Testosterone is somewhat thought of as the holy grail of exercise, especially in the dude circles, but is it really?

In this article I go full tilt science and while I wanted it to be entertaining, it must convey important information and to do that we must go down the rabbit hole.

To start this conversation you must have an understanding of the male hypothalamic pituitary gonadal (HPG) axis aka how the male body signals the testicles to produce testosterone. This all starts in the brain with the Hypothalamus secreting gonadotropin-releasing hormone GnRH which it does like all hormones in a pulsatile fashion. GnRH then tells the pituitary to release follicle stimulating hormone (FHS) and luteinizing hormone (LH). FSH acts on the Sertolli cells and says hey guys light up some sperm production. LH on the other hand tells the Leydig cells to ramp up androgenesis AKA testosterone production.

Here is a diagram of this process.

HPGNow this is an oversimplification and as you would guess the whole story is a lot more complicated as to what other factors regulate this axis and there are also things we undoubtedly don’t know yet. Below is the more complicated version of that diagram. On these two diagrams I want to highlight two things.

  • The major regulator of GnRH secretion is Testosterone itself, this is called negative feedback inhibition. This means if testosterone is high the signal to make more testosterone would go down. This is why we must be absoluetly certain that a male needs exogenous testosterone because it will shut down this communication at the level of the brain. The body is efficient above all else, so if it is getting something exogenously it won’t see a need to produce it endogenously.
  • The other highlight is that corticotropin-releasing hormone (CRH) also inhibits GnRH secretion. CRH is the master hormone released by the hypothalamus of the hypothalamic-pituitary adrenal (HPA) axis. Furthermore, cortisol one of the end products of the HPA axis also inhibits androgenesis at both the gonadal and hypothalamic areas. Thus, you can begin to see how dysregulation of the stress response can inhibit testosterone production. And this makes sense physiologically because if we are running from a real or proverbial tiger we are not worried about things like reproduction, muscle growth, or the lushishness of our beards (this is actually more related to DHT, but still).

 

HPG2

* from Constantini NW, Hackney AC. Endocrinology of physical activity and sport. 2nd ed.

 

Now that we have an understanding of how the HPG axis functions, let’s ask the big question.

 

How does exercise affect Testosterone levels?

 

Globally, that’s actually fairly simple, short, acute, intense sessions (lifting and even sprinting) usually increase testosterone (transiently), while prolonged exercise usually reduces serum testosterone levels acutely and chronically. Go ahead read that last sentence again. It’s important. Men both young and old get this acute hormonal spike in testosterone 15-30 min following an appropriate exercise bout, but the spike has been found to be larger in younger men.

Now the bigger question.

 

Do acute post-exercise hormonal secretions mediate increases in muscle size?

 

This is called the hormone hypothesis and to understand it we need some understanding of how muscles grow.

“Postexercise hypertrophic adaptations are mediated by a complex enzymatic cascade whereby mechanical tension is molecularly transduced into anabolic and catabolic signals that ultimately lead to a compensatory response, shifting muscle protein balance to favor synthesis over degradation.”

-Brad Schoenfeld

This one sentence is grounds for articles on articles and I would refer you to Dr. Pat Davidson’s series What Causes Muscle to Grow. Also, Coach Davis is neck deep and sprinting through this research all the time, always striving to look at personalizing the amount of damage (accumulation of metabolic waste, reduction in pH, and hypoxia being the main three) needed to produce the desired physiologic response.

Now how does testosterone fit into this process? As most of you know from the media, testosterone is in fact anabolic (gasp) in that it attenuates protein breakdown and promotes protein synthesis, as well as promotes the release of other anabolic hormones like growth hormone (GH) and insulin-like growth factor 1 (IGF-1). The hypothesis now being that if you have more testosterone hanging around after exercise more will bind to the androgen receptor and this will turn the ship around faster and produce a heightened response to said training load. At this point some of you may be wondering why I am talking so much about this post-exercise transient increase in testosterone concentrations, this is because in the research, strength training has not been found to raise basal (resting) levels of testosterone and this in my mind is where functional medicine (more just being smart and accumulating the right data) comes into play for both male and female athletes.

The science on the importance of the post-exercise rise in anabolic hormones is far from black and white and studies have found that muscle growth can occur in the absence of this post-exercise hormonal increase and that increases in post exercise hormone concentrations may not be related to further increases in muscle growth in response to resistance training. Thus, these hormonal elevations may heighten muscular growth (and even increase androgen receptor concentrations) but may not be absolutely necessary. These increases have also not been found to be mediated by LH secretion and are more likely a result of the activation of the sympathetic nervous system during training. Anecdotally, we have seen that some CrossFitters who are obviously over-trained and can still gain muscle in a state where low  and low-normal testosterone is present, whether they are still getting a transient rise in testosterone in this overtrained state we cannot say.

