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

Full 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.

Author information

Author/s: Tamaki, Tetsuro (T); Uchiyama, Yoshiyasu (Y); Okada, Yoshinori (Y); Tono, Kayoko (K); Nitta, Masahiro (M); Hoshi, Akio (A); Akatsuka, Akira (A);

Affiliation: Muscle Physiology and Cell Biology Unit, Department of Regenerative Medicine, Division of Basic Clinical Science, Tokai University School of Medicine, 143 Shimokasuya, Isehara, Kanagawa 259-1143, Japan. tamaki(-atsign-)is.icc.u-tokai.ac.jp

Journal and publication information

Publication Type: Journal Article; Research Support, Non-U.S. Gov't

Journal: Histochemistry and cell biology (Histochem Cell Biol), published in Germany. (Language: eng)

Reference: 2009-Jul; vol 132 (issue 1) : pp 71-81

Dates: Created 2009/06/09; Completed 2009/08/31;

PMID: 19319558, status: MEDLINE (last retrieval date: 8/31/2009, IMS Date: )

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