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Anabolic-androgenic steroid does not enhance compensatory muscle hypertrophy but significantly diminish muscle damages in the rat surgical ablation model

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Abstract

Cellular responses in the compensatory hypertrophied (plantaris) muscle induced by surgical ablation of synergistic muscles (soleus and gastrocnemius) were determined during 10-week anabolic androgenic steroid (AAS) treatment. Adult Wistar male rats were divided randomly into the Control and Steroid groups, and contralateral surgery was performed. Nandrolone decanoate was administered to the Steroid group. [3H]thymidine and [14C]leucine labeling were used to determine the serial changes in cellular mitotic activity and amino acid uptake. Myogenic cells and cellular responses in blood vessels and nerve fibers were analyzed by immunohistochemistry. Significantly lower cellular mitotic activity associated with lower volume of muscle fiber necrosis was observed in the Steroid group during the first week. However, amino acid uptake and final muscle wet weight gain did not differ between the groups. Marked activation/proliferation of muscular, vascular, and peripheral nerve-related cells was seen with the inflammatory responses in both groups. However, this activation was dependent on the volume of muscle fiber damage and was not preferentially accelerated by AAS loading. These results indicated that AAS loading significantly diminished muscle fiber damages, but they did not accelerate final muscle wet weight gain and activation of myogenic, vascular, and peripheral nerve related cells in the compensatory enlarged muscles.

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Acknowledgment

This work was supported by a Grant-in-Aid for Scientific Research (B-12480012) from the Ministry of Education, Science and Culture of Japan.

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Correspondence to Tetsuro Tamaki.

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Tamaki, T., Uchiyama, Y., Okada, Y. et al. Anabolic-androgenic steroid does not enhance compensatory muscle hypertrophy but significantly diminish muscle damages in the rat surgical ablation model. Histochem Cell Biol 132, 71–81 (2009). https://doi.org/10.1007/s00418-009-0584-2

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  • DOI: https://doi.org/10.1007/s00418-009-0584-2

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