# Gw50156 log



## Lordsks (Jun 2, 2012)

I'm excited to be running this log on GW50156 it's from Purchase Peptides, from what I have been reading on other logs the increased endurance and fat burning are it's main effects. I will be running 5mg ED for 2 months. That's one 60ml bottle. I have seen others running upwards of 15-20mg's a day but read a 3 month log that someone only use 5mg and was happy with the results. Apparently there is a build up period that needs to happen of a week or two before things really get going. 

The packaging was great, the product protected from possible shipping damage. It got here fast, the label on the bottle was straight. It came with an eye dropper however the dropper isn't marked for dosing but typically a full dropper is 1ml. I like to break the needle off of a slin pin and use that for precise dosing anyway. 

1st dose was this morning and the solution it's suspended in wasn't to bad. Diffidently a OJ chaser helps, but that's typical of most research products. Not to much to comment on after dosing, no immediate effects where noticed. 

I don't do alot of cardio but I'm looking for increased recovery between sets and between workouts. This as ALWAYS been an issue for me, I can only hit one body part a week, occasionally I'll hit it twice. Increased fat burning and energy during the day would be nice also. 


Currently the protocol is looking like this:

test e 500mg weekly. +(In two weeks starting 700mg's primo weekly) 
aromasin 12.5mg daily+10mg nolvadex
50mcg t3 nightly
igf des 200mcg preworkout IM, MGF 500mcg 15 mins post workout IM, Igf1r3 100mcg 15mins later IM, ghrp-6/cjc 1295 200mcg subq pre bed. 
GW50156 every morning 5mg's. (Purchase Peptides)



Here's a current pic.


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## meow (Jun 2, 2012)

Taken orally? Anymore info on this compound you could share?


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## BFHammer (Jun 2, 2012)

It's suppose to raise HDL as well.  It's in clinicals for anti obesity and a few other things.


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## crackrbaby (Jun 2, 2012)

Sub'd...


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## Lordsks (Jun 2, 2012)

I believe the clinicals it's in now is phase II and for improving Cholesterol. 

Meow, I just googled GW 50156 and started reading.


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## meow (Jun 2, 2012)

Sounds promising. Ill be following your log!


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## TwisT (Jun 2, 2012)

Awesome buddy!


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## Lordsks (Jun 2, 2012)

I should note that I'm a little tired today and running hotter than normal. So far so good!


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## Lordsks (Jun 4, 2012)

Just an update, I think its still to early to tell how its effecting recovery. Feel good throughout the day. No effect on sleeping.


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## Lordsks (Jun 4, 2012)

some good info

*Study on Obese Humans*
OBJECTIVE— Pharmacological use of peroxisome proliferator–activated  receptor (PPAR)δ agonists and transgenic overexpression of PPARδ in mice  suggest amelioration of features of the metabolic syndrome through  enhanced fat oxidation in skeletal muscle. We hypothesize a similar  mechanism operates in humans.

RESEARCH DESIGN AND METHODS— The PPARδ agonist (10 mg o.d. GW501516), a  comparator PPARα agonist (20 μg o.d. GW590735), and placebo were given  in a double-blind, randomized, three-parallel group, 2-week study to six  healthy moderately overweight subjects in each group. Metabolic  evaluation was made before and after treatment including liver fat  quantification, fasting blood samples, a 6-h meal tolerance test with  stable isotope fatty acids, skeletal muscle biopsy for gene expression,  and urinary isoprostanes for global oxidative stress.

RESULTS— Treatment with GW501516 showed statistically significant  reductions in fasting plasma triglycerides (−30%), apolipoprotein B  (−26%), LDL cholesterol (−23%), and insulin (−11%), whereas HDL  cholesterol was unchanged. A 20% reduction in liver fat content (P <  0.05) and 30% reduction in urinary isoprostanes (P = 0.01) were also  observed. Except for a lowering of triglycerides (−30%, P < 0.05),  none of these changes were observed in response to GW590735. The  relative proportion of exhaled CO2 directly originating from the fat  content of the meal was increased (P < 0.05) in response to GW501516,  and skeletal muscle expression of carnitine palmitoyl-transferase 1b  (CPT1b) was also significantly increased.

CONCLUSIONS— The PPARδ agonist GW501516 reverses multiple abnormalities  associated with the metabolic syndrome without increasing oxidative  stress. The effect is probably caused by increased fat oxidation in  skeletal muscle. 

