Strategies to manage post-exercise glycaemia in type 1 diabetes

Campbell, Matthew (2014) Strategies to manage post-exercise glycaemia in type 1 diabetes. Doctoral thesis, Northumbria University.

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Abstract

For patients with type 1 diabetes, a fear of hypoglycaemia and a concern over a loss of control with wider diabetes management are the most salient barriers to exercise participation and adherence. A large proportion of patients report a lack of advice for preventing post-exercise hypoglycaemia, and many feel largely uninformed about insulin administration and carbohydrate intake around aerobic-based exercise. Presently, recommendations within the literature are based predominantly on anecdotal and observational, but not empirical or interventional data. Therefore, this thesis aimed to develop a strategy that enables patients to effectively self-manage glycaemia following exercise, supported by evidence pertaining to the deeper physiological implications and consequences.

Study one (chapter 3) revealed that under conditions of reduced pre-exercise rapid-acting insulin dose, it is also necessary to reduce post-exercise rapid-acting insulin administration by 50% to prevent early-onset hypoglycaemia (≤ 8 hours post-exercise). Consequently, some patients experienced post-prandial hyperglycaemia with this intervention, although this was not associated with any other metabolic, counter-regulatory hormonal, or inflammatory disturbances. The results of study two (chapter 4) demonstrate that post-exercise meal composition, under conditions of reduced pre- and post-exercise rapid-acting insulin dose, carry important implications for post-prandial glycaemia. Specifically, consumption of low GI post-exercise carbohydrates normalise post-prandial hyperglycaemia, whilst protection from early onset hypoglycaemia is maintained. In addition, post-exercise meal composition heavily influences inflammatory markers; a high GI meal results in a pronounced inflammatory response, but a low GI meal completely prevented any rise in measured inflammatory markers. Lastly, study three (chapter 5) assessed the efficacy of a combined basal-bolus insulin reduction and low GI carbohydrate post-exercise feeding strategy. A 20% reduction in basal insulin provided full protection from hypoglycaemia for a total of 24 hours after exercise. Furthermore, ketonaemia did not increase to clinically meaningful levels, nor did inflammatory markers rise above concentrations seen at rest or when exercising under usual basal dose. No other metabolic or counter-regulatory hormonal disturbances were observed following a combined dose reduction to basal-bolus insulin and low GI carbohydrate post-exercise feeding.

Collectively, this thesis has shown that acute prandial adjustments in rapid-acting insulin and carbohydrate feeding, in combination with alterations in basal dose, are effective for managing post-exercise glycaemia and protecting patients from hypoglycaemia for a total of 24 hours after exercise. Moreover, this strategy aims to maintain euglycaemia by reducing post-prandial hyperglycaemia. This is not associated with clinically significant rises in ketonaemia, nor does it induce inflammatory, counter-regulatory hormonal, or other metabolic disturbances. Clinicians are advised to tailor these recommendations to a patient’s individual exercise preferences, fitness and exercise ability, level of diabetes management, and treatment regimen.

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