Testosterone level in body with activites

Does ejaculation lower level of testosterone in body, Conflicting reports on internet, a firm answer would help a lot?

There are two studies that shows that level of testosterone is higher during abstinence.

A research on the relationship between ejaculation and serum testosterone level in men:

The authors found that the fluctuations of testosterone levels from the 2nd to 5th day of abstinence were minimal. On the 7th day of abstinence, however, a clear peak of serum testosterone appeared, reaching 145.7% of the baseline ( P < 0.01). No regular fluctuation was observed following continuous abstinence after the peak.

The results showed that ejaculation-caused variations were characterized by a peak on the 7th day of abstinence; and that the effective time of an ejaculation is 7 days minimum.

Endocrine response to masturbation-induced orgasm in healthy men following a 3-week sexual abstinence:

These effects were observed both before and after sexual abstinence. In contrast, although plasma testosterone was unaltered by orgasm, higher testosterone concentrations were observed following the period of abstinence. These data demonstrate that acute abstinence does not change the neuroendocrine response to orgasm but does produce elevated levels of testosterone in males.

Sex in Sport: Men Don’t Always Have the Advantage

Research shows that real differences exist in athletic capacities, on average, between men and women. But they cut both ways.

A s the Summer Olympics gear up to kick off in Tokyo, Japan, on July 23—delayed a year thanks to the pandemic—sexism in sports has again become a hot topic. In February, Olympic organizing committee president Yoshiro Mori resigned after saying he thought women talked too much in March, the games’ creative director Hiroshi Sasaki stepped down after directing demeaning comments at a female celebrity in Japan.

A lso in March, an Instagram photo of training equipment provided to the men’s teams versus the women’s teams for the National Collegiate Athletic Association (NCAA) basketball players went viral, with the post’s author, and many commentators, scandalized by the meager offerings for women.

O ne need only scroll social media comment sections to find claims that this was not a case of sexism because, commentators argue, men are better athletes and generate more revenue than women. The money argument is a strange and weak one, given that the women’s NCAA basketball Division I reportedly pulled in nearly a billion dollars in revenue for 2018–2019. As a biological anthropologist, I find the “men are better athletes” stereotype—which turns up in so many places, in so many ways—particularly frustrating.

A thletic performance differences can be caused by all manner of things across four broad categories: anatomical (physical features such as height), physiological (functional factors like the body’s ability to deliver oxygen to muscles), psychological, and socioeconomic (such as access to equipment and training knowledge). A number of myths and misconceptions exist within each of these categories that tend to ascribe overwhelming advantages to men.

I am here to dispel those myths and misconceptions.


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A quick aside: There are different ways to define biological sex (based on the presence of gonads, internal and external genitalia, chromosomes, or hormones). None of these consistently present a clear and hard boundary between male and female instead, each presents a range of variation. The binary scheme of sex categorization is a false dichotomy: a dichotomy that is misunderstood and misappropriated in ways that can cause harm. This is the dichotomy that I must work within, as most—if not all research—on athletes considers sex a binary attribute.

T hat said, there are some real, uncontroversial average differences between groups typically categorized as women and men. And the ones conferring an advantage to women, as opposed to men, tend to be less well-known.

A natomically, on average, men have larger hearts, larger lungs, less body fat, and more muscle mass than women. With the exception of body fat (which is linked to reproduction), many of these anatomical differences are due to the fact that men are typically larger than women. In muscular people, muscle mass tends to be more exaggerated in the upper body for men, whereas women often have greater lower body muscle mass. These differences do sometimes confer an athletic advantage to men, especially in sports that rely on power or being of a larger size, such as rugby. But size isn’t everything.

I mportantly, there is no significant difference in strength between women and men with the same muscle mass. Furthermore, there appears to be no difference between women and men in terms of being able to activate muscle, known as neuromuscular recruitment. This matches up with more and more research that indicates there are no meaningful neurological differences between women and men.

A long with larger hearts and lungs, men also have a greater number of red blood cells (linked to the production of testosterone), which can give them an advantage in terms of oxygen delivery throughout the body—particularly for endurance sports such as running or cycling. Yet women appear to be metabolically better suited for endurance.

Research indicates that women are better able to manage glucose—a simple sugar used by the body for energy—and store it in muscle, where it can be quickly used when taking part in endurance events. Women also have more adiponectin (a hormone that regulates fat metabolism) and a higher concentration of fatty acids and intramuscular triglycerides. These factors can all enhance glucose use and fat-burning capacities during endurance exercise, and may delay the phenomenon of “hitting the wall”—the point at which an athlete feels they cannot go any further.

A natomically, women tend to have a greater proportion of “slow-twitch” muscle fibers: These are less powerful but more fatigue resistant. Conversely, men on average have more “fast-twitch” fibers that produce quick, powerful bursts of strength but fatigue quickly. (Although in one study of weightlifters, women had more fast-twitch muscles than men, suggesting that training and other factors are more important determinants than sex when it comes to muscle composition.) Slow-twitch fibers are associated with success in endurance sports, like long-distance running, whereas fast-twitch fibers are more associated with power sports, such as sprinting and weightlifting.

Fast-twitch muscles convey an advantage to weightlifters. Peter Dean/Flickr

I n addition to the greater abundance of slow-twitch fibers, women overall seem to be better at enduring in the face of continued exertion and stress—whether that’s due to physical or psychological factors. Two analyses of speed change over the course of marathon races, for example, found that women were able to maintain a more consistent pace than men. And a study examining serve performance among tennis players found that men consistently “choked” under high pressure situations far more regularly than women did.

T his, of course, flies in the face of the idea that men are better at “toughing it out.” It’s complicated, though: Recent studies, for example, hint that men and women feel pain differently. It’s not clear how that might affect athletic performance.