*Study on Lean Individuals*
Objectives— Exercise increases fatty acid oxidation (FAO), improves  serum high density lipoprotein cholesterol (HDLc) and triglycerides  (TG), and upregulates skeletal muscle peroxisome proliferator activated  receptor (PPAR)δ expression. In parallel, PPARδ agonist-upregulated FAO  would induce fatty-acid uptake (via peripheral lipolysis), and influence  HDLc and TG-rich lipoprotein particle metabolism, as suggested in  preclinical models.

Methods and Results— Healthy volunteers were allocated placebo (n=6) or  PPARδ agonist (GW501516) at 2.5 mg (n=9) or 10 mg (n=9), orally,  once-daily for 2 weeks while hospitalized and sedentary. Standard  lipid/lipoproteins were measured and in vivo fat feeding studies were  conducted. Human skeletal muscle cells were treated with GW501516 in  vitro and evaluated for lipid-related gene expression and FAO. Serum TG  trended downwards (P=0.08, 10 mg), whereas TG clearance post fat-feeding  improved with drug (P=0.02). HDLc was enhanced in both treatment groups  (2.5 mg P=0.004, 10 mg P<0.001) when compared with the decrease in  the placebo group (−11.5±1.6%, P=0.002). These findings complimented in  vitro cell culture results whereby GW501516 induced FAO and upregulated  CPT1 and CD36 expression, in addition to a 2-fold increase in ABCA1  (P=0.002). However, LpL expression remained unchanged.

Conclusions— This is the first report of a PPARδ agonist administered to  man. In this small study, GW501516 significantly influenced HDLc and  TGs in healthy volunteers. Enhanced in vivo serum fat clearance, and the  first demonstrated in vitro upregulation in human skeletal muscle fat  utilization and ABCA1 expression, suggests peripheral fat utilization  and lipidation as potential mechanisms toward these HDL:TG effects.


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## Lordsks (Jun 4, 2012)

More info I found for those wanting to know....

GW-501516 is a PPARδ modulator compound is currently being investigated for drug use by GlaxoSmithKline. It activates the same pathways activated through exercise, including PPARδ and AMP-activated protein kinase. It is being trialed as a potential treatment for a few conditions consisting mainly of obesity, diabetes, dyslipidemia and heart disease. GW-501516 has a synergistic effect when combined with the AMP-K agonist AICAR:  the combination has been shown to significantly increase exercise  endurance in animal studies more than 40%. And from My own experience  yes it works my friends.

