Over the last few years, controversy has surrounded the World Athletics judgment that female hyperandrogenic athletes — female athletes with naturally high levels of testosterone — are banned from competing in certain monitor events.

The controversy is perhaps best exemplified by the case of South African runner Caster Semenya.

This rule relies on the hypothesis that total testosterone levels directly determine athletic performance in females. But our new research challenges this assumption.

Remind me, what’s the controversy about?

Testosterone is the major androgenic (male) hormone and one of the most common doping agents. Athletes who participate in strength and power-based sports, including athletics, bodybuilding, wrestling and cycling, have used testosterone for decades for its muscle-building properties.

Contemporary anti-doping tests can detect and distinguish between the presence of pharmaceutical (“exogenous”) testosterone and organic (“endogenous”) testosterone using a high degree of certainty. The existence of exogenous testosterone is vital to return a positive result.

However, some people, males and females, present with elevated levels of natural testosterone without having ever taken androgenic hormones. These people are “hyperandrogenic. ”

Male athletes with naturally occurring high testosterone levels can compete normally. In contrast, female hyperandrogenic athletes are at the center of a controversy of regulations.

Because their natural blood testosterone levels are above an arbitrary threshold of five nanomoles of testosterone per liter (nmol/L), hyperandrogenic females are banned from competing in a series of World Athletics events ranging from 400m to the mile.

They can only compete if they opt to take anti-androgen drugs to reduce their testosterone levels.

How does testosterone improve performance?

Testosterone acts on muscle cells by binding to a specific receptor protein, the androgen receptor. Upon testosterone binding, the androgen receptor signals to the muscle cell to activate the pathways that activate an increase in muscle mass, called muscle hypertrophy. Because of this, the muscle grows and becomes more powerful.

But let’s look at what occurs when testosterone can ’t perform its job in the muscle. “Androgen receptor knockout mice” are genetically modified mice which do not produce this receptor. In comparison to normal male mice, male androgen receptor knockout mice get rid of up to 20% of the muscle mass and strength. This makes sense because testosterone doesn’t possess a receptor to bind to anymore.

Surprisingly though, this doesn’t occur in female mice. Female androgen receptor knockout mice are as strong and muscular as their control counterparts. This suggests testosterone may not be necessary to reach peak muscle mass and strength in females.

Our new human data align with this hypothesis. We used a large, publicly available database and showed total testosterone levels were not correlated with muscle mass or strength in 716 pre-menopausal females.

This is in contrast to men, where higher testosterone concentrations are associated with increased muscle mass and strength.

We’re also doing experimental research on this subject. Weve recruited 14 young female volunteers with natural testosterone levels along a spectrum from low to hyperandrogenism.

Although this part of our research isn’t yet printed in a peer-reviewed journal, our results so far appear to confirm the findings in the epidemiological data. We’ve found testosterone levels don’t correlate with thigh muscle size, strength and power even after 12 months of resistance training aimed at maximising muscle density and building strength.

Our laboratory-based study allows us to tightly control for external factors that may influence muscle mass and strength, such as sleep, diet, training status and menstrual cycle.

Why mightn’t testosterone improve athletic performance in females?

Previous research suggests the female sex hormones estrogen and progesterone may take over some of their muscle-building role of testosterone in young females.

Another important factor is natural testosterone exists in 2 forms: “free” inside the bloodstream, or “ bound ” to a protein that reduces its ability to signal to the muscle. Our research indicates “free” testosterone gets the greater role in regulating female muscle mass and performance.

Unfortunately, the present World Athletics rules are based on the entire testosterone pool (the sum of “free” and “ jumped ” testosterone).

A limitation of our studies is most of our participants would not be classified as hyperandrogenic based on World Athletics. Past a certain threshold, testosterone may have a different effect on female muscle structure.

A recent study tested this hypothesis by administering pharmaceutical testosterone to females to approach the 5nmol/L threshold. After ten weeks of the treatment, the authors found that volunteers receiving testosterone had gained more muscle mass and could run for longer on a treadmill before getting exhausted compared to the volunteers that didn’t receive testosterone.

Surprisingly though, there were no between-group gap in muscle power, muscle strength, explosive power (sprinting) and the highest rate of oxygen consumption measured during exercise, that’s the best indicator of cardiorespiratory fitness.

These parameters are important for short- and middle-distance track events. These findings support our hypothesis that overall testosterone isnt a direct determinant of muscle strength and performance in females and reiterates the need to challenge the World Athletics rules.

What now?

Our research is important as it struggles for the right of a cohort of naturally talented female athletes to compete in their chosen athletics events, despite their naturally high testosterone levels.

By challenging the present assumption that “the more the better”, we hope our project will offer the building blocks for new regulations aimed at treating hyperandrogenic athletes more fairly.

Severine Lamon, Associate professor, Nutrition and Exercise Physiology, Deakin University

This article is republished from The Conversation under a Creative Commons license. Read the first article.

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