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

Abstract

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.

A skeletal muscle model of extreme hypertrophic growth reveals the influence of diffusion on cellular design

“…Myonuclear domain size is thought to remain constant during the life of a muscle fiber (2,3,7,8,12,17,21), as nuclear number changes in response to hypertrophy (9,28,31,44,57,59,62) and/or atrophy (1,25,50,70). Although comparable data for crustaceans are not available, Skinner (64) showed a ϳ50% increase in DNA content per gram of protein during extreme atrophy coordinated with ecdysis.…”

Muscle memory and a new cellular model for muscle atrophy and hypertrophy

“…It seems generally accepted that myonuclei are added under many hypertrophic conditions (Allen et al, 1995Bruusgaard et al, 2010;Cabric et al, 1987;Cabric and James, 1983;Cheek et al, 1971;Enesco and Puddy, 1964;Giddings and Gonyea, 1992;Kadi et al, 1999;Lipton and Schultz, 1979;McCall et al, 1998;Moss, 1968;Moss and Leblond, 1970;Roy et al, 1999;Schiaffino et al, 1976;Seiden, 1976;Winchester and Gonyea, 1992). However, the growth differs from the model shown in Fig.…”

Effect of radiation on satellite cell activity and protein expression in overloaded mammalian skeletal muscle

“…Satellite cells, the normally inactive myogenic nuclei that participate in developmental and regenerative growth of skeletal muscle (reviewed in Schultz and McCormick, 1994), may play an important role in some of these events. Activation of satellite cells has been observed in stretch-overloaded avian muscle (Winchester et al, 1991;Winchester and Gonyea, 1992;Schultz, 1992, 1994); in weight-trained cat muscle (Giddings and Gonyea, 1992); and in functionally overloaded rodent muscle (Hanzlikova et al, 1975;Schiaffino et al, 1976). Since activated satellite cells fuse to each other to form new fibers during regeneration (Snow, 1977), they might also form new fibers during hypertrophy.…”