 GW-50156 regulates fat burning through a number of different pathways which includes exercise mimetic effects.  It increases glycogen retention in skeletal muscle  tissue while increasing muscle gene expression. This shift changes the  body’s metabolism to allow for more fat burning and for energy instead  of carbohydrates or protein as the source of fuel. This is why the main  reason why it’s being looked into as a treatment for diabetes.  As it  will not allow the patients to endure and overly catabolic state, thus  allowing energy levels and health to be stable at all times. GW-501516  clearly demonstrates that it increases muscle mass while keeping glucose  from touching the adipose tissue sort of like Need2Slin  but need2slin does much more then just this. Treatments with GW-501516  have been shown to increase HDL cholesterol by up to 79% and the  compound is now undergoing Phase II trials to improve HDL cholesterol in  humans. We dive into its attributes further later in the article But  again let me speak from personal experience. I did a test with this drug  and Winstrol. I know for my self when I take wonstrol it always kills  my cholesterol levels. Last time I took it I ended up with an HDL of ten  and a LDL over two hundred and it only took less then 2 weeks for this  to happen. So knowing this I took wintrol for 4 weeks and also took  GW-501516 along with it and I was amazed at the results. My cholesterol  levels were BETTER at the end of the 4 week trial. So if cholesterol is  of concern for you then you need to get some of this stuff my friend  because trust me it works.
 Concerns had been raised right before the 2008 Beijing Olympics that GW-501516 could be used by athletes as a performance enhancing drug  which was not detectable nor tested for during the doping test. The  main reason why athletes would use it is because of the increase in  endurance through the increase of glycogen storage leading to increased  muscular endurance, again ring a bell. Need2Slin does THE SAME THING!  GW-501516 has yet to be label a controlled or banned substance by any  national drug enforcement agency including Wada. Obviously no one will  test positive for this drug, so if I were an Olympic athlete looking for  a boost; this would be at the top of the list considering its much  outweighed pros over cons. Any Athletes looking for a edge can use this  drug and never have to worry about popping hot. They can not test for it  my friends so you are golden. Some new testing is coming out in the  next 3-5 years that will allow them to basically test your DNA to see if  your bosy as been drug altered in anyway but this is years in the  making. For now you are safe to take GW-501516 and not have to worry  about popping hot.
​ The benefits of endurance exercise on general health make it  desirable to identify orally active agents that would mimic or  potentiate the effects of exercise to treat metabolic diseases. Although  certain natural compounds, such as reseveratrol, have  endurance-enhancing activities, their exact metabolic targets remain  elusive. We therefore tested the effect of pathway-specific drugs on  endurance capacities of mice in a treadmill running test. Researchers  found that PPARbeta/delta agonist and exercise training synergistically  increase oxidative myofibers and running endurance in adult mice.  Because training activates AMPK and PGC1alpha, they then tested whether  the orally active *AMPK agonist AICAR might be sufficient to  overcome the exercise requirement. Unexpectedly, even in sedentary mice,  4 weeks of AICAR treatment alone induced metabolic genes and enhanced  running endurance by 44%. These results demonstrate that AMPK-PPARdelta  pathway can be targeted by orally active drugs to enhance training  adaptation or even to increase endurance without exercise.  *Now how does this peptide cause mice to lose weight without activity? Simple, theActivation  of PPARβ/δ by GW501516 in skeletal muscle cells induces the expression  of genes involved in preferential lipid utilization, β-oxidation,  cholesterol efflux, and energy uncoupling. In addition, the treatment of  muscle cells with GW501516 increases apolipoprotein-A1 specific efflux  of intracellular cholesterol, thus identifying this tissue as an  important target of PPARβ/δ agonists. Interestingly, fenofibrate induces  genes involved in fructose uptake, and glycogen formation. In contrast,  rosiglitazone-mediated activation of PPARγ induces gene expression  associated with glucose uptake, fatty acid synthesis, and lipid storage.  Furthermore, we show that the PPAR-dependent reporter in the muscle  carnitine palmitoyl-transferase-1 promoter is directly regulated by  PPARβ/δ, and not PPARα in skeletal muscle cells in a PPARγ  coactivator-1-dependent manner. This study demonstrates that PPARs have  distinct roles in skeletal muscle cells with respect to the regulation  of lipid, carbohydrate, and energy homeostasis. Overall the peptide  GW501516 (PPARβ/δ agonists) would increase fatty acid catabolism,  cholesterol efflux, and energy expenditure in muscle, and speculate  selective activators of PPARβ/δ may have therapeutic utility in the  treatment of hyperlipidemia, atherosclerosis, and obesity.  (Dressel et  al. 17 (12): 2477).. However I would advice only using this drug orally  IMO..

Proof that GW5010516 increases insulin sensitivity​ Elevated plasma free fatty acids cause insulin resistance in skeletal  muscle through the activation of a constant chronic inflammatory  process. This process involves nuclear factor (NF)-kappaB activation as a  result of diacylglycerol (DAG) accumulation and following protein  kinase Ctheta (PKCtheta) phosphorylation. At present, it is unknown  whether peroxisome proliferator-activated receptor-delta (PPARdelta)  activation prevents fatty acid-induced inflammation and insulin  resistance in skeletal muscle cells. In C2C12 skeletal muscle cells, the  PPARdelta agonist GW501516 prevented phosphorylation of insulin  receptor substrate-1 at Ser(307) and the inhibition of  insulin-stimulated Akt phosphorylation caused by exposure to the  saturated fatty acid palmitate. This latter effect was reversed by the  PPARdelta antagonist GSK0660. Treatment with the PPARdelta agonist  enhanced the expression of two well known PPARdelta target genes  involved in fatty acid oxidation, carnitine palmitoyltransferase-1 and  pyruvate dehydrogenase kinase 4 and increased the phosphorylation of  AMP-activated protein kinase, preventing the reduction in fatty acid  oxidation caused by palmitate exposure. In agreement with these changes,  GW501516 treatment reversed the increase in DAG and PKCtheta activation  caused by palmitate. Consistent with these findings, PPARdelta  activation by GW501516 blocked palmitate-induced NF-kappaB DNA-binding  activity. These findings indicate that PPARdelta attenuates fatty  acid-induced NF-kappaB activation and the subsequent development of  insulin resistance in skeletal muscle cells by reducing DAG  accumulation. The results of the study clearly demonstrate that  PPARdelta activation is a pharmacological target to prevent insulin  resistance. (Endocrinology 2010 Apr; 151(4) :1560-9.)

