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Jean-Jacques Grimm

2.1 Introduction

Regular exercise in people with diabetes does not necessarily lead to improved control. Indeed, the metabolic disturbances associated with sustained exercise may lead to worsening control unless great care is taken to adjust carbohydrate intake and the insulin dosage.

Type 1 diabetes frequently affects children, adolescents and young adults in whom health improvement does not feature highly among the reasons for exercising. The desire to play, or to become a member of a team, is often more important, and is driven by social reasons and the need not to appear ‘different’ from the peer group. The aim of the medical team is to allow the diabetic child or adult to participate in the sport of his or her choice and to avoid any form of discrimination during school sports or when playing on a team.

This chapter deals with the way a person with type 1 diabetes could manage their condition independently and safely during various kinds of sports and recreation.

Recent literature 1-2 acknowledges that ‘all levels of exercise, including leisure activities, recreational sports, and competitive professional activities (www.steveredgrave.com/), can be performed by people with type 1 diabetes’. It must be stressed, however, that high-intensity endurance exercise (e.g. marathon, triathlon, cross-country skiing) is not required to achieve maximal health benefits from exercise.3 Regular, moderate-intensity exercise.1-4 has the best risk-benefit ratio.

The advantages of exercise in type 1 diabetes relate more to its protective cardiovascular effects than to improved glycemic control. Exercise is not a tool for improving blood glucose control in type 1 diabetes. However, the diabetes education team needs to be knowledgeable about all treatment adjustments required to enable their patients to exercise safely and with maximum health benefits; regular exercise may improve insulin sensitivity in the overweight type diabetic person and therefore render blood glucose control easier.

2.2 Exercise Physiology

As well as an increase in oxygen availability, exercise requires rapid mobilization and redistribution of metabolic fuels to ensure adequate energy supply for the working muscles (see Chapter 1). This necessitates a cascade of neural, cardio- vascular and hormonal adjustments.

Fuels metabolized by skeletal muscle

Skeletal muscle metabolizes mainly glucose, free fatty acids (FFA) and triglycerides. Ketones do not participate in the oxidative metabolism of the active muscle, in the healthy human.5 Amino acids derived from catabolism within the muscle can be used as an energy source by muscles during very long and very intense effort. Nevertheless, amino acids never contribute more than 10 per cent of the total energy expenditure.6

Sources and proportions of fuels used during exercise

During the first 20-30 min of effort, muscle glycogen is the main source of energy.’ Later, blood-borne glucose derived from hepatic glycogenolysis, gluco-neogenesis and intestinal absorption is metabolized followed by muscle triglycer- ides and circulating FFA derived from adipose tissue (Figure 2.1)

At rest almost no blood glucose enters the muscle cell. During the first 10 min of exercise, blood glucose represents 10-15 per cent of oxidative metabolism, and after 90 min it can increase to 40 per cent of the total fuel utilization.9 After 4 h of exercise, blood glucose provides approximately one-third and FFA two-thirds of the oxidative fuels.lO After 8 h of moderate exercise. FFAs are responsible for 80- 85 per cent of the oxidative fuel, the rest being derived from glucose with a small contribution from branched-chain amino acids.11

Figure 2.1 Regulation of energy sources during mild exercise of long duration. Experimental situation without glucose ingestion8

Regulation of fuel delivery during exercise

During exercise of moderate intensity, insulin and zlucazons are the main regulators of hepatic glucose production. A low level of plasma insulin is required to allow hepatic glycogenolysis, and an increase in glucagon concentration is necessary for both glycogenolysis and gluconeogenesis.12 The glucagon-insulin ratio correlates better with hepatic glucose production than insulin or glucagon levels alone.13 Itseems that a decrease in insulin level enhances hepatic sensitivity to the action of glucagon. Without the presence of glucagon, however, the decrease in insulin concentration alone does not stimulate hepatic glycogenolysis.14

Adrenaline stimulates hepatic glucose production during intense effort of long duration by facilitating mobilization of the precursors of gluconeogenesis. Catecholamines are also responsible for extra glucose production during very intense exercises of short duration.15-16

Lypolysis is stimulated by increased catecholamine levels, which also suppress insulin secretion. Increased ex-adrenergic stimulation from noradrenaline released from sympathetic nerves seems to be the most prominent stimulus to lipolysis, 17 together with increased sensitivity of the adipocytes to catecholamines.18

Figure 2.2 Main energy fluxes during exercise, and their regulation in blood qlucose homeostasis. In the non-diabetic exercising subject, the plasma insulin level decreases, whereas the adrenaline and glucagon levels increase. Adapted from Zinman19 by permission of Lilly Research Laboratories

Consequences of diabetes on the metabolic reponse to exercise

The problems relating to blood glucose control in physically active insulin-treated people can be explained by imbalances between the plasma insulin level and the available plasma glucose. Very often the plasma insulin, derived from injected insulin, is too high during exercise compared with the insulin level of a non-diabetic person in the same situation. At the same time, the carbohydrate supply is often too low because hepatic glycogenolysis is blocked by high insulin levels (Figure 2.2).

