Important sources of energy for living organisms are carbohydrates and especially glucose, and low blood glucose can cause loss of consciousness, seizures, and death. On the other hand, chronically elevated concentrations in blood glucose can result in blindness, renal failure, cardiac and peripheral vascular diseases, and neuropathy [17]. Therefore, blood glucose concentrations should be maintained within narrow limits to prevent complications. During fasting, the physiological blood concentrations of glucose are maintained by the liver. In the postprandial state, the rise in blood glucose concentration stimulates insulin secretion, which reduces hepatic glucose production and increases membrane glucose transporters (GLUT) in peripheral tissues, thus reducing blood glucose [11, 13, 24, 26].
During exercise, and compared to the basal status, recruited skeletal muscles require four- to fivefold more energy for contraction, using blood glucose, muscle glycogen, and fatty acids derived from adipose tissue as metabolic fuel [37]. Muscle glycogen serves as the main fuel source during strenuous and short-term exercise in healthy subjects. When the duration of exercise is prolonged, muscle energy is predominantly derived from blood-born glucose and from fatty acids produced in the adipose tissue [37, 49, 52]. Enhanced plasma levels of adrenalin, glucagon, cortisol, and growth hormone promote both an increased glucose production and a mobilization of fatty acid from adipose tissue [37, 49, 52]. In addition, gluconeogenesis maintains glucose homeostasis by synthesizing glucose from substrates like pyruvate. These changes may increase fuel supply to the skeletal muscle contraction during exercise and prevent hypoglycemia as a result of excessive utilization of glucose by the contracting muscles.
Physical exercise is a recommended treatment for patients with type II DM because it enhances the GLUT4 expression in trained skeletal muscle with a consequent increase in the glucose transport capacity [48]. This mechanism may explain the enhanced sensitivity to insulin observed in physically active DM patients [11, 13, 16, 22, 24, 26]. Increased mass in skeletal muscle, enhanced blood flow in muscle, greater density of insulin receptors, enhanced disposal of glucose in skeletal muscle, and a reduction in body fat could also contribute to this insulin sensitivity and improved glucose tolerance induced by physical training in DM patients [25, 49].
As mentioned above, the aim of exercise in type II diabetic patients is to induce acute and chronic physiological changes, which improve insulin sensitivity and glucose tolerance [11, 13, 22, 23, 24, 26]. To maintain glucose homeostasis, glucagon and adrenalin are released during acute exercise, which increases hepatic glucose production; simultaneously, the insulin secretion by pancreatic β cells is reduced [37, 40, 52]. Thus, an increase in glucose utilization during acute exercise is accompanied by an increase in hepatic glucose production, an improved insulin sensitivity enhancing the binding of insulin to sarcolemmal receptors, and an increased GLUT4 expression [15]. From a chronic perspective, the improvement in insulin sensitivity is positively correlated with the intensity of aerobic endurance training, which is in accordance with the fact that insulin resistance in type II diabetic patients is associated with diminished physical fitness [15]. Regular exercise, combined with dietary control training, leads to changes in body composition, namely, a reduction in body fat and an increase in muscle mass [9, 15]. This association of dietary control with physical training seems to improve the glycemic control better than exercise alone [9, 15], and this assumption offers an explanation to why obese subjects with type II DM, when compared to non-obese patients, show no beneficial effects in insulin sensitivity from training alone [36].
When patients with type II DM participate in physical training programs, metabolic control is improved, as evidenced for example by a decrease in serum triglyceride (TG) and very low density lipoprotein (VLDL) cholesterol and an increase in high density lipoprotein cholesterol at rest [2]. However, some studies have found that middle-aged subjects (age 40–54 years) who exercise regularly have a better response in metabolic control when compared to older subjects (age 57–61 years), perhaps due to different pretraining levels of metabolic control or to differences in the intensity of the training program or magnitude of chronic complications with advanced age [48].
Precautions before starting a training program
Before starting an exercise program, patients should submit to a medical examination. Because these patients have an increased risk of coronary artery disease and silent cardiac ischemia, the examination should screen the presence of macro- and microvascular complications that may be worsened during acute exercise [2, 17, 19, 34, 40, 48]. In general, physical exercise could be safely performed by patients with good glycemic control and without any manifested chronic complications [8]. However, before starting any training program, a laboratory-graded exercise test is recommended for all diabetic patients over 35 years [7, 8] and must be performed in high-risk cardiovascular patients based on one of the following criteria [5, 7]: (1) age ≥35 years or age ≥25 years with a history of type II DM diagnosed more than 10 years earlier, (2) presence of any additional risk factors for coronary artery disease, (3) presence of microvascular diseases (retinopathy, nephropathy, microalbuminuria), peripheral vascular disease, or autonomic neuropathy.
Moreover, this test is used to define exercise intensity, duration, and frequency as well as other modalities of the training program.
The monitoring of blood glucose concentration before, during, and after any acute exercise is considered a necessary procedure to prevent unpleasant situations (Table 4). Blood glucose ranging from 150–249 mg/dl is considered a safe amount for practicing exercise [7, 28]. If these levels exceed 250 mg/dl, exercise is contraindicated. Immediately after exercise, patients should monitor blood glucose to prevent low concentrations (lower than 70 mg/dl). In fact, one of the most common causes of low blood glucose is the exaggerated practice of physical activity. To prevent low blood glucose or even hypoglycemia, diabetic patients should avoid hot environments, like saunas or steam rooms immediately after exercise, as these favor the maintenance of an increased metabolic rate and may be responsible for lower blood glucose. Patients should also avoid the consumption of alcohol before or immediately after exercise, as well as exercising at the peak of insulin action [12]. Although exercise-induced hypoglycemia is a less common problem in type II DM than in type I DM, the risk is increased in patients who are using insulin [15]. Changes in dosage or in the timing of insulin administration, as well as modifications, in meal habits are usually efficient procedures to correct the problem.
Table 4 Summary of preexercise blood glucose values (adapted from Leutholtz and Ripoll [28])
A standard recommendation of the American Diabetes Association and the American College of Sports Medicine for diabetic patients includes a warm up and a cool down period that should consist of 5–10 min of aerobic activity at low intensity, as well as a stretching period [7]. The aim of the warm up session is to prepare skeletal muscle and the cardiovascular and respiratory systems for a progressive increase in exercise intensity, and the cool down period allows a gradual adjustment to baseline of heart rate and blood pressure [7]. Stretching should be performed for 5–10 min, especially in muscles used during the training session. It is important for DM patients to prevent foot blisters by use of adequate socks and appropriate shoes; any potential damage to their feet must be monitored before and after any exercise session. Because dehydration can affect blood glucose levels and cardiovascular function, it is recommended to ingest 500 ml of fluid until 2 h before starting the exercise. During exercise, the fluid ingestion should compensate all losses taking place by sweat and ventilation, to avoid a loss of bodyweight at the end of acute exercise [7].