Ritti‐Dias, Raphael Mendes

This study compared the effects of self-selected exercise intensity (SEI) versus predetermined exercise intensity (PEI) on blood pressure (BP) and arterial stiffness in adolescents with obesity. A total of 37 adolescents, 14.7 (1.6) years old, body mass index ≥95th percentile were randomly allocated into SEI (n = 18; 12 boys) or PEI (n = 19; 13 boys). Both groups exercised for 35 minutes on a treadmill, 3 times per week, for 12 weeks. The SEI could set the speed at the beginning of the sessions and make changes every 5 minutes. The PEI adolescents were trained at an intensity set at 60% to 70% of heart rate reserve. Brachial and central BP, pulse pressure, augmentation index, and carotid–femoral pulse wave were determined at baseline and after 12 weeks. Both groups reduced brachial systolic BP (SEI, Δ = −9 mm Hg; PEI, Δ = −4 mm Hg; P < .01), central systolic BP (SEI, Δ = −4 mm Hg; PEI, Δ = −4 mm Hg; P = .01), and central pulse pressure (SEI, Δ = −4 mm Hg; PEI, Δ = −3 mm Hg; P = .02) without differences between groups. No changes in the augmentation index and carotid–femoral pulse wave were observed in either group. The SEI induced similar changes in various cardiovascular outcomes compared with PEI in adolescents with obesity.

AbstractBackground and AimThis study aimed to evaluate the impact of physical activity (PA) on the course of hepatic steatosis (HS) in adults.MethodsHepatic steatosis status (ultrasonography) and PA levels were evaluated in 5860 subjects at baseline and after approximately 2.5 years (range: 19–50 months). At follow up, possible exposures to different PA levels were those who remained inactive, became inactive, became active, and remained active. After follow up, subjects were then classified according to the four possible states (outcomes): “remained without HS,” “developed HS” (subjects without HS at baseline), “remained with HS,” or “reverted HS.”ResultsAfter multivariate adjustments, individuals without HS that became or remained physically active were less likely to develop HS compared with those who remained physically inactive (odds ratio = 0.75, P = 0.04 and 0.75, P = 0.03, respectively). Among those with HS at baseline, becoming and remaining physically active beneficially improved the HS status (odds ratio = 0.64, P = 0.01 and 0.66, P = 0.01, respectively). However, the significance was lost when adjusted for changes in body mass index.ConclusionHigher levels of PA were associated with prevention and treatment of HS, with evidence of effect mediation by changes in body mass index.

Purpose: To investigate the effects of a low- versus high-intensity aerobic training on biomarkers of inflammation and endothelial dysfunction in adolescents with obesity. Methods: Sixty-two adolescents with obesity [age = 15 (14) y, body mass index = 34.87 (4.22) kg·m−2] were randomized to receive either a high-intensity training (HIT, n = 31) or a low-intensity training (LIT, n = 31) for 24 weeks. All participants also received nutritional, psychological, and clinical counseling. Leptin, total and subtype leukocyte counts, tumor necrosis factor-alpha, interleukin-6, myeloperoxidase, soluble intercellular adhesion molecule-1, and soluble vascular cell adhesion molecule-1 were obtained at baseline and after 24 weeks. Results: HIT reduced neutrophils [from 4.4 (1.9) to 3.6 (1.3) µL−1 × 103; P = .01] and monocytes [from 7.2 (2.5) to 5.2 (1.8) µL−1 × 102; P < .01], but LIT increased neutrophils [from 4.5 (1.7) to 5.2 (3.3) µL−1 × 103; P = .01]. Although tumor necrosis factor-alpha increased in LIT [from 13.3 (7.5) to 17.7 (10.8) pg·mL−1; P = .01], it decreased in HIT [from 12.4 (7.5) to 11.3 (6.2) pg·mL−1; P = .01]. No changes in leukocyte counts, soluble intercellular adhesion molecule-1, soluble vascular cell adhesion molecule-1, and homeostasis assessment model for insulin resistance were observed. Conclusions: Both HIT and LIT improved the inflammatory profile. The study, however, indicated that the number of biomarkers and the magnitude of changes were higher in the HIT compared with LIT.