{"title":"糖尿病运动员的护理","authors":"Vanessa A. Curtis, A. Peterson","doi":"10.1249/fit.0000000000000215","DOIUrl":null,"url":null,"abstract":"Patients with type 1 diabetes mellitus (T1DM) should be encouraged to live full and healthy lives. For many patients with T1DM, this includes sports participation. This review provides an overview of T1DM and its treatment with emphasis on challenges that are encountered frequently by the athlete and his or her health care providers. Glucose homeostasis requires a dynamic balance that includes mechanisms to raise and lower blood glucose. Normally, beta cells in the pancreas respond to dietary carbohydrate intake and release insulin to maintain blood glucose within a narrow target for optimal health. Insulin allows blood glucose to be used for energy or stored for future use. Later, when the blood glucose begins to fall, the pancreas quickly halts insulin release. In an exercising or fasted state, when cells need more energy than is available, the body releases counterregulatory hormones (glucagon, epinephrine, norepinephrine, cortisol, and growth hormone) to help mobilize glucose that has been stored and promote energy release from fat stores. In addition, working skeletal muscle expresses transporters that allow it to take in glucose from the blood without the help of insulin. This is very important for glucose homeostasis in athletes. T1DM is caused by the autoimmune destruction of the pancreatic beta cells. The condition has a prevalence of approximately 1 in 500 Americans less than 20 years of age, with the highest prevalence in non-Hispanic whites (1). This results in an insulin deficiency that prevents the blood glucose from entering cells and providing energy, which, in turn, leads to increases in blood glucose (hyperglycemia) while depriving the cell of its main energy source. The body responds to the lack of available energy by mobilizing energy stored as fat. The unchecked breakdown of the body's fat stores (fatty acid oxidation) results in weight loss and the production of ketones as a byproduct. Ketones do provide an energy substrate but also are strongly anionic and can lead to dangerous acidosis (ketoacidosis). Patients with T1DM are dependent on injections or infusions of exogenous insulin. For many years, the two available forms of insulin were short-acting regular insulin and intermediateacting neutral protamine Hagedorn (NPH) insulin. These insulins are given at set doses and times, typically in three daily injections. With this plan, the patient must eat a constant amount of carbohydrates at prescribed times to maintain euglycemia. Although effective and relatively inexpensive, the regular/NPH regimen requires adherence to a rigid lifestyle. 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Normally, beta cells in the pancreas respond to dietary carbohydrate intake and release insulin to maintain blood glucose within a narrow target for optimal health. Insulin allows blood glucose to be used for energy or stored for future use. Later, when the blood glucose begins to fall, the pancreas quickly halts insulin release. In an exercising or fasted state, when cells need more energy than is available, the body releases counterregulatory hormones (glucagon, epinephrine, norepinephrine, cortisol, and growth hormone) to help mobilize glucose that has been stored and promote energy release from fat stores. In addition, working skeletal muscle expresses transporters that allow it to take in glucose from the blood without the help of insulin. This is very important for glucose homeostasis in athletes. T1DM is caused by the autoimmune destruction of the pancreatic beta cells. The condition has a prevalence of approximately 1 in 500 Americans less than 20 years of age, with the highest prevalence in non-Hispanic whites (1). This results in an insulin deficiency that prevents the blood glucose from entering cells and providing energy, which, in turn, leads to increases in blood glucose (hyperglycemia) while depriving the cell of its main energy source. The body responds to the lack of available energy by mobilizing energy stored as fat. The unchecked breakdown of the body's fat stores (fatty acid oxidation) results in weight loss and the production of ketones as a byproduct. Ketones do provide an energy substrate but also are strongly anionic and can lead to dangerous acidosis (ketoacidosis). Patients with T1DM are dependent on injections or infusions of exogenous insulin. For many years, the two available forms of insulin were short-acting regular insulin and intermediateacting neutral protamine Hagedorn (NPH) insulin. These insulins are given at set doses and times, typically in three daily injections. With this plan, the patient must eat a constant amount of carbohydrates at prescribed times to maintain euglycemia. Although effective and relatively inexpensive, the regular/NPH regimen requires adherence to a rigid lifestyle. 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Patients with type 1 diabetes mellitus (T1DM) should be encouraged to live full and healthy lives. For many patients with T1DM, this includes sports participation. This review provides an overview of T1DM and its treatment with emphasis on challenges that are encountered frequently by the athlete and his or her health care providers. Glucose homeostasis requires a dynamic balance that includes mechanisms to raise and lower blood glucose. Normally, beta cells in the pancreas respond to dietary carbohydrate intake and release insulin to maintain blood glucose within a narrow target for optimal health. Insulin allows blood glucose to be used for energy or stored for future use. Later, when the blood glucose begins to fall, the pancreas quickly halts insulin release. In an exercising or fasted state, when cells need more energy than is available, the body releases counterregulatory hormones (glucagon, epinephrine, norepinephrine, cortisol, and growth hormone) to help mobilize glucose that has been stored and promote energy release from fat stores. In addition, working skeletal muscle expresses transporters that allow it to take in glucose from the blood without the help of insulin. This is very important for glucose homeostasis in athletes. T1DM is caused by the autoimmune destruction of the pancreatic beta cells. The condition has a prevalence of approximately 1 in 500 Americans less than 20 years of age, with the highest prevalence in non-Hispanic whites (1). This results in an insulin deficiency that prevents the blood glucose from entering cells and providing energy, which, in turn, leads to increases in blood glucose (hyperglycemia) while depriving the cell of its main energy source. The body responds to the lack of available energy by mobilizing energy stored as fat. The unchecked breakdown of the body's fat stores (fatty acid oxidation) results in weight loss and the production of ketones as a byproduct. Ketones do provide an energy substrate but also are strongly anionic and can lead to dangerous acidosis (ketoacidosis). Patients with T1DM are dependent on injections or infusions of exogenous insulin. For many years, the two available forms of insulin were short-acting regular insulin and intermediateacting neutral protamine Hagedorn (NPH) insulin. These insulins are given at set doses and times, typically in three daily injections. With this plan, the patient must eat a constant amount of carbohydrates at prescribed times to maintain euglycemia. Although effective and relatively inexpensive, the regular/NPH regimen requires adherence to a rigid lifestyle. With the advent
期刊介绍:
ACSM''s Health & Fitness Journal®, an official publication from the American College of Sports Medicine (ACSM), is written to fulfill the information needs of fitness instructors, personal trainers, exercise leaders, program managers, and other front-line health and fitness professionals. Its mission is to promote and distribute accurate, unbiased, and authoritative information on health and fitness. The journal includes peer-reviewed features along with various topical columns to cover all aspects of exercise science and nutrition research, with components of ACSM certification workshops, current topics of interest to the fitness industry, and continuing education credit opportunities.