Morphological observations supporting muscle fiber hyperplasia following weight-lifting exercise in cats

Although exercise-induced muscle fiber hyperplasia has been demonstrated through direct fiber counts following nitric-acid digestion of muscle, morphological studies to determine the mechanism of hyperplasia have not been performed previously. In this study, light and electron microscopy were used to evaluate evidence of muscle fiber splitting or de novo formation of new muscle fibers. Since both fiber hypertrophy and hyperplasia may result in alterations in the muscle nuclear populations, myonuclear number and satellite cell frequency were assessed quantitatively to determine their role in regulating muscle fiber size. Ten adult cats performed weight-lifting exercise, and the right (exercised) and left (control) forelimbs were fixed by vascular perfusion. Spaced serial sections were used to evaluate muscle fiber morphology along the length of fibers, and muscle fiber areas were measured. Myonuclei and satellite cells were counted using electron microscopy. Morphological evidence supporting muscle fiber hyperplasia was observed in exercised muscles. These observations included the presence of small fibers which may signify de novo fiber formation. Myonuclear counts indicate that myonuclear density is not a primary regulator of fiber size. Satellite cell frequency was unchanged following exercise. Autoradiographic studies revealed satellite cell activation by uptake of tritiated thymidine in exercised muscles. Satellite cell activation appears to result from increased activity in exercised muscles. These findings confirm previous studies demonstrating muscle fiber hyperplasia following weight-lifting exercise, and suggest that de novo fiber formation is the major mechanism contributing to muscle fiber hyperplasia in this model.