Research in Endocrinology, Muscle & Tendon Physiology, PEDs. Main: @0xVM7.

Joined October 2024
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 resistance!
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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 in more detail later). For many reasons the acute HYPOglycaemic risk ought to be brought to attention to all rhGH users but I suggest a special emphasis for younger demographics.
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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 associated with a signal which sets off processes via mechanotransduction, which, after happening ONLY THEN, leads to progressive overload. You (~) only perform the signal here; the rest is contingent on factors external to that. This is why you have some people who are not that great at training, e.g. Paul Dillett, be able to build such a physique, and why someone with Tay Sachs disease with amazing training and amazing PED stack would be smaller than a natural Phil Heath before he even started bodybuilding. You (~) only send the signal. You only take in resources, e.g., food. You only provide other signals, e.g. with PEDs, and increase various other signals with sleep. What your body does with them is contingent on genetics.
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 like Phil Heath with current technology. I am tired of people pretending and lying to people that you can achieve what someone else can achieve when there are HARD, GENETIC limiting factors preventing them with current technology. I am tired of people ruining their health and lives trying to achieve what they are biologically not built for and dying in the process.
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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 muscle (which is heavily limited by genetics). Creating tends to be harder than destroying (this applies to fat loss vs muscle gain, too). UCP1 and PPARGC1A are some pretty acceptable candidates for genes affecting metabolism and lipolysis (to address your question somewhat).
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 like Phil Heath with current technology. I am tired of people pretending and lying to people that you can achieve what someone else can achieve when there are HARD, GENETIC limiting factors preventing them with current technology. I am tired of people ruining their health and lives trying to achieve what they are biologically not built for and dying in the process.
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Replying to @art_is_found
Seems the significance of genetics might be quite underrated by many commenters here.
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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 such loads or are not so susceptible to injury may decrease the time of the eccentrics, as the concentric portion is more important, and in assigning energy to each part of the movement, we should prioritise the most stimulating, as we seek to maximise the stimulus-to-fatigue ratio in order to achieve the most growth).
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More on hypertrophy (enhancedbb.com):
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 enhancedbb.com to ask any questions). Why does muscle grow, and why is this the sort of training that causes it to grow the most? When muscle fibres controlled by the high threshold motor units (remember when I mentioned MUR) experience an adequately high level of mechanical tension as a result of slowing contraction velocities (look at force-velocity relationship image: credit to Chris Beardsley from S&C Research), we have what we will call “stimulating reps.” Quickly explaining the importance of high threshold motor units: they are largely composed of type II (fast-twitch) muscle fibres, which have the higher intrinsic capacity/potential for force production and hypertrophy. As the name explains, they are only recruited at high force demands, during ONLY brief, intense training; they have a greater density of contractile proteins and more potential for MPS compared to type I fibres. Motor units are recruited from smallest to largest (lowest threshold to highest threshold) based on force required; low to moderate intensities recruit the low threshold units (type I and endurance based); consequently, ONLY brief, intense exercise recruits high threshold motor units. Now, these reps occur at approximately 90% (roughly equivalent to 5RM loads) of maximal unfatigued isometric force production (so you can see how repetitions of cardio are not going to be stimulating in a way which is scalably anabolic — have to be specific here because of untrained -> beginner cardio is slightly anabolic but in a way which isn’t sufficiently scalable due to novel stimulus and more MUR than before). As those who strength train or bodybuild (or engage in similar resistance training) are already familiar with, such rep ranges when taken to “failure” (hence, INTENSE) result in an INVOLUNTARY SLOWING OF CONTRACTILE VELOCITY — meaning as we approach the end of the set, the rep gets slower and harder, and we can’t do anything about it. Next, I’m going to explain why high threshold motor units experiencing high mechanical tension is what’s required for adequate training stimulus to cause sufficient anabolic adaptations to increase BMR in a scalable way via muscle growth: Mechanical tension is determined by the force-velocity relationship as applied to a single muscle fibre. Under quick shortening, the fibre produces a small force (few myosins attach to actin), however, under slow shortening (REMEMBER what I say about INVOLUNTARY SLOWING CONTRACTILE VELOCITY and how this is achieved only with INTENSE training, meaning high effort per repetition of which approximately the last 5 are meaningful or more precisely that 90% of max force production figure? Well, you’re not going to generate such forces with ultra-high-rep exercise or cardio, because you will be too fatigued to be able to produce 90% of your maximal unfatigued isometric force with the loads which allow you to perform that many reps in such a fashion) a large force is produced (more myosins attach to actin). Now, when contraction velocity is significantly slowed (remember that ONLY BRIEF INTENSE TRAINING allows for this because if the training is not brief then you are fatigued by the point that you get to these reps and therefore cannot produce sufficient force for your high threshold motor units to experience adequate mechanical tension), the dwell time (the time where the myosin heads remain attached to actin) increases ∴ increasing the duty ratio which is the fraction of the contraction cycle during which a cross-bridge — connection between myosin and actin — is active. enhancedbb.com/explaining-wh… ENHANCEDBB.COM. @VMHypertrophy.
