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Andreo Fernando AguiarINTRODUCTIONSkeletal muscle displays a wide ability to alter the morphology and phenotypicfeatures in response to specific stimuli, such as physical training (12). Whereasendurance training frequently leads to minor changes in muscle mass, strength traininginduces marked muscle hypertrophy (15). For example, the resistance training (RT)during 10 and 12 weeks promoted a 10 to 30% increase in muscle fiber cross-sectionalarea (CSA) in sedentary subjects (55); this rise reaching about 80% in weightliftingathletes (29). Muscle hypertrophy is directly associated with increased myofibrillarprotein content (17) by increase in protein synthesis which enables new contractilefilaments to be added to the pre-existing muscle fiber; this, in turn, enables the muscleto generate greater force (16). While the exact mechanisms involved in the increasedexpression of contractile proteins are unclear, two of the major molecular pathway inregulation of muscle hypertrophy are myogenic regulatory factors (MRFs) and insulinlikegrowth factor-I (IGF-I).The MRFs are a superfamily of transcription factors that regulate the expressionof several skeletal muscle-specific genes (44). The family is composed of fourmembers: myogenin, MRF4, MyoD and Myf5. These proteins belong to a larger basichelix-loop-helix (bHLH) class of transcription factors that, after dimerization with aubiquitous E protein, bind to an E-box domain and promote the expression of musclespecificgenes (11), thus potentially influencing hypertrophy. The MRFs areupregulated during muscle hypertrophy when satellite cells (SC) are required to repairthe load-induced muscle damage. The steps associated with the proliferation,differentiation and fusion of SC to damaged myofibers (hypertrophy) are generally wellestablished (for review see ref. 13). Briefly, MyoD is predominantly upregulated duringthe SC proliferation (54), which from new cells known as myoblasts. Myoblastsdifferentiation is marked by the upregulation of the MRF4 and Myogenin (54). Then,MRFs are often used as markers of myogenic cell differentiation in settings associatedwith muscle formation or muscle hypertrophy (22, 47).Increased MyoD and myogenin gene expression has been shown in human andanimal studies that investigated the acute response to RT (47, 8, 58). Psilander et al.(47) conducted an acute exercise protocol involving eight sets of 8–12 repetitions, andbiopsy samples were collected serially (pre- and 0, 1, 2, 6, 24, and 48 h postexercise)after exercise. The authors showed that the Myogenin, MyoD and mRNA expression43