It is generally accepted that the primary mechanisms governing skeletal muscle hypertrophy are satellite cell activation, proliferation, and differentiation. Specific growth factors and hormones modulate satellite cell activity during normal muscle growth, but as a consequence of resistance exercise additional regulators may stimulate satellite cells to contribute to gains in myofiber size and number. Present knowledge of the regulation of the cellular, biochemical and molecular events accompanying skeletal muscle hypertrophy after resistance exercise is incomplete. We propose that resistance exercise may induce satellite cells to become responsive to cytokines from the immune system and to circulating hormones and growth factors. The purpose of this paper is to review the role of satellite cells and growth factors in skeletal muscle hypertrophy that follows resistance exercise.

Eight steers from a group of 14 were fed ad libitum from 240 to 510 kg live weight, gaining at 1.4 +/- .2 kg/d. The six other steers were diet-restricted and grew at .37 +/- .09 kg/d from 240 to 307 kg, prior to ad libitum realimentation on the same diet to a final weight of 510 kg. Blood samples taken during the growth phases from both treatments were analyzed for insulin-like growth factor-I (IGF-I), triiodothyronine (T3), thyroxine (T4), glucose (GLU), nonesterified fatty acids (NEFA), and blood urea nitrogen (BUN) and (or) growth hormone (GH). During restricted growth, mean serum concentrations of GH were elevated (45.6 vs 23.4 ng/ml; P less than .05), serum concentrations of IGF-I decreased (108 vs 167 ng/ml; P less than .05) compared with control steers with ad libitum access to feed. Levels of T4 and GLU also were lower (P less than .05) during restricted than during normal growth. During early realimentation, levels of GLU (P less than .05), IGF-I (P less than .01), T4 and BUN (P less than .01) increased. Levels of T3 remained unchanged, whereas concentration of NEFA declined (P less than .001). Blood urea nitrogen decreased during early realimentation despite a large increase in diet protein intake and in protein storage, suggesting an increased efficiency of nitrogen use for protein synthesis. During realimentation, IGF-I levels rose above those of control steers and remained higher at the final weight of 510 kg (P less than .05).(ABSTRACT TRUNCATED AT 250 WORDS)

Primary cultures of skeletal muscle satellite cells, the postnatal myogenic precursor cells, were induced to proliferate by exposure to physiological levels of somatomedins (Sms)/insulin-like growth factors (IGFs) and pharmacological levels of insulin. These polypeptides were included in medium containing horse serum as well as serum-free defined medium. Dexamethasone inclusion in the serum-containing medium facilitated the ovine Sm (oSm; P less than 0.05) and the multiplication-stimulating activity/rat IGF-II (MSA/rIGF-II; P less than 0.25) responses, but not the insulin proliferative response. In addition, data from defined medium studies indicate that satellite cells are more sensitive to both IGF moieties than insulin and that the proliferations induced by half-maximal concentrations of oSm and insulin were similar (P less than 0.05), but both were different from the proliferation induced by MSA/rIGF-II (P less than 0.05). In the presence of insulin concentrations that promote maximum proliferation, the addition of oSm did not produce an additive effect, whereas the addition of MSA/rIGF-II did produce a significant increase in satellite cell proliferation above that induced by insulin. MSA/rIGF-II may, therefore, be stimulating proliferation of satellite cells through a receptor system different from that serving insulin and oSm. Collectively, these data support the hypothesis that Sms/IGFs play an important role in the control of postnatal muscle growth by providing a link between these hormones and one of the significant target cells involved in this process.

Insulin-like growth factors (IGFs) and their binding proteins play an essential role in regulating animal growth and metabolism. The initial portion of the current review focuses on the physiological effects of the IGFs and delineates their role as regulators of animal growth and metabolism. The role of IGFs as mediators of growth hormone effects, as insulin-like metabolic regulators and as foetal growth regulators is discussed. The remainder of the review is devoted to the IGF binding proteins, their modulation of IGF action and their role in foetal and postnatal regulation of growth.Keywords: binding proteins, insulin-like growth factor. Overexpression of human insulin-like growth factor-II in transgenic mice causes increased growth of the thymus.