The sirtuins form a family of evolutionarily conserved nicotinamide adenine dinucleotide (NAD)-dependent deacetylases. Seven sirtuins (SIRT1–SIRT7) have been described in mammals, with specific intracellular localization and biological functions associated with mitochondrial energy homeostasis, antioxidant activity, proliferation and DNA repair. Physical exercise affects the expression of sirtuin in skeletal muscle, regulating changes in mitochondrial biogenesis, oxidative metabolism and the cellular antioxidant system. In this context, sirtuin 1 and sirtuin 3 have been the most studied. This review focuses on the effects of different types of exercise on these sirtuins, the molecular pathways involved and the biological effect that is caused mainly in healthy subjects. The reported findings suggest that an acute load of exercise activates SIRT1, which in turn activates biogenesis and mitochondrial oxidative capacity. Additionally, several sessions of exercise (training) activates SIRT1 and also SIRT3 that, together with the biogenesis and mitochondrial oxidative function, jointly activate ATP production and the mitochondrial antioxidant function.
Sirtuin 3 enzyme (SIRT3) is involved in the regulation of mitochondrial energy homeostasis by activating Peroxisome proliferator-activated receptor-gamma coactivator (PGC-1α). Murine models have shown that the protein SIRT3 was modified by exercise and diet, however, the effect of exercise without diet in humans has not been examined. Propose of this paper was to analyze the effect of aerobic training on SIRT3 and PGC-1α in skeletal muscle of overweight adolescents without change in caloric intake. Fourteen overweight or obese male adolescents (15.5 ± 0.8 years) trained 3 days-week/50 min × session, at 70-80% of maximal heart rate for 12 weeks. Anthropometrics and skeletal muscle biopsies from the vastus lateralis were taken before and after the exercise program to measure adiposity, SIRT3, and PGC-1α proteins. Peak aerobic capacity (VO2peak) was estimated before and after training. The participants did not change their eating habits during the intervention. SIRT3 (1.05 ± 0.11 vs. 1.25 ± 0.14 AU, p = .014) and PGC-1a (1.06 ± 0.15 Vs 1.39 ± 0.20 AU, p = .009) increased. Fat percentage and waist circumference decreased (p < .05). VO2peak increased after training (p < .001). There was a significant association between SIRT3 and PGC-1α after training program. These data suggest that aerobic training increased SIRT3 and PGC-1a expression levels in sedentary, overweight, or obese adolescents.
BackgroundExercise stimulates the production of fibronectin type III domain-containing protein 5 (FNDC5), which is cleaved to release a protein called irisin. This protein induces browning of white adipose tissue resulting in increased thermogenesis. Different studies have measured circulating irisin at baseline and in response to exercise among a wide variety of individuals; yet, regarding the effect of different exercise intensities in obese adolescent girls, limited insight is available. This study compares the effect of acute aerobic exercise of moderate intensity and high-intensity interval training (HIIT) on irisin levels in skeletal muscle and plasma of sedentary overweight or obese female adolescents.MethodsThe aerobic group (n = 15) and HIIT group (n = 15) underwent anthropometric and metabolic measurements, electrocardiogram, peak oxygen uptake (VO2peak), and two vastus lateralis muscle biopsies before and after session of workout. The session of aerobic exercise included cycling at 65% of their peak heart rate (HRpeak) for 40 min. In the HIIT group, exercise included six bouts of 1 min at 85–95% HRpeak separated by 1 min of recovery. Irisin levels were evaluated in samples of skeletal muscle (western blot) and plasma (ELISA).ResultsThe levels of expression of irisin in skeletal muscle increased significantly after a session of HIIT (p < 0.05), while aerobic exercise no affect irisin levels. No significant differences between the groups in plasma irisin levels were found.ConclusionsThe increase in muscle irisin levels was observed only following HIIT session. No increases in plasma irisin concentration were observed.
Background: Lifestyle changes can reduce the risk of T2D; however, no study has evaluated the effect of a lifestyle intervention involving patients´family. The aim of this study was to compare the impact of an interdisciplinary family (FI) Vs individual intervention (II) on glucose metabolism, insulin resistance (IR), pancreatic β-cell function and cardiovascular risk markers in patients with prediabetes, as well as to measure the impact on their families' metabolic risk. Methods: Randomized Clinical Trial (RCT) to compare the impact of FI and II on IR and pancreatic β-cell function in subjects with prediabetes. There were 122 subjects with prediabetes (and 101 family members) randomized to FI or II. Data were collected in 2015-2016 and analyzed in 2017-2018. FI group had the support of their family members, who also received personalized diet and exercise recommendations; patients and their family members attended monthly a lifestyle enhancement program. II group received personalized diet and exercise recommendations. The follow-up was for 12 months. Glucose, IR, pancreatic β-cell function and secondary outcomes (body composition and lipid profile) were assessed at baseline, 6 and 12 months. Results: FI group improved area under the glucose curve (AUC) (from 18,597 ± 2611 to 17,237 ± 2792, p = 0.004) and the Matsuda index (from 3.5 ± 2.3 to 4.7 ± 3.5, p = 0.05) at 12 months. II group improved Disposition Index (from 1.5 ± 0.4 to 1.9 ± 0.73, p < .0001) at 12 months. The improvements achieved in weight and lipids at 6 months, were lost in II group at 12 moths, whereas in FI persisted. Adherence up to 12 months was not different between the study groups (FI 56% Vs II 60%). Conclusions: FI intervention was more effective by improving glucose AUC, insulin sensitivity and lipid profile, besides that, metabolic risk in family members of the FI group was maintained, while the risk of II group was increased. Trial registration: This study was retrospectively registered at clinicaltrials.gov on December 15, 2015 (NTC026365646).
In recent years, prevalence of obesity in children and adolescents has increased. A strategy for prevention and management of obesity is aerobic training (AT) due to its effectiveness to decrease fat mass. AT increases the content of SIRT3, a mitochondrial protein that increases the expression of PGC-1α and NFR1, thereby enhances mitochondrial function and metabolic health. Resistance training (RT) provides metabolic benefits but its effect on SIRT3 content is unknown. To compare the effect of AT and RT on SIRT3, PGC-1α and NRF-1 protein levels in skeletal muscle of sedentary obese adolescents. Twenty-seven sedentary obese male adolescents (age: 16.7 ± 0.9 years; BMI: 33.7 ± 4.3 kg/m) completed a 1-month control period prior to randomization to one of two supervised exercise protocols: AT (3 days/week, 40 min/day, 70-80% peak heart rate) or RT (3 days/week, 11 exercises, 2 sets/exercise, 12 repetitions/set) for 12 weeks. Biopsies were obtained from the vastus lateralis muscle before and after 12 weeks to analyse SIRT3, PGC-1α and NRF-1 proteins content. Peak oxygen consumption (VO and anthropometric variables were evaluated before and after training. AT increased SIRT3 content, which was associated with improvements in PGC-1α content and body fat percentage. RT did not affect SIRT3 or PGC-1α. VO increased only in AT. The increase in muscle mitochondrial SIRT3 was observed only following AT. In contrast, RT increased muscle mass without improving SIRT3 in obese male adolescents.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
customersupport@researchsolutions.com
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
This site is protected by reCAPTCHA and the Google Privacy Policy and Terms of Service apply.
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.