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RESEARCH PAPER
Exercise-induced abnormal recovery of heart rate and ventricular repolarization parameters among smokers without known cardiovascular disease: A cross-sectional study
1
Cardiology Department, Sincan State Hospital, Ankara, Turkey
2
Department of Cardiology,
Cihanbeyli State Hospital,
Konya, Turkey
3
Department of Cardiology, Ankara Bilkent City Hospital, Ankara, Turkey
These authors had equal contribution to this work
Submission date: 2025-09-30
Final revision date: 2025-11-07
Acceptance date: 2026-01-04
Publication date: 2026-03-19
Corresponding author
Ayhan Cosgun
Cihanbeyli State Hospital, Atçeken, Hastane Cd. No:13, 42850, Cihanbeyli, Konya, Turkey
Cihanbeyli State Hospital, Atçeken, Hastane Cd. No:13, 42850, Cihanbeyli, Konya, Turkey
Tob. Induc. Dis. 2026;24(March):39
KEYWORDS
TOPICS
ABSTRACT
Introduction:
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.
Methods:
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.
Results:
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).
Conclusions:
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.
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.
Methods:
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.
Results:
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).
Conclusions:
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.
CONFLICTS OF INTEREST
The authors have completed and submitted the ICMJE Form for
Disclosure of Potential Conflicts of Interest and none was reported.
FUNDING
There was no source of funding for this research.
ETHICAL APPROVAL AND INFORMED CONSENT
Ethical approval was obtained from the Ankara Bilkent City Hospital
Administration (Approval number: TABED 2-25-1603; Date: 12 November 2025).
Participants provided informed consent.
DATA AVAILABILITY
The data supporting this research are available from the authors on
reasonable request.
PROVENANCE AND PEER REVIEW
Not commissioned; externally peer reviewed.
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