In this large cross-sectional samples of apparently healthy Korean adults, we found that three adiposity measures reflecting either general or abdominal adiposity were differentially associated with the HRV measures. WHR was more likely than BMI or PBF to be strongly associated with almost all of the HRV indices that are thought to be modulated by both the sympathetic and parasympathetic nervous systems. In addition, these associations were significant when age, gender, and CV risk factors were considered, and they were only significant in the overweight subgroup. Increased PBF, reflecting overall fat, also appeared to be a better predictor for decreased HRV indices than BMI, which does not discriminate fat from muscle. Therefore, increased abdominal fat appeared to be an independent indicator of decreased ANS balance regardless of age, gender, and CV risk factors, particularly in the overweight subgroup. Additionally, abdominal fat is a better predictor of low HRV than overall fat.
In previous studies, associations between obesity and low HRV were reported mainly in small case-control or cross-sectional studies. Our findings extend this knowledge to a population comprised of many people of normal weight and a small subgroup of obese participants (1.8% had a BMI of >30 kg/m2
). Laederach-Hofmann, et al.1
showed that BMI and WHR were inversely correlated with sympathetic activity in 42 subjects with a BMI of 28-83 kg/m2
. Associations between body fat percentage and depression in sympathetic and parasympathetic activity were also found in 56 men with various percentages of body fat.4
In an another study with 44 obese patients and normal-weight controls, obese patients had HRV indices reflecting lower sympathetic activity and higher parasympathetic activity compared with non-obese controls.2
Similarly, a decrease in HRV was found in morbidly obese group compared with controls in 80 women, and significant associations between metabolic and hormonal factors and HRV measures disappeared after adjusting for body fat mass.5
It has also been suggested that HRV is reversible. In a handful of studies about change in ANS activity after weight loss in obese patients, an increase in HRV was noted after weight loss by gastroplasty,7
increased physical activity and calorie restriction,8-10
and anti-obesity medication.11
An association between abdominal fat and ANS imbalance has also been reported. Lindmark, et al.24
reported that there was a positive association between visceral abdominal fat and sympathetic/parasympathetic ratio in HRV assessment, while subcutaneous abdominal fat was not associated with HRV measures in 18 subjects, including first-degree relatives of patients with type 2 diabetes and controls. A positive association between intra-abdominal adiposity and sympathetic activity was also found among male adolescents.25
The exact mechanisms linking increased abdominal adiposity with low HRV are unclear. A plausible explanation for the association involves compartment-specific alterations in the balance of sympathetic/parasympathetic outflow. Increased parasympathetic dominance in the visceral compartment and increased sympathetic tone in the thoracic and movement compartments could contribute to the metabolic syndrome, including visceral fat accumulation.24,26
Several limitations in the present study should be considered. First, the study sample consisted of a relatively small number of obese participants, which might have led to an underestimation of the associations between adiposity and HRV measures. Second, this study had a cross-sectional design, which does not allow for an evaluation of temporal relationships. Third, HRV has been known to be very vulnerable to diurnal, postural, and emotional changes. Therefore, it is necessary to carefully adjust the data acquiring conditions to get valid HRV, though it is as short as 5 minutes. In the current study, we obtained stationary HRV by keeping the following conditions: recording ECG in the morning to be free from diurnal change; keeping supine position to make effects of posture change small; and selecting stationary 5-min segment from 10-min HRV to avoid nonstationarity. However, we might not have completely controlled conditions related to HRV such as psychological status, acute illness, and medications that could influence HRV measurements. Fourth, as we conducted this study using stationary 5-minute segment from 10-minute HRV, the current results might not extend to the findings that were derived from long-term HRV extracted from 24-hour ECG that gives some important information about long-term variability and fluctuation. However, it is not easy to acquire long-term ECG/HRV from a large population of more than 1000 subjects. Also, there has been sufficient evidence to support that this short-duration stationary HRV can reflect cardiac ANS function.18
Finally, despite adjustment for potential confounders, residual and unmeasured confounders may affect the results.
In conclusion, our data confirm an association between increased adiposity and low HRV. However, we found that the strength of association is not uniform; it is rather specific to different adiposity measures and weight subgroups. WHR and PBF are better indicators of low HRV than BMI. In addition, our data provide evidence that, irrespective of age, gender, and CV risk factors, these associations were consistent and stronger in overweight subgroup. These findings support clinical importance of abdominal obesity as a risk factor for CV disease.