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GH and The Athlete - is there a point to it???

  • Thread starter Thread starter Juice Authority
  • Start date Start date
Juice Authority said:
I'm not sure what all that means. I posted an article I found to be very informative along with other related abstracts and associated links. If you have nothing positive to contribute to the discussion other than to call me the "cut and paste king" then please refrain from posting on this thread. I’d hate to see the quality of the information posted compromised by denigrating statements such as yours.

I meant that as a compliment :rainbow:
 
DrJMW said:
HGH directly stimulates beta-3 receptors which makes it the superior fat burner. There is no other compound that does so.

You know, this is very interesting point since I looked into this and apparently the pharmaceutical industry has not been successful in developing a beta 3-adrenoceptor agonist for use in the treatment of human obesity. The major question seems to be whether the number of biologically active beta 3-adrenoceptors in adult humans is sufficient to produce relevant metabolic effects and, if so, whether their long-term stimulation is safe and free of unwarranted side effects. The following study shows that the beta3-adrenoceptor agonist, L-796568, directed at the human receptor has been shown to increase lipolysis.


Clin Pharmacol Ther. 2002 Apr;71(4):272-9. Related Articles, Links


Acute effect of L-796568, a novel beta 3-adrenergic receptor agonist, on energy expenditure in obese men.

van Baak MA, Hul GB, Toubro S, Astrup A, Gottesdiener KM, DeSmet M, Saris WH.

Nutrition and Toxicology Research Institute (NUTRIM), Department of Human Biology, Maastricht University, The Netherlands. [email protected]

OBJECTIVE: Our objective was to investigate the thermogenic efficacy of single oral doses of the novel beta(3)-adrenergic receptor agonist L-796568 [(R )-N -[4-[2-[[2-hydroxy-2-(3-pyridinyl)ethyl]amino]ethyl]-phenyl]-4-[4-[4-(trifluoromethyl)phenyl]thiazol-2-yl]-benzenesulfonamide, dihydrochloride] in humans. METHODS: Twelve healthy overweight to obese men participated in this 2-center, 3-period, randomized, placebo-controlled, crossover trial. In each period subjects received 250 mg L-796568, 1000 mg L-796568, or placebo. Energy expenditure and respiratory quotient were determined by indirect calorimetry; blood samples were taken; and ear temperature, heart rate, and blood pressure were measured at baseline and during the 4-hour period after administration. RESULTS: Energy expenditure increased significantly after the 1000-mg dose (about 8%) and this was accompanied by an increase in plasma glycerol and free fatty acid concentrations. Systolic blood pressure also increased significantly. No changes in heart rate, diastolic blood pressure, ear temperature, plasma catecholamine, potassium, or leptin were found. CONCLUSIONS: Single-dose administration of 1000 mg of the novel beta(3)-adrenergic receptor agonist L-796568 increased lipolysis and energy expenditure in overweight men. This is the first study to show such an effect of beta(3)-adrenergic receptor agonists in humans without significant evidence for beta(2)-adrenergic receptor involvement.

Publication Types:
Clinical Trial
Multicenter Study
Randomized Controlled Trial

PMID: 11956510 [PubMed - indexed for MEDLINE]
 
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DrJMW said:
Even the HGH experts (docs, gurus, what-have-you) prefer using Long R3 IGF-1 to HGH for raising IGf-1 levels. Some even suggest that using both Long R3 and HGH is the way to go for maximizing levels of IGF-1. HGH, alone, is useless for building muscle, but excellent for fat loss. There is a company in Australia developing an oral that basically mimics HGH's fat burning effect. It is in Phase II FDA trails now. Unfortunately, Long R3 isn't classified a drug by the FDA and it isn't being manufactured by pharmaceutical companies..maybe some day.

All true, but have you seen this : http://www.insmed.com/Prod_Pipeline/Studies/Somatokine/SomatoKine.htm :chomp:
 
Juice I hadn't seen the hyperplasia article, so I need to digest it. I'll come back when I've gone through.

