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    Lightbulb Gw50156 log

    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.
    Last edited by TwisT; 06-02-2012 at 02:05 PM.

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

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

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    Sub'd...

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    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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    Sounds promising. Ill be following your log!

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    Awesome buddy!


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

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    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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    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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    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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    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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    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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    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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    How would u compare to clen?


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

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    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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    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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    interested in this

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    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.
    Last edited by sdf38; 06-11-2012 at 07:07 PM.

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    Quote Originally Posted by fsoe View Post
    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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    Quote Originally Posted by sdf38 View Post
    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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    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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    Quote Originally Posted by Lordsks View Post
    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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    Quote Originally Posted by sdf38 View Post
    PS: T3 at night would keep me up, I would only take in morning

    ditto


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    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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    Quote Originally Posted by sdf38 View Post
    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.

    Quote Originally Posted by DEE151 View Post
    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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    Quote Originally Posted by Lordsks View Post
    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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    so how long are u going to run GW for?


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