 The peroxisome proliferator-activated receptor δ (PPARδ) regulates  the expression of genes involved in cellular lipid and cell energy  metabolism in many metabolically active tissues, such as liver, muscle,  and fat, and plays a role in the cellular response to stress and  environmental stimuli. The particular role of PPARδ in insulin-secreting  β-cells, however, is not well understood; we recently identified the  cell-specific role of PPARδ on mitochondrial energy metabolism and  insulin secretion in lipotoxic β-cells. After treatment of HIT-T15  cells, a syrian hamster pancreatic β-cell line, with high concentrations  of palmitate and/or the specific PPARδ agonist GW501516, we detected  the gene expression changes for transcripts, such as peroxisome  proliferator-activated receptor gamma co-activator 1 (PGC-1α), nuclear  respiratory factor 1 (NRF-1), mitochondrial transcription factor A  (mtTFA), the protein levels of the mitochondria uncoupling protein 2  (UCP2), mitochondrial morphology, the insulin secretion capacity and  ATP/ADP ratio. Our results show that GW501516 treatment promoted  generation of mitochondrial ATP, as well as expression levels of PGC-1α,  NRF-1 and mtTFA, decreased basal insulin secretion, but had no effect  on glucose-stimulated insulin secretion (GSIS), increased amounts of  UCP2 and changed ATP-to-ADP ratio, improved mitochondrial morphology in  palmitate-treated β-cells. GW501516-induced activation of PPARδ enhanced  mitochondrial energy metabolism, but also promoted a concomitant  mitochondrial uncoupling and resulted in decreased basal insulin  secretion and restricted GSIS; this observation indicated the possible  action of a protective mechanism responding to the alleviation of  excessive lipid load and basal insulin secretion in lipotoxic β-cells. (Volume 343, Numbers 1-2,  249-256, DOI: 10.1007/s11010-010-0520-8) As you can see this peptide  has a profound effect on the liver and pancreas resulting in lower blood  sugar and controlled insulin output.
GW501516 prevents brain aging.​ 
 Brain inflammation plays a central role in numerous brain  pathologies, including multiple sclerosis (MS). Microglial cells and  astrocytes are the effector cells of neuroinflammation. They can be  activated also by agents such as interferon-γ (IFN-γ) and  lipopolysaccharide (LPS). Peroxisome proliferator-associated receptor  (PPAR) pathways are involved in the control of the inflammatory  processes, and PPAR-β seems to play an important role in the regulation  of central inflammation. In addition, PPAR-β agonists were shown to have  trophic effects on oligodendrocytes _in vitro_, and to give  partial protection in experimental autoimmune encephalomyelitis (EAE),  an animal model of MS. In the present work, a three-dimensional brain  cell culture system was used as _in vitro _model to study  antibody-induced demyelination and inflammatory responses. GW 501516 is a  specific PPAR-β agonist that researchers chose to  examine for its  capacity to protect from antibody-mediated demyelination and to prevent  inflammatory responses induced by IFN-γ and LPS. GW 501516 decreased the  IFN-γ-induced up-regulation of TNF-α and iNOS in accord with the  proposed anti-inflammatory effects of this PPAR-β agonist. However, it  increased IL-6 m-RNA expression. In demyelinating cultures, reactivity  of both microglial cells and astrocytes was observed, while the  expression of the inflammatory cytokines and iNOS remained unaffected.  Furthermore, GW 501516 did not protect against the demyelination-induced  changes in gene expression.  This suggests that the protective effects  of PPAR-β agonists observed _in vivo _can be attributed to their  anti-inflammatory properties rather than to a direct protective or  trophic effect on oligodendrocytes.  We all know that both alzheimer’s  and Dementia are caused by chronic inflammation within the brain.  Further research is still needed but this peptide displays promise in  preventing the aging of the brain. (_Journal of Neuroinflammation_ 2009, *6*:15 doi:10.1186/1742-2094-6-15)
