D.M.1 FEBBRAIO 1986 PDF

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M anagement of patients with type 1 diabetes T1D during and after exercise continues to be a challenge for care providers and patients alike in terms of approach both to insulin therapy and to hypoglycemia prevention and rescue. These issues pose significant limitations from the providers' standpoint of hypoglycemia prevention and from the patients' standpoint of seeking to achieve desirable level of fitness to improve general metabolic and cardiovascular health.

The purpose of this editorial therefore is 1 to summarize available knowledge of carbohydrate physiology during and after exercise in healthy and T1D individuals, 2 to elucidate possible physiological mechanisms predisposing to hypoglycemia, 3 to describe current approaches to prevent and manage exercise-induced hypoglycemia in T1D, and 4 to identify knowledge gaps in our understanding of exercise physiology in T1D that require further study.

Blood glucose concentration at any given time point is a reflection of the net balance between the rates of glucose appearance R a into and disappearance R d from the circulation. It is well established that exercise increases muscle glucose uptake through insulin-dependent and insulin-independent mechanisms and that EGP must increase to meet the increased metabolic demands of the exercising muscle to prevent hypoglycemia. Skeletal muscle glucose uptake increases dramatically in response to exercise together with a drop in plasma insulin concentrations in healthy individuals to overnight fasted levels.

Exercise also increases the energetic demands of skeletal muscle, resulting in increased glycolytic flux and demand for glucose as an energy substrate. Endogenous glucose production increases, making blood glucose more available as a result of elevations in circulating glucagon and catecholamine concentrations. Finally, increased skeletal muscle blood flow as a result of elevations in cardiac output and increased capillary blood flow together with local vasodilation increase glucose delivery to active tissues.

The rise in EGP during exercise was observed to be due to increases in both gluconeogenesis and glycogenolysis in a series of elegant experiments in intact and pancreatectomized dogs. When these data are taken together, the falling glucose concentrations during exercise was due to the fact that the combined effect of meal glucose appearance and EGP R a was unable to keep pace with exercise-induced changes in whole-body glucose uptake R d.

There have also been prior publications that have reported on the effect s of exercise of varying intensity on glucose physiology. These have included ground-breaking work by exercise physiologists using isotope dilution techniques and glucose clamps. In healthy adults, Friedlander et al. Furthermore, the increased efficiency of R d was related to up-regulation of muscle glycogen synthesis secondary to increased stimulation of glucose transport across the skeletal muscle cell membrane.

Interesting gender differences in glucose kinetics and hormonal responses during exercise have also been observed, 16 , 18 with women shifting substrate oxidation from carbohydrates to lipids and showing lesser rises in post-exercise glucagon and epinephrine concentrations than men at submaximal workloads common to endurance levels and daily activity. Likewise, during endurance exercise and exercise training, women utilize lipids more than carbohydrates when compared at the same relative exercise intensity with equally trained men.

In contrast, the effect size of menstrual cycle on exercise-related substrate metabolism is modest at best. In an early study, the effects of menstrual phases on glucose turnover during moderate- and high-intensity exercise were negligible in healthy young women. Insulin sensitivity, in the purist term, is defined as the ability of insulin to stimulate uptake of glucose by target tissues viz. Hence, by definition, an increase in insulin sensitivity implies a shift of the dose—response curve of insulin to the left such that a lower concentration of insulin results in an equivalent amount of glucose uptake by the target tissue s.

Although some studies had suggested that insulin was indeed required and had a permissive effect on muscle glucose uptake during and after exercise, 25 , 26 others demonstrated similar findings on glucose uptake in the muscle both during and after exercise even in the absence of insulin. Mechanical factors that modulate muscle glucose uptake include, among others, tissue permeability to glucose and changes in blood flow to exercising muscles.

In an elegant and pioneering series of experiments in isolated frog muscle, Hollozsy and Narahara 27 demonstrated that both muscle contractions and insulin separately stimulated muscle glucose uptake, presumably through a common transport pathway.

However, further mechanistic studies in isolated rat skeletal muscle revealed that effects of insulin and muscle contractions on glucose uptake were additive but caused glucose transporter type 4 GLUT4 translocation via independent pathways in contracting skeletal muscle. A single endurance exercise bout increased insulin action on skeletal muscle 36 , 37 predominately because of an increase in GLUT4 protein content. Muscle blood flow, a factor beside blood glucose concentration that determines delivery to skeletal muscle, markedly increases during exercise.

Strategies to prevent exercise-induced hypoglycemia could prolong exercise ability and delay exhaustion. In a series of experiments, various investigators 49 , 50 demonstrated that carbohydrate feeding and water ingestion during prolonged exercise delay fatigue and increase neuromuscular power, at least in part by preventing hypoglycemia, by avoiding muscle glycogen depletion. A similar effect of carbohydrate ingestion on cycling time trial performance was also reported.

