Aims: Hypoglycemia induced at rest enhances susceptibility to cardiac arrhythmias by increasing the QTc-interval. Although exercise is a common cause of hypoglycemia in insulin-treated patients, its acute effects on hypoglycemia-induced QTc-interval prolongation remain unknown. Therefore, we aimed to investigate changes in cardiac repolarization during exercise-related hypoglycemia compared to hypoglycemia induced at rest in people type 1 diabetes.

Material and methods: In a randomized crossover study, 15 men with type 1 diabetes underwent two separate hyperinsulinemic euglycemic-hypoglycemic clamp experiments during Holter-ECG monitoring. One experiment included a bout of moderate intensity cycling exercise (60 minutes) along with declining plasma glucose (PG) (Clamp-exercise), while on the other experiment, hypoglycemia 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) a hypoglycemic phase (PG < 3.0 mmol/L), and iii) a recovery phase (PG 4.0 - 8.0 mmol/L).

Results: Both the QTc-interval and Tpe-interval increased significantly from baseline during the hypoglycemic phase but with no significant difference between test days. These changes were accompanied with an increase in plasma adrenaline and a decrease in plasma potassium on both days. During the recovery phase, the ΔQTc-interval was longer on Clamp-rest compared to Clamp-exercise whereas the ΔTpe-interval remained similar between test days.

Conclusions: We found that both exercise-related hypoglycemia and hypoglycemia 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. This article is protected by copyright. All rights reserved.