GW501516 helps prevent the onset of Diabetes​ In contrast to the well-established roles of PPARgamma and PPARalpha  in lipid metabolism, little is known for PPARdelta in this process. We  show here that targeted activation of PPARdelta in adipose tissue  specifically induces expression of genes required for fatty acid  oxidation and energy dissipation, which in turn leads to improved lipid  profiles and reduced adiposity. Importantly, these animals are  completely resistant to both high-fat diet-induced and genetically  predisposed (Lepr(db/db)) obesity. As predicted, acute treatment of  Lepr(db/db) mice with a PPARdelta agonist depletes lipid accumulation.  In parallel, PPARdelta-deficient mice challenged with high-fat diet show  reduced energy uncoupling and are prone to obesity. In vitro,  activation of PPARdelta in adipocytes and skeletal muscle cells promotes  fatty acid oxidation and utilization. Our findings suggest that  PPARdelta serves as a widespread regulator of fat burning and identify  PPARdelta as a potential target in treatment of obesity and its  associated disorders. (Cell. 2003 Apr 18;113(2):159-70. PMID:12705865)
PPAR Agonist help prevent Dyslipidemia​ _In vitro_ and_ in vivo_ genetic and  pharmacological studies have demonstrated PPARα regulates lipid  catabolism. In contrast, PPARγ regulates the conflicting process of  lipid storage. However, relatively little is known about PPARβ/δ in the  context of target tissues, target genes, lipid homeostasis, and  functional overlap with PPARα and -γ. PPARβ/δ, a very low-density  lipoprotein sensor, is abundantly expressed in skeletal muscle, a major  mass peripheral tissue that accounts for approximately 40% of total body  weight. Skeletal muscle is a metabolically active tissue, and a primary  site of glucose metabolism, fatty acid oxidation, and cholesterol  efflux. Surprisingly, the role of PPARβ/δ in skeletal muscle has not  been investigated. We utilize selective PPARα, -β/δ, -γ, and liver X  receptor agonists in skeletal muscle cells to understand the functional  role of PPARβ/δ, and the complementary and/or contrasting roles of PPARs  in this major mass peripheral tissue. Activation of PPARβ/δ by GW501516  in skeletal muscle cells induces the expression of genes involved in  preferential lipid utilization, β-oxidation, cholesterol efflux, and  energy uncoupling. Furthermore, we show that treatment of muscle cells  with GW501516 increases apolipoprotein-A1 specific efflux of  intracellular cholesterol, thus identifying this tissue as an important  target of PPARβ/δ agonists. Interestingly, fenofibrate induces genes  involved in fructose uptake, and glycogen formation. In contrast,  rosiglitazone-mediated activation of PPARγ induces gene expression  associated with glucose uptake, fatty acid synthesis, and lipid storage.  Furthermore, we show that the PPAR-dependent reporter in the muscle  carnitine palmitoyl-transferase-1 promoter is directly regulated by  PPARβ/δ, and not PPARα in skeletal muscle cells in a PPARγ  coactivator-1-dependent manner. This study demonstrates that PPARs have  distinct roles in skeletal muscle cells with respect to the regulation  of lipid, carbohydrate, and energy homeostasis. Moreover, we surmise  that PPARβ/δ agonists would increase fatty acid catabolism, cholesterol  efflux, and energy expenditure in muscle, and speculate selective  activators of PPARβ/δ may have therapeutic utility in the treatment of  hyperlipidemia, atherosclerosis, and obesity.  (Dressel et al. 17 (12):  2477)

