VM Hypertrophy
@VMHypertrophy
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Research & Coaching | Endocrinology, Muscle & Tendon Physiology, PEDs. Main: @0xVM7.
Joined October 2024
Be careful, please, especially as younger demographics are becoming more interested in rhGH and as such may be more likely to attempt higher doses and more rapid uptitration due to their naturally higher GH and IGF-1 levels, as well as due to other factors (which I may write upon
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RhGH carries an ACUTE HYPOglycaemic risk! A recent conversation has shown me how few are aware of this, even in professional circles. So I have decided to raise awareness of this here, also. The risk isn’t only in the long term management of hyperglycaemia and insulin
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In response to a claim that you can “force” progressive overload and that genetics is an “excuse”: That is untrue because myofibrillar hypertrophy is limited by so many factors which dictate the response to stimuli and cap growth. By training, you are only performing a behaviour
@viveresanus16 @art_is_found What dictates the response to stimuli? What dictates nutrient uptake? What dictates tolerability of pharmacology? What dictates recoverability? What dictates myostatin expression? What dictates baseline and potential? Someone with infantile Tay Sachs disease will not look
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@KirinSays @CryptoSteven88 @art_is_found Anyone can lose fat. It’s not that difficult to do and isn’t really limited as much by genetics (mostly just thermodynamics with some additional variables) as building muscle is. Building a decent physique is quite literally more than about losing fat; it’s also about BUILDING
@viveresanus16 @art_is_found What dictates the response to stimuli? What dictates nutrient uptake? What dictates tolerability of pharmacology? What dictates recoverability? What dictates myostatin expression? What dictates baseline and potential? Someone with infantile Tay Sachs disease will not look
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@art_is_found Seems the significance of genetics might be quite underrated by many commenters here.
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More on hypertrophy ( https://t.co/HSXw4Twb49):
@DanAdvantage @locknload1337 @yacineMTB Part 2/4: The best way to induce hypertrophy is with brief, intense training. This is simply because of the way hypertrophy works (I recommend following my account @VMHypertrophy for more information or getting a membership at https://t.co/PmJpZVgJQe to ask any questions). Why
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Execution: The Eccentric and Concentric: Do we need to exaggerate the eccentric? No. Although some of JP’s eccentrics may seem longer in other sets, with heavy loads, minimising injury risk via somewhat longer eccentrics is appropriate (however, individuals who are not using
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@cremieuxrecueil It seems Crémieux didn’t interpret this study correctly! FFM ≠ muscle; this led him to make an incorrect conclusion. Perhaps he should limit his comments to areas where he has a decent understanding. Cremieux may seem intelligent at first until you see him post something
@DrCamRx @maxhertan The number of times I have already addressed that exact study and had to correct people that water retention increases are significantly responsible for the rapid FFM jump is laughable. Also, you can’t extrapolate rapid increases in FFM, which then taper off to a constant rate of
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@Soli729 What Mike Israetel promotes is not “science-based” lifting and science-based lifting actually aligns more with the brief, intense training that Israetel seems to do almost anything to avoid.
@DanAdvantage @locknload1337 @yacineMTB Part 2/4: The best way to induce hypertrophy is with brief, intense training. This is simply because of the way hypertrophy works (I recommend following my account @VMHypertrophy for more information or getting a membership at https://t.co/PmJpZVgJQe to ask any questions). Why
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@BelleauskyeRN @Chris32171566 @misfitpatriot_ “Corticosteroids which have ZERO effect on muscle mass”. FALSE. Corticosteroids have a NEGATIVE effect on muscle mass. They are catabolic and cause MP breakdown, inhibit MPS, can increase myostatin expression, inhibit mTOR and reduce IGF-1 signalling. Have you heard of
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Regarding "desensitisation" and seemingly low IGF-1 (but actually not, e.g., expecting more than 1000 ng/mL), the serum levels and PO with up-titration beyond a certain point could be attributed to serum IGF-1 saturation and non-serum-IGF-1-mediated growth.
Anti-HGH antibody formation, immunogenicity risk is very real. Frequency ( https://t.co/KYprKLRRbk) isn’t the only factor.
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@RupertLowe10 I don’t want to detract from your position, but that’s quite evidently the case for success in a great many sports, regardless of gender/sex. The genetic component is extremely important and a primary factor for success and isn’t limited to sex differences but a variety of
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Regarding "desensitisation" and seemingly low IGF-1 (but actually not, e.g., expecting more than 1000 ng/mL), the serum levels and PO with up-titration beyond a certain point could be attributed to serum IGF-1 saturation and non-serum-IGF-1-mediated growth.
Anti-HGH antibody formation, immunogenicity risk is very real. Frequency ( https://t.co/KYprKLRRbk) isn’t the only factor.
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Anti-HGH antibody formation, immunogenicity risk is very real. Frequency ( https://t.co/KYprKLRRbk) isn’t the only factor.
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@odhagan @wrycountenance @mhartl @cremieuxrecueil Even though you can’t completely target AR only in skeletal muscle or reduce every side effect to zero, you can get them pretty close to that, especially with TRT or “TRT+” levels of steroids. E.g. heart example: Blocking angiotensin II type 1 receptor with telmisartan
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@DrJesseMorse @FogelSylvia @RFMpropagandist Around 20-30% if I had to choose a blanket figure. Significantly less in enhanced bodybuilders due to massive upregulation of anabolic pathways. Still, even as someone enhanced, I don’t take metformin and have stellar BG, despite taking HGH quantities greater than any
@EmporerSuperior @AJA_Cortes Wrong and potentially dangerous misunderstanding. I address this here: https://t.co/Dfz3dq2TYC. "Addressing Insulin and HGH+AAS: I recently talked to someone about the relationship of insulin and HGH+AAS, and it seems there is a misunderstanding about the role of insulin here.
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@DanAdvantage @locknload1337 @yacineMTB Discussion: explaining why desirable, highly scalable BMR elevation via muscle anabolism through training is only possible with BRIEF, INTENSE exercise. Part 1/4: “Brief, intense training leads to the most mechanical tension, consequently the most stimulus relative to fatigue,
@yacineMTB @locknload1337 If you think 3,600kcals is insane, wait until you see what some IFBB pros, pro strongmen, and other athletes especially ones with naturally higher metabolisms eat. Obviously, I am not saying the average American is like this or that their diet is healthy — just mentioning
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@DanAdvantage @locknload1337 @yacineMTB Part 2/4: The best way to induce hypertrophy is with brief, intense training. This is simply because of the way hypertrophy works (I recommend following my account @VMHypertrophy for more information or getting a membership at https://t.co/PmJpZVgJQe to ask any questions). Why
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@DanAdvantage @locknload1337 @yacineMTB @VMHypertrophy Part 3/4: Btw, the contraction cycle is a repeating series of the following molecular events: Attachment: myosin head binds to actin filament, forming cross-bridge Power Stroke: myosin head pivots; pulls actin filament; generates force Detachment: ATP binds to myosin head ∴
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