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Acute hypertrophic response of skeletal muscle to removal of synergists

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1979

Year

TLDR

The study aimed to examine the rapid hypertrophic response of skeletal muscle following removal of synergistic muscles and to determine whether inflammation drives this initial enlargement. Researchers conducted a series of experiments to test an inflammation hypothesis, track its time course, and identify causative factors, hypothesizing that surgical trauma or increased muscle stretch triggers the inflammatory response. Plantaris muscle weight rose 14 % within 1 h after gastrocnemius removal, peaked 1–5 days post‑surgery, and returned to baseline by day 16, with inflammation—edema, leukocyte infiltration, and increased hexose monophosphate shunt activity—identified as the driving factor and surgical trauma confirmed as its cause.

Abstract

The purpose of this project was to study the initial rapid enlargement phase of skeletal muscle in response to ablation of synergistic muscles. The first experiment tested the hypothesis that this initial phase is due to inflammation in the enlarging muscle. The wet weight of the plantaris muscle increased significantly (14%) within 1 h after removal of the ipsilateral gastrocnemius muscle. This increase was due to inflammation, as evidenced initially by edema, and within the next few hours, by leukocyte invasion of the interstitium and enhanced hexose monophosphate shunt-reducing capacity. In the second experiment we followed the time course of this inflammatory reaction. The response peaked at 1–5 days following surgery, after which it subsided to control levels by 16 days postsurgery. The final experiments were designed to uncover the factor(s) causing the inflammatory response. Two possible mechanisms were hypothesized: 1) trauma resulting from surgical manipulation of the tissue, and 2) trauma due to elevated stretch and/or tension on the muscle following removal of the synergists. The data indicate that surgical trauma is the causative factor of the inflammatory response in this hypertrophy model.