The Most Effective Growth Hormone Protocol for Hypertrophy

MGF has been shown in cell culture models to increase the proliferation and migration of myoblasts, as well as being involved in satellite cell activation. Whether or not this is something that translates into real-world applicability is still a source of contention however. This behavior has been seen even in the presence of IGF-1 inactivation, which suggests MGF has the ability to operate independently of mature IGF-1 [438]. With that said, all IGF-1 isoforms do require a functional IGF-1 receptor to actually produce muscle hypertrophy as they do not affect the receptor in the absence of mature IGF-1 [439-440]. Actual response to MGF relies upon having an environment with active pools of satellite cells, as aged muscle tissues are normally in a state of dormancy. Finally, although finding legitimate injectable MGF is almost unicorn-like in bodybuilding circles, understand that full-length MGF appears to produce less activity in muscle than mature IGF-1, so its inherent value to bodybuilders may actually be overestimated [442].

Somatopause

Studying elderly subjects brings a somewhat unique perspective to the table as it is well-known that sarcopenia, another term for degenerative muscle loss, occurs as we age. It is also well-established that levels of secreted GH and circulating IGF-1 gradually decline over one’s lifetime after peaking during puberty [159-162]. The decline in hormone levels is quite severe, with GH secretion declining by as much as 10-15% every decade after the age of 20 [163]. It was suggested many years ago that these senescent changes in body composition and metabolic functions are directly related to the decrease in hormone levels within the GH/IGF axis. The research community has actually coined the term “somatopause” to describe this phenomenon [159,164]

More succinctly stated, the somatopause hypothesis proposal [128] states:

• Changes in lifestyle and genetic predispositions promote accumulation of body fat with advancing age
• This increased fat mass increases FFA availability and thus induces insulin resistance
• High insulin levels suppress IGFBP-1 resulting in a relative increase in free IGF-1 levels
• Systemic elevations in FFA, insulin, and free IGF-1 suppress pituitary GH release, which further increases fat mass
• Endogenous GH is cleared more rapidly in subjects with increased fat mass

As you can see, this is a bit of a chicken and egg scenario. We gain body fat as we age, which causes insulin resistance, which suppresses GH secretion, which makes us more fat. It is kind of interesting to see that GH pulse frequency remains essentially intact though. The age-related attenuation is actually just a marked reduction in pulse amplitude alongside increased SRIF secretion [165].

The changes associated with somatopause very much resemble those seen in younger adults with clinical growth hormone deficiency (GHD). Although similar, elderly folks are normally not as severely impacted as GHD individuals and somatopause is not considered a disease state [160,166-167]. Examples of some of the changes associated with somatopause include reduced muscle and bone mass, reduced strength, diminished exercise and cardiac capacity, increased body fat (particularly in the visceral region), and cognitive deterioration.

Because of the desire to reverse the many detrimental effects related to aging, there is widespread speculation that GH administration may help as part of a complete hormone replacement therapy (HRT) program. A complete review of HRT and the elderly is beyond the scope of this article, but those who are interested can find a recent discussion on the topic here [168].

Does Growth Hormone Enhance Athletic Performance?

The emergence of GH as a performance enhancing drug (PED), outside of underground bodybuilding circles, is largely attributed to the release of the now infamous “Underground Steroid Handbook” in the early 1980s [169]. Subsequently, GH hit more of a mainstream audience when 1988 Olympic gold medal winner Ben Johnson admitted to using it alongside AAS after being stripped of his title following a failed blood test [170]. During this era, it was popularly believed that GH would increase muscle mass while simultaneously improving aspects of athletic performance [171]. And, as a response to this belief, in 1989 the IOC banned GH while labeling it as a PED as part of a new doping class of “peptide hormones and analogs”. It banned GH despite there being a lack of a legitimate test for rHGH at the time [172]. Despite all this, the question still remains – even with evidence suggesting that GH has been used in competitive athletics for decades, does it truly provide any measurable performance enhancing effects?

There have actually been multiple systematic reviews that have attempted to answer this question, but unfortunately they have all been far from conclusive as it relates to the ergogenic effects of GH [173-175]. And despite various scandals over the years, as well as the prevalence of GH usage by pro athletes, there is still very little clinical evidence to suggest that GH in isolation has any significant impact on performance enhancement in either healthy adults or younger subjects [173,176-179].

There have been a handful of tightly controlled trials which more directly attempted to look for its impacts on physical performance in healthy and trained subjects. Arguably the most interesting of the bunch demonstrated that supraphysiological doses of GH alongside AAS provided no significant improvements on VO2 consumption, strength, or explosive power as measured by jump height [180]. It did note a slight improvement in anaerobic sprint capacity, which was more noticeable on men and especially in those using the combined treatment. Considering this is an event where fractions of a second could mean the difference between winning and losing, it is certainly something worth noting.

By and large though, no increased aerobic performance is observed with GH administration when looking at the body of literature as a whole. This is the case when GH is administered at physiological doses to healthy subjects [181-182] as well as when it is administered in supraphysiological doses [180,183-184]. Aerobic capacity is also not affected by acute GH administration prior to training [185]. Any and all aerobic performance enhancements by GH actually appear to be mediated via androgens, and this is further supported by the results of a trial demonstrating former AAS users showing increased VO2 max, maximum inspiratory, and maximum expiratory pressure. Although it had been a few months since their last exposure to AAS, this was likely not enough time to entirely rule out any sort of AAS bleed over effect [186].