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High dose rHGH+AAS: Systemic stress indicated by HRV drop and RHR increase. Stabilisation then reversal with breathwork and telmisartan. More details (email) and read: enhancedbb.com/stack-update-…. For telmisartan: try to take it far away from training sessions (telmisartan has a negative role in angiotensin II signalling regarding hypertrophy). [email protected] enhancedbb.com
High dose rHGH+AAS: Systemic stress indicated by HRV drop and RHR increase. Speculation: caused by the body’s massive focus on muscle anabolism at the cost of other processes due to recorded increases in strength and muscle mass. [email protected] enhancedbb.com
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VM Hypertrophy retweeted
Replying to @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 ridiculous in a field where you are very knowledgeable, and suddenly, this image is shattered. Scrutinise what this account says, as we now know he is prone to making easily avoidable mistakes! Perhaps Cremieux should delete his tweets on this topic and follow me like Dr. Cameron Maximus did when I corrected him. That would help him avoid such mistakes again, and perhaps he could learn some interesting new things.
Replying to @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 progress — especially when you’re looking at a 10 week study. You guys should actually read the studies you talk about. I am probably one of the most informed people on the planet in some aspects of PED research (you can check out @VMHypertrophy), and I am also the first to research the HRV/IGF-1/HGH/BG relationship at highly supraphysiological levels. Please tell me you have some experience with PED research beyond skimming the abstract of one study; otherwise, what’s the point even talking to you?
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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.
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 enhancedbb.com to ask any questions). Why does muscle grow, and why is this the sort of training that causes it to grow the most? When muscle fibres controlled by the high threshold motor units (remember when I mentioned MUR) experience an adequately high level of mechanical tension as a result of slowing contraction velocities (look at force-velocity relationship image: credit to Chris Beardsley from S&C Research), we have what we will call “stimulating reps.” Quickly explaining the importance of high threshold motor units: they are largely composed of type II (fast-twitch) muscle fibres, which have the higher intrinsic capacity/potential for force production and hypertrophy. As the name explains, they are only recruited at high force demands, during ONLY brief, intense training; they have a greater density of contractile proteins and more potential for MPS compared to type I fibres. Motor units are recruited from smallest to largest (lowest threshold to highest threshold) based on force required; low to moderate intensities recruit the low threshold units (type I and endurance based); consequently, ONLY brief, intense exercise recruits high threshold motor units. Now, these reps occur at approximately 90% (roughly equivalent to 5RM loads) of maximal unfatigued isometric force production (so you can see how repetitions of cardio are not going to be stimulating in a way which is scalably anabolic — have to be specific here because of untrained -> beginner cardio is slightly anabolic but in a way which isn’t sufficiently scalable due to novel stimulus and more MUR than before). As those who strength train or bodybuild (or engage in similar resistance training) are already familiar with, such rep ranges when taken to “failure” (hence, INTENSE) result in an INVOLUNTARY SLOWING OF CONTRACTILE VELOCITY — meaning as we approach the end of the set, the rep gets slower and harder, and we can’t do anything about it. Next, I’m going to explain why high threshold motor units experiencing high mechanical tension is what’s required for adequate training stimulus to cause sufficient anabolic adaptations to increase BMR in a scalable way via muscle growth: Mechanical tension is determined by the force-velocity relationship as applied to a single muscle fibre. Under quick shortening, the fibre produces a small force (few myosins attach to actin), however, under slow shortening (REMEMBER what I say about INVOLUNTARY SLOWING CONTRACTILE VELOCITY and how this is achieved only with INTENSE training, meaning high effort per repetition of which approximately the last 5 are meaningful or more precisely that 90% of max force production figure? Well, you’re not going to generate such forces with ultra-high-rep exercise or cardio, because you will be too fatigued to be able to produce 90% of your maximal unfatigued isometric force with the loads which allow you to perform that many reps in such a fashion) a large force is produced (more myosins attach to actin). Now, when contraction velocity is significantly slowed (remember that ONLY BRIEF INTENSE TRAINING allows for this because if the training is not brief then you are fatigued by the point that you get to these reps and therefore cannot produce sufficient force for your high threshold motor units to experience adequate mechanical tension), the dwell time (the time where the myosin heads remain attached to actin) increases ∴ increasing the duty ratio which is the fraction of the contraction cycle during which a cross-bridge — connection between myosin and actin — is active. enhancedbb.com/explaining-wh… ENHANCEDBB.COM. @VMHypertrophy.
