scholarly journals Heart Rate Variability Reactivity to Food Image Stimuli is Associated with Body Mass Index

2021 ◽  
Author(s):  
Jung-Chi Chang ◽  
Wei-Lieh Huang ◽  
Chao-Yu Liu ◽  
Meg Mei-Chih Tseng ◽  
Cheryl C. H. Yang ◽  
...  
Keyword(s):  
Body Mass Index ◽  
Heart Rate ◽  
Heart Rate Variability ◽  
Disordered Eating ◽  
Body Mass ◽  
Sympathetic Activity ◽  
Eating Behaviors ◽  
Visual Stimuli ◽  
Disordered Eating Behaviors ◽  
Frequency Power

AbstractAppetitive control is driven by the hedonic response to food and affected by several factors. Heart rate variability (HRV) signals have been used to index autonomic activity and arousal levels towards visual stimuli. The current research aimed to examine the influence of body mass index (BMI), disordered eating behaviors, and sex on the HRV reactivity to food in a nonclinical sample. Thirty-eight healthy male and sixty-one healthy female participants completed questionnaires assessing disordered eating symptoms. HRV was recorded when the participants received visual stimuli of high-calorie food, neutral and negative emotional signals. Generalized estimating equation models were used to investigate the associations between HRV, BMI, disordered eating behaviors, and sex across the three stimulus types. Male participants demonstrated a higher ratio of low-frequency power to high-frequency power (LF/HF) than females across all the stimulus types. An increase in LF/HF reactivity to food signals was observed in all the study subjects. The moderation effect of BMI on LF/HF in response to food signals was also observed. Our study suggests that body weight may play a role in the interaction between sympathetic activity and food stimuli; however, how the interaction between sympathetic activity and food stimuli contributes to diet control warrants further investigation.

scholarly journals Effects of Metformin Added to Insulin in Adolescents with Type 1 Diabetes: An Exploratory Crossover Randomized Trial

2020 ◽  
Vol 2020 ◽  
pp. 1-10
Author(s):  
Daizhi Yang ◽  
Jinhua Yan ◽  
Hongrong Deng ◽  
Xubin Yang ◽  
Sihui Luo ◽  
...  
Keyword(s):  
Body Mass Index ◽  
Heart Rate ◽  
Heart Rate Variability ◽  
Type 1 Diabetes ◽  
Insulin Sensitivity ◽  
Body Mass ◽  
Autonomic Function ◽  
Insulin Dose ◽  
Glucose Variability

Background. To comprehensively assess the effects of metformin added to insulin on metabolic control, insulin sensitivity, and cardiovascular autonomic function in adolescents with type 1 diabetes. Materials and Methods. This was an exploratory, crossover, randomized trial conducted in adolescents with type 1 diabetes aged 12-18 years old. Participants were randomly received metformin (≤1000 mg/d) added to insulin for 24 weeks followed by insulin monotherapy for a subsequent 24 weeks or vice versa. Blood pressure, body mass index, insulin dose, estimated insulin sensitivity, glycated hemoglobin A1c (HbA1c), and lipid profiles were measured, with a 72-hour continuous glucose monitoring and 24-hour Holter monitoring performed at baseline, 24, and 50 weeks for the assessments of glucose variability and heart rate variability. Results. Seventeen patients with mean ± SD age 14.4 ± 2.3   years , body mass index 18.17 ± 1.81   kg / m 2 , median (IQR) diabetes duration 4.50 (3.58, 6.92) years, and HbA1c 9.0% (8.5%, 9.4%) were enrolled. The between-group difference in HbA1c of 0.28% (95% CI -0.39 to 0.95%) was not significant ( P = 0.40 ). Changes in body mass index, insulin dose, blood pressure, lipid profiles, and estimated insulin sensitivity were similar for metformin add-on vs. insulin monotherapy. Glucose variability also did not differ. Compared with insulin monotherapy, metformin add-on significantly increased multiple heart rate variability parameters. Conclusions. Metformin added to insulin did not improve metabolic control or glucose variability in lean/normal-weight adolescents with type 1 diabetes. However, metformin added to insulin significantly increased heart rate variability, suggesting that metformin might improve cardiovascular autonomic function in this population.

Low-frequency component of the heart rate variability spectrum: a poor marker of sympathetic activity

1999 ◽  
Vol 276 (1) ◽  
pp. H215-H223 ◽  
Author(s):  
Melanie S. Houle ◽  
George E. Billman
Keyword(s):  
Heart Rate ◽  
Heart Rate Variability ◽  
Ventricular Fibrillation ◽  
Sympathetic Activity ◽  
Low Frequency ◽  
Frequency Component ◽  
Atropine Sulfate ◽  
Low Frequency Power ◽  
Heart Rate Variability Spectrum ◽  
Frequency Power

The low-frequency component of the heart rate variability spectrum (0.06–0.10 Hz) is often used as an accurate reflection of sympathetic activity. Therefore, interventions that enhance cardiac sympathetic drive, e.g., exercise and myocardial ischemia, should elicit increases in the low-frequency power. Furthermore, because an enhanced sympathetic activation has been linked to an increased propensity for malignant arrhythmias, one might also predict a greater low-frequency power in animals that are susceptible to ventricular fibrillation than in resistant animals. To test these hypotheses, a 2-min coronary occlusion was made during the last minute of exercise in 71 dogs with healed myocardial infarctions: 43 had ventricular fibrillation (susceptible) and 28 did not experience arrhythmias (resistant). Exercise or ischemia alone provoked significant heart rate increases in both groups of animals, with the largest increase in the susceptible animals. These heart rate increases were attenuated by β-adrenergic receptor blockade. Despite the sympathetically mediated increases in heart rate, the low-frequency power decreased, rather than increased, in both groups, with the largest decrease again in the susceptible animals: 4.0 ± 0.2 (susceptible) vs. 4.1 ± 0.2 ln ms2 (resistant) in preexercise control and 2.2 ± 0.2 (susceptible) vs. 2.9 ± 0.2 ln ms2 (resistant) at highest exercise level. In a similar manner the parasympathetic antagonist atropine sulfate elicited significant reductions in the low-frequency power. Although sympathetic nerve activity was not directly recorded, these data suggest that the low-frequency component of the heart rate power spectrum probably results from an interaction of the sympathetic and parasympathetic nervous systems and, as such, does not accurately reflect changes in the sympathetic activity.

Sign in / Sign up

Export Citation Format

Share Document