The Truth on Insulin and HGH.
The real reason for increased size of new age pros, insulin, not HGH.
Why aren’t you growing? Insulin resistance/hgh, glucose no longer able to efficiently get into the muscles.
Hgh doesn’t build muscle, Hgh can ruin muscular growth, And the real cause of “palumboism” hgh induced insulin resistance. Hgh induces insulin resistance which can cause the limb(arms/legs) muscles to atrophy.
Ever hear many state hgh isn’t good for muscle building? But when you add insulin it is? No the insulin itself is going to help muscle growth due to multiple mechanisms. The hgh use has nothing to do with it. And insulin does not make you fat without hgh use. Scientifically this does not make sense in any form. Insulin itself is going keep the same ratio you currently have at shuttling said nutrients into muscle/fat. The ratio you gain right now bulking will be the same ratio on insulin of fat to muscle gain… The only thing that will affect that would be insulin resistance. Which is why it matters the type of insulin you pick. Since some insulin forms cause insulin resistance.. And some are shown to increase insulin sensitivity, lower ac1 levels. Body builders… Don’t use humalin R…
So hgh, the expensive fat burner that ruins muscle gains. Where do we start? The copious studies showing muscle tissue has never been increased in any hgh study? The fact that bone growth and collagen growth takes longer then muscle tissue, yet in studies on hgh show all these factors happening.. Yet zero muscle tissue growth… Many like to live in fantasy landing claiming of muscle cells take a long time to mature.. Well so does collagen/connective tissue and bone… Yet these seem to grow just fine in HGH studies. All these studies show how hgh has its impact on bone and connective tissue and has no real affinity for the muscle.
Yes studies show muscle mass increase on hgh studies. But know the difference here, lean body mass increase etc or muscle mass speficially stated means a increase in the mass which can be due to various reasons. Which those reasons are here are water retention via potassium/sodium retention. Which steroids also do. But read the studies and you will see that actual ZERO tissue growth itself of the muscle is seen. Hence why you come off hgh you lose that extra 10-15lbs water weight that you loved so much making you look fuller/thicker yet that bone growth stays…
It is seen in acromegaly patients as well. Research any study you want on hgh and muscle tissue growth. It doesn’t happen yet we clearly see other areas grow regardless of dose up to 27iu a day in studies yet still, zero muscle tissue growth.
Hgh will however in those high doses let insulin resistance set in. Like in a recent interview where dave palumbo was discussed, on how he stopped growing on hgh he just couldn’t grow. Where he was told insulin resistance had set in and he needed insulin to start growing again to actually have those nutrients pushed into the muscles like they once were able to.
Another fun fact when insulin resistance sets in. Blood sugar stays high, and nerves start getting damaged. Diabetic neuropathy. Hence the shrunken limbs, the legs and arms, and the guts. It is well documented in diabetics, the nerve damage in these areas the limbs and gut. The damaged gut nerves leading to intestinal muscles that don’t contract as well, just like the arms. There is no absurd visceral fat growth. That is just ridiculous. If this was true all the diabetics that refuse to eat better that have to keep increasing their insulin needs to 200iu, 300iu, 500iu… etc eating very fatty meals like they never had diabeties would have insane amounts of visceral fat. But again… that’s not the case.. However many do support the “palumboism” look or the “kovacs” look. The nerve damaged shrunk limbs, legs/arms. The hugely distended abdominal. Again you only see this in the diabetics that refuse to eat better and let insulin resistance get worse and worse to where nerve damage takes place.
Put the diabetic neuropathy nerve damage look, the shrunk legs/arms with the bone growth in the face/feet/hands and you get the so called “palumboism”.
So many people like to make up this fancy lack of science theories, that make absolute no sense… With zero science to back it. Like some predisposed to hgh causing this effect. Everything is just made up fairy tale from people who didn’t use a little knowledge based off of the drugs these bodybuilders are using.
On our end note here. The picture above is a young hobbyist bodybuilder who happens to be a diabetic. He has what many call the “HGH look”, The extremely full muscles all around, namely delt/trap muscle area, while also looking like mini pro bodybuilder that a few years ago if you had seen him would never have thought the same person could carry this much muscle.
