Igf1-Lr3/tadalafil log...

Hahaha it's good igf1 hahaha. Yep, I weigh 231

Brooklynn said:

JJ... Hey thanks for the advise. I can see my forarms getting bigger already. And the pump is crazy.

Click to expand...

It's frustrating at first because you can obviously shrug, dead lift, and row more by using wrist wraps, but without them your forearms have to bare a lot of weight which causes them to grow and grow stronger. I glad it's helping.

Alright, put 100mcg in pecs and delts in 8 micro injects. Took 40mg tadalafil. Trained arms, delts, upper chest, and calves. Had a killer pump!!! I'm still coughing nonstop from this big but it felt good to pump things up.

I ran into one of my clients at the gym. I have him taking 20mg tadalafil before each workout. He kept coming up to me in between sets saying he couldn't believe the pump he had in his arms. He kept asking, What the hell is that stuff? I tried to explain vasodialation and blood flow.

I took two z pak tabs after work and took a nap. I actually felt like training when I woke up. I haven't felt that way in a long time.

I took 100mcg igf1-Lr3 preworkout in a series of 6 micro injections all in my chest. Damn, acetic acid hurts!!! I also took 40mg tadalafil. My weight went up one pound. I was 232Lbs. My strength was way up on hammer strength bench press and seated back rows. A lot of people told me I got bigger. The pump from the Igf/tadalafil is always incredible!!!

Research subject has noticed a much more full look to his chest. Today the micro injects will all go into chest again as it needs more size. Research subject is bulking and has noticed since strength is jumping up from igf1-Lr3 it is best to do one or two chest exercises eod with the Igf to really stimulate the muscle and force new growth. The added weight to each chest exercise is tearing fibers deep in the tissue which is what we want to increase thickness.

I trained at work yesterday so I didn't have access to my igf1-Lr3. I just administered it now, all 100mcg into pecs in 8 micro injections. I swear my pecs swell up damn near immediately. Going to take my tadalafil before legs today. Time to get legs back up to par so I can hit the stage again.

Tomorrow, I lift weights at work so I'll pin the igf1-Lr3 later in the evening.

Both Igf1-des and Igf1-Lr3 have a different number of amino acids than normal Igf1 making them resistant to igf1-Binding Protein 3 which makes them more anabolic and more applicable to bodybuilding.


Unbound (bioavailable) IGF1 enhances somatic growth.

AuthorsElis S, et al. Show all Journal
Dis Model Mech. 2011 Sep;4(5):649-58. doi: 10.1242/dmm.006775. Epub 2011 May 31.

Affiliation
Abstract
Understanding insulin-like growth factor-1 (IGF1) biology is of particular importance because, apart from its role in mediating growth, it plays key roles in cellular transformation, organ regeneration, immune function, development of the musculoskeletal system and aging. IGF1 bioactivity is modulated by its binding to IGF-binding proteins (IGFBPs) and the acid labile subunit (ALS), which are present in serum and tissues. To determine whether IGF1 binding to IGFBPs is necessary to facilitate normal growth and development, we used a gene-targeting approach and generated two novel knock-in mouse models of mutated IGF1, in which the native Igf1 gene was replaced by Des-Igf1 (KID mice) or R3-Igf1 (KIR mice). The KID and KIR mutant proteins have reduced affinity for the IGFBPs, and therefore present as unbound IGF1, or 'free IGF1'. We found that both KID and KIR mice have reduced serum IGF1 levels and a concomitant increase in serum growth hormone levels. Ternary complex formation of IGF1 with the IGFBPs and the ALS was markedly reduced in sera from KID and KIR mice compared with wild type. Both mutant mice showed increased body weight, body and bone lengths, and relative lean mass. We found selective organomegaly of the spleen, kidneys and uterus, enhanced mammary gland complexity, and increased skeletal acquisition. The KID and KIR models show unequivocally that IGF1-complex formation with the IGFBPs is fundamental for establishing normal body and organ size, and that uncontrolled IGF bioactivity could lead to pathological conditions.

Just got a pm from a member. He said he took 12.5mg Superior tadalafil last night and had an erection all night long. It's the strongest tadalafil I've ever researched!!!

I was down to the end of my igf1-Lr3 vial so I took out the last of it which turned out to be 150mcg. I micro injected it all into my pecs. I also took 40mg tadalafil. At the gym I trained chest, tris, bis, delts, and calves. Every muscle got a good pump, but OMG did my chest get an insane pump!!! You definitely get the best pump where you micro inject the igf1-Lr3. I can tell that the higher you dose it, the better the pump you get. My AAS dose is the lowest it's been, for the most part, in 19 years, but the pump was incredible. I plan to blast in the near future and only use Igf on the weekends. I also believe the less frequently you use Lr3, the better it works. Since I missed a lot of workouts lately due to illness, I've only been using the Lr3 a couple times a week which definitely has kept my igf1 receptors clean.

Igf1-Lr 3 does not cause the heart to enlarge according to this study.

Extracellular signal-regulated kinase and phosphoinositol-3 kinase mediate IGF-1 induced proliferation of fetal sheep cardiomyocytes.

AuthorsSundgren NC, et al. Show all Journal
Am J Physiol Regul Integr Comp Physiol. 2003 Dec;285(6):R1481-9. Epub 2003 Aug 28.

Affiliation
Abstract
Growth of the fetal heart involves cardiomyocyte enlargement, division, and maturation. Insulin-like growth factor-1 (IGF-1) is implicated in many aspects of growth and is likely to be important in developmental heart growth. IGF-1 stimulates the IGF-1 receptor (IGF1R) and downstream signaling pathways, including extracellular signal-regulated kinase (ERK) and phosphoinositol-3 kinase (PI3K). We hypothesized that IGF-1 stimulates cardiomyocyte proliferation and enlargement through stimulation of the ERK cascade and stimulates cardiomyocyte differentiation through the PI3K cascade. In vivo administration of Long R3 IGF-1 (LR3 IGF-1) did not stimulate cardiomyocyte hypertrophy but led to a decreased percentage of cells that were binucleated in vivo. In culture, LR3 IGF-1 increased myocyte bromodeoxyuridine (BrdU) uptake by three- to five-fold. The blockade of either ERK or PI3K signaling (by UO-126 or LY-294002, respectively) completely abolished BrdU uptake stimulated by LR3 IGF-1. LR3 IGF-1 did not increase footprint area, but as expected, phenylephrine stimulated an increase in binucleated cardiomyocyte size. We conclude that 1) IGF-1 through IGF1R stimulates cardiomyocyte division in vivo; hyperplastic growth is the most likely explanation of IGF-1 stimulated heart growth in vivo; 2) IGF-1 through IGF1R does not stimulate binucleation in vitro or in vivo; 3) IGF-1 through IGF1R does not stimulate hypertrophy either in vivo or in vitro; and 4) IGF-1 through IGF1R requires both ERK and PI3K signaling for proliferation of near-term fetal sheep cardiomyocytes in vitro.