Synthesis of Best Practice

Abstract

In the preceding chapters, we have seen elegant discussions of the hormonal and metabolic responses to exercise and how these responses are altered by type 1 diabetes and insulin therapy. In Chap. 1, we have seen how exercise exerts a great demand on the capacity of the human body to maintain blood glucose homeostasis. The normal physiological counterregulatory hormone response generated by exercise produces coordinated endocrine response which switches the physiological state from the postabsorptive to the exercise state, enabling release of the nutrients required to support increased work. Increased glucose utilization by skeletal muscle proportionate to the duration and intensity of exercise is counteracted by a complex and well-coordinated endocrine response. Hepatic glucose production (through increased glycogenolysis and gluconeogenesis) mediated through increased glucagon and a fall in insulin concentrations in the portal vein are important stimulators of hepatic glucose production during low- and moderate-intensity exercise. Further counterregulatory catecholamine responses during high-intensity exercise are important in intense exercise and with modest hypoglycemia in nondiabetic intervals. It is perhaps surprising that even in nondiabetic individuals, preexercise hypoglycemia is associated with blunted counterregulation during subsequent exercise, and prior exercise blunts the counterregulatory response to subsequent hypoglycemia. There are further age-, gender-, and obesity-related difference in these responses. It is therefore entirely predictable that diabetes and insulin treatment is likely to have very significant effects on the ability to perform exercise though changes in glycemic and counterregulatory responses.