In contrast, recently, Fahey et al. In the free-living condition, humans frequently participate in sports activities e. Systematic assessments and comparisons of glucose turnover and insulin sensitivity during intermittent versus sustained exercise have been sparse in people with and without diabetes.

Early investigations 54 did not demonstrate differences between sustained and intermittent exercise on intramuscular glycogen content and lactate accumulation, but subsequent studies by the same investigators 55 suggested lower rates of glycolysis with intermittent compared with sustained exercise in healthy adults.

In an intriguing study, 56 , 57 fat oxidation was threefold lower and carbohydrate oxidation was 1. A recent study 58 in type 2 diabetes subjects revealed improved insulin sensitivity, as measured by the homeostasis model of insulin resistance, during intermittent exercise performed with mild hypoxia.

Unfortunately, this study did not compare intermittent versus sustained exercise at normoxia. Although it has been suggested 63 that there is sufficient evidence to recommend PA in the management of T1D, the duration, intensity, and form of exercise that should be recommended and whether such interventions would translate to better outcomes are presently unclear. A recent meta-analysis 64 suggests benefits of regular aerobic training, interspersed with brief bouts of sprinting, on glycated hemoglobin concentrations and incidence of delayed hypoglycemia in T1D.

Systematic examinations of carbohydrate physiology and substrate metabolism during exercise are sparse in T1D. Increased risk of hypoglycemia during exercise in T1D individuals could be due to factors that either lower rates of EGP or increase rates of glucose uptake or a combination of both.

In contrast, in a study comparing individuals with and without T1D during moderate- and high-intensity exercise, Petersen et al. However, to further complicate matters, defective activation of skeletal muscle and adipose tissue lipolysis during hypoglycemia in T1D subjects, as a result of insufficient catecholamine response, 68 could potentially further prolong the duration and severity of exercise-induced hypoglycemia in these individuals.

Apart from applying common-sense tactics to prevent hypoglycemia during and after exercise, there have been few reports that have systematically examined therapeutic approaches to mitigate hypoglycemia during and after PA in T1D. An observational field study 60 demonstrated the efficacy of real-time continuous glucose monitoring and carbohydrate loading in preventing post-exercise hypoglycemia in adolescents with T1D. Recently, short-term studies incorporating PA have shown improvements in glucose control in T1D patients.

These studies have compared multiple daily insulin injections with open-loop continuous subcutaneous insulin infusion, 69 open-loop continuous subcutaneous insulin infusion with single-hormone insulin closed-loop control, 70 and open-loop continuous subcutaneous insulin infusion with single-hormone modular closed-loop control. The recommendation of daily PA by the American Diabetes Association refers to all patients with diabetes. Specific PA recommendations for T1D are not available simply because of lack of good evidence of the effect of PA on glucose control or outcomes.

In an intriguing study 74 conducted in healthy sedentary men, reductions in daily step count from approximately 10, steps to approximately 2, steps led to reductions in fat free mass with lowering of insulin sensitivity measured before and after a 2-week period.

A recent review 75 has identified exercise as a major obstacle in current closed-loop control efforts. Even if exercise is announced during closed-loop therapy, maintenance of optimal glucose control during and after exercise may be challenging despite dual-hormone systems without a flexible and learning program of concomitant carbohydrate ingestion.

As elucidated above, even healthy trained and untrained individuals without diabetes need to resort to periodic carbohydrate ingestion during and after exercise to prevent exhaustion, fatigue, and symptomatic hypoglycemia and to improve performance, especially during prolonged, unusual, or intense physical activity or sports. Hence, it would be impractical and unnatural to expect to rely solely on closed-loop control with dual-hormone insulin and glucagon systems to prevent hypoglycemia without exogenous simple carbohydrate ingestion.

Furthermore, the considerable intra- and interindividual variability of insulin sensitivity in T1D individuals, even in the absence of exercise under carefully controlled experimental conditions , as we have recently demonstrated, 76 is expected to be far greater during exercise , posing additional challenges to a generic closed-loop control algorithm.

Physiological effects of exercise on glucose metabolism have been extensively studied in healthy humans, over the last several decades. However, detailed and systematic investigations into exercise effects on glucose homeostasis and resultant hypoglycemia, pertaining especially to T1D, are scarce.

Studies exploring the effects of exercise of varying intensities and duration on counter-regulatory hormonal responses, substrate carbohydrate and fat predominantly metabolism, muscle and hepatic glucose, glycogen, and lipid kinetics, lactate threshold, etc. The roles of short- and long-term glycemic control, duration of diabetes, and accompanying comorbidities and complications of diabetes on exercise physiology in T1D are also unknown.