But I want to edit my above scientific stance on GH and add a personal anecdote. In a current jin experience, in about a month my bench (at 5 reps) has gone up 10 lbs a week (no exaggeration at all!), three times. This was after a plateau at 275 for over a month and a half. I was on deca/dbol/test for 6 weeks prior to the growth, and had gained well, but leveled off. How is such a strength gain possible when such synergy was not noticed to so great a degree in the lab? On a cybex press . . . Or at 6 weeks pre- and post- a growth cycle? Or a failure to spike protein synthesis with GH? I think therein lies the answer. The lab is too controlled. In big power lifts, technique is very important, probably more important the GH, IGF or whatever. Different technique or a different shirt can lead to almost unbelieveable poundage gains. In my case, the twinge in my right wrist from an old wrestling injury and a wiggly shoulder from another time always limited big weight. With growth, these areas have subjectively tightened. Perhaps, in other words, collagen synthesis, actually proven with GH, enables the strength athlete to lift big on the compound movements. Moving more weight is certainly going to provide a stronger overload stimulus, leading to greater growth, especially in the presence of AAS to enhance protein synthesis and encourage the formation of thicker muscle fibers. Something like this could explain the inability to measure of significant increase in protein synthesis with the addition of GH in a lab, while understanding the presence of many, many subjective stories of fantastic gains with GH.

In many compound movements, the athlete's ability to coordinate the whole body, so that each part contributes to the lift perfectly, is limited by tendon and ligament strength. GH allows for growth in these elements, allowing the athlete to lift heavier weight. Lifting heavier weight leads to greater hypertrophy. Therefore growth + AAS would seem to work synergisticly to build mass. Especially for the powerlifter or heavy-weight style bodybuilder, it would seem.
 
I agree, and it's nice to see the subject brought up again here JA, that if you are young and are looking soley to build mass that GH is not worth the money. But I don't think that's the only use for it. Neither is fat loss. Many people young and not so young grow LBM so quickly while on that their connective tissue doesn't keep up. This usually results in injury at some point for a lot of guys. I think GH helps your bones and connective tissue grow and handle the strain better as your muscle grows. How many times have I seen... "my forearms hurt" or "my elbows, wrists hurt" while guys are cycling?


Also, when it comes to GH's healing properties, once the damage is done, it's worth every penny. The bone fusion I had last July healed 3-4 times faster than normal because I used GH, my surgeon was absolutely amazed when he saw the X-ray 6 weeks post op and the bones had completely fused and developed over growth as though 6 months had gone by.
No, I didn't tell him though if you're wondering.
 
majutsu and ulter -

Great points. Here's a study that speaks to your point(s). Unfortunately it was performed on rats but it does show that rhGH administration stimulated dense fibrous connective tissue growth. The important thing to note is that it also caused a reduction in collagen maturation. This is an important point not to be overlooked since a reduction in collagen maturation affects the stability of the carpal bones and can ultimately lead to carpal tunnel.

Growth Horm IGF Res. 2002 Oct;12(5):367-73. Related Articles, Links


Growth and maturational changes in dense fibrous connective tissue following 14 days of rhGH supplementation in the dwarf rat.

Kyparos A, Orth MW, Vailas AC, Martinez DA.

Connective Tissue Physiology Laboratory, Department of Biology and Biochemistry, University of Houston, Houston, TX 77204-5001, USA.

The purpose of this study was to investigate the impact of recombinant human growth hormone (rhGH) on patella tendon (PT), medial collateral ligament (MCL), and lateral collateral ligament (LCL) on collagen growth and maturational changes in dwarf GH-deficient rats. Twenty male Lewis mutant dwarf rats, 37 days of age, were randomly assigned to Dwarf + rhGH (n = 10) and Dwarf + vehicle (n = 10) groups. The GH group received 1.25 mg rhGH/kg body wt twice daily for 14 days. rhGH administration stimulated dense fibrous connective tissue growth, as demonstrated by significant increases in hydroxyproline specific activity and significant decreases in the non-reducible hydroxylysylpyridinoline (HP) collagen cross-link contents. The increase in the accumulation of newly accreted collagen was 114, 67, and 117% for PT, MCL, and LCL, respectively, in 72 h. These findings suggest that a short course rhGH treatment can affect the rate of new collagen production. However, the maturation of the tendon and ligament tissues decreased 18-25% during the rapid accumulation of de novo collagen. We conclude that acute rhGH administration in a dwarf rat can up-regulate new collagen accretion in dense fibrous connective tissues, while causing a reduction in collagen maturation.

Copyright 2002 Elsevier Science Ltd.

PMID: 12213190 [PubMed - indexed for MEDLINE]
 
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I think we're getting a little warmer as far as the connection between GH and AAS for strength and size when taken together. Here's a study where both men and women were given GH and AAS to evaluate the changes in body composition, strength and endurance. You'll notice the one group of men had increases in LBM and strength with the combination of both GH and AAS as opposed to just AAS or GH alone. So, one could conclude from this that AAS and GH are synergistic and if taken together produce greater gains in strength and LBM than they do if taken separately. The downside to this study is that the test subjects were between 65 to 88 years old.

Growth hormone and sex steroid administration in healthy aged women and men: a randomized controlled trial.

