The importance of cardiorespiratory fitness vs. adiposity in determining heart rate variability (HRV) is unclear.
From CARDIA, an observational cohort study, we included 2,316 participants (mean age 45.2±3.6 years at Year 20, 57% female, 43% black) with HRV measured in 2005–06 (Year 20), and graded exercise test duration (GXTd) and adiposity measures (BMI, waist circumference) obtained in 1985–86 (baseline) and 2005–06. HRV measures (standard deviation of all normal RR intervals [SDNN] and square root of the mean of the squares of differences between all successive RR intervals [RMSSD]) were obtained from resting 30-second 12-lead ECGs. Cross-sectional associations between GXTd, adiposity and HRV were assessed at Year 20. Longitudinal changes in GXTd and adiposity measures were categorized as ≥10% increase, <10% change (no change), or ≥10% decrease. We used multivariable logistic regression to assess associations of GXTd and adiposity measures with unfavorable vs. more favorable HRV (lower 25th percentile vs. upper 75th percentile).
A 1-SD increment in GXTd was associated with 22% and 32% lower odds of unfavorable SDNN and RMSSD, respectively; associations remained significant after adjustment for adiposity. A 1-SD increment in adiposity measures was associated with 16–28% higher odds of unfavorable RMSSD; associations were not significant after adjustment for GXTd. Compared with no change/increase in GXTd, longitudinal decrease in GXTd was significantly associated with 55% and 94% higher odds of unfavorable SDNN and RMSSD, respectively, at Year 20. These associations remained significant after adjusting for adiposity.
Cardiorespiratory fitness may be a stronger determinant of HRV than adiposity. Intervention studies are needed to better determine the differential effects of improved cardiorespiratory fitness vs. weight loss on HRV.
1Cardiovascular Division, Department of Medicine, University of Minnesota Medical School, Minneapolis, MN;
2Division of Epidemiology and Community Health, School of Public Health, University of Minnesota, Minneapolis, MN;
3Division of Diabetes, Endocrinology and Metabolism, Department of Medicine, University of Minnesota Medical School, Minneapolis, MN;
4Department of Preventive Medicine, Feinberg School of Medicine, Chicago, IL
Corresponding author: Lin Y. Chen, MD, MS, Cardiovascular Division, Department of Medicine, University of Minnesota Medical School, 420 Delaware Street SE, MMC 508, Minneapolis, MN 55455, USA. Phone: 1-612-625-4401, Fax: 1-612-624-4937, E-mail: email@example.com
Dr. Chen receives grant funding from the National Heart, Lung, and Blood Institute (NHLBI) as PI of R01HL126637 and R01HL141288. The Coronary Artery Risk Development in Young Adults Study (CARDIA) is conducted and supported by NHLBI in collaboration with the University of Alabama at Birmingham (HHSN268201300025C & HHSN268201300026C), Northwestern University (HHSN268201300027C), University of Minnesota (HHSN268201300028C), Kaiser Foundation Research Institute (HHSN268201300029C), and Johns Hopkins University School of Medicine (HHSN268200900041C). CARDIA is also partially supported by the Intramural Research Program of the National Institute on Aging (NIA) and an intra-agency agreement between NIA and NHLBI (AG0005). This manuscript has been reviewed by CARDIA for scientific content.
CONFLICT OF INTEREST
None. The results of the present study are presented clearly, honestly, and without fabrication, falsification, or inappropriate data manipulation. In addition, the results of the present study do not constitute endorsement by ACSM.
Accepted for Publication: 12 September 2018