Such large and critical knowledge gaps need to be filled so that patients and their physicians are better informed to provide logical, evidence-based therapeutic options so that this patient population becomes fitter through regular exercise and training while simultaneously minimizing the constant and sometimes disabling fear of hypoglycemia that prevents these individuals from leading healthier and fitter lives.

Such an understanding of physiological effects of exercise could also inform next-generation closed-loop control algorithms currently being designed for the artificial endocrine pancreas to treat T1D. There are no competing financial interests to declare for any of the authors. National Center for Biotechnology Information , U. Diabetes Technol Ther. Johnson , PhD, Yogish C. Author information Copyright and License information Disclaimer. Corresponding author.

Copyright , Mary Ann Liebert, Inc. This article has been cited by other articles in PMC. Physical Activity, Glucose Physiology, and Hypoglycemia Blood glucose concentration at any given time point is a reflection of the net balance between the rates of glucose appearance R a into and disappearance R d from the circulation.

Effects of Exercise in Healthy Individuals. Open in a separate window. Intermittent Exercise and Glucose Physiology In the free-living condition, humans frequently participate in sports activities e. PA in T1D: Management Strategies Apart from applying common-sense tactics to prevent hypoglycemia during and after exercise, there have been few reports that have systematically examined therapeutic approaches to mitigate hypoglycemia during and after PA in T1D.

Closed-Loop Strategies for Exercise A recent review 75 has identified exercise as a major obstacle in current closed-loop control efforts. Summary and Conclusions Physiological effects of exercise on glucose metabolism have been extensively studied in healthy humans, over the last several decades.

Acknowledgments R. Author Disclosure Statement There are no competing financial interests to declare for any of the authors. References 1. Felig P, Wahren J: Fuel homeostasis in exercise.

Andersen P, Saltin B: Maximal perfusion of skeletal muscle in man. Dissociation of signaling pathways for insulin- and contraction-activated hexose transport. Diabetes ; 41 — [ PubMed ] [ Google Scholar ]. J Clin Endocrinol Metab ; 90 — Erratum in J Clin Endocrinol Metab ; Changes in permeability to 3-methylglucose associated with contraction of isolated frog muscle. Wallberg-Henriksson H, Holloszy JO: Activation of glucose transport in diabetic muscle: responses to contraction and insulin.

Diabetes ; 39 — [ PubMed ] [ Google Scholar ]. Diabetes ; 52 — [ PubMed ] [ Google Scholar ]. Essen B, Hagenfeldt L, Kaijser L: Utilization of blood-borne and intramuscular substrates during continuous and intermittent exercise in man.

Essen B, Kaijser L: Regulation of glycolysis in intermittent exercise in man. Christmass MA, Dawson B, Arthur PG: Effect of work and recovery duration on skeletal muscle oxygenation and fuel use during sustained intermittent exercise. Riddell MC, Milliken J: Preventing exercise-induced hypoglycemia in type 1 diabetes using real-time continuous glucose monitoring and a new carbohydrate intake algorithm: an observational field study.

A literature review. Diabetologia ; 55 — [ PubMed ] [ Google Scholar ]. Standards of medical care in diabetes— A 13 C nuclear magnetic resonance spectroscopy study.

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FERRAR FENTON PDF

Skeletal muscle as a therapeutic target for delaying type 1 diabetic complications.

M anagement of patients with type 1 diabetes T1D during and after exercise continues to be a challenge for care providers and patients alike in terms of approach both to insulin therapy and to hypoglycemia prevention and rescue. These issues pose significant limitations from the providers' standpoint of hypoglycemia prevention and from the patients' standpoint of seeking to achieve desirable level of fitness to improve general metabolic and cardiovascular health. The purpose of this editorial therefore is 1 to summarize available knowledge of carbohydrate physiology during and after exercise in healthy and T1D individuals, 2 to elucidate possible physiological mechanisms predisposing to hypoglycemia, 3 to describe current approaches to prevent and manage exercise-induced hypoglycemia in T1D, and 4 to identify knowledge gaps in our understanding of exercise physiology in T1D that require further study. Blood glucose concentration at any given time point is a reflection of the net balance between the rates of glucose appearance R a into and disappearance R d from the circulation. It is well established that exercise increases muscle glucose uptake through insulin-dependent and insulin-independent mechanisms and that EGP must increase to meet the increased metabolic demands of the exercising muscle to prevent hypoglycemia. Skeletal muscle glucose uptake increases dramatically in response to exercise together with a drop in plasma insulin concentrations in healthy individuals to overnight fasted levels.

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