospitalized twice as often as their peers without the condition.3 Heart disease is the leading cause of death in the USA and the risk for cardiovascular disease and mortality increases two-three-fold in individuals with diabetes. Following an appropriate exercise program and doing it safely is a critical component to preventing and treating type 2 diabetes. The elderly frequently have co-morbid diseases like: arthritis, gait apraxia, dysequilibrium, and presbycusis that make proper instruction on preventive medicine imperative. Not to mention, timing different anti-hypoglycemic agents to exercise. For example, a shot of insulin into a muscle you plan on exercising will cause a quicker release, higher peak level, and a shorter duration of action. Sulfonurea type drugs may need to be weaned down with planned exercise.
What is diabetes mellitus?
 Diabetes mellitus (DM) is a controllable disorder that is characterized by chronic hyperglycemia (blood glucose level > 126 mg/dL).1,4 Associated with this disease is the irregular metabolism of carbohydrates, protein, and fat.1 It is often referred to as "drowning in a sea of plenty" to highlight the fact that the serum glucose is high while the intracellular glucose is low. In addition, diabetes can result in vascular and neurological complications, including retinopathy, nephropathy, peripheral vascular disease (PVD), coronary heart disease, and cerebrovascular disease.1
Major types of diabetes
 While the classifications of diabetes are numerous, the two main types are insulin-dependent diabetes mellitus (IDDM) and non-insulin-dependent diabetes mellitus (NIDDM).1 While not discussed in this paper, other forms include gestational and malnutrition-related diabetes mellitus. Insulin-dependent diabetes mellitus is commonly referred to as type 1 or juvenile-onset DM. It is characterized by the destruction of pancreatic beta cells, which are responsible for the body's production of insulin.1 The cause is not fully understood, but seems to be of genetic, autoimmune, or viral origin. A diagnosis is usually made before the age of 30. Individuals with IDDM tend to be of average weight and require external sources of insulin to survive.1
 Non-insulin dependent diabetes mellitus is the most common form of the disorder, accounting for 90% of all cases.1 It is also known as type 2 or adult-onset DM. Individuals with NIDDM may have normal, high, or low insulin levels, but their bodies do not use the insulin efficiently due to an abnormal resistance to it.1 These individuals will often be overweight. A diagnosis is usually made after the age of 30. External insulin may or may not be necessary to alter blood glucose levels.1
Medical management of diabetes
 Diabetes does not have to progressively worsen.4 In fact, it may be effectively managed by a combination of pharmacological intervention, exercise, and proper diet. Insulin is a hormone that is commonly used for drug therapy. It is responsible for lowering blood glucose levels either by suppressing the release of stored glucose from the liver or by directing blood glucose to be used in peripheral tissues such as muscle.1 Insulin for drug therapy is typically obtained from the pancreas of animals and is subcutaneously injected into its human recipients.1 Combinations of different types of insulin are used to treat diabetes. Different types will vary in terms of how quickly effects will occur and the duration and intensity of these effects.1 In general, effects will be seen within a half hour to four hours and will last between eight to 36 hours.1
 Exercise also decreases blood glucose levels by increasing glucose transport to peripheral tissues. This is achieved by creating a mechanical muscular pump and by enhancing blood circulation.1 As many people with diabetes are overweight, exercise and a proper diet can help them to control weight. In people with NIDDM, weight loss has been shown to reduce abnormal insulin resistance.1 In addition, people with NIDDM, weight loss has been shown to reduce abnormal insulin resistance.1 In addition, dietary management is used to control fluctuating blood glucose levels, especially hypoglycemia.1
Complications of diabetes
 Diabetes can affect nearly every system of the human body, having such sequelae as the damage or destruction of blood vessels and nerves.5 Physical therapists are likely to treat patients with diabetic complications, including peripheral neuropathies and PVD. The causes of these complications are not fully understood and are beyond the scope of this paper. However, it has been recognized that diabetes impairs the efficiency of oxygen transport to tissues.6 Hyperglycemia may result in an increase in hemoglobin, causing oxygen to remain bound to the hemoglobin rather than circulating to surrounding tissues.6 In addition, capillary membranes appear to be thicker in people with diabetes, thus inhibiting oxygen difussion.6 Such alterations can lead to hypoxia of structures such as nerve axons and myelin sheaths, contributing to neuropathy.7
 Vascular changes are also apparent. Atherosclerosis of large blood vessels is, for some unknown reason, more frequent and occurs sooner in individuals with diabetes.7 This may be related to hyperlipidemia secondary to diabetes.1,7 Structural alterations such as thickening of blood vessels membranes and increased blood viscosity may contribute to PVD.1,7
Clinical implications for physical therapy: Diabetic foot care
 Peripheral neupathy and PVD can result in limb amputation in the diabetic population. Approximately 50% of all non-traumatic amputations in America are related to diabetes.7 With proper medical management and patient education, however, extreme measures such as amputation can be avoided.
