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BackgroundSarcopenic obesity is characterized by low muscle mass and high body fat; prevalence increases with age, particularly after age 65 years. For this systematic literature review we searched scientific databases for studies on exercise interventions for improving physical performance in adults with sarcopenic obesity; also, we identified potential gaps in clinical practice guidelines that need to be addressed.MethodsWe followed the recommendations of the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA). The databases were searched for studies published through November 2021 that measured physical performance in adults with sarcopenic obesity.ResultsMost of the studies applied a strength training protocol in which improvement was noted post-treatment on the Time Chair Rise (TCR), 30-s Chair Stand, and Single Leg Stance (SLS) tests. Discrepancies between the studies were observed when resistance training was combined with or without elastic bands or electromyostimulation, as measured with the Short Physical Performance Battery (SPPB), Physical Performance Test (PPT), Gait Speed, and Timed Up & Go (TUG) test. Post-intervention SPPB, PPT, and gait speed scores showed an increase or maintenance of performance, while TUG test scores were higher according to one study but lower according to another.ConclusionsEngagement in physical exercise, and resistance training in particular, can improve or maintain physical performance in adults with sarcopenic obesity. Study samples should include more men. A future area of focus should be the impact of different types of training (aerobic, power training, combined modalities). Finally, studies with longer intervention periods and follow-up periods are needed to gain a better understanding of the effectiveness of exercise on physical function in adults with sarcopenic obesity.

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Type 2 diabetes (T2D) is a multisystem disease that is the subject of many studies, but the earliest cause of the disease has yet to be elucidated. Mitochondrial impairment has been associated with diabetes in several tissues. To extend the association between T2D and mitochondrial impairment to blood cells, we investigated T2D-related changes in peripheral mononucleated blood cells’ (PBMCs) mitochondrial function in two groups of women (CTRL vs. T2D; mean age: 54.1 ± 3.8 vs. 60.9 ± 4.8; mean BMI 25.6 ± 5.2 vs. 30.0 ± 5), together with a panel of blood biomarkers, anthropometric measurements and physiological parameters (VO2max and strength tests). Dual-energy X-ray absorptiometry (DXA) scan analysis, cardio-pulmonary exercise test and blood biomarkers confirmed hallmarks of diabetes in the T2D group. Mitochondrial function assays performed with high resolution respirometry highlighted a significant reduction of mitochondrial respiration in the ADP-stimulated state (OXPHOS; −30%, p = 0.006) and maximal non-coupled respiration (ET; −30%, p = 0.004) in PBMCs samples from the T2D group. The total glutathione antioxidant pool (GSHt) was significantly reduced (−38%: p = 0.04) in plasma samples from the T2D group. The fraction of glycated hemoglobin (Hb1Ac) was positively associated with markers of inflammation (C-reactive protein-CRP r = 0.618; p = 0.006) and of dyslipidemia (triglycerides-TG r = 0.815; p < 0.0001). The same marker (Hb1Ac) was negatively associated with mitochondrial activity levels (OXPHOS r = −0.502; p = 0.034; ET r = −0.529; p = 0.024). The results obtained in overweight postmenopausal women from analysis of PBMCs mitochondrial respiration and their association with anthropometric and physiological parameters indicate that PBMC could represent a reliable model for studying T2D-related metabolic impairment and could be useful for testing the effectiveness of interventions targeting mitochondria.