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“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 corticosteroid-induced myopathy? Please don’t act like you’re an authority on this topic because you’re a nurse and then say such evidently incorrect things.
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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 (academic.oup.com/jcem/articl…) isn’t the only factor.
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VM Hypertrophy retweeted
Replying to @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 factors, such as ACTN3, the length of CAG repeats, PPARGC1A, ACE, MSTN and more.
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High dose rHGH+AAS: Systemic stress indicated by HRV drop and RHR increase. Speculation: caused by the body’s massive focus on muscle anabolism at the cost of other processes due to recorded increases in strength and muscle mass. [email protected] enhancedbb.com
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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 (academic.oup.com/jcem/articl…) isn’t the only factor.
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Anti-HGH antibody formation, immunogenicity risk is very real. Frequency (academic.oup.com/jcem/articl…) isn’t the only factor.
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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 decreases vasoconstriction and aldosterone secretion, which drive hypertension -> lower bp reducing afterload on heart -> reduces LVH. Reduces negative cardiac remodelling via activation of PPAR-γ. Also dampens pro-fibrotic signalling via TGF-β pathways and can reduce ox stress and inflammation in cardiac tissue, further mitigating maladaptive remodelling. Even if selective blocking of AR to counter their targeting by AAS doesn’t occur here, you’ve still addressed the vast majority of the negatives that would have otherwise come from that regarding maladaptive left ventricular hypertrophy REGARDLESS of AR specificity. Take this approach for all aspects of your body. Mitigate sides and take advantage of benefits. So, what exactly is the major asymmetric drawback?
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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 recorded in a (yet) published study and eating over 800-1,000+g carbs daily.
Wrong and potentially dangerous misunderstanding. I address this here: enhancedbb.com/stack-update-…. "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. If you have no major insulin bottleneck (e.g. optimal bg whilst running high doses of HGH), you will benefit from enormous increases in anabolism from adding in HGH much more than from AAS solo, even without exogenous insulin if you avoid insulin resistance (as I have for now — no insulin, no metformin and 4.2 mmol/l blood glucose level about 2 hours postprandial) and about ~70 of generic HGH a day (decreasing soon). Some people develop significant insulin resistance from HGH quickly; some do not. Frequency, age, diet, health, lifestyle, and genetics all affect this. You do NOT need exogenous insulin or even metformin to benefit from HGH (including hypertrophy and hyperplasia-wise, not simply via recovery and so forth); if you have a bottleneck or are absolutely maximising everything, then it will lead to more results, but the jump from AAS to AAS+HGH is massive and not simply due to recovery/sleep/synergy as some believe. It is significantly more anabolic than AAS alone. If there is enough interest, I may write a post on this." HbA1c-(IFCC) on about 70 iu of generic HGH a day, btw. Bloodwork here: enhancedbb.com/bloodwork-upd…. HGH+AAS also, in my personal experience, produces far more anabolism than AAS solo. Do bear in mind that HGH solo for muscle building is largely a waste (at these levels, anyway), but "HGH+AAS no insulin" isn't, in the same way that "AAS solo" isn't. I can explain non-anecdotally why the thread is wrong, but only if it's worthwhile and you are interested. IGF-1 test may come later. [email protected] enhancedbb.com
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VM Hypertrophy retweeted
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, and therefore the most growth, which in turn leads to higher maintenance.” Ok, this was my response to your claim: “More than active. Cmon bro, be honest: that’s a lot of vigorous physical activity per day” in response to someone saying 3000kcals was maintenance for active 180cm+ individuals. Now, I didn’t say anything about running a 10K w/ 7min miles. I didn’t mention cardio at all. My point was that your claim that a lot of vigorous physical activity per day to have a maintenance of over 3,000 was wrong; I said: “A “lot” of physical activity every day isn’t a requirement. Don’t conflate volume with intensity.” Why? Because the sort of training that gets your maintenance caloric requirements that high, if we’re doing that by elevating your BMR that high, is going to be predominantly anabolic. Sure, you can burn those calories with lots of vigorous physical activity every day — my point is that’s not the only way to get such a high maintenance. In fact, pretty much the main way to get your maintenance that high without lots of volume every day is to increase your BMR. This is done by inducing muscle anabolism (mainly by hypertrophy) because, as we know, more mass requires more energy to maintain, especially muscle mass. I’m no Greg Kovacs; however, my maintenance is significantly above 3,000 kcals a day, even when mostly sedentary. enhancedbb.com/explaining-wh… ENHANCEDBB.COM. @VMHypertrophy.
