Rudy Bilous, MD, FRCP
Richard Donnelly, MD, PHD, FRCP, FRACP
Regular physical exercise is an important component of the management and prevention of type 2 diabetes (Figure 26.1). Aerobic exercise, in particular, and resistance exercise improve insulin sensitivity and glycemic control. Blood glucose and lipid profiles improve, as well as insulin sensitivity, but in type 2 diabetes, exercise does not usually cause hypoglycemia and extra carbohydrate is unnecessary. Regular exercise accelerates weight loss, but it should be combined with an appropriate diet and tailored to the individual patient’s capabilities. Moderate exercise in the form of walking (e.g. 30–60 minutes per day) is often the most practical recommendation. Subjects with type 2 diabetes and moderate or high fitness have a long-term mortality that is 50%–60% lower than individuals with diabetes and low cardiorespiratory fitness.
Supervised, progressive resistance exercise training may be of greater benefit in Asian patients with type 2 diabetes. For example, a typical protocol supervised by physiotherapists three times per week might include a range of movements, e.g. biceps and hip flexion, shoulder flexion, finger grip, knee extension and heel rise, and be gradually increased over time (Figure 26.2). Exercise of any type increases glucose transporter levels (GLUT-4) in the cell membrane of skeletal muscle, and resistance training seems to increase fat-free mass. There may be added benefits for patients who adopt a program of exercise that combines aerobic activity with resistance training.
In type 1 diabetes, short-term glycemic changes during exercise depend largely on circulating insulin levels, which in turn depend on the type of insulin used and the interval between insulin injection and exercise. For example, hyperinsulinemia that occurs when exercise is taken shortly after the injection of short-acting insulin (and particularly when the site of insulin injection is an exercising limb) causes blood glucose levels to fall. Other factors that determine the effects of exercise are the intensity of the exercise and the intake of food (Box 26.1).
Most studies have not found that exercise improves the long-term glycemic control in patients with type 1 diabetes, perhaps because patients tend to consume extra carbohydrate to prevent hypoglycemia. However, as with type 2 diabetes, patients with type 1 diabetes who exercise regularly have lower long-term morbidity and mortality compared with their sedentary counterparts, so regular exercise carries benefits that may not be reflected in short-term markers of glycemic control (Figure 26.3).
Patients with type 1 diabetes can reduce the risk of hypoglycemia during exercise by following specific guidelines, which include close blood glucose monitoring, extra carbohydrate taken before and hourly during exercise, avoiding exercising muscle territories used for injection (such as the legs) and reducing the pre-exercise insulin dose by 30%–50% if necessary (Box 26.2).
Numerous drugs can affect diabetic control and cause hyper- or hypoglycemia by interfering with insulin secretion or action, or both, or by interacting with antidiabetic agents (Table 26.1). Hyperglycemia can be caused or worsened by many drugs. Corticosteroids, which are widely prescribed for numerous medical conditions, have an especially potent diabetogenic effect and act by inducing insulin resistance. Dosages equivalent to 30 mg/day of prednisolone are especially likely to raise blood glucose in diabetic patients, and may cause glucose intolerance or overt diabetes in previously normoglycemic individuals. Oral contraceptives rarely worsen diabetic control; the risks of hyperglycemia are highest with the now obsolete high-dose oestrogen pills, combined pills that contain the progestogen levonorgestrel and in women with a history of gestational diabetes. High-dose thiazide diuretics (e.g. 5 mg/day of bendroflumethiazide) cause insulin resistance and impair insulin secretion, whereas lower dosages (2.5 mg/day bendroflumethiazide), which are still effective in controlling blood pressure, do not. Diabetogenic drugs that damage the 13 cell include pentamidine (an antiprotozoal agent) and cyclosporin.
Several drugs can cause or exacerbate hypoglycemia (Box 26.3). Important examples are alcohol, sulphamethoxazole (combined with trimethoprim in co-trimoxazole), quinine, aspirin and paracetamol (acetaminophen) in over-dosage, and the numerous drugs that enhance the action of sulphonylureas (e.g. probenecid, sulphonamides, monoamine oxidase inhibitors, chloramphenicol, fluconazole).
(See also Diabetes In Control’s complete list of Drugs That Can Affect Blood Glucose Levels.)
Diabetes is associated with a wide range of infections (Box 26.4), which are more frequent than in the general population (e.g. urinary tract infections, UTI), occur almost exclusively in subjects with diabetes (e.g. malignant otitis externa) or run a different or more aggressive course in the host with diabetes (e.g. respiratory tract infections). The multiple defects in immunity in diabetes may explain the susceptibilty to infection, including impaired polymorphonuclear leukocyte function. Other contributory causes in some patients include frequent hospitalization, delayed wound healing and chronic renal failure. Common infections include UTI, respiratory tract infections and soft tissue infections.
About 25% of women with diabetes have asymptomatic bacteriuria (this is four times more common than in the population without diabetes). Escherichia coli is the most common pathogen. UTI may be asymptomatic or present with dysuria, frequency or urgency (lower UTI), or flank pain, fever and vomiting (upper UTI). Perinephric abscess and papillary necrosis are rare complications (Figure 26.4).
With respiratory tract infections in diabetes, bacteraemia, delayed resolution and recurrence are more common than in the general population, though the overall frequency is probably no greater. Respiratory infection caused by certain microorganisms, including Staphylococcus aureus, gram-negative bacteria, Mycobacterium tuberculosis and Mucor, is more common in diabetes. Respiratory infection with Streptococcus, Legionella and influenza virus is associated with more morbidity and mortality in diabetes. Cough and fever are the usual presenting complaints, although ketoacidosis can be the first manifestation. Deep soft tissue infections with bacteria (e.g. pyomyositis, a muscle abscess that occurs after trauma and haematoma and is caused by Staph. aureus) and fungi (e.g. cutaneous mucormycosis) are more common in diabetes.