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Article Abstract

Metabolic syndrome (MetS) development is associated with insulin resistance and obesity, with the progression of visceral adipose tissue playing a crucial role. Excessive adipose tissue is accompanied by an increase in the asprosin (ASP), which is responsible for carbohydrate metabolism and the regulation of hunger and satiety. Exercise affects the release of ASP, which may regulate metabolism accordingly. Due to the inconclusive results of the effect of exercise on ASP concentration in men with MetS, 12-week interventions were carried out in the following groups: EG1-aerobic training (n = 21, age: 34.21 ± 6.06, WC; waist circumference: 114.7 ± 10.93) and EG2-a combination of aerobic and resistance training (n = 21, age: 37.37 ± 7.08, WC: 114.8 ± 11.64) and compared with a control group (CG) of men with MetS without any intervention (n = 20, age: 38.26 ± 7.43, WC: 115.3 ± 10.54). Body composition, indicators of carbohydrate-lipid metabolism, and ASP were assessed four times: before the intervention, at 6 and 12 weeks of training, and 4 weeks after the training sessions. A comparison of the intervention influence on changes in the analyzed variables between the groups was performed using ANOVA test for dependent groups with post-hoc comparison. The effect size (ES) was also assessed using squared eta (η). The implementation of aerobic training resulted in a decrease in ASP concentration (p = 0.03) within 6 weeks of the intervention, while in the CG a gradual increase in ASP was confirmed (p < 0.001). Aerobic-resistance training did not induce significant changes in ASP concentration but resulted in an increase in fat-free mass/fat mass (FFM/FM) ratio (p < 0.001), and a decrease (p = 0.04) in Homeostasis Model Assessment of Insulin Resistance (HOMA-IR). Changes in the visceral adipose tissue level indicate a gradual decrease in both the EG1 (p = 0.01) and EG2 (p = 0.04) groups. Both aerobic and aerobic-resistance exercises may have a regulatory effect, mainly by reducing visceral adipose tissue, on the improvement of metabolic disorders.

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10782011PMC
http://dx.doi.org/10.1038/s41598-024-51473-1DOI Listing

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