Muscle Growth Flowchart

Discussion in 'General Training' started by imported_dkm1987, Nov 8, 2004.

  1. Internal tension rises as the muscle fiber contracts. External tension rises more slowly as the series elastic elements are stretched. (a) During a single-twitch contraction, external tension cannot rise as high as internal tension before the relaxation phase begins. (b) During a tetanic contraction, external tension soon plateaus at a level roughly equivalent to internal tension. External tension remains elevated for the duration of the contraction.
  2. Muscle fibers of different motor units are intermingled, so the forces applied to the tendon remain roughly balanced regardless of which muscle groups are stimulated. (b) The tension applied to the tendon remains relatively constant even though individual motor units cycle between contraction and relaxation.
  3. Possible mechanism of activation of ERK1/2 and AP-1 in skeletal muscles. Schematic representation of the potential mechanism of activation of ERK1/2 and AP-1 transcription factor in response to mechanically loading of skeletal muscles either axially or transversely as supported by the data. Despite activation of ERK1/2 by either form of mechanical stress, the MEK1/2, PI3K, and PKC are involved in the activation of ERK1/2 in response to axial mechanical stress whereas PKA is involved only in response to applied transverse stress.
  4. Allright that comprises the bulk of what I can contribute. The rest is in study papers and if anyone would like links or copies just let me know. I do have some stuff on the influence of endogeneous hormone introduction if anyone wishes.

    If anyone can fill in the blanks please do as I am very interested, obvioulsy :D
  5. I dug deeper in my filing system and came up with this, this I like I wish I had more.

    The mitogen-activated protein (MAP) kinase intracellular signaling pathway (adopted from Ref. 74). After stimulation, a variety of known and unknown upstream regulators lead to the sequential phosphorylation and activation of a MAP kinase kinase kinase (MAPKKK) and subsequently a MAP kinase kinase (MAPKK). The MAPKK can then phosphorylate (P) and activate MAP kinase (MAPK) on conserved threonine and tyrosine residues. Activated MAP kinase phosphorylates numerous substrates, resulting in various biological effects.
  6. Contraction effects on MAP kinase signaling pathways in skeletal muscle. Physical exercise and muscle contraction activate the c-Jun NH2-terminal kinase (JNK), extracellular signal-regulated kinase (ERK), and p38 signaling cascades in rodent and human skeletal muscle. The mechanism(s) that leads to activation of MAP kinase signaling with exercise could involve mechanical, systemic, autocrine, or paracrine factors, as well as a change in the energy status of the contracting muscle fibers. Established and putative cytosolic and nuclear substrates of MAP kinases in skeletal muscle are shown. RSK, 90-kDa ribosomal S6 kinase; MSK, mitogen and stress-activated protein kinase; MNK, MAP kinase-interacting kinase; ATF-2, activating transcription factor 2; CHOP, CCAAT/enhancer-binding protein (C/EBP) homologous protein; CREB, cAMP-dependent response element-binding protein; MEF2, myocyte enhancer-binding factor 2.
  7. Putative substrates and biological consequences of AMP-activated protein kinase (AMPK) activation in response to muscle contraction. Contraction alters the fuel status of skeletal muscle, which leads to the activation of AMPK by allosteric and phosphorylation-dependent mechanisms. Activated AMPK phosphorylates various known and unknown targets and induces multiple cellular responses. AMPKK, AMP-activated protein kinase kinase; eNOS, endothelial nitric oxide synthase; ACC, acetyl-CoA carboxylase; ?, unidentified molecule.
  8. Exercise regulates multiple intracellular signaling molecules in skeletal muscle. Putative cellular functions that may be regulated by each molecule are shown. The top row includes processes that may utilize these signaling proteins in response to an acute bout of exercise in skeletal muscle; the bottom row list functions putatively regulated by these proteins for chronic adaptations to exercise. GSK3, glycogen synthase kinase-3; p70S6K, 70-kDa S6 protein kinase; +, positive regulation; , negative regulation.
  9. Even though it deals with smooth muscle many of the transcriptional processes overlap into striated muscle from what I understand, so yeah I would say it does, Thanks guy :D
  10. More IGF and related info from Adams, I forgot I had this one [​IMG]