 The feet are generally the first area to be affected by neuropathy and PVD in the individual with diabetes.4 The therapist may need to educate the patient on the inspection of the feet for indications of these conditions. The patient should look out for decreased temperature of the foot: dry, scaly skin; weakness of the foot; callus or blister formation; and decreased sensation or pain awareness in the foot.4 In addition, the therapist should note any loss of deep tendon reflexes and loss of vibratory or position sense in the foot and ankle.4 Daily inspections should be encouraged.4
 If physical therapy involves immersing the foot of a patient with diabetes in water, the therapist should thoroughly dry the foot and use lotion to moisturize the area following treatment. This is wise because a wet foot can promote bacterial growth, and dry skin can crack and eventually ulcerate.4 The physical therapist may or may not be involved in the treatment of diabetic foot ulcers, as this is commonly addressed by podiatrists. However, with proper education and self-management, patients may never need to be treated for ulcers.
Clinical implications for physical therapy: Use of modalities
 In patients with diabetes who are using insulin injections, the physical therapist must be aware of the effects that modalities can have upon the absorption of insulin. Studies have demonstrated that heat can accelerate absorption due to increased vasodilation and circulation.1 Therefore, therapists should avoid the use of heating agents such as hot packs, ultrasound, and paraffin over areas recently injected with insulin.1
 The effects of cold agents and massage on insulin absorption have not been adequately investigated. Logic would suggest that massage would also hasten absorption due to increased circulation and that ice would slow the absorption due to vasoconstruction.1 Therefore, it may be safest to also avoid the application of these modalities to recently injected sites.1
Clinical implications for physical therapy: Responses to exercise
 While the exercise management of diabetes will be directed by physicians, physical therapists commonly use therapeutic exercise as a component of treatment. For this reason, therapists should be familiar with the potential effects that exercise can have upon patients with diabetes.
Cardiovascular differences
 Many studies have indicated that exercise poses greater cardiovascular demands on people with diabetes than on those without it. This may be due largely to the decreased efficiency of oxygen delivery discussed earlier.6 With submaximal levels of exercise, individuals with diabetes have been found to have higher heart rates and lower maximal heart rates than non-diabetic controls of the same age.6 In addition, caution should be taken when exercising individuals with retinopathy at high intensities because hypertension could result in hemmorage of the eye vessels.6
Effects of exercise on insulin and glucose levels
 In non-diabetic people, serum insulin levels fall during exercise, allowing the liver to provide increased glucose to the working muscles.1,6 Blood glucose levels also fall, as glucose is drawn to peripheral tissues for energy.6 In addition, exercise increases delivery of glucose and insulin to muscle due to increased blood flow and mechanical contraction.1 Blood glucose also decreases with exercise but to a greater extent in people with controlled diabetes.6 However, in individuals with uncontrolled diabetes, blood glucose levels tend to rise with exercise.6 This could result in ketoacidosis (increased blood acidity) and severe dehydration, which could be harmful if not fatal.6 Serum insulin levels could increase during exercise in some diabetics. Glucose production by the liver is then inhibited, and hypoglycemia could result.6 For this reason, it is important for people with diabetes to have access to dietary sources of glucose during exercise.
 The effects of exercise will vary according to the type of diabetes; type of insulin delivery; the coordination of insulin, exercise, and meals; fitness level; and nature of the exercise.1,6 Exercise can be effectively performed if it follows a consistent pattern in relation to carbohydrate and insulin intake.1,6 In addition, exercise training in patients with IDDM and NIDDM seems to improve the body's sensitivity to insulin, thus decreasing the need for external sources of insulin.1 In general, exercise if beneficial to people with diabetes but should be avoided in individuals with uncontrolled diabetes.