Blackman MR, Sorkin JD, Munzer T, Bellantoni MF, Busby-Whitehead J, Stevens TE, Jayme J, O'Connor KG, Christmas C, Tobin JD, Stewart KJ, Cottrell E, St Clair C, Pabst KM, Harman SM.

Division of Endocrinology and Metabolism, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD, USA. [email protected]

CONTEXT: Hormone administration to elderly individuals can increase lean body mass (LBM) and decrease fat, but interactive effects of growth hormone (GH) and sex steroids and their influence on strength and endurance are unknown. OBJECTIVE: To evaluate the effects of recombinant human GH and/or sex steroids on body composition, strength, endurance, and adverse outcomes in aged persons. DESIGN, SETTING, AND PARTICIPANTS: A 26-week randomized, double-blind, placebo-controlled parallel-group trial in healthy, ambulatory, community-dwelling US women (n = 57) and men (n = 74) aged 65 to 88 years recruited between June 1992 and July 1998. INTERVENTIONS: Participants were randomized to receive GH (starting dose, 30 micro g/kg, reduced to 20 micro g/kg, subcutaneously 3 times/wk) + sex steroids (women: transdermal estradiol, 100 micro g/d, plus oral medroxyprogesterone acetate, 10 mg/d, during the last 10 days of each 28-day cycle [HRT]; men: testosterone enanthate, biweekly intramuscular injections of 100 mg) (n = 35); GH + placebo sex steroid (n = 30); sex steroid + placebo GH (n = 35); or placebo GH + placebo sex steroid (n = 31) in a 2 x 2 factorial design. MAIN OUTCOME MEASURES: Lean body mass, fat mass, muscle strength, maximum oxygen uptake (VO(2)max) during treadmill test, and adverse effects. RESULTS: In women, LBM increased by 0.4 kg with placebo, 1.2 kg with HRT (P =.09), 1.0 kg with GH (P =.001), and 2.1 kg with GH + HRT (P<.001). Fat mass decreased significantly in the GH and GH + HRT groups. In men, LBM increased by 0.1 kg with placebo, 1.4 kg with testosterone (P =.06), 3.1 kg with GH (P<.001), and 4.3 kg with GH + testosterone (P<.001). Fat mass decreased significantly with GH and GH + testosterone. Women's strength decreased in the placebo group and increased nonsignificantly with HRT (P =.09), GH (P =.29), and GH + HRT (P =.14). Men's strength also did not increase significantly except for a marginally significant increase of 13.5 kg with GH + testosterone (P =.05). Women's VO(2)max declined by 0.4 mL/min/kg in the placebo and HRT groups but increased with GH (P =.07) and GH + HRT (P =.06). Men's VO(2)max declined by 1.2 mL/min/kg with placebo and by 0.4 mL/min/kg with testosterone (P =.49) but increased with GH (P =.11) and with GH + testosterone (P<.001). Changes in strength (r = 0.355; P<.001) and in VO(2)max (r = 0.320; P =.002) were directly related to changes in LBM. Edema was significantly more common in women taking GH (39% vs 0%) and GH + HRT (38% vs 0%). Carpal tunnel symptoms were more common in men taking GH + testosterone (32% vs 0%) and arthralgias were more common in men taking GH (41% vs 0%). Diabetes or glucose intolerance occurred in 18 GH-treated men vs 7 not receiving GH (P =.006). CONCLUSIONS: In this study, GH with or without sex steroids in healthy, aged women and men increased LBM and decreased fat mass. Sex steroid + GH increased muscle strength marginally and VO( 2)max in men, but women had no significant change in strength or cardiovascular endurance. Because adverse effects were frequent (importantly, diabetes and glucose intolerance), GH interventions in the elderly should be confined to controlled studies.

Publication Types:
Clinical Trial
Randomized Controlled Trial

PMID: 12425705 [PubMed - indexed for MEDLINE]
 
An Australian company, Metabolic Pharmaceuticals LTD, is in Phase II trials with an oral that duplicates the HGH fragment that stimulates Beta-3's in adipose tissue. They have a website www.metabolic.com.au. You can read up on their experimental drug. There are still some mysteries that aren't solved, but I find it hard to argue with results.
 
DrJMW said:
An Australian company, Metabolic Pharmaceuticals LTD, is in Phase II trials with an oral that duplicates the HGH fragment that stimulates Beta-3's in adipose tissue. They have a website www.metabolic.com.au. You can read up on their experimental drug. There are still some mysteries that aren't solved, but I find it hard to argue with results.

Doc,

If GH is not mediated through the beta-3 receptor then how exactly does it stimulate it?
 
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