Associations of Sedentary Time with Heart Rate Variability
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Abstract
Heart rate variability (HRV) is the gold standard non-invasive measure of cardiac-parasympathetic activity that is modulated by respiration. Lower resting HRV or cardiac-parasympathetic activity was proposed as a major linking mechanism between sedentary time (ST) and cardiovascular diseases (CVD). Several studies have examined associations of ST with HRV and reported favorable, unfavorable, or no associations. As such, it was challenging to draw a conclusion about the relationship of ST with HRV and cardiac-parasympathetic regulation. Thus, this dissertation sought to advance scientific knowledge by systematically reviewing and adding new investigations of ST with HRV.
First, we undertook a systematic review and meta-analysis (manuscript 1) which summarized the available observational literature and identified current research limitations and gaps. We found an unfavorable, but not clinically meaningful, association of ST with heart rate in males only; no correlations were observed with other HRV indices. Then, we conducted two original analyses (manuscripts 2 and 3) in a cohort of women and addressed many, but not all, of the observed limitations and gaps. We hypothesized that higher ST would be associated with unfavorable HRV. Our new analyses of self-reported activity and ST (manuscript 2) revealed that higher leisure moderate-to-vigorous intensity physical activity (MVPA) was associated with favorable HRV in women, while leisure ST was associated with unfavorable HRV only among inactive women. Occupational MVPA and ST were not associated with HRV. Our second originalanalysis (manuscript 3) found that statistically replacing accelerometer-measured ST with long-bouts of MVPA resulted in favorable effects on HRV in women. Further, statistically replacing short- with long-bouts of MVPA was associated with more favorable HRV among women without preexisting conditions that may affect HRV.
Overall, the current literature as well as our new analyses found largely null or small associations between ST and HRV. Hence, lower resting HRV or cardiac-parasympathetic dysregulation does not appear to be a major linking mechanism between ST and CVD. To strengthen this conclusion, future research should address major limitations of the available literature including exclusive use of cross-sectional designs, rare implementation of gold standard approaches to evaluate ST and HRV, and lack of cardiac-sympathetic activity measurement.