The Effect Of Exercise In Gastrocnemius Muscle Alterations-induced By Obesity

Abstract

In the management of obesity, exercise has been proposed as one of the first line strategies and skeletal muscle a key organ in energy expenditure. However, the role of exercise in biogenesis and oxidative stress, both key mechanisms in obesity development, remain unclear. PURPOSE: Analyze the effect of exercise on mitochondrial biogenesis and oxidative stress alterations-induced by obesity in gastrocnemius muscle. METHODS: Male Sprague–Dawley rats (n=24) were divided in two groups: a standard diet (SS, n=11) and a high-fat diet sedentary group (HS, n=13). Following 9 weeks of diet treatment, half of SS and HS group were engaged in an exercise program on treadmill for 8 weeks, 5 days/week and 1hour/day (ST, n=5 and HT, n=7). Skeletal muscle oxidative damage markers (MDA and SH) and pro-oxidant signaling proteins (SIRT3 and P66shc) content were evaluated. The content of biogenesis-related proteins (Tfam and PGC-1α) and mitochondrial complex sub-units were also assessed. RESULTS:High-fat diet treatment (HT) induced an increase of thiol groups (0,041+0,003 vs. 0,031+0,003 mmol.mg protein-1, p<0.05), Sirt3 (161+19,99 vs. 100+33,01%, p<0.05), PGC-1α (195,4+41,04 vs. 100+28,57%, p<0.05) and complex III (195,70%+13,43 vs. 100+48,43%, p<0.05) content compared to SS. The HT animals showed a decreased Sirt3 (85,41+10,65 vs. 161+19,99%, p<0.05), PGC-1α (85,10+21,66 vs. 195,4+41,04%, p<0.05) and complex III content (99,35+18,39 vs. 195,7+13,43%, p<0.05) compared to HS, whereas complex IV was significantly increased (242,40+38,94 vs. 93,14+7,1%, p<0.05). No changes were observed in MDA levels or P66shc and Tfam content. CONCLUSIONS:Obesity might induce skeletal muscle mitochondrial biogenesis as an attempt to increase fatty acid oxidation, ultimately contributing to ameliorate redox pressure. In turn, the increased expression of complex IV in HT group, might have contributed to improve the oxidation of mitochondrial substrates.