Exercise‐related hypoglycaemia induces QTc‐interval prolongation in individuals with type 1 diabetes

Abstract

AbstractAimsTo investigate changes in cardiac repolarisation during exercise‐related hypoglycaemia compared to hypoglycaemia induced at rest in people with type 1 diabetes.Material and methodsIn a randomised crossover study, 15 men with type 1 diabetes underwent two separate hyperinsulinaemic euglycaemic‐hypoglycaemic clamp experiments during Holter‐ECG monitoring. One experiment included a bout of moderate‐intensity cycling exercise (60 min) along with declining plasma glucose (PG; Clamp‐exercise). In the other experiment, hypoglycaemia was induced with the participants at rest (Clamp‐rest). We studied QTc interval, T‐peak to T‐end (Tpe) interval and hormonal responses during three steady‐state phases: (i) baseline (PG 4.0–8.0 mmol/L); (ii) hypoglycaemic phase (PG <3.0 mmol/L); and (iii) recovery phase (PG 4.0–8.0 mmol/L).ResultsBoth QTc interval and Tpe interval increased significantly from baseline during the hypoglycaemic phase but with no significant difference between test days. These changes were accompanied by an increase in plasma adrenaline and a decrease in plasma potassium on both days. During the recovery phase, ΔQTc interval was longer during Clamp‐rest compared to Clamp‐exercise, whereas ΔTpe interval remained similar on the two test days.ConclusionsWe found that both exercise‐related hypoglycaemia and hypoglycaemia induced at rest can cause QTc‐interval prolongation and Tpe‐interval prolongation in people with type 1 diabetes. Thus, both scenarios may increase susceptibility to ventricular arrhythmias.