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mTOR pathway
By: Hypertrophy
The mTOR (Mechanistic target of rapamycin) pathway is a serine-threonine protein kinase that regulates cell growth, cell proliferation, cell motility, cell survival, autophagy, protein synthesis and transcription. It belongs to the PIKK (phosphatidylinositol 3 kinase related kinase) family. It also indirectly promotes the activation of insulin receptors and IGF1 receptors through the downstream pathways.
mTOR comes in two complexes, mTORC1 and mTORC2. MTORC1 is composed of mTOR, Raptor (regulatory associated protein of mTOR), mLST8 (mammalian lethal with SEC13 protein 8) and non core components (PRAS40 and DEPTOR). This functions as a redox/nutrient/energy sensor and controls protein synthesis. The activity for this complex is regulated by insulin, growth factors, phosphatidic acid, some amino acids, rapamycin, mechanical stimuli and oxidative stress. Now moving on to mTORC2, this complex is made up of mTOR, RICTOR (rapamycin insensitive companion of mTOR), Protor 1 and 2, MLST8, and mSIN1 (mammalian stress activated protein kinase interacting protein 1). This complex is involved in cell survival, metabolism and cytoskeletal organization.
So mTORC1 is the protein that is responsible for muscle hypertrophy and is what test activates in order to promote protein synthesis and bigger muscles. Testosterone binds to the AR then moves to the nucleus, from there it promotes production of IGF1. The IGF1 then binds to the IGF1 receptor on the outside of the muscle cell. This activates PI3K which then activates AKT. The active AKT phosphorylates TSC 1 and 2 (aka the proteins that inhibit rheb). So with the phosphate group added to TSC 1/2 it gets inhibited, meaning that TSC 1/2 is no longer inhibiting rheb and rheb can interact with and activate mTORC1 (Thank you akt jfl). Now with mTORC1 activated it can phosphorylate downstream targets such as S6K and 4EBP1. When S6K is phosphorylated it enhances protein synthesis of specific mRNAs. Moving on to 4EBP1, when this is phosphorylated it releases eIF4E which is essential for binding to the cap of mRNA which then starts the process of translating mRNA into proteins. (btw all phosphorylating is, is just adding a phosphate group to a molecule which can change its activity). This then leads to increased muscle proteins which leads to muscle growth.
(yes ik this image uses the IR and not the IGF1R dont kill me)
There is alot that also plays into mTOR and much more factors that activates it or inhibits it, it's fairly complex and interesting. So ill leave it at that because this thread is only talking about testosterone.
That's all bhais, rep it up
By: Hypertrophy
The mTOR (Mechanistic target of rapamycin) pathway is a serine-threonine protein kinase that regulates cell growth, cell proliferation, cell motility, cell survival, autophagy, protein synthesis and transcription. It belongs to the PIKK (phosphatidylinositol 3 kinase related kinase) family. It also indirectly promotes the activation of insulin receptors and IGF1 receptors through the downstream pathways.
mTOR comes in two complexes, mTORC1 and mTORC2. MTORC1 is composed of mTOR, Raptor (regulatory associated protein of mTOR), mLST8 (mammalian lethal with SEC13 protein 8) and non core components (PRAS40 and DEPTOR). This functions as a redox/nutrient/energy sensor and controls protein synthesis. The activity for this complex is regulated by insulin, growth factors, phosphatidic acid, some amino acids, rapamycin, mechanical stimuli and oxidative stress. Now moving on to mTORC2, this complex is made up of mTOR, RICTOR (rapamycin insensitive companion of mTOR), Protor 1 and 2, MLST8, and mSIN1 (mammalian stress activated protein kinase interacting protein 1). This complex is involved in cell survival, metabolism and cytoskeletal organization.
So mTORC1 is the protein that is responsible for muscle hypertrophy and is what test activates in order to promote protein synthesis and bigger muscles. Testosterone binds to the AR then moves to the nucleus, from there it promotes production of IGF1. The IGF1 then binds to the IGF1 receptor on the outside of the muscle cell. This activates PI3K which then activates AKT. The active AKT phosphorylates TSC 1 and 2 (aka the proteins that inhibit rheb). So with the phosphate group added to TSC 1/2 it gets inhibited, meaning that TSC 1/2 is no longer inhibiting rheb and rheb can interact with and activate mTORC1 (Thank you akt jfl). Now with mTORC1 activated it can phosphorylate downstream targets such as S6K and 4EBP1. When S6K is phosphorylated it enhances protein synthesis of specific mRNAs. Moving on to 4EBP1, when this is phosphorylated it releases eIF4E which is essential for binding to the cap of mRNA which then starts the process of translating mRNA into proteins. (btw all phosphorylating is, is just adding a phosphate group to a molecule which can change its activity). This then leads to increased muscle proteins which leads to muscle growth.
(yes ik this image uses the IR and not the IGF1R dont kill me)
There is alot that also plays into mTOR and much more factors that activates it or inhibits it, it's fairly complex and interesting. So ill leave it at that because this thread is only talking about testosterone.
That's all bhais, rep it up