 Another consideration regarding exercise is that of its effects on insulin absorption. Exercising an area that has recently been injected with insulin increased absorption and thus increased serum insulin levels.1,6,8 Bicycling, for example, should therefore not be performed after having injected the thigh with insulin.1 Patients should be encouraged to select injection sites, such as the abdomen, that are not the focus of the exercise activity.6
Muscular differences
 Alterations in muscle secondary to diabetes have the potential to affect exercise performance. Levels of glycogen, the body's anerobic energy source, appear to be diminished in the muscles of people with diabetes when compared to non-diabetics.6 Another difference is that skeletal muscle fibers seem to be larger in individuals with diabetes; however, the blood supply to these fibers is less. This can result in a decreased aerobic capacity in patients with diabetes.
Fatigue during anerobic versus aerobic exercise
 Although not thoroughly researched, one may expect some individuals with diabetes to have different fatigue rates during exercise than non-diabetics. This is a reasonable hypothesis considering the inhibitive effects of insulin on hepatic glucose production, reduced oxygen transport efficiency, and greater cardiovascular demands seen in diabetes. Physical therapists should consider this possibility when treating patients with diabetes since it can affect a patient's performance in and tolerance of therapeutic exercise.8
 One study examined the differences in fatigue rates between individuals with IDDM (n=8) and non-diabetics (n=8) during anaerobic and aerobic exercise.8 In two trials, subjects pedaled on an ergometer at 90% of their VO2max and at 60% of their VO2max until fatigue. Vital signs and time until the point of fatigue were recorded. Although not statistically significant, the mean time to fatigue during anaerobic (90% VO2max) exercise was 18% longer in the diabetic group, while the mean time during aerobic (60% VO2max) exercise was 26% longer in the non-diabetic group. This suggests that patients with diabetes may better tolerate anaerobic exercise since oxidative energy processes are less active during anaerobic activity.8 It is possible that people with diabetes must compensate for inefficient oxygen delivery by developing greater anaerobic capacities.8 However, further research is necessary considering the small sample sizes and the contradictory evidence that individuals with diabetes have lower levels of glycogen in muscle. Until then, it may serve physical therapists to recognize that patients with diabetes may fatigue sooner with aerobic activity than non-diabetics.
Conclusion
 Diabetes Mellitus is a common disorder of chronic hyperglycemia seen especially often in the elderly population. Due to its widespread effects on many systems and tissues of the human body, diabetes can result in serious medical complications, including stroke and peripheral vascular disease. Physical therapists are likely to treat patients for diabetes-related complications or will encounter patients who have diabetes. Therapists may also have a role in preventing complications secondary to diabetes. Understanding the effects of diabetes upon the cardiovascular, musculoskeletal, and metabolic systems will allow physical therapists to better design safe and effective treatment plans for their patients with diabetes.

References
  1. Betts EF, Betts JJ, Betts CJ. Pharmacological management of hyperglycemia in diabetes mellitus: Implications for physical therapy. Physical Therapy. 1995; 75(5): 415-425.
  2. Funnell MM, Merritt JH. The challenges of diabetes and older adults. Nursing Clinics of North America. 1993; 28(1): 45-60.
  3. Departments of Labor, Health and Human Services, Edication. Approp. for 1993 (Part 3). Hearing. Washington, DC: United States House Committee on Appropriations, 1992. 958.
  4. Frantz S, Lawton R, Schmagel C, Zimmerman C. The physical therapist's role in the treatment of diabetes. Clinical Management in Physical Therapy. 1987; 7(1): 30-31.
  5. Fain JA. National trends in diabetes: Anepidemiologic perspective. Nursing Clinics of North America. 1993; 28(1): 1-7.
  6. Jette DU. Physiological effects of exercise in the diabetic. Physical Therapy. 1984; 64(3): 339-342.
  7. Haas LB. Chronic complications of diabetes mellitus. Nursing Clinics of North America. 1993; 28(1): 71-85.
  8. Wolfe PI, DiCarlo S. Fatigue rate during anaerobic and aerobic exercise in insulin-dependent diabetics and nondiabetics. Physical Therapy. 1983; 63(4): 500-504.