We investigated the extent to which obesity could identify autonomic dysfunction of heart control in a cross-sectional study with 65 women (aged 18-45 years), categorized as eutrophic, overweight or obese. We collected anthropometric measures and measures of heart rate variability (HRV) between March 2015 and March 2017. Low frequency in normalized units (LF (nu) ) over 46 was considered a marker of autonomic imbalance and high frequency in normalized units (HF (nu) ) below 38 a marker of depressed vagal modulation. Overweight (mean difference MΔHF (nu) = −13.11 [95% confidence interval (CI) of difference, −25.88, −0.34], Hedges's g = 0.65, common language effect size (CL) = 68.1%) and obese (MΔHF (nu) = −21.22 [95% CI, −31.89, −10.55], Hedges's g = 1.17, CL = 79.2%) women presented depressed vagal modulation compared to eutrophic women. Autonomic imbalance increased as body mass index increased (eutrophic-to-overweight MΔLF (nu) = 13.06 [95% CI, 1.65, 24.47], g = 0.65, CL = 67.9%, and overweight-to-obese MΔLF (nu) = 21.07 [95% CI, 10.32, 31.82], g = 1.15, CL 78.9%). The odds ratio for depressed HF (nu) among overweight women was 2.36 (95% CI 0.77, 7.29) and 2.18 among obese women (95% CI 0.79, 5.99), as well as 9.17 (95% CI 2.62, 32.04) and 17.39 for increased LF (nu) (95% CI 2.13, 141.76), respectively. The parasympathetic activity is diminished and autonomic imbalance of the cardiac control increased with increasing BMI categories.

Background/purpose: There is an increasing discussion concerning the deleterious effect of hyperglycemia on the wound healing. Patients with sepsis are subjected not only to high risk of death, but are also vulnerable to developing problems related to deficient healing. The aim of this study was to examine the interference of abdominal sepsis and diabetes on the healing of skin in a rat experimental model. Methods: Wistar rats (Rattus norvegicus) weighing 282±34g randomly distributed into 4 groups of 6 animals each. Twelve animals were subjected to abdominal sepsis with cecal ligation and puncture (CLP) and 12 without sepsis. Six animals from each subgroup had induction of diabetes induced with streptozotocin 50 mg/kg, i.p. and six were non-diabetic. Six days after sepsis induction, a tensile strength test of skin scar from abdominal wall and histopatology of skin wound were carried out. Results: The tensile strength showed a significant difference between groups. The control group rats had a tensile strength of 219.0±12.4 gf/cm2, significantly higher than in the diabetes group (185.2±5,9gf/cm2) and in the sepsis group (107.0±9,8mg/cm2) respectively. The group of animals subjected to sepsis + diabetes had the lowest mean tensile strength (86.3±6,6gf/cm2), significantly lower than the results from other groups (p<0.0001). The isolated sepsis was more detrimental to wound healing than the isolated diabetes. The existence of the two comorbidities resulted in the lower tensile strength of the scar tissue. The control group rats exhibited an inflammatory reaction score (4.67±0.16) significantly lower (p=0.002) than the scores exhibited by the sepsis + diabetes group (5.98 ± 0.27), the sepsis group (5.04 ± 0.23) and the diabetes group (4.95 ± 0.32). Conclusion: Sepsis and diabetes, alone or in combination, negatively influenced the healing of skin wounds in rats. Therefore, the data indicates that sepsis and diabetes may operate as deleterious to the wound healing.