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The distribution of Type I and Type II fibers, as determined from histochemical estimation of myofibrillar ATPase activity, was studied within and among the locomotory muscles of the forelimb, trunk, and hindlimb of three mongrel dogs. All Type II fibers had high oxidative capacities as estimated from the histochemical assay for reduced nicotinamide adenine dinucleotide tetrazolium reductase, so they were not further divided into subpopulations. Furthermore, Type I and Type II fibers had similar oxidative potentials as indicated by both histochemistry and biochemistry. Type I fiber populations ranged between 14% and 100% in the muscles sampled. The highest percentages of Type I fibers were found in deep muscles of physiological extensor groups in the arm and thigh that serve to resist gravity (antigravity muscles) when the dog is in the quadrupedal standing position. More superficial muscles in these same groups had fewer Type I fibers. The patterns of Type I fiber distribution among muscles in the antigravity groups of the forearm and leg were the opposite of those in the arm and thigh, with the more superficial muscles of the distal limb segments having more Type I fibers than the deeper muscles. In all limb segments, muscle groups that do not serve to resist gravity did not show as much intermuscular variation. Type I fiber populations in these muscles did not exceed 50%. A stratification of fiber types also existed within muscles, both in extensor and flexor groups, with the deeper portions of the muscles having more Type I fibers than the more superficial portions.

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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.

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