GW5015016 decreases chances of Heart Disease​ The peroxisome proliferator-activated receptors (PPARs) are dietary  lipid sensors that regulate fatty acid and carbohydrate metabolism. The  hypolipidemic effects of the fibrate drugs and the antidiabetic effects  of the glitazone drugs in humans are due to activation of the alpha  (NR1C1) and gamma (NR1C3) subtypes, respectively. In macrophages,  fibroblasts, and intestinal cells, GW501516 increases expression of the  reverse cholesterol transporter ATP-binding cassette A1 and induces  apolipoprotein A1-specific cholesterol efflux. When dosed to  insulin-resistant middle-aged obese rhesus monkeys, GW501516 causes a  dramatic dose-dependent rise in serum high density lipoprotein  cholesterol while lowering the levels of small-dense low density  lipoprotein, fasting triglycerides, and fasting insulin. These results  suggest that PPARdelta agonists may be effective drugs to increase  reverse cholesterol transport and decrease cardiovascular disease which  is typically associated with the metabolic syndrome X. (Proc Natl Acad Sci U S A. 2001 Apr 24;98(9):5306-11. Epub 2001 Apr 17. PMID:11309497)


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## fsoe (Jun 4, 2012)

put me dwn as watching this ---- and placing an order to PP 

- You think a cruise of 200-300 cyp per week - with this stuff and some mast at 300mg ew for 8-10 weeks is good, oh and dont forget my ghrp - 2 and cjc1295 will use that as well


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## Lordsks (Jun 4, 2012)

maybe....there seems to be alot of positives. Endurance, fat burning, better lipid profile, lowers blood presure. I can't personally say it's great stuff as I'm only on day 3. From what I have been reading week 2 you start seeing some benefits. Reading a log on another board and he was taking 15mg-20mg a day and saying it's by far the best fat burner there is over DNP, t3, clen, ect/... Don't think I'll hit those doses just yet...


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## Lordsks (Jun 7, 2012)

So I have upped the dose to 10mg's the last few days. I have been feeling like crap, just tired and sore. Took today's dose and it woke me up a bit, I took the whole 10mg one dose. One thing I noticed is I took 40mcg's of clen yesterday before working out chest and tri's. My heart rate was very calm after the workout. Normally it would be beating through my chest. I wondering if that's why I'm tired is heart rate and BP are down?? I have a wrist BP monitor I'll have to check it a few times through out the day.


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## TwisT (Jun 8, 2012)

How would u compare to clen?


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## TheEighthDwarf (Jun 9, 2012)

Have you feeling like crap due to increased workouts/intensity or due from the GW?  When are your taking it in relation to your workouts?  I was considering taking it prior to working out, but have read a few other people just having rediculous amounts of energy and that wouldn't be so good since I don't finish my workouts till about 7:30 at night.  LAST thing I need is to be wanting to pain the house at 10 at night.


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## fsoe (Jun 9, 2012)

S__T i need my Heart Rate and BP down - I gotta get some of this


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## Lordsks (Jun 9, 2012)

Not even close to clen, clen will get me going fast. Not sure on the tiredness if its from GW or not, the jury is still out on that..Could be unrelated, one thing I did notice today cause like I said I don't really do alot of cardio but I did a 5 mile hike thru the mountains took 4 hours to give you an idea of the terrain but the whole time I was never really breathing hard, I was really blow away at the calm steady pace I had the whole time, mouth wasn't open breathing heavy. I normally would be gasping for air the whole time. I'm sold on the endurance part of GW for sure. Haven't seen any lost of weight yet.


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## fsoe (Jun 9, 2012)

hell - I will take it just for endurance - I am sucking wind all the time just walking - 5'11 - 230 ... I should not be sucking wind - I do 40 mins cardio 5 x a week --- Must be the Tren


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## dirtwarrior (Jun 10, 2012)

interested in this


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## sdf38 (Jun 11, 2012)

Lordsks, 
on post #11, first paragraph, is this you saying this or someone else... "And from My own experience yes it works my friends." ? 
Seems weird you would say this anyway.....being only day 2 of your log,that's why I ask.


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## BFHammer (Jun 11, 2012)

fsoe said:


> hell - I will take it just for endurance - I am sucking wind all the time just walking - 5'11 - 230 ... I should not be sucking wind - I do 40 mins cardio 5 x a week --- Must be the Tren



How to Shrink Lungs | eHow.com  Gerbil on a wheel cardio actually decreases lung capacity.


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## Lordsks (Jun 11, 2012)

sdf38 said:


> Lordsks,
> on post #11, first paragraph, is this you saying this or someone else... "And from My own experience yes it works my friends." ?
> Seems weird you would say this anyway.....being only day 2 of your log,that's why I ask.



I copied that from another board cause it had some good info in there. Someone must have thrown there own comments in there. This is the first time running GW for me.


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## sdf38 (Jun 12, 2012)

Thanks, Lordsks .  Any chance you would throw the AMP-K agonist AICAR into the mix to see if they trully are synergistic?
Purchase Peptides has it I see....