We all know the theory on growth hormones effect on muscle growth. We see a person gain 10lbs water weight, looking fuller, loses body fat. Losing body fat anytime will make you look bigger as a bodybuilder then when body fat is higher. But if the theory was true, continually using the same high dose would just keep “splitting” those muscle cells and lead to continuous growth just it does with bone/tendons, again which is fully proven its growth effects on bone/tendon, science has proven it, and it does happen like science says it happens. Now muscle growth however is not proven in adults, and if it did happen, it would be very well documented in studies that see significant bone/tendon growth.
What do we see in the bodybuilding world with insulin? We see continuous growth. HGH is not needed nor is it the factor behind insulin working on muscle growth, like many claim it is. Nor is HGH needed to prevent fat gain on insulin. Again… if this was true every diabetic would be at the hand of continuous absurd fat gain. Whatever your insulin resistance factors are currently at now allowing you to gain said amount of muscle and fat ratio is on your current diet, will stay the exact same ratio with insulin. Only both will be at a higher rate as if you sped up time to get there. 25lbs of muscle at the end of the year with 5lbs of fat vs 25lbs of muscle in 6 months with 5lbs of fat is still the same outcome but in a shorter time frame. The only thing that would change this ratio you are currently gaining at is changing your diet or ruining your insulin sensitivity.
Main cause of kidney failure in bodybuilders, insulin resistance due to hgh abuse.
Diabetic nephropathy (DN) is a serious and progressive complication of both type 1 DM and type 2 DM. The first manifestation of DN is typically microalbuminuria, which progresses to overt albuminuria (ie, increased albumin levels in the urine, indicating more severe renal dysfunction) and eventually to renal failure54 and is the leading cause of end-stage renal disease (ESRD).55 Approximately one fourth of people with type 2 diabetes have microalbuminuria or a more advanced stage of DN that worsens at a rate of 2% to 3% per year.56 Other characteristic features of DN include thickening of glomerular basement membranes (Fig. (Fig.1)1) and glomerular hyperfiltration, leading to mesangial (central part of the renal glomerulus) extracellular matrix expansion and further increases in urinary albumin excretion57 and progressing to glomerular and tubular sclerosis and renal failure.58,59 Like those for DR and PN, the risk factors for DN include hyperglycemia, duration of diabetes, age of onset, tobacco use, dyslipidemia, hypertension,60,61 and obesity (Table(Table).62
Enlarged gut smooth muscle cell dysfunction(intestines)/nerve damage.
Finally, diabetes is associated with smooth muscle cell dysfunction.74 Although the precise mechanism for smooth muscle cell dysfunction in diabetes is unclear, it may be associated with similar mechanisms for endothelial cell dysfunction, including activation of the PKC pathway, AGE deposition, and AGE receptor activation as well as overproduction of growth factors.136
When insulin resistance occurs, neuropathy and limb(arms/legs) muscles atrophy.