References:

American Diabetes Association. Diabetes mellitus and exercise: position statement. Diabet Care 1997; 20: 1908-1912 Rudermann N, Devlin IT (eds), Handbook of Exercise in Diabetes. Alexandria, VA: American Diabetes Association, 2002. Grimm II, Fontana E, Gremion G et al. Diabete de type 2: Quel exercice pour quel diabetique et comment le prescrire? In: lournees de Diaberologie de f’Hote1-Dieu 2004. Paris: Flammarion Medecine-Sciences, 2004, pp. 95-104. Kang I, Robertson RI et al. Effect of exercise intensity on glucose and insulin metabolism in obese individuals and obese NIDDM patients. Diabet. Care 1996; 19: 341-349. Hagenfeldt L, Wahren I. Human forearm muscle metabolism during exercise uptake, release and oxidation of individual FFA and glycerol. Scand. 1. Clin. Lab. Invest. 1968; 21: 263-276. Lemon PWR, Nagle FI. Effects of exercise on protein and amino acid metabolism. Med. Sci. Sports Exerc. 1981; 13: 141-149. Koivisto VA. Diabetes and exercise. In: Alberti KGMM, Krall LP (eds), The Diabetes Annual 6. Amsterdam: Elsevier Science, 1991: pp. 169-183. Moesch H, Decombaz I. In: Nutrition et Sport Vevey: Nestle, 1990. Wahren I, Felig P, Ahlborg G, Jorfeldt L. Glucose metabolism during leg exercise in man. J. Clin. Invest. 1971; 50: 2715-2725. Ahlborg G, Felig P, Hagenfeld L, Hendler R, Wahren I. Substrate turnover during prolonged exercise in man. Splanchnic and leg metabolism of glucose, FFA and amino acids. 1. Clin. Invest. 1974; 53: 1080-1090. Stein TP, Hoyit RW, O’Toole M et al. Protein and energy metabolism during prolonged exercise in trained athletes. Int. 1. Sports Med. 1989; 10: 311-316. Wasserman DH, Lacy DB. Goldstein RE. Wiliams PE, Cherrington AD. Exercise-ind.fall in insulin and hepatic carbohydrate metabolism during exercise. Am. 1. Physiol. 1-256: E500-508. Wasserman DH. Control of glucose fluxes during exercise in the absorptive state. A.Phvsiol, 1985: 191-218. Wasserman DH, Zinnmann B. Fuel Homeostasis. In: Rudennann N, Devlin IT (eds). Health Professional’S Guide to Diabetes and Exercise. Alexandria: American Dial-: Association, 1995. pp. 27–47. Mitchell TH, Abraham G. Schiffrin A Leiter LA, Marliss EB. Hyperglycaemia : intense exercise in IDDM subjects during continuous subcutaneous insulin infus: Diabet. Care 1988: 11: 311-317. Purdon C. Brousson M. Nyreen SL et al. The roles of insulin and catecholamines in glucoregulatory response during intense exercise and early recovery in insulin-dependent diabetic and control subjects. 1. Clin. Endocinol. Metab. 1993; 76: 566-573. Hoelzer DR. Dalsky GP, Schwartz NS et al, Epinephrine is not critical to prevention of hypoglycemia during exercise in humans. Am. 1. Physio/1986; 251: El04-11O. Wahrenberg H. Engfeldt P. Bolinder J. Arner P. Acute adaptation in adrenergic control in lipolysis during physical exercise in humans. Am. 1. Phvsiol, 1987; 253: E383-390. Zinman B. Exercise in the patient with diabetes mellitus. In: Galloway lA, Potvin JH., Shuman CR (eds), Diabetes Mellitus. Indianapolis, IN: Lilly Research Laboratories, 1988, pp. 216-223. Frid A. Linde B. Intraregional differences in the absorption of unmodified insulin from the abdominal wall. Diabet. Med. 1992: 9: 236-239.

The new edition of this acclaimed title provides a practical guide to the risks and benefits of undertaking sport and general exercise for patients with diabetes.

Fully updated to reflect the progress and understanding in the field, the book features new chapters and material on insulin pump therapy and exercise, physical activity and prevention of type 2 diabetes, dietary advice for exercise and sport in type 1diabetes, and fluid and electrolyte replacement.

Next week: New Joslin Diabetes Deskbook excerpt!

For more information on this book and how to get a copy, just follow this link to Amazon.com, Exercise and Sport in Diabetes (Practical Diabetes) , Dinesh Nagi 2nd Edition.

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