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## sdf38 (Jun 12, 2012)

Lordsks said:


> So I have upped the dose to 10mg's the last few days. I have been feeling like crap, just tired and sore. Took today's dose and it woke me up a bit, I took the whole 10mg one dose. One thing I noticed is I took 40mcg's of clen yesterday before working out chest and tri's. My heart rate was very calm after the workout. Normally it would be beating through my chest. I wondering if that's why I'm tired is heart rate and BP are down?? I have a wrist BP monitor I'll have to check it a few times through out the day.



You could be right, I've taken supplements that lowered BP unexpectedly(one example is agmatine) and when my BP lowers rapidly I do feel fatigued and tired....not sure how heart rate would figure in though.

PS: T3 at night would keep me up, I would only take in morning


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## TwisT (Jun 12, 2012)

sdf38 said:


> PS: T3 at night would keep me up, I would only take in morning




ditto


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## DEE151 (Jun 12, 2012)

I never heard of the build up in the body from GW before you see any good results this is the first I have heard of this I also rep for gtgchem.com so i have tried this allready kept my dose at 10mg ed 5mg at 6am and another 5mg at 1pm, Now i am using there MK osta right now. I know 2 site were ppl have run this, one guy got it for his wife and she lost 3 pounds in 5 days and she did not even work out, I would only run GW for 5wks no longer.


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## Lordsks (Jun 13, 2012)

sdf38 said:


> Thanks, Lordsks .  Any chance you would throw the AMP-K agonist AICAR into the mix to see if they trully are synergistic?
> Purchase Peptides has it I see....



No just going to run GW right now. If there's another pep/RC I would add it would be MYO HMP. 



DEE151 said:


> I never heard of the build up in the body from GW before you see any good results this is the first I have heard of this I also rep for gtgchem.com so i have tried this allready kept my dose at 10mg ed 5mg at 6am and another 5mg at 1pm, Now i am using there MK osta right now. I know 2 site were ppl have run this, one guy got it for his wife and she lost 3 pounds in 5 days and she did not even work out, I would only run GW for 5wks no longer.



I was reading on promuscle and a few have commented results started coming in after a few weeks. It may have some truth to it, the last few days I have been hot and sweating, the first week didn't feel to much other than being tired. Tomorrow I climb 1500 steps 4x's with 100lbs material on my back, I have done this multipule times in the past before taking GW so I know I'm normally bent over gasping for air when I get to the top. I have a feeling it's going to be easier this time.


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## DEE151 (Jun 13, 2012)

Lordsks said:


> No just going to run GW right now. If there's another pep/RC I would add it would be MYO HMP.
> 
> 
> 
> I was reading on promuscle and a few have commented results started coming in after a few weeks. It may have some truth to it, the last few days I have been hot and sweating, the first week didn't feel to much other than being tired. Tomorrow I climb 1500 steps 4x's with 100lbs material on my back, I have done this multipule times in the past before taking GW so I know I'm normally bent over gasping for air when I get to the top. I have a feeling it's going to be easier this time.


my next run is going to be GW and osta MK stack


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## DEE151 (Jun 14, 2012)

so how long are u going to run GW for?


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## crackrbaby (Jun 14, 2012)

Lordsks said:


> No just going to run GW right now. If there's another pep/RC I would add it would be MYO HMP.
> 
> 
> 
> I was reading on promuscle and a few have commented results started coming in after a few weeks. It may have some truth to it, the last few days I have been hot and sweating, the first week didn't feel to much other than being tired. Tomorrow I climb 1500 steps 4x's with 100lbs material on my back, I have done this multipule times in the past before taking GW so I know I'm normally bent over gasping for air when I get to the top. I have a feeling it's going to be easier this time.



Sounds like fire fighter training ...


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## Lordsks (Jun 14, 2012)

I do put out fires all day long just a different type. Was just going to run one bottle but could extend it if things are going good. Which currently is 35days.


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## Lordsks (Jun 17, 2012)

Just an update, I have been sweating alot more than normal still. Things are going well, not fatigued as much throughout the day. Weight is about the same.


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## TwisT (Jun 21, 2012)

Keep up the good log bud


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## Lordsks (Jun 22, 2012)

Feeling really good which is nice normally there's always some side I'm dealing with one way or anther in the pursuit of bodybuilding. My last cycle I got to the point where tren wasn't making me sweat anymore and now I remember what sweating is. The endurance if diffidently there with GW. I have been getting backacne like crazy normally I never get acne no matter what I'm running. Diet hasn't been the best the last few days flying around the country will do that. Always like hitting a new gym in another place, "hey man what's your secret" lol. I uped the test to 800mg a week and haven't started the primo yet. Dropped the igfr3 to a lower dose of 50mcg on workout days. Site injections deff work with it as I always just hit the outer bicep head and it's much larger than the inner. I going to be out in 100+ deg. temps in all of July and August running around like a madman working. I'm really hoping GW is going to help me out.


