# Exercise-induced abnormal recovery of heart rate and ventricular repolarization parameters among smokers without known cardiovascular disease: A cross-sectional study

## TL;DR

Smoking affects heart recovery after exercise, increasing the risk of sudden cardiac death even in people without known heart disease.

## Contribution

This study identifies abnormal heart rate and repolarization recovery in smokers using specific indices, linking smoking to autonomic and myocardial dysfunction.

## Key findings

- Smokers showed significantly lower heart rate recovery index (HRR-I) during recovery periods compared to non-smokers.
- Smokers exhibited higher Tp-eR-I and QTR-I values, indicating impaired ventricular repolarization recovery.
- Smoking intensity was positively correlated with Tp-eR-I and QTR-I and negatively correlated with HRR-I.

## Abstract

Smoking is a major preventable risk factor for cardiovascular disease and is strongly associated with sudden cardiac death (SCD). This study investigated the relationship between the heart rate recovery index (HRR-I), T peak–end recovery index (Tp-eR-I), and QT interval recovery index (QTR-I) in smokers compared with non-smokers.

This cross-sectional study, conducted in Bilkent City Hospital, Ankara, Turkey, between May 2017 and June 2025, included 150 healthy smokers (120 males, 30 females) and 123 healthy non-smokers (97 males, 26 females). Smoking data are self-reported. All participants underwent symptom-limited treadmill exercise testing using the Bruce protocol. Heart rate (HR), QT, and Tp-e intervals were measured at baseline, peak exercise, and during recovery periods. HRR-I was calculated as the difference between peak HR and HR at the 1st, 2nd, and 3rd minutes of recovery. Tp-eR-I and QTR-I were calculated as the differences between baseline values and those obtained during peak, 1st, 2nd and 3rd minutes recovery times.

Smokers exhibited significantly lower HRR-I values at the 1st [18.6 ± 7.1 vs 24.2 ± 6.9, p<0.001; 17.9 (95% CI: 12.9–22.9)], 2nd [27.4 ± 7.3 vs 33.1 ± 7.1, p<0.001; 10.7 (95% CI 7.3–14.1)], and 3rd minutes [33.8 ± 7.9 vs 39.5 ± 8.3, p<0.001; 13.4 (95% CI: 9.6–17.2)] of recovery compared with non-smokers. Tp-eR-I and QTR-I values were significantly higher in smokers [Tp-eR-I: 7.8 ± 2.6 vs 5.2 ± 2.1, p<0.001; 18 (95% CI: 12–24)] [QTR-I: 24.5 ± 6.3 vs 18.9 ± 5.8, p<0.001; 12 (95% CI: 6–18)]. Smoking intensity was positively associated with Tp-eR-I (r=0.41, p<0.001) and QTR-I (r=0.36, p<0.001), and negatively associated with HRR-I (r= -0.39, p<0.001).

Cigarette smoking impairs autonomic regulation as reflected by reduced HRR-I and abnormal ventricular repolarization recovery, shown by increased Tp-eR-I and QTR-I. These findings suggest that smoking disrupts sympathetic–parasympathetic balance and myocardial repolarization, potentially explaining the higher incidence of arrhythmias and sudden cardiac death among smokers.