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 outliers for fun/info. For me, this is probably quite an average (gaining) day up until I snapped my humerus this January. Just under 7,000kcals. I’ve also lost a lot of weight whilst being a lot more sedentary than usual (major surgery about a week ago) whilst eating an average of over 4,000kcals a day. So, my maintenance is quite a bit in excess of that under uninjured conditions. Ignore “targets” for the macros.
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VM Hypertrophy retweeted
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 enhancedbb.com to ask any questions). Why does muscle grow, and why is this the sort of training that causes it to grow the most? When muscle fibres controlled by the high threshold motor units (remember when I mentioned MUR) experience an adequately high level of mechanical tension as a result of slowing contraction velocities (look at force-velocity relationship image: credit to Chris Beardsley from S&C Research), we have what we will call “stimulating reps.” Quickly explaining the importance of high threshold motor units: they are largely composed of type II (fast-twitch) muscle fibres, which have the higher intrinsic capacity/potential for force production and hypertrophy. As the name explains, they are only recruited at high force demands, during ONLY brief, intense training; they have a greater density of contractile proteins and more potential for MPS compared to type I fibres. Motor units are recruited from smallest to largest (lowest threshold to highest threshold) based on force required; low to moderate intensities recruit the low threshold units (type I and endurance based); consequently, ONLY brief, intense exercise recruits high threshold motor units. Now, these reps occur at approximately 90% (roughly equivalent to 5RM loads) of maximal unfatigued isometric force production (so you can see how repetitions of cardio are not going to be stimulating in a way which is scalably anabolic — have to be specific here because of untrained -> beginner cardio is slightly anabolic but in a way which isn’t sufficiently scalable due to novel stimulus and more MUR than before). As those who strength train or bodybuild (or engage in similar resistance training) are already familiar with, such rep ranges when taken to “failure” (hence, INTENSE) result in an INVOLUNTARY SLOWING OF CONTRACTILE VELOCITY — meaning as we approach the end of the set, the rep gets slower and harder, and we can’t do anything about it. Next, I’m going to explain why high threshold motor units experiencing high mechanical tension is what’s required for adequate training stimulus to cause sufficient anabolic adaptations to increase BMR in a scalable way via muscle growth: Mechanical tension is determined by the force-velocity relationship as applied to a single muscle fibre. Under quick shortening, the fibre produces a small force (few myosins attach to actin), however, under slow shortening (REMEMBER what I say about INVOLUNTARY SLOWING CONTRACTILE VELOCITY and how this is achieved only with INTENSE training, meaning high effort per repetition of which approximately the last 5 are meaningful or more precisely that 90% of max force production figure? Well, you’re not going to generate such forces with ultra-high-rep exercise or cardio, because you will be too fatigued to be able to produce 90% of your maximal unfatigued isometric force with the loads which allow you to perform that many reps in such a fashion) a large force is produced (more myosins attach to actin). Now, when contraction velocity is significantly slowed (remember that ONLY BRIEF INTENSE TRAINING allows for this because if the training is not brief then you are fatigued by the point that you get to these reps and therefore cannot produce sufficient force for your high threshold motor units to experience adequate mechanical tension), the dwell time (the time where the myosin heads remain attached to actin) increases ∴ increasing the duty ratio which is the fraction of the contraction cycle during which a cross-bridge — connection between myosin and actin — is active. enhancedbb.com/explaining-wh… ENHANCEDBB.COM. @VMHypertrophy.
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VM Hypertrophy retweeted
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 ∴ causes it to detach from actin Reactivation: myosin hydrolyses ATP; preparing for another cycle Now, the higher proportion of time in this cycle that myosin remains bound to actin (actively generating force) indicates more myosin-actin interactions occur during a given time period, meaning greater overall force production by the muscle fibre Simply, by slowing down the contraction, you allow more myosin-actin interactions to occur ∴ increasing the overall force produced by the muscle fibre. So, to summarise, the higher proportion of time myosin is bound to actin, the higher number of active cross-bridges during each contraction cycle, which amplifies the mechanical tension within that fibre). Now, this concentration of mechanical tension is the key to the activation of various mechanosensitive signalling complexes (via protein detection), e.g. integrin-associated focal adhesion kinase (FAK) — enzyme converting mechanical tension into biochemical signal; kinase domain of titin (large protein with role in muscle elasticity, however, more relevantly here, it also acts as a sensor), etc… enhancedbb.com/explaining-wh… ENHANCEDBB.COM. @VMHypertrophy.
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