Lívia P Carvalho1, Luciana Di Thommazo-Luporini1, Renata G Mendes1, Ramona Cabiddu1, Paula A Ricci1, Renata P Basso-Vanelli1, Manoel C Oliveira-Junior2, Rodolfo P Vieira3, José C Bonjorno-Junior4, Cláudio R Oliveira4, Rafael L Luporini4, Audrey Borghi-Silva5. 1. Department of Physical Therapy, Federal University of Sao Carlos, Sao Carlos, Sao Paulo, Brazil. 2. Laboratory of Pulmonary and Exercise Immunology (LABPEI), Brazilian Institute of Teaching and Research in Pulmonary and Exercise Immunology (IBEPIPE), Nove de Julho University, Sao Paulo, Sao Paulo, Brazil. 3. Brazilian Institute of Teaching and Research in Pulmonary and Exercise Immunology (IBEPIPE), School of Medical Sciences of Sao Jose dos Campos Humanitas, Universidade Brasil, Sao Jose dos Campos, Sao Paulo, Brazil. 4. Department of Medicine, Federal University of Sao Carlos, Sao Carlos, Sao Paulo, Brazil. 5. Department of Physical Therapy, Federal University of Sao Carlos, Sao Carlos, Sao Paulo, Brazil. Electronic address: audrey@ufscar.br.
Abstract
Obesity is often associated with increased risk of cardiometabolic morbidities and mortality. However, evidence shows that some obese individuals are more likely to develop such risk factors early in life, including those with Metabolic Syndrome (MetS). Whether the presence of MetS in obese people impairs cardiac autonomic modulation (CAM) remains to be investigated. METHODS: Cross-sectional study. Sixty-six subjects were classified as normal-weight (NW, n = 24) or obese (BMI ≥ 30 kg·m-2): metabolically healthy (MHO, n = 19) vs unhealthy (MUHO, n = 23: NCEP/ATPIII-MetS criteria). Body composition (bioimpedance), metabolic (glucose-insulin/lipid) and inflammatory profiles were determined. Linear and nonlinear heart rate variability (HRV) indices were computed at rest and during the submaximal six-minute step test (6MST). Blood pressure (BP) and metabolic and ventilatory variables were assessed (oxygen uptake, VO2; carbon dioxide production, VCO2; minute ventilation, VE) during the 6MST and the maximal cardiopulmonary exercise testing (CPX). RESULTS: All groups reached the same 6MST intensity (VO2 ~ 80% and HR ~ 87% of CPX peak values). Both obese groups, independently of MetS, presented higher BP and lower maximal VO2 than NW. However, HRV differed between groups according to MetS at rest and during exercise: MUHO had lower meanRRi and SD1 than NW and lower RMSSD and pNN50 than MHO at rest; during exercise, the lowest SDNN, TINN, SD1 and Shannon entropy were observed for MUHO. Significant correlations were found between MetS, insulin resistance and HRV indices; and between insulin resistance and aerobic capacity (VO2peak). CONCLUSION: Obesity per se impairs aerobic-hemodynamic responses to exercise. However, MetS in obese young adults negatively impacts overall HRV, parasympathetic activity and HRV complexity.
Obesity is often associated with increased risk of cardiometabolic morbidities and mortality. However, evidence shows that some obese individuals are more likely to develop such risk factors early in life, including those with Metabolic Syndrome (MetS). Whether the presence of MetS in obese people impairs cardiac autonomic modulation (CAM) remains to be investigated. METHODS: Cross-sectional study. Sixty-six subjects were classified as normal-weight (NW, n = 24) or obese (BMI ≥ 30 kg·m-2): metabolically healthy (MHO, n = 19) vs unhealthy (MUHO, n = 23: NCEP/ATPIII-MetS criteria). Body composition (bioimpedance), metabolic (glucose-insulin/lipid) and inflammatory profiles were determined. Linear and nonlinear heart rate variability (HRV) indices were computed at rest and during the submaximal six-minute step test (6MST). Blood pressure (BP) and metabolic and ventilatory variables were assessed (oxygen uptake, VO2; carbon dioxide production, VCO2; minute ventilation, VE) during the 6MST and the maximal cardiopulmonary exercise testing (CPX). RESULTS: All groups reached the same 6MST intensity (VO2 ~ 80% and HR ~ 87% of CPX peak values). Both obese groups, independently of MetS, presented higher BP and lower maximal VO2 than NW. However, HRV differed between groups according to MetS at rest and during exercise: MUHO had lower meanRRi and SD1 than NW and lower RMSSD and pNN50 than MHO at rest; during exercise, the lowest SDNN, TINN, SD1 and Shannon entropy were observed for MUHO. Significant correlations were found between MetS, insulin resistance and HRV indices; and between insulin resistance and aerobic capacity (VO2peak). CONCLUSION: Obesity per se impairs aerobic-hemodynamic responses to exercise. However, MetS in obese young adults negatively impacts overall HRV, parasympathetic activity and HRV complexity.