How muscles grow

Discussion in 'General Bodybuilding' started by Jamie555, Feb 28, 2013.

  1. Jamie555

    Jamie555 Moderator Moderator

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    Whilst posting up another article I noticed this little gem on the same site. Although I have copied in the introduction, there is a discussion of cell signalling (hormones, etc) on the site (see the source link for details). It gives a nice introduction to those bodybuilders without a bio background who want to get a better grip on mechanisms going on in muscle growth.

    Lets Get Hypertrophic
    October 3, 2012
    Lets review how muscles actually grow!

    Mechanisms of Exercise-Induced Muscle Hypertrophy

    Dr Jason Cholewa

    Skeletal muscle is a postmitotic tissue and does not undergo significant cell replacement through the course of human life. Cellular repair in skeletal muscle depends primarily on the dynamic balance between muscle protein synthesis and degradation (Toigo & Boutellier, 2006). Increases in muscle CSA occur nearly exclusively through hypertrophy when protein synthesis exceeds that of protein breakdown (Brooks, Fahey, & Balwin, 2005c). Skeletal muscle hypertrophy occurs via an increase in contractile proteins, increase in non-contractile intracellular volume, and an expansion of the extracellular matrix (Schoenfeld, 2010). Myofibril hypertrophy, the addition of sarcomeres in parallel, accounts for the majority of skeletal muscle growth (Paul & Rosenthal, 2002). Exposure of a myofiber to overload stimulates protein synthesis, leading to an increase in the size and volume of myosin and actin filaments, resulting in a greater number and volume of parallel sarcomeres, and thereby results in an increase muscle CSA (Toigo & Boutellier, 2006).

    Sarcoplasmic hypertrophy occurs through increases in intracellular elements and fluid (Flück & Hoppeler, 2003), and has been suggested to lead to an increase in muscle CSA without significant increases in strength (Siff & Verkhoshansky, 1999). Satellite cells (myogenic stem cells) located between the basal lamina and sarcolemma of the myofiber have been identified as responsible for mediating a significant portion of sarcoplasmic hypertrophy (Rosenblatt, Yong, & Parry, 1994). When activated by mechanical or chemical stimuli, myogenic stem cells proliferate and fuse to existing skeletal muscle fibers, emptying their contents into the muscle fiber, and thus facilitating repair and growth (Toigo & Boutellier, 2006). Myogenic stem cell fusion leads to skeletal muscle hypertrophy via two mechanisms. First, myogenic stem cell fusion donates nuclei to the skeletal muscle fiber (Moss & Leblond, 1971), increasing the number of myonuclear domains, and enhancing mRNA expression throughout the muscle fiber (Toigo & Boutellier, 2006). Second, myogenic stem cells express various myogenic factors that bind to the muscle gene promoter, thereby aiding in regeneration and growth (Sabourin & Rudnicki, 2000).

    Cellular hyper-hydration (cellular swelling) is influenced by aniso-osmolarity, hormones, nutrients, and oxidative stress (Usher-Smith, Huang, & Fraser, 2009), and may also contribute to muscle hypertrophy beyond the acute increase in intracellular fluid by creating a more anabolic environment. Cellular swelling has been shown to stimulate protein synthesis in mammary (Grant, Gow, Zammit, & Sheenan, 2000) and hepatic cells (Stoll, Gerok, Lang, & Häussinger 1992). The increased pressure exerted against the sarcolemma with cellular swelling may pose a threat to cellular integrity, and thereby initiate a signaling response that results in the reinforcement of intracellular structures (Schoenfeld, 2011). Häussinger (1996) hypothesized that cellular swelling is sensed by integrins and transduced down stream to signal protein synthesis, gene transcription, and inhibit proteolysis via mitogen activated protein kinase (MAPK). Additionally, cellular hyperhydration may augment protein stimulus by enhancing amino acid uptake via phosphatidylinositol 3-kinase activation (Low, Rennie, & Taylor, 1997).

    Performance of resistance exercise leads to an anabolic environment through mechanical and chemical signaling cascades. An acute bout of resistance training results in the elevation of both anabolic and catabolic hormones and growth factors (Leite et al., 2011). The metabolic stress and resultant accumulation of metabolites associated with resistance exercise has been suggested to promote anabolism by altering the hormonal milieu (Goto, Ishii, Kizuka, & Takamatsu, 2005), inducing cellular swelling, and promoting the expression of growth factors (Takarada et al., 2000). Mechanical perturbations are sensed and molecularly transduced downstream to a number of pathways that couple myofiber contraction with chemical signals, shifting the intracellular protein balance to stimulate synthesis over degradation (Schoenfeld, 2010). Additionally, sarcolemma deformation and myofibril damage during high degrees of muscle tension attracts macrophages and lymphocytes. As macrophages phagocytize extracellular debris they produce cytokines which activate myoblasts and stimulate myogenic stem cell proliferation and differentiation, leading to a hypertrophic response (Vierck et al., 2000).

    To better understand how betaine may improve body composition via muscle hypertrophy, downstream cellular signaling and the role of hormones in the hypertrophic response will be discussed.

    Downstream Cellular Signaling

    [ Source: Jason Cholewa Let's get hypertrophic ]

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