I’ve got an ABC (Ask Bret Contreras) question for you. Can someone be consistently on the lower end of the normal range for testosterone and still be muscular? And if so, why?
Hey Bobby! Testosterone is valuable for hypertrophy for many reasons, including increased protein synthesis, increased growth factor activity (growth hormone, IGF-1, etc.), and increased satellite cell activation. In addition to its anabolic effects on muscle, testosterone also acts on the nervous system and can increase neurotransmitter release and nerve regeneration. So testosterone is definitely a good thing. But high levels are not mandatory for muscular growth, which is why some women are able to grow larger muscles than some men despite the fact that they produce one-tenth to one-twentieth the testosterone levels of men. Here’s why:
According to research, satellite cell efficiency appears to be the most important factor in muscular growth. Some folks have efficient satellite cell systems while others don’t. Satellite cells are located between the basil lamina and sarcolemma toward the periphery of the myofibers and function like stem cells. Once a nucleus and its surrounding sarcoplasm reaches approximately 2,000 square micrometers per nucleus (or 17-25% of the fiber’s initial size), a threshold is reached and additional nuclei are required for further growth (this has been coined the “myonuclear domain”). Efficient satellite cell systems are generous with their donation of nuclei to myofibers, and they’re also very expedient at replenishing themselves so the available pool stays bountiful. Poor satellite cell systems are stingy with their nuclei and inefficient at renewing themselves.
While testosterone is indirectly related to satellite cell efficiency through increased IGF-1 production (which has been shown to activate satellite cells) and increased androgen receptor density (which has been shown to be abundant in satellite cell nuclei), it appears that mechanical tension and muscular damage (and the associated macrophage/cytokine release) are closely related to satellite cell behavior as well. Mechanical tension also stimulates growth through increased mechanogrowth factor release and activation of the Akt/mTOR pathway, which appears to be a dominant pathway leading to muscular hypertrophy.
Another important consideration is how the low testosterone levels come about. To illustrate a point, let’s consider two examples at opposite ends of the extremes.
Male number one trains hard six days per week via heavy squatting, pulling, and pressing. He’s consistently oscillating between stimulating and overreaching. He eats and sleeps well and has low stress levels, but since he trains so hard his testosterone levels are usually on the low end.
Male number two doesn’t lift weights. All day long he sits on the couch, drinks beer, takes pain killers, smokes weed, eats cheetos, drinks red bull, doesn’t sleep well, is stressed out all the time because he can never pay his bills, and is sick all the time. Furthermore, he lives in an area where xanoestrogens are abundant and he’s sucking down PCB and BPA by the liter. Here would be the differences between the two guys:
As you can see, there are multiple (and many redundant) pathways to muscular hypertrophy, and even though testosterone helps tremendously, one can still see dramatic gains despite suffering from low testosterone levels.