QTc interval dynamics and heart rate variability response to submaximal exercise in normotensive young adults with and without parental hypertension

BACKGROUND: Prolonged QTc interval and reduced heart rate variability (HRV) are independent predictors of postexercise sudden cardiac death (SCD) in apparently healthy individuals. Offspring of hypertensive parents may exhibit early autonomic dysfunction, placing them at higher risk for future cardiovascular disease. This study evaluated the impact of submaximal aerobic exercise on QTc interval and its correlation with HRV in normotensive individuals with and without parental hypertension. MATERIALS AND METHODS: A cross-sectional study was conducted on 100 healthy medical students (18–25 years), divided into normotensive offspring of hypertensive parents (NOHPs, n = 50) and sex-matched offspring of normotensive parents (NONPs, n = 50). HRV and lead-II ECG were recorded in supine rest and 10 minutes postexercise. Participants underwent a standardized submaximal treadmill test using a modified Bruce protocol, targeting 50% VO₂max to ensure uniform workload. HRV indices (LFnu, HFnu, LF/HF ratio) and QTc (Bazett’s correction) were analyzed with statistical significance set at P < 0.05. RESULTS: Following exercise, NOHPs exhibited significantly prolonged QTc, higher LFnu, and elevated LF/HF ratio, alongside a reduction in HFnu compared with NONPs, indicating sympathovagal imbalance characterized by sympathetic predominance and vagal withdrawal. Correlation analysis revealed strong positive associations of QTc with LFnu and LF/HF ratio, and a negative association with HFnu in NOHPs during recovery. CONCLUSION: Submaximal exercise unmasks latent autonomic dysfunction in NOHPs, reflected as impaired vagal reactivation and augmented sympathetic drive, which is closely linked to prolonged QTc during recovery. The study highlights that combined QTc-HRV assessment, particularly after standardized exercise using the modified Bruce protocol, may serve as a sensitive early marker of repolarization instability and elevated arrhythmic risk in young individuals with genetic predisposition to hypertension.