The purpose of the present study was to investigate whether peripheral brain-derived neurotrophic factor (BDNF) treatment induced metabolic adaptations in mouse skeletal muscle. BDNF (20 mg/kg/day) was injected subcutaneously for successive 14 days. BDNF treatment significantly reduced the total food intake and inhibited the weight gain in comparison to the control group. The glucose transporter 4 (GLUT4) protein expression in the gastrocnemius muscle was significantly increased by BDNF treatment in comparison to the control and pair-fed groups. Neither the oxidative nor the glycolytic enzyme activities in the gastrocnemius muscle changed after the BDNF treatment. These results suggest that the peripheral BDNF treatment promotes the skeletal muscle GLUT4 protein expression as well as hypophagia., M. Suwa ... [et al.]., and Obsahuje bibliografii a bibliografické odkazy
This study aimed to examine how regular aerobic training can affect the muscle hypertrophy induced by overloading. Male C57BL/6J mice were randomly divided into three groups: rest group, low-intensity aerobic exercise group, and high-intensity aerobic exercise group. Mice in the exercise groups were assigned to run at a speed of 10 m/min (low-intensity) or 25 m/min (high-intensity) for 30 min/day, five days/week, for four weeks. Then, the right hind leg gastrocnemius muscles were surgically removed to overload the plantaris and soleus muscles, while the left hind leg was subjected to a sham-operation. Both the plantaris and soleus muscles grew larger in the overloaded legs than those in the sham-operated legs. Muscle growth increased in the plantaris muscles in the low-intensity exercise group compared to that in the rest or high-intensity exercise groups at one and two weeks after overloading. This enhancement was not observed in the soleus muscles. Consistently, we observed changes in the expression of proteins involved in anabolic intracellular signaling, including Akt, mechanistic target of rapamycin (mTOR), and p70S6K, in the plantaris muscles. Our data showed for the first time that chronic low-intensity aerobic exercise precipitates overload-induced muscle growth., Siriguleng, T. Koike, Y. Natsume, S. Iwama, Y. Oshida., and Obsahuje bibliografii
Hypoxia-inducible factor-1α (HIF-1α) transcriptionally regulates expression of several target genes in protecting tissues against hypoxia. With hypoxic stress, vascular endothelial growth factor (VEGF) is a signal protein produced by cells and further contributes to improvement of vascular functions and restoring the oxygen supply to tissues. In this current study, we first hypothesized that the protein levels of HIF-1α and VEGF are reduced in skeletal muscles of plateau animals [China Qinghai- Tibetan plateau pikas (ochotona curzoniae)] in response to hypoxia as compared with control animals [normal lowland Sprague-Dawley (SD) rats]. We further hypothesized that HIF-1α plays a role in regulating expression of VEGF in skeletal muscle. Note that HIF-1α and VEGF were determined by using two-site immunoenzymatic assay (ELISA) methods. Our results demonstrated that hypoxic stress induced by exposure of lower O2 (6 h) significantly increased the levels of HIF-1α and VEGF in the oxidative and glycolytic muscles of SD rats and pikas (P<0.05 vs. normoxic conditions). Notably, the increases in HIF-1α and VEGF were significantly less in pikas (P<0.05, vs. SD controls) than in SD rats. In addition, a linear relationship was observed between amplified HIF-1α and VEGF in oxidative muscle (r=0.76 and P<0.01) and glycolytic muscle (r=0.72 and P<0.01) and inhibiting HIF-1α significantly decreased expression of VEGF induced by hypoxic stress in skeletal muscles (P<0.05). Overall, our findings suggest that (1) responsiveness of HIF-1α and VEGF in skeletal muscles to hypoxic stress is blunted in plateau animals, and (2) HIF-1α has a regulatory effect on VEGF under hypoxic environment., H.-C. Xie, J.-P. He, J.-F. Zhu, J.-G. Li., and Obsahuje bibliografii
This study aimed to compare the effects of three different resistance exercise models on the quadriceps muscle crosssectional area, as well as on mTOR phosphorylation and other pivotal molecules involved in the upstream regulation of mTOR. Twenty-four male Wistar rats were divided into untrained (control), endurance resistance training, strength resistance training, and hypertrophy resistance training (HRT) groups (n=6). After 12 weeks of training, the red portion of the quadriceps was removed for histological and Western blot analyses. The results showed that the quadriceps weight and cross-sectional areas in the exercised groups were higher than those of the untrained rats. However, the HRT group presented better results than the other two experimental groups. This same pattern was observed for mTOR phosphorylation and for the most pivotal molecules involved in the upstream control of mTOR (increase of PKB, 14-3-3, ERK, p38 MAPK, and 4E-BP1 phosphorylation, and reduction of tuberin, sestrin 2, REDD1, and phospho AMPK). In summary, our study showed that HRT leads to high levels of mTOR phosphorylation as well as of other proteins involved in the upstream regulation of mTOR., T. F. Luciano, S. O. Marques, B. L. Pieri, D. R. de Souza, L. V. Araújo, R. T. Nesi, D. L. Scheffer, V. H. Comin, R. A. Pinho, A. P. Muller, C. T. de Souza., and Obsahuje bibliografii