Medicine and sport science最新文献

Exercise in people with type 1 diabetes (T1DM) can produce large changes in blood glucose, with hypo- and hyperglycaemia before and following exercise. Different exercise types, intensity and duration have significantly different effects on blood glucose control, and on the endocrine response to exercise. Exercise performance can also be impaired in T1DM. There have been significant recent improvements in the knowledge of what underlies these changes and in the appropriate management to support the maintenance of euglycaemia. Further advances in insulin infusion pump therapy and continuous subcutaneous glucose monitoring are likely to be useful in the management of people with T1DM who want to exercise.

It is well known that obesity is a major risk factor for type 2 diabetes (T2D), while exercise is known to reduce body fatness and attenuate the risk of T2D. The aim of this chapter is to examine the interactions between exercise, obesity and body fat distribution, and the risk for T2D. Firstly, we show that body fatness, in particular visceral adipose tissue (VAT) accumulation, is associated with insulin resistance and incident T2D. We then show that aerobic exercise of sufficient intensity and volume results in a decrease in body fat and VAT. Conversely, sedentary behavior and physical inactivity are associated with increased body fat and VAT. Finally, the chapter examines the interaction between physical activity (PA), obesity and risk for T2D and shows that both obesity and PA are significant independent predictors of incident T2D, but the magnitude of risk imparted by high levels of body fat is much greater than that of low levels of PA. Further, we show that obese physically active individuals are at greater risk for incident T2D than normal-weight physically inactive individuals. The mechanisms underlying this complex interaction include the ability of exercise to increase free fatty acid oxidation to match high rates of lipolysis associated with obesity, as well as the effects of exercise on adipokine, cytokine and myokine secretion. Exercise, of sufficient volume and intensity, is therefore recommended to reduce obesity, centralization of body fat, and risk of T2D.

Skeletal muscle is the major site of insulin-stimulated glucose utilization in the body. Central to this process is oxidative metabolism, which is controlled by mitochondria. Therefore, defects in the biogenesis of this organelle can impact the ability of muscle to oxidize substrates and can have grave consequences on the action of insulin on glucose uptake. In healthy muscle, glucose and free fatty acids (FFAs) are efficiently metabolized preventing the accumulation of harmful lipid by-products. In contrast, in pre-diabetic conditions, reduced oxidative capacity, high levels of reactive oxygen species, and chronic elevations in FFAs culminate in greater intramyocellular lipids and lipid metabolites that interfere with insulin signaling pathways, and contribute to lower insulin sensitivity. While the extent of the involvement of mitochondria in insulin resistance and type 2 diabetes (T2D) is still an ongoing debate, there is compelling evidence to suggest that dysfunction in mitochondria, mediated by changes in gene expression, morphology, and mitochondrial turnover, contributes to the dysregulation of insulin signaling pathways observed with this metabolic syndrome. In the present review, we discuss our current understanding of mitochondrial biogenesis and highlight how dysfunction in key mitochondrial biogenesis pathways may play an important role in the pathogenesis of T2D. Moreover, we provide evidence supporting the therapeutic value of exercise in the prevention and treatment of metabolic syndromes such as T2D.

Type 2 diabetes mellitus is highly prevalent among the elderly. Age-associated changes in body composition, obesity and sedentary behavior are some of the main factors responsible for the increased prevalence of diabetes in this population. Elderly patients experience important and specific issues, including the association of comorbidities and geriatric syndromes, use of many medications, the presence of dependencies and frailty. Physical activity has been shown to be as effective for the treatment of diabetes in the elderly as in younger patients, so that its practice must be strongly encouraged. Resistive activities are preferable for the frail and vulnerable diabetic elderly. Aerobic activities should be prescribed whenever possible, and the association of both modalities is the best choice. Moderate- to high-intensity exercises are more effective for glycemic control and, unlike previously thought, are generally safe for the elderly population. The frequency of exercising should be at least 3 days/week for aerobic and 2 days/week for resistance activities. Balance exercises may be beneficial in special situations. In the elderly patient, special care must be taken for: the presence of contraindications for the practice of each exercise modality; the interactions and limitations imposed by medications, chronic comorbidities and geriatric syndromes; the higher possibility of developing hypoglycemia, especially if insulin is used for treatment, and the prevention of orthostatic hypotension that may be worsened by dehydration. The prescription of exercises tailored for each patient's preferences and limitations is highly effective not only for glycemic control, but also for improving independence, self-esteem and quality of life.