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## crackrbaby (Jun 22, 2012)

Gw gives you Wings!


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## Lordsks (Jun 26, 2012)

I dropped the t3 a few days ago and I seem to be getting tighter now and thinning out. GW is in full swing, still running hotter than normal but that means I'm burning fat!


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## sdf38 (Jun 28, 2012)

If it was as hot as it is here(100 F) you would be hot as h*ll outside anyway, us northeners are not used to heat like this...

Keep up the log bro as I want to see also if you lose the endurance immediatly or not right away.


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## Lordsks (Jun 28, 2012)

yep for sure. From what I hear it hangs around with you for awhile.


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## sdf38 (Jul 6, 2012)

any updates Lordsks?


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## Lordsks (Jul 6, 2012)

Ya I'm sweating my balls off.
I need to get some bloodwork done and see where my hdl is at. If i get time in the next few weeks ill do it. Just taking 5mg a day right now.


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## birket (Jul 7, 2012)

good job.


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## strickamania (Jul 7, 2012)

since this makes me tired, would it be safe to run an eca stack with it.


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## teezhay (Jul 7, 2012)

Awesome log, thanks for doing this!

From your experience so far, what do you think about combining this compound with IGF-1 Lr3 or Des for the purpose of maintaining body composition while off cycle?


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## Goldenera (Jul 7, 2012)

Nice log!  I just stumbled on this stuff last few week. That's for the info!

Any update ?  Melting the fat off you?


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## sdf38 (Jul 9, 2012)

I thought you were in the UK, like Londen or something?


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## Lordsks (Jul 12, 2012)

teezhay said:


> Awesome log, thanks for doing this!
> 
> From your experience so far, what do you think about combining this compound with IGF-1 Lr3 or Des for the purpose of maintaining body composition while off cycle?



Yes would be very good for that. Just make sure your getting enough carbs.



strickamania said:


> since this makes me tired, would it be safe to run an eca stack with it.



Don't see why it wouldn't be safe. Whats your dose at? maybe taper down a bit. I noticed the tiredness went away after 3 weeks or so. 




Goldenera said:


> Nice log!  I just stumbled on this stuff last few week. That's for the info!
> 
> Any update ?  Melting the fat off you?



No more like maintaining, I didn't notice to much fat loss. I mean when I started this I was just finishing a long crazy cycle and was at my lowest bf% to date already. But it does work good at reducing bf. 




sdf38 said:


> I thought you were in the UK, like Londen or something?


What.. a guy can't go on vacation?


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## Lordsks (Jul 12, 2012)

I should note that I'm done running the 30ml bottle. I think this stuff is good enough to continue running it at 5mg daily.


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## TwisT (Jul 16, 2012)

bumps


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## sdf38 (Jul 17, 2012)

thought there maybe was a city called Pheonix in England....


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## Goldenera (Jul 29, 2012)

Lordsks said:


> No more like maintaining, I didn't notice to much fat loss. I mean when I started this I was just finishing a long crazy cycle and was at my lowest bf% to date already. But it does work good at reducing bf.



Hmm that's not the answer I was hoping for. I can maintain fine. I'm usually around 10-12% bf with no cardio. Was hoping this stuff worked per the hype for fat loss. 

U used 10 or 5 mg Ed?


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## BIGBEN2011 (Jul 30, 2012)

yea i dont understand you said this stuff is good and then you said i have not lost any weight .which is it i mean for close to 100 bucks a bottle i would want some damn results thats a vial of tren a and then some.


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## Goldenera (Jul 30, 2012)

BIGBEN2011 said:


> yea i dont understand you said this stuff is good and then you said i have not lost any weight .which is it i mean for close to 100 bucks a bottle i would want some damn results thats a vial of tren a and then some.



My thoughts as well.

 I'm hearing pros are dropping hgh for fat loss and using this. However that same read said they are using 20-25mg daily lol.


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## Him123 (Aug 21, 2012)

Hey bro how did you journey with gw end?  Good Log.


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