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.

These experiments were designed to test the hypothesis that locomotory gait transitions occur when some critical cross-sectional area of active muscle is reached as animals increase speed within a gait. We used glycogen depletion as evidence of muscle fiber activity and selected an experimental animal in which all muscle fibers in the locomotory muscles rely extensively on glycogen as a substrate--the lion. We found a high correlation between biochemically and histochemically determined rates of glycogen depletion (r = 0.906). Rates of glycogen depletion in the biceps femoris and triceps brachii muscles increased logarithmically with speed with no discontinuities at the gait transitions. However, we found large discontinuities both in the total cross-sectional area of muscle that showed depletion and in the rates at which the different types of fibers depleted glycogen at the trot-gallop transition. Our results indicate that 1) gait transition did not occur at a maximum tension level either for a particular type of fiber or the whole muscle, and 2) different configurations of motor units within an individual muscle may be recruited as an animal changes gait.

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