    The Ras-ERK signaling cascade. A simplified diagram of one intracellular signaling pathway associated with tyrosine kinase activity of the type 1 insulin-like growth factor receptor (IGFR1). A number of studies have linked this pathway with the control of muscle cell proliferation in vitro. The phosphorylation targets of ERKs include transcription factors and additional protein kinases. ERK, extracellular signal-regulated kinase; MEK, mitogen-activated protein kinase (MAPK)/ERK kinase; Raf, MAPK kinase kinase; Ras protein, member of the Ras GTPase family; Shc, SH2-containing collagen-related proteins (couples IGFR1 tyrosine kinase to Ras).
  11. The IRS-PI3K signaling cascade. Signaling through PI3K is central to a large number of processes in mammalian cells. In this greatly simplified diagram, one of the primary pathways leads to increased translation initiation and increased production of components of the transnational system. Also shown is the pathway for protection from apoptosis and that which can mediate increased cytoplasmic calcium levels. DAG-induced increases in PKC activity have the potential to feed back and prevent the phosphorylation of IRS-1. For clarity, potential interactions between the Ras/ERK pathway (Fig. 1) and calcineurin and G-protein receptor signaling have been omitted. Akt, protein kinase B; BAD, proapoptotic regulator of programmed cell death; Bcl2, regulator of programmed cell death, promotes cell survival; DAG, diacylglycerol; 4E-BP1, eukaryotic initiation factor 4 binding protein; eEF2, eukaryotic elongation factor-2 (k = kinase); GSK3, glycogen synthase kinase 3; IRS, insulin receptor substrate; mTOR, mammalian target of rapamycin; PI3-kinase (PI3K), phosphotidylinositol 3-kinase; PIP2, phosphatidylinositol 3,4-bisphosphate; PIP3, phosphatidylinositol 3,4,5-trisphosphate; PDK1, PI3K-dependent kinase; PKC, protein kinase C; S6K1, p70 S6 kinase.
  12. IGF-I and "myogenesis" during compensatory hypertrophy. Increased loading leads to satellite cell proliferation, differentiation, and fusion. IGF-I has been shown to stimulate these myogeninc processes in skeletal muscles. It is postulated that IGF-I, and/or the loading-sensitive IGF-I isoform mechanogrowth factor (MGF), is produced and released by myofibers in response to increased loading or stretch. The increased local concentration of IGF-I (MGF) would then stimulate the myogenic processes needed to drive the hypertrophy response.
  13. Old and Grey

    Old and Grey Super Moderator Staff Member

    And if you can summarize this in 25 words or less, you win a super duper top secret HST Decoder Ring. [​IMG]
  14. mikeynov

    mikeynov Super Moderator Staff Member

    Wow, this thread is dynamite good. It should be a sticky imho.

    Glad to see you've also earned your wings with the 'HST Expert' distinction. This is very well earned, in my esitmation :)
  15. With the Green Hornet Mask? You got a deal, yeah right.
  16. Thanks Michael. Coming from someone as educated as you, I feel blessed. Now add to it. [​IMG]
  17. Keep Frequency High at least every 48 hours
    Increase the weight each workout
    Supply the Tension for enough time
    Strategically Decondition when growth stops


    Where is my Preciousssss, I want my Precioussss
  18. Old and Grey

    Old and Grey Super Moderator Staff Member

    It's in the mail! [​IMG] [​IMG] [​IMG]
  19. RotatorCuff

    RotatorCuff New Member

    Some of your diagroms stated that some of these chemicals regulate gene regulation and transcription. How exactly do they do this? What do they do to genes?
  20. First they are not MY diagrams, these I pulled from various studies that I have compiled when following what Bryan suggested, read the reviews then work through the recitations to get a good understanding of the hypertrophy processes.

    From my limited understanding, genes are either turned on or off by outside events, in hypertrophy all the events have not been identified, but many have, as you've seen in the diagrams from the studies above. As far what exactly turns them on to induce growth is complicated and I don't fully understand it all, as it would take someone who is educated more than myself in molecular biology. But here is a quick down and dirty synopsis that I have in my files.

    Now to see how all this deals with Hypertrophy, you might want to read these studies.

    <a href="" target="_blank">Integrin signaling's potential for mediating gene expression in hypertrophying skeletal muscle

    Clark, E. A., and J. S. Brugge. Integrins and signal transduction pathways: the road taken. Science 268: 233-239, 1995

    Giancottin, F. G., and E. Ruoslahti. Integrin signaling. Science 285: 1028-1032, 1999

    Ingber, D. E. Tensegrity: the architectural basis of cellular mechanotransduction. Annu. Rev. Physiol. 59: 575-599, 1997

    Schwartz, M. A., M. D. Schaller, and M. H. Ginsberg. Integrins: emerging paradigms of signal transduction. Ann. Rev. Cell. Dev. Biol. 11: 549-599, 1995

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