BACKGROUND: Obese people have a higher prevalence of cardiovascular disease, but the mechanism of this result remains obscure. The purpose of this study was to prove heart rate variability (HRV) response at rest and during stimuli in these persons. METHODS: The subjects were 41 healthy persons (19 men, 22 women) ranging in age from 20 to 65 years. HRV was measured at rest and at given stresses with noise and standing. RESULTS: Higher levels of fat mass, percentage fat content, and waist/hip ratio were significantly associated with lower low frequency (LF) (r = -0.34, r = -0.43; P < .01, r = -0.33, P < .05), and lower root mean square differences of successive NN intervals (RMS standard deviation) (r = -0.33, r = -0.35, r = -0.38, P < .05). During rest, noise, and standing, the change amount of the standard deviation of NN interval (SDNN) and low frequency/high frequency ratio were not different between normal and obese groups (P > .05). CONCLUSION: Although there was no significant HRV response to stimuli, root mean square of successive differences (which reflects parasympathetic acivity) and low frequency (which mainly reflects sympathetic activity) were negatively correlated with fat mass, fat percentage, and waist-to-hip ratio at rest in obese persons. These results mean obesity can change cardiac autonomic nervous response, meaning that the mechanism by which obesity increases cardiac mortality would be explained, at least partially.
BACKGROUND:Obesepeople have a higher prevalence of cardiovascular disease, but the mechanism of this result remains obscure. The purpose of this study was to prove heart rate variability (HRV) response at rest and during stimuli in these persons. METHODS: The subjects were 41 healthy persons (19 men, 22 women) ranging in age from 20 to 65 years. HRV was measured at rest and at given stresses with noise and standing. RESULTS: Higher levels of fat mass, percentage fat content, and waist/hip ratio were significantly associated with lower low frequency (LF) (r = -0.34, r = -0.43; P < .01, r = -0.33, P < .05), and lower root mean square differences of successive NN intervals (RMS standard deviation) (r = -0.33, r = -0.35, r = -0.38, P < .05). During rest, noise, and standing, the change amount of the standard deviation of NN interval (SDNN) and low frequency/high frequency ratio were not different between normal and obese groups (P > .05). CONCLUSION: Although there was no significant HRV response to stimuli, root mean square of successive differences (which reflects parasympathetic acivity) and low frequency (which mainly reflects sympathetic activity) were negatively correlated with fat mass, fat percentage, and waist-to-hip ratio at rest in obesepersons. These results mean obesity can change cardiac autonomic nervous response, meaning that the mechanism by which obesity increases cardiac mortality would be explained, at least partially.
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