Effects of pediatric adiposity on heart rate variability

The relationship between obesity and heart rate variability (HRV) has been studied in adults and adolescents, but is not determined in young pediatrics. The purpose of this study was to assess autonomic activity using HRV in a pediatric population. We hypothesized that obese children would have reduced parasympathetic and increased sympathetic activity compared to age-matched subjects. 42 pediatric subjects (ages 3-5) were classified into 3 groups based on body mass index-for-age; normal, overweight and obese. HRV and respiratory rate were recorded during 3 minute baseline, 2 minute isometric handgrip and 3 minute recovery. HRV was analyzed in the time domain [heart rate (HR), RR interval (RRI) and RRI standard deviation (RRISD)] and frequency domain [low frequency (LF), high frequency (HF) and LF/HF ratio] using repeated measures ANOVA. Spearman’s correlations were used to examine the relations between BMI and HRV at rest. Significant condition effects were found between baseline, exercise and recovery, but these responses were not significantly different between the normal, overweight and obese children. BMI was negatively correlated with LF/HF, while BMI was positively correlated with RRISD, LF, HF and nHF. Our data demonstrate that higher BMI in the pediatric population is correlated with higher parasympathetic and lower sympathetic activity. These findings are contrary to HRV responses observed in adults and adolescents, suggesting complex relationships between age, obesity and autonomic control of the heart. The data supports the concept of an age reliance of HRV and a novel relationship between adiposity and body mass index in 3-5 year olds.

INFLUENCE OF 24-HOUR SLEEP DEPRIVATION ON CARDIOVASCULAR AND NEURAL CONTROL AT REST AND DURING ACUTE STRESS IN HUMANS

Recent epidemiological studies report a consistent association between short sleep and incidence of hypertension, as well as short sleep and cardiovascular disease-related mortality. While the association between short sleep and hypertension appears to be stronger in women than men, the mechanisms underlying the relations between sleep deprivation, stress, risks of cardiovascular diseases, and sex remain unclear. We conducted two studies to investigate the underlying neural mechanisms of these relations. In study 1, we examined sympathetic neural and blood pressure responses to experimentally-induced sleep deprivation in men and women. We further investigated the influence of sleep deprivation on cardiovascular reactivity to acute stress. In study 2, we examined the neural and cardiovascular function throughout the ovarian cycle in sleep deprived women. Twenty-eight young healthy subjects (14men and 14 women) were tested twice in study 1, once after normal sleep (NS) and once after 24-h total sleep deprivation (TSD). We measured the blood pressure, heart rate (HR), muscle sympathetic nerve activity (MSNA) and forearm blood flow (FBF) during 10min baseline, 5min of mental stress (MS) and 2 min cold pressor test (CPT). We demonstrated that TSD increased resting arterial blood pressure to a similar extent in both men and women, but MSNA decreased only in men following TSD. This MSNA response was associated with altered baroreflex function in women and divergent testosterone responses to TSD between men and women. Regarding TSD and cardiovascular reactivity, TSD elicited augmented HR reactivity and delayed recovery during both MS and CPT in men and women, and responses between sexes were not statistically different. Fourteen young healthy women participated in study 2. Subjects were tested twice, once during their early follicular (EF) phase after TSD, once during their mid-luteal (ML) phase after TSD. Blood pressure, HR, MSNA, and FBF were recorded during 10min baseline, 5 min MS, and 2 min CPT. We observed an augmented resting supine blood pressure during EF compared to ML in sleep deprived women. In contrast, resting MSNA, as well as cardiovascular responses to stressors, were similar between EF and ML after TSD. In conclusion, we observed sex differences in MSNA responses to TSD that demonstrate reductions of MSNA in men, but not women. TSD elicited augmented HR reactivity and delayed HR recovery to acute stressors similarly in men and women. We also reported an augmented supine blood pressure during EF compared to ML in sleep deprived women. These novel findings provide new and valuable mechanistic insight regarding the complex and poorly understood relations among sleep deprivation, sex, stress, and risk of cardiovascular disease.