In recent years, controversy has surrounded the Judgment of the World Athletics Championships that hyperandrogenic athletes (female athletes with natural testosterone levels) are prohibited from competing in certain track events.
The controversy is perhaps the best example of the case of the South African corridor Caster Semenya.
This rule is based on the assumption that total testosterone levels directly determine women’s athletic performance. But ours new research challenges this assumption.
Remember me, what is the controversy about?
Testosterone is the main androgenic hormone (male) and one of the hormones the most common doping agents. Athletes involved in strength and power-based sports, including bodybuilding, athletics, wrestling, and cycling, have used testosterone for decades because of its muscular properties.
Contemporary anti-doping tests can detect and distinguish between the presence of pharmaceutical testosterone (“exogenous”) and natural testosterone (“endogenous”). with a high level of certainty. The presence of exogenous testosterone is essential for a positive result.
However, some people, men and women, present high levels of natural testosterone without ever taking androgenic hormones. These people are “hyperandrogenic.”
Male athletes with high levels of naturally occurring testosterone can compete normally. In contrast, hyperandrogenic women athletes are at the center of a controversy over sports regulations.
Because their natural blood testosterone levels are above an arbitrary threshold of five nanomoles of testosterone per liter (nmol / L), hyperandrogenic females are forbidden to compete in a series of world athletics events ranging from 400 meters to the mile.
They can only compete if they choose to take it anti-androgen drugs to lower your testosterone levels.
How does testosterone improve performance?
Testosterone acts on muscle cells by binding to a specific receptor protein, the androgen receptor. When testosterone binds, the androgen receptor signals to the muscle cell to activate the pathways that trigger a increased muscle mass, called muscle hypertrophy. As a result, the muscle grows and becomes stronger.
But let’s see what happens when testosterone can’t do its job on the muscle. “Androgen receptor elimination mice” are genetically modified mice that do not produce this receptor. Compared to normal male mice, mice removed from the male androgen receptor lose up to 20% of your muscle mass and strength. This makes sense as testosterone no longer has any receptor to bind to.
Surprisingly, this does not happen in female mice. Female androgen receptor elimination mice are as strong and muscular as their control counterparts. This suggests that testosterone may not be needed to achieve maximum muscle mass and strength in women.
Our novelty human data align with this hypothesis. We used a large publicly accessible database and demonstrated that total testosterone levels are not associated with muscle mass or strength in 716 pre-menopausal women.
This contrasts with males, where there are higher concentrations of testosterone are associated with increased muscle mass and strength.
We are also doing experimental research on this topic. We recruited 14 young volunteer women with natural testosterone levels along a spectrum from low to hyperandrogen.
Although this part of our research has not yet been published in a peer-reviewed journal, our results so far seem to confirm the results of epidemiological data. We found that testosterone levels did not correlate with thigh muscle size, strength, and endurance, even after 12 weeks of resistance training aimed at maximizing muscle mass and increasing strength.
Our laboratory study allows us to closely monitor external factors that may influence muscle mass and strength, such as diet, sleep, training status, and menstrual cycle.
Why can’t testosterone improve women’s athletic performance?
Previous research suggests female sex hormones estrogen and progesterone may play a part in the muscular role of testosterone in young women.
Another important consideration is that natural testosterone exists in two forms: “free” in the bloodstream, or “bound” to a protein that reduces its signaling ability to muscle. Our research suggests that “free” testosterone plays the most important role in regulating female muscle mass and performance.
Unfortunately, the current one World Athletics Standards they are based on the total set of testosterone (the sum of “free” and “bound” testosterone).
One limitation of our studies is that most of our participants would not be classified as hyperandrogenic according to World Athletics. Beyond a certain threshold, testosterone can have a different effect on female muscle physiology.
A recent study tested this hypothesis administering pharmaceutical testosterone to women to approach the 5 nmol / L threshold. After ten weeks of this treatment, the authors found that volunteers receiving testosterone had gained more muscle mass and could run longer with a treadmill. before exhaustion compared to volunteers who did not receive testosterone.
Surprisingly, however, there were no differences between groups in muscle strength, muscle strength, explosive force (speed) and the maximum rate of oxygen consumption measured during exercise, which is the best indicator of cardiorespiratory form. .
All of these parameters are important for short and medium distance track events. These results support our hypothesis that total testosterone is not a direct determinant of women’s muscle strength and performance and reiterates the need to challenge the rules of the world of athletics.
Now what?
Our research is important as it fights for the right of a cohort of naturally talented athletes to compete in the chosen athletic tests, despite their natural testosterone levels.
Challenging the current assumption that “the more the better,” we hope our project provides the basis for new regulations aimed at treating hyperandrogenic athletes more equitably.
Severine Lamon, Associate Professor, Nutrition and Exercise Physiology, Deakin University
This article is republished from The conversation under a Creative Commons license. Read the original article.