On the other end of the spectrum, there is no debating that exogenous testosterone administration can produce increases in muscle size and decreases in body fat and these effects are increased when strength training is added. Yet,  I have not seen a study that looks at differences in increases in muscle size in response to resistance exercise based on natural basal hormonal values inside of physiological ranges. Interestingly, no difference in testosterone (both free and total) was seen between top-class athletes and untrained controls. But would having a basal testosterone level of 850 ng/dL compared to 500 ng/dL result in an elevated response to the same resistance training program, when keeping all other things constant (nutrition, sleep, stress, etc)? To my knowledge, we don’t know the answer to that question and we may never know as running this type of randomized controlled trial (RCT) would be extremely difficult to run/control and the selection process would also be quite costly from both a financial and time standpoint.

However, we do very much know that prolonged chronic endurance exercise leads to dysfunction in the HPG axis. Cross-sectionally, many studies have found depressed testosterone levels in endurance trained athletes compared to sedentary controls and these levels are consistently in the low-normal range. Interesting, this lowering of basal testosterone levels is not accompanied by a rise in LH (which would be expected), in fact LH has been found to stay the same or even decrease in response to chronic endurance training. The mechanism of this reduction in basal testosterone levels has yet to be determined, but is likely to involve a milieu of other hormonal changes, like the increase in CRH and cortisol which have been found to inhibit the HPG axis at both the brain and testicular level.

 

So what’s the final rub?

 

Testosterone is important. It follows a circadian rhythm (why you stand at attention in the early morning hours) and levels peak in the late teens or early twenties and then plateau until the 30s or 40s when testosterone starts decreasing by 1-2% per year. However, I have become less and less apt to just accept this fate as I have tested plenty of men in their 50s and even 60s who have natural testosterone levels in the ideal range of 700-900 and I now believe that this commonly cited population wide reduction in testosterone may be more of a factor of our current environment than guaranteed “death” sentence.

Yet, testosterone is not be the end all be all for what we do in the weight room but if you asked any man if he wanted high physiological or low physiological levels you can guess his response. And low or even low-normal levels can be indicative of more overall stress than the system can handle as we know both chronic physical and psychosocial stress will wreak havoc on the HPG axis. Thus, the inclusion of testing basal levels in one’s eval process is highly recommended to establish if someone is tanked or tanking. This can then add buy-in for what you can do from a functional medicine standpoint to potentially bring that level back up. We have seen men raise their basal levels anywhere from 200 to 500ng/dL in 90 day protocols with lifestyle changes and organic, natural supplements. Continued testing is then advisable throughout the life course as a barometer of total accumulated stress (environmental, physical, and psychosocial) and the functioning of the HPG axis. Science is displayed in populations and averages and what matters is individuals and this is why knowing both the research and the state of your own system is so important. When or if I have a son I will start getting annual testosterone levels on him starting at puberty so he knows physiologically where he stands and then he can track that value as he ages if he so chooses. If you want more information on this topic check out the references below. Get educated on something that most men leave to hearsay instead of things like facts, science, and objective data.

By: Ben House

References:

  1. Constantini NW, Hackney AC. Endocrinology of physical activity and sport. 2nd ed. New York: Humana Press; 2013.
  2. Schoenfeld BJ. Postexercise hypertrophic adaptations: a reexamination of the hormone hypothesis and its applicability to resistance training program design. J Strength Cond Res. Jun 2013;27(6):1720-1730.
  3. Hayes LD, Bickerstaff GF, Baker JS. Interactions of cortisol, testosterone, and resistance training: influence of circadian rhythms. Chronobiology international. Jun 2010;27(4):675-705.
  4. Vingren JL, Kraemer WJ, Ratamess NA, Anderson JM, Volek JS, Maresh CM. Testosterone physiology in resistance exercise and training: the up-stream regulatory elements. Sports medicine. Dec 1 2010;40(12):1037-1053.
  5. Kraemer WJ, Ratamess NA. Hormonal responses and adaptations to resistance exercise and training. Sports medicine. 2005;35(4):339-361.
  6. Rubin DA, Pham HN, Adams ES, et al. Endocrine response to acute resistance exercise in obese versus lean physically active men. European journal of applied physiology. Jan 30 2015.
  7. Hackney AC, Szczepanowska E, Viru AM. Basal testicular testosterone production in endurance-trained men is suppressed. European journal of applied physiology. Apr 2003;89(2):198-201.
  8. Daly W, Seegers CA, Rubin DA, Dobridge JD, Hackney AC. Relationship between stress hormones and testosterone with prolonged endurance exercise. European journal of applied physiology. Jan 2005;93(4):375-380.
  9. Hackney AC. Effects of endurance exercise on the reproductive system of men: the “exercise-hypogonadal male condition”. J Endocrinol Invest. Oct 2008;31(10):932-938.
  10. West DW, Phillips SM. Anabolic processes in human skeletal muscle: restoring the identities of growth hormone and testosterone. The Physician and sportsmedicine. Oct 2010;38(3):97-104.

 

 

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