The Most Effective Growth Hormone Protocol for Hypertrophy

Healthy elderly subjects who were provided combined doses of testosterone and GH, designed to put them back into youthful hormone ranges, did experience improvements in certain measures of balance and physical performance [187]. These performance improvements seem to be more pronounced in men though, and are marginal at best, even with the combined treatments [188]. As has been discussed earlier, supraphysiological doses of GH may increase anaerobic capacity [180]. This is something that has also been seen on occasion when GHD subjects were treated with GH, putting them back into “normal” hormone ranges [182,189].

The GH/IGF axis may also play a role in the regulation of vascular tone, or the degree of constriction as compared to a blood vessel’s maximally dilated state, thereby regulating peripheral resistance [190-191]. IGF-1 has been identified as a potent vasodilator, an effect partly mediated by increased nitric oxide release from the endothelium, the tissue that forms a layer of cells lining organs such as the heart and lymphatic vessels [192-194]. This potential for increased blood flow capacity has a myriad of hypothetical benefits on athletic endeavors.

The bottom line here is that, despite the lack of compelling evidence in the literature [434], athletes are often using doses and protocols that are not being replicated in trials. With that said, caution should still be exercised before completely dismissing GH as a performance enhancer simply based upon what the body of literature suggests to us. It is very possible that it is going to be a contributor to elite level athletes, and may be doing so via direct or indirect means.

Direct Effects of GH and IGF-1 – Skeletal Muscle Hypertrophy

Let’s cut right to the chase – in and of itself, GH does not directly cause skeletal muscle hypertrophy. This has been studied extensively for decades and, so far, no credible study has been able to show a clear effect of medium-to-long term rHGH administration on hypertrophy – even in supraphysiological doses provided to high level athletes participating in rigorous resistance training.

The fact that this correlation has not been made is certainly not due to lack of trying. Plenty of research teams through the years have attempted to identify GH-mediated hypertrophy in healthy adult subjects [48,184,195-199] or elderly subjects [188,198,200-203] either unsuccessfully, or inconclusively. Furthermore, the acute exercise-induced increases in GH secretion have also been demonstrated to produce no changes in MPS or hypertrophy [204-205]. Interestingly, although the amount of trials occurring within the literature are significantly less common than those where GH was administered, systemic administration of rhIGF-1 has also been shown to result in no measurable hypertrophic effect in both young [63,206] and elderly [207-208] subjects.

There is recent evidence which suggests that chronic GH exposure increases the expression of the intramuscular pathways responsible for atrophy [209]. It stands to reason that many of the anabolic characteristics demonstrated by GH may be offset by this increased catabolic pathway expression, which could be why chronic exposure to GH does not lead to hypertrophy. It could also be responsible for why chronic GH exposure may produce less efficient and weaker muscles [210]. Quite simply, this may be yet another in long line of negative regulations built into the GH/IGF axis, but further studies are going to need to be conducted to further elucidate this hypothesis.

For those that plan on digging into the literature themselves after reading this article, which I highly encourage by the way, I want to make a very important distinction here which goes all the way back to my opening statement. Most GH trials do report an increase of lean body mass in their subject groups who were administered GH. So, at this juncture, one may be unclear how I can still be making these anti-hypertrophy claims? Well, we must remember that GH is very adept at causing water retention, as well as increasing soft tissue mass which I’ll talk about momentarily. Specifically, GH increases whole-body sodium retention, and consequently extracellular water, in a dose-dependent manner, via its effects on the renin-angiotensin system [211]. These increases in sodium and water retention have also been seen with IGF-1 administration, as IGF-1 itself seems to be a key regulator of renal sodium excretion rate [83,212-213]. So the real takeaway point here is to just be careful when drawing conclusions between reports of increased lean body mass and actual skeletal tissue growth.

Indirect Effects of GH and IGF-1 – Skeletal Muscle Hypertrophy

We’ve just spent the entirety of the last section talking about how both GH and IGF-1 have no direct impact on hypertrophy. However, this does not mean they do not contribute at all. My primary goal for this section of the article is to explain a few of the many mechanisms occurring behind the scenes, many of which will still be big factors to someone that is interested in maximizing their hypertrophy potential.

Growth hormone is a potent stimulator of collagen synthesis in both tendons and skeletal muscle. This effect is likely mediated via autocrine IGF-1’s ability to stimulate fibroblasts to synthesize it [214-215]. It actually does this without affecting skeletal muscle protein synthesis, despite both circulating and local IGF-1 being enhanced significantly. This effect is also induced independent of resistance training, and even seen in immobilized subjects provided with GH administration [216]. The connective component of skeletal muscle is vital for the transmission of force, which is produced by muscle fibers, to the tendons and bones for actual movement. Specifically, collagen is an important strength-carrying component of the extracellular matrix, which is continually being loaded during intense movements.

Because of GH’s potent effects on the components of the extracellular matrix, we may now begin to understand why anecdotes over the years suggested that adding GH into a hormone stack produced positive impacts on things like nagging aches and pains. On the other end of the spectrum, this also could be a primary contributing factor to why various side effects are reported by GH users such as soft tissue edema, joint pain, and carpal tunnel syndrome [217-219]. There are also many who believe GH can accelerate injury recovery time, however that is a complex topic that will be discussed another day.

GH’s impacts on collagen synthesis could also be of great interest to strength athletes who are not necessarily motivated by hypertrophy, but whose goals are creating an environment conducive to moving the absolute maximum weight from point A to point B. Stimulating collagen synthesis would potentially help strengthen the entire skeletal muscle support system. Now, it is worth adding a little clarifying side-note here. Despite this sounding great in principle, GH supplementation has never directly resulted in strength gains in any of the trials on otherwise healthy subjects, spanning various groups [48,50,184,196-198,200-201,203,220-221]. Of course, if GH was being used alongside something that did increase strength, it isn’t much of a leap to postulate that it may be a valuable accessory compound.