Endocrine Abstracts

Myostatin (MSTN) is a negative regulator of skeletal muscle growth, while androgens are strong positive regulators of muscle growth and strength. Follistatin (FS) is a binding protein which inhibits MSTN action. Evidences suggest that MSTN and testosterone actions in muscle may be associated. However, the mechanisms of androgens actions are not fully elucidated. The objective of this study was to evaluate the influence of exercise training in the expression of MSTN and FS in orchidectomized rats submitted to exercise. Adult male Wistar rats were housed under controlled conditions (20–220 C, 12 h light-dark cycle) and were allowed free access to standard rodent chow. After 3 days of acclimation, rats were orchidectomized (O) or sham-operated (S). One group of animals was maintained intact (I). After 1 week, animals were randomly assigned to a training group (O-Train, S-Train and I-Train) or a sedentary group (O-Sed, S-Sed and I-Sed). O-Train, S-Train and I-Train were submitted to resistance training for 8 weeks. In the training protocol, animals climbed a 1.1-m vertical ladder with weights attached to their tails. The sessions were performed three times a week, with 4–9 climbs and 8–12 dynamic movements per climb. After this period, rats were decapitated and white gastrocnemius muscle were dissected, immediately frozen in liquid nitrogen and stored at −700 C for subsequent analysis. MSTN and FS mRNA was quantified by real time RT-PCR. The animals were maintained according to the local University Committee guidelines for the care and use of laboratory animals. P<0.05 was considered statistically significant. MSTN mRNA expression was significantly higher in gastrocnemius muscle of O-Sed group than in I-Sed group. FS mRNA expression did not vary among the groups. The results indicate that MSTN expression increases in skeletal muscle of orchidectomized rats and is not influenced by resistance training.

Declaration of interest: The authors declare that there is no conflict of interest that could be perceived as prejudicing the impartiality of the research project.

Funding: This research did not receive any specific grant from any funding agency in the public, commercial or not-for-profit sector