Parenting

Optimal Metabolic Control

Optimal Metabolic Control

The diabetic person exercising in a state of good metabolic control (adequate levels of insulin and normal blood glucose concentration), typically shows a gradual decrease in plasma glucose with prolonged exercise, which can lead eventually produce symptomatic hypoglycemia. In this situation, consumption of glucose by the muscle increases adequately, but the blood sugar levels decrease, since the absence of a decrease in exercise-induced plasma insulin inhibits hepatic glucose production (glycogenolysis, gluconeogenesis) as well as mobilizing fatty acids from fat reserves. That is, the exercise equipment works normally, but the power supply line is cut.

Several factors determine the extent of the decrease in blood glucose and risk of hypoglycemia. The fall of blood sugar precipitates if the exercise is performed at the time of peak action of insulin injected. This occurs in 2 to 4 hours after injection of insulin regular and intense exercise is more likely to cause hypoglycemia at the time. As shown in Figure 2, there is evidence that the rate of absorption of insulin is magnified, and the rate of decline of blood glucose is higher if the injection is made in the member exercise (Koivisto & Felig, 1978 .) For example, brokers may recommend that insulin be injected in the abdomen before exercise, and not in the thigh. The later is the period after the injection, the less likely that this effect occurs. The diabetic child must also know that a decreased blood glucose is exaggerated by the exercise of longer duration and greater severity (Hagan, Marks, & Warren, 1979).

Under conditions of adequate insulin, the level of blood sugar drop also depends on the initial level of glucose. Higher concentrations predispose to increased glucose decreased physical activity, an effect that can be seen as beneficial to the diabetic control (Persson & Thoren, 1980). However, even prolonged exercise can lead to hypoglycemia, with excessive fatigue, dizziness, disorientation, syncope, and seizures. In addition, some patients may produce low blood glucose levels up to 15 hours after completion of the exercise, continuing effects of glucose uptake by muscle cells that have been exercising, as they replenish their intracellular stores of glucose (MacDonald, 1987 .) Every diabetic patient needs to know your own personal response to exercise through blood glucose monitoring, since the risk of hypoglycemia with exercise can vary greatly from one person to another. Based on this information, we can develop strategies to increase carbohydrate intake and insulin dose adjustments, in order to allow full participation in sports. These tactics will be discussed later in this article.

METABOLIC EFFECTS OF ACUTE EXERCISE

METABOLIC EFFECTS OF ACUTE EXERCISE

The child with diabetes is a particular difficulty in regulating blood glucose during exercise, better understood in relation to the normal metabolic responses to physical activity in individuals without diabetes (Kemmer & Berger, 1983; Larsson, 1984; Vranic & Berger, 1979). During acute exercise series, the energy demands for more muscular contraction are met through increased oxygen delivery (increase in ventilation and cardiac output), and largest source of fuel (glucose, fatty acids). When you start the exercise, glucose derived from glycogen stored within muscle cells serves as the main source of energy. With increasing exercise intensity, this source is empty, and muscles and blood glucose seek circulating fatty acids.

With high stress loads, the energy requirements reach 10 to 20 sometimes needs rest, and this high rate of consumption of glucose in the blood quickly cause hypoglycaemia, if not for the constant replenishment of glucose by the liver. This is critical, since the maintenance of normal blood glucose levels is essential during exercise, both for normal brain function in maintaining the level of muscle energy substrates. The liver serves as a donor of glucose necessary during prolonged exercise, with its output quite similar to its use through the breakdown of liver glycogen (glycogenolysis) and the conversion of glucose formation from protein (gluconeogenesis) . A failure in hepatic glucose production during exercise, lead hipoglucermia and exhaustion.

This sequence of events is mediated a complex hormonal interplay involving decreased insulin and increased contraregulatorias hormones (catecholamines, cortisol, and glucagon). The drop in insulin levels with acute exercise increases the release of fatty acids from peripheral depots, and stimulates hepatic glycogenolysis and gluconeogenesis. Despite these low levels of insulin, it is clear a high consumption of glucose by muscle, a phenomenon perhaps explained by the increased sensitivity of muscle cells to insulin during exercise.

These metabolic events are not as well orchestrated by the diabetic patient. In these individuals, insulin levels are not determined by physiological responses to exercise, but for the moment and the amount of injected daily. Consequently, diabetic subjects experience no period of stable blood glucose levels, their levels vary according to the plasma insulin concentration, duration and intensity of exercise, site of injection, diet, and other factors.

Physical Activity and Diabetes

Physical Activity and Diabetes

It has been over half a century since insulin became available for the treatment of diabetes mellitus, and yet this disease remains a serious health problem. Significant morbidity and early mortality will happen to the majority of 5 to 10 million people with diabetes in the United States. Diabetes is considered the sixth leading cause of death in this country, which is almost certainly an underestimate, since many deaths related to cardiovascular system in these patients are categorized as no deaths due to diabetes, but with other covers (eg., congestive heart failure or attack.) Although type I diabetes (juvenile-onset or) represents the minority of cases, this chapter refers exclusively to this group as it covers virtually all young people with diabetes.
Keywords: insulin, training, health, diabetes, Type I.

TYPE I DIABETES

Type I diabetes is characterized by inadequate pancreatic insulin secretion, and the consequent need for replacement of the hormone daily via subcutaneous injections. In the absence of insulin, glucose transport into cells is impaired, causing a progressive hyperglycemia and ketoacidosis. Individuals with type II diabetes (or adult-onset) are usually older than 45 years and normally suffer from insulin resistance, rather than a quantitative failure. Typically, oral medications and weight loss are able to control hyperglycemia in type II diabetes without insulin application.

The main objective in the daily treatment of patients with type I diabetes is to maintain a state of euglycemia – preventing hyper-and hypoglycemia – balancing the influences of diet, exercise and insulin on blood glucose levels. But ultimately, morbidity and mortality of this disease are related to vascular and neurological complications usually manifest as clinical in young adulthood, and include (Figure 1):

A generalized thickening of basement membranes of capillaries (microangiopathy) that affects various organs, with greater prominence of the eye (diabetic retinopathy) and kidneys (diabetic nephropathy).
An accelerated atherosclerotic vascular disease (macroangiopathy), presented as early disease of the coronary arteries and heart attack.
Peripheral neuropathy affects sensory function, motor, and autonomous.