This chapter summarizes current knowledge regarding the interaction between lipid availability, endurance exercise, and insulin sensitivity. We discuss the role of lipid availability as a key mediator of insulin resistance in obesity, the proposed cellular mechanisms underlying this relationship, recent studies demonstrating that acute exercise protects against lipid-induced insulin resistance, how fatty acid partitioning may contribute to this protective effect of endurance exercise and finally remaining questions and future directions in the field.

In the last 50 years, sub-Saharan Africa has witnessed a significant increase in the prevalence of type 2 diabetes mellitus (T2DM), from <1% recorded in some countries in the 1960s to a regional prevalence of 4.3% in 2012 (compared with a current global prevalence of 6.4%). There is great variability in prevalence of T2DM among the African communities with some countries, such as Réunion, recording an average of 16% and others, such as Uganda registering <1% in rural communities. The greatest increase in prevalence has been registered among urban dwellers. The cause of the rapid increase in T2DM prevalence is not clear. However, studies in both rural and urban areas have found that physical activity is not an independent risk factor for the disease in the region. Physical activity level was found to be adequate in Africa, with 83.8% of men and 75.7% of women meeting the WHO recommendation of at least 150 min of moderate- to vigorous-intensity physical activity per week. The paper argues that the rapidly growing number of people >40 years old, increasing urbanization, adaptation of lifestyle behaviors that accompany urbanization and the interaction of these with a genetic predisposition to T2DM, are plausible reasons for the increasing prevalence of T2DM.

Physical activity exerts beneficial effects on glucose homeostasis that are channeled through our genes. Where variation in the target genes of physical activity exists, gene-physical activity interactions may occur, such that individual genetic profiles inflict differing physiological responses to an equal bout of physical activity. Individuals with specific genetic profiles are also expected to be more responsive to the beneficial effects of physical activity in the prevention of type 2 diabetes. Identification of such gene-physical activity interactions could give new insights into the biological mechanisms of how type 2 diabetes develops, which could open up new avenues for the development of novel treatments. It has also been postulated that knowledge of interactions could improve the prevention and treatment of type 2 diabetes by enabling targeted interventions. The present chapter will introduce the reader to the recent advances in the genetics of type 2 diabetes, summarize the current evidence on gene-physical activity interactions in relation to type 2 diabetes, and outline how information on gene-physical activity interactions might help improve the prevention and treatment of type 2 diabetes. Finally, we will discuss the existing and emerging strategies that might enhance our ability to identify and exploit gene-physical activity interactions in the etiology of type 2 diabetes.

Type 2 diabetes mellitus and its precursor, insulin resistance, are metabolic disease states characterized by impaired regulation in the delivery, transport, and/or storage of energy substrates (primarily carbohydrate- and fat-based fuels). A hallmark feature of patients with type 2 diabetes is prolonged periods of hyperglycemia due to a decreased responsiveness of metabolically active peripheral tissues to the actions of insulin (i.e., metabolic inflexibility). Accordingly, efforts to modify skeletal muscle substrate handling in type 2 diabetes patients so that the capacity for fat oxidation and metabolic flexibility is improved should be a primary goal for the treatment of these disorders. Two potent interventions for improving whole-body glucose homeostasis are exercise and diet. A single bout of either resistance or endurance exercise reduces the prevalence and duration of hyperglycemic excursions in patients with type 2 diabetes, an effect lasting well into the next day. With regard to diet, the carbohydrate content of a meal and the glycemic index (GI) of the carbohydrate consumed are both major determinants of the postprandial glycemic response. Diets containing high-GI carbohydrates have been shown to be independent risk factors for type 2 diabetes onset, while in obese insulin-resistant individuals, low-GI diets are effective for inducing both weight loss and improving insulin action and glucose tolerance. The implementation of physical activity and dietary modifications are effective low-cost treatment options for controlling hyperglycemic episodes in patients with type 2 diabetes.

There is strong evidence that increased physical activity is beneficial for blood glucose homeostasis and the prevention of obesity and type 2 diabetes mellitus. This chapter takes a life course approach with an emphasis on the intrauterine and childhood stages of life. Firstly, growth and development at critical periods with a focus on skeletal muscle and adipose tissue; then, obesity and type 2 diabetes mellitus are considered in relation to physical activity and sedentary behaviour. The importance of the development of fundamental movement skills in early childhood for both physical fitness and also growth and development is emphasised. Physical activity guidelines in westernised countries are examined for commonalities. Finally, the effective translation of the evidence base for the benefits of physical activity into randomised controlled trials and then into real-world public health services that are sustainable is addressed with a case study from New Zealand of Project Energize--a through-school physical activity and nutrition intervention. Physical activity, alongside a 'healthy diet' is arguably the best preventive measure and treatment for both obesity and type 2 diabetes. It is an essential and normal activity of daily life, and all aspects of the life course and the environment should support physical activity.