It is without doubt that certain hormones and growth factors positively influence muscle growth.
However, the exact way those substances affect human muscle is not completely understood.
The prevalent opinion was, until recently, that the IGF-I (Insulin-like Growth Factor 1) is playing main role in this mechanism. There are legitimate reasons to reassess this hypothesis.
The role of testosterone (full article here)
Higher levels of testosterone lead to higher increases in lean muscle growth. It is generally accepted that this is also the reason why males possess larger muscle mass than females.
The same is true about various testosterone derivates, whether naturally occurring or artificially produced (these substances are known as Anabolic Androgenic Steroids or AAS).
Testosterone is partially tied to SHBG (Sex Hormone Binding Globulin) which makes it biologically unavailable and partially turned into estradiol and other estrogens by the ester aromatase (the amount is insignificant under normal conditions but very significant if testosterone is administered exogenously).
About 7% of testosterone is turned into DHT (Dihydrotestosterone), a potent androgen.
It is well known that testosterone binds to androgen receptor (AR) and glucocorticoid receptors.
Testosterone-induced increase in muscle mass is associated with hypertrophy of both type I and type II muscle fibers and an increase in the number of myonuclei and satellite cells. Testosterone promotes the differentiation of mesenchymal, multipotent cells into the myogenic (muscle) lineage and inhibits their differentiation into the adipogenic (fat cells) lineage. Androgens regulate mesenchymal multipotent cell differentiation by binding to ARs, and promoting the association of ARs with β-catenin and translocation of the AR–β-catenin complex into the nucleus, resulting in activation of T-cell-specific transcription factor 4 (TCF-4). The activation of TCF-4 modulates a number of wnt-regulated genes that promote myogenic differentiation and inhibit adipogenic differentiation. (http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2072878/ )
Testosterone also occupies glucocorticoid receptors without activating them. This may be important since glucocorticoids normally induce strong catabolic reaction.
Some researchers presume that this mechanism may lead to strong anti-catabolic effects of testosterone. However, this would mean that other substances that also occupy glucocorticoid receptors will have similar anabolic effects.
This is not the case – DHEA, for example, is one such substance but its anabolic effects on young people are negligable or non-existent.
There is strong evidence that testosterone and DHT induce muscle growth by stimulating the androgen receptors (AR). Resistance exercise increases the concentration of AR in skeletal muscle (http://www.ncbi.nlm.nih.gov/pubmed/21070797 ). Japanese team led by Kazuo Inoue tried to block the AR receptors by oxendolone (an AR antagonist) and the results were very clear: much smaller muscle growth in rats with blocked AR despite muscle stimulation that induced muscle growth in a control group (http://www.springerlink.com/content/l651840550t56gm3/ ).
Growth Hormone effects on muscle growth (full article here)
There is a wide belief among bodybuilders (and even some medical professionals) that GH supplementation leads to muscle growth in normal individuals. This assumption is wrong and it has been refuted by many clinical studies.
Human Growth Hormone (HGH or simply GH) leads to muscle growth when supplemented to individuals with deficiency of this hormone. It also helps strengthening connective tissue but not muscle fibers.
Make no mistake – you will find many scientific papers concluding that Human Growth Hormone has a profound anabolic effect on muscle mass (especially when administered together with insulin). But under closer examination you will find that the subjects of those studies were persons with some kind of hormonal deficiency, seniors, malnourished persons or people recovering from disease/injury.
During the process of muscle repair following the catabolic phase of microinjury, host of various growth factors is released locally.
They include the fibroblast growth factors (FGFs), hepatocyte growth factor (HGF), transforming growth factor-betas (TGF-betas), insulin-like growth factors (IGFs), tumour necrosis factor alpha (TNFalpha) and others.
Until recently, IGF’s, especially the IGF-I, have been associated with muscle anabolism. This theory, as it seems, must be reevaluated. For the time being we can safely claim that various growth factors have important role in lean muscle growth but this role must be subject of further research.
Insulin effects on muscle growth
Insulin is a human hormone naturally secreted by the pancreas beta-cells. It is a crucial regulator of metabolic processes: people with no natural insulin secretion (Type 1 Diabetes) must be given exogenous insulin for life.
Insulin has a number of anabolic and anti-catabolic effects:
Decreased proteolysis – insulin causes lower protein breakdown
Increased protein synthesis – insulin causes the cells to absorb circulating amino acids
Vascularization – insulin forces the arterial wall muscle to relax thus causing increased blood flow to the muscles
Higher glycogen synthesis – insulin causes storage of glucose in the liver in the form of glycogen
While proper insulin function is indispensible for muscle growth and indeed for our survival, exogenous insulin supplementation is one of the most displaced and dangerous ideas ever proposed by some bodybuilders.