The results showed that the ultrasonographic transverse diameter, thickness, and cross-sectional area of EDB and the thickness of MILs in patients of T2DM with DPN were significantly smaller than those in patients of T2DM without DPN (all P < 0.01) and those in the control subjects (all P < 0.01). The transverse diameter and cross-sectional area of the EDB and thickness of MILs in patients of T2DM without DPN were significantly smaller than those of the control subjects (all P < 0.01). In conclusion, the atrophy of foot muscle in Chinese T2DM patients can be detected by high-frequency ultrasonography. Notably, ultrasonography may detect early atrophy of foot muscles in patients without DPN. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4140103/ In the present study, we explored the possibility that insulin resistance would cause muscle atrophy and examined potential proteolytic pathways that could cause accelerated loss of muscle protein. - See more at: http://press.endocrine.org/doi/full/10.1210/en.2006-0251… The primary findings on biopsy are muscle edema and necrosis. It is important to examine patients for possible motor weakness from median nerve compression. Assessment of thenar muscle strength and examination of the hand for the presence of the muscle atrophy help accomplish this task. It is important that clinicians intercede in CTS before the development of this type of atrophy .https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1839979/ both a sural nerve biopsy and a gastrocnemius biopsy were performed. A reduction in large myelinated fibers was observed on nerve biopsy, and muscle showed neurogenic atrophy, as well as a few necrotic fibers and some perivascular lymphocytes and histiocytes. all had distal muscle chronic denervation changes and distal more than proximal weakness and wasting; electrophysiologically the majority had motor conduction block, slow conduction velocities, prolonged distal latencies, and all had F-wave abnormalities. EMG may show abnormalities of denervation in the thoracic paraspinal muscles or in abdominal muscles. The association of these with other forms of radiculoplexus neuropathies was noted by Bastron and Thomas and termed diabetic polyradiculopathy For additional information related to the effects of peripheral neuropathy on skin and muscle, see related articles by Mueller et al,40 LeMaster et al,41 and Hilton et al42 in this issue. HGH on muscle growth. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2439518/ Supraphysiological GH in the young leads to pituitary gigantism, whereas adult-onset GH tumours result in a condition called acromegaly characterized by overgrowth of bony tissue (brow and lower jaw protrusion, enlargement of the extremities), osteoarthritis, carpal tunnel syndrome, headaches, cardiomyopathies, hyperglycaemia, hypertension and diabetes mellitus (Ayuk and Sheppard, 2006). Observations in people with acromegaly suggest that chronic high levels of circulating GH and IGF-I may actually be detrimental to muscle function. (Nagulesparen et al., 1976; Woodhouse et al., 2006). Despite the observations of an effect of GH and IGF-I on protein synthesis, the fact remains that gains in muscle mass are not observed in healthy subjects after long-term GH administration so any benefits are unlikely to be due to muscle mass gains. In the GH plus exercise groups, circulating IGF-I levels and fat-free mass were consistently increased in comparison to placebo groups. Thus, it is possible to extrapolate that increasing circulating IGF-I would also be without consequence for muscle mass in healthy humans. Administration of IGF-I acutely activates muscle protein synthesis (Fryburg et al., 1995), but similarly to GH a 1-year administration did not result in increased lean body mass (Friedlander et al., 2001). The effects of GH on fat-free mass may be due to water retention, which is a known side effect of GH administration, or to an increase in soft tissue due to the stimulatory effects of GH on collagen synthesis. Welle et al. (1996) reported differences in strength following 12 weeks GH administration in older men (mean age 66 years), but did not observe differences between GH and placebo groups in terms of mean fractional rates of myofibrillar protein breakdown or mean postabsorptive fractional rate of myofibrillar protein synthesis. Superior increases in whole body protein synthesis have been observed in both young (mean age 23 years; Yarasheski et al., 1992) and old (mean age 67 years; Yarasheski et al., 1995) untrained subjects undertaking resistance exercise in combination with GH relative to those on placebo, but interestingly, this effect was not mirrored in quadriceps protein synthesis rates, suggesting that the GH effects are not on muscle tissue. Yarasheski et al. (1993) also demonstrated that there was no effect of 2 weeks GH administration on quadriceps protein synthesis rates or whole body protein breakdown in young experienced weight lifters (mean age 23 years). The data suggest that there is no beneficial effect of administering GH in combination with an exercise programme for muscle mass gains. In line with the autocrine–paracrine theory of IGF-I action, the endocrinological status of animals and humans does not seem to affect the ability of muscles to hypertrophy following exercise. Hypophysectomized rats that have decreased circulating GH and IGF-I are able to hypertrophy to the same extent as controls (DeVol et al., 1990). Humans with GH deficiency or the very elderly with low GH and IGF-I also adapt to resistance exercise by increasing muscle mass and strength. In adult humans, GH administration is lipolytic and causes increase in serum-free fatty acids. In turn, this inhibits glucose uptake to the heart, adipose tissue and muscle and may underlie the hyperglycaemia and insulin resistance associated with acromegaly. GH also causes an increase in water absorption by the gut and sodium retention leading to extracellular fluid accumulation, (Woodhouse et al., 2006; Gibney et al., 2007).