Key result
Exercise-related hypoglycaemia and resting hypoglycaemia both significantly prolonged QTc and Tpe intervals in men with type 1 diabetes, with no significant difference between the two conditions.
Why the study?
The study was conducted to investigate changes in cardiac repolarisation during exercise-related hypoglycaemia compared with hypoglycaemia induced at rest in people with type 1 diabetes.
Does exercise-related hypoglycaemia compared to rest-induced hypoglycaemia affect QTc-interval prolongation in men with type 1 diabetes?
RCT (n=15)
Crossover
Does exercise-related hypoglycaemia compared to rest-induced hypoglycaemia affect QTc-interval prolongation in men with type 1 diabetes?
Hypoglycaemia, whether induced at rest or during exercise, causes significant QTc and Tpe interval prolongation in men with type 1 diabetes, highlighting a potential mechanism for increased ventricular arrhythmia risk.
Exercise-related hypoglycaemia may prolong QTc and raise arrhythmia risk in T1D; hypothesis-generating, needs confirmation before practice change.
AIMS: To investigate changes in cardiac repolarisation during exercise-related hypoglycaemia compared to hypoglycaemia induced at rest in people with type 1 diabetes. MATERIAL AND METHODS: In 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). RESULTS: Both 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. CONCLUSIONS: We 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.
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Hagelqvist et al. (2023) conducted an RCT in Type 1 diabetes (n=15). Exercise-related hypoglycaemia vs. Hypoglycaemia induced at rest was evaluated on Changes in QTc interval and T-peak to T-end (Tpe) interval. Exercise-related hypoglycaemia and resting hypoglycaemia both significantly prolonged QTc and Tpe intervals in men with type 1 diabetes, with no significant difference between the two conditions.
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