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While mounting evidence suggests that sleep plays an important role in the etiology of obesity, the underlying pathogenic pathways are complex and unresolved. Experimental sleep deprivation studies demonstrate sympathovagal imbalance, indicative of diminished parasympathetic activity and/or heightened sympathetic activity, is consequent to poor sleep. Further, obese children exhibit sympathovagal imbalance, particularly during the night, compared to non-obese children. The question remains whether sympathovagal imbalance is one potential pathophysiological pathway underlying the association between sleep and obesity. The aim of the present study was to examine whether sympathovagal imbalance contributed to the association between sleep and obesity in children. Participants included 564 children aged 10 to 12 years (M = 11.67, SD = 0.95; 43.5 % girls) from the QUALITY Cohort, a longitudinal study of children at-risk for the development of obesity. While children were at-risk due to confirmed parental obesity status, 57.7 % of children were of normal body mass index (5-85th percentile). Sleep duration, sleep timing, and sleep disturbances were based on child- and parent-report. Anthropometrics were measured for central adiposity (waist circumference) and body composition (body mass index, fat mass index). Sympathovagal imbalance was derived from heart rate variability spectral analyses. Estimated path coefficients revealed that sympathovagal imbalance partially contributed to the association between poor sleep (later bedtimes, sleep-disordered breathing) and obesity. These findings highlight the importance of better understanding sympathovagal imbalance and its role in the etiology and maintenance of obesity. Future research should consider investigating nocturnal sympathovagal balance in youth. [ABSTRACT FROM AUTHOR]

Heart rate variability (HRV) is a non-invasive quantitative marker of cardiac autonomic function derived from continuous electrocardiogram (ECG) recordings. Normative HRV values and development factors have not been established in pediatric populations. The objective was to derive referent time- and frequency-domain HRV values for a population-based sample of children. Children aged 9-11 years ( N = 1,036) participated in the Québec Longitudinal Study of Child Development cohort cardiovascular health screening. Registered nurses measured anthropometrics (height, weight) and children wore an ambulatory Holter monitor to continuously record an ECG signal. HRV variables included time (SDNN, pNN50, RMSSD, SDANN) and frequency (HF, LF, LF/HF ratio) domain variables. Normative HRV values, stratified by age, sex, and heart rate, are presented. Greater heart rate ( β = −0.60, R = 0.39), pubertal maturation ( β = −0.11, R = 0.01), later ECG recording times ( β = −0.19, R = 0.07), and higher diastolic blood pressure ( β = −0.11, R = 0.01) were significantly associated with reduced HRV in 10-year-old children. The normative HRV values permit clinicians to monitor, describe, and establish pediatric nosologies in primary care and research settings, which may improve treatment of diseases associated with HRV in children. By better understanding existing values, the practical applicability of HRV among clinicians will be enhanced. Lastly, developmental (e.g., puberty) and procedural (e.g., recording time) factors were identified that will improve recording procedures and interpretation of results. [ABSTRACT FROM AUTHOR]