M any people will likely point out that men are still outperforming women in long-distance events. This is true, but it is also changing. Women are now regularly finishing ultra-endurance events before men: like Jasmin Paris, who won the Montane Spine Race—an epic, week-long run of more than 260 miles from England to Scotland—in 2019 while still breastfeeding her child. As more women take part in these ultra-endurance events, we are likely going to see a greater number of women outperforming men.

T here is a pernicious and persistent sex-based hormone myth that says testosterone is exclusively male, estrogen exclusively female, and that testosterone is the secret ingredient for athletic success.

F irst, women and men need both hormones in order to function properly. When women ovulate, testosterone plays a critical role, just as estradiol (a predominant form of estrogen) is crucial in men for sperm formation. Second, while it is true that women tend to have more estrogen and men more testosterone, there is a great deal of individual variation and an overlap in ranges—particularly among athletes. A study among close to 700 elite athletes found that about 5 percent of women had testosterone levels in the typical male range and about 2 percent of men had levels in the typical female range.

Women appear to be metabolically better suited for endurance.

T estosterone, like all hormones, has multiple effects throughout the body. While it is true that testosterone can, in very large doses, lead to increased muscle mass, the link between natural levels of testosterone and muscle mass is not consistent across populations. Furthermore, evidence unequivocally linking natural testosterone levels to improved athletic performance remains elusive.

E strogen, on the other hand, seems to play a critical role in endurance performance, potentially due to its role in glucose metabolism. One research study found that endurance-trained men had significantly more estrogen receptors on their muscles than moderately active men.

D espite all this, World Athletics regulations, which are followed by the International Olympic Committee, determine eligibility of certain athletes in the female classification of some athletic events based on testosterone levels. These protocols assume that testosterone always confers an advantage, and these organizations apply this rule only to a handful of sports, like middle-distance running, for which testosterone may not confer an advantage at all.

T he result is often a travesty on many levels, with women being barred from competing (based on a questionable reading of the science) or having to undergo potentially detrimental medical treatment to lower their natural testosterone levels, which can have multiple negative effects.

E verything I just told you about female and male differences may be wrong.

W hy? Women are horribly underrepresented in exercise physiology—both as researchers and research participants.

B ecause of this lack of representation, we know comparatively little about the best training and nutritional practices for women much less their performance limits. Furthermore, we know very little about how the menstrual cycle (for women who menstruate) impacts performance, as current studies are plagued by a small number of participants, a lack of actual hormone measurements, and poor accounting for hormonal contraceptive use.

H ere are the differences in amenities/provisions between the Women’s & Men’s NCAA Tournament I’ve seen so far

– Weight room/equipment
– Food
– Swag Bags

P hotos from: @Cpav15, @sedonaprince_, @danhenry3, @alikershner

— AJ McCord (@AJ_McCord) March 19, 2021

C urrent recommendations for best practices for women usually fall into the category of “shrink it and pink it”: the common tactic in marketing (and even medicine) of “customizing” products for women by simply making things smaller (such as dosing amounts) and changing the color. Women are typically treated like little men. This is a biased way to treat women that is unrepresentative of reality.

T here are true differences, though a great deal of variation, between women and men. These may, on average, give men an advantage in strength and power-based activities, and women an advantage in endurance sports.

M any of the differences we have learned are wrong, while the biologically meaningful differences are often understudied or ignored. That needs to change if we are to banish sexism in sport and take seriously the training and nutrition of female athletes the world over.

Correction: June 11, 2021
This article has been corrected to avoid implying that the average anatomical difference in muscle mass between men and women is entirely due to differences in body size.

Can a man's testosterone be boosted naturally?

Yes, but probably not in the way you are thinking, and only if the man has a healthy testosterone hormone system to begin with. Testosterone is an important hormone that plays many roles. In adult males, testosterone promotes muscle growth, physical energy, assertive and competitive moods, sperm development, libido, and emotional bonding. A man with abnormally low testosterone therefore experiences low energy, muscle weakening, mood problems, infertility, low libido, and emotional distance. In contrast, a man with a significantly higher-than-normal testosterone level can enjoy high energy, strong muscles, constructive moods, increased libido, and emotional closeness. For these reasons, boosting testosterone is generally desirable. However, if the testosterone level is too high, it can cause liver damage, uncontrollable moods, and cardiovascular disease. The ideal level of testosterone is therefore in the high end of the normal range. Fortunately, a man can only get dangerously high levels of testosterone if he dopes or if he has a rare disease. Testosterone doping, which involves internally taking in testosterone from an external source without medical necessity, is inherently dangerous and unhealthy because it raises testosterone levels too high. Testosterone doping is therefore illegal. As long as you don't resort to illegal drugs, any action that boosts your testosterone will elevate your levels while keeping you safely in the normal range, thereby allowing you to enjoy the benefits without the risks.

Let's look at various agents and actions that do and do not boost testosterone. Keep in mind that all of the concepts below assume that the man has a healthy testosterone hormone system, which includes a properly functioning hypothalamus, pituitary gland, and testicles. If a man has a non-functioning testosterone hormone pathway, no amount of effort will naturally boost his testosterone levels. Such a man has to undergo hormone replacement therapy in order to have normal health. Also note that testosterone is a hormone with a long-term action. This means that a higher testosterone level will only lead to higher energy, bigger muscles, and better moods if the testosterone levels remain consistently elevated for several weeks to months. Agents that may lead to a temporary elevation of testosterone followed by a dip have no effect on long-term testosterone levels and therefore do not give the desired long-term benefits.

Testosterone precursor pills do not boost long-term testosterone levels.
Testosterone precursor pills are commonly sold on the shelves of pharmacies and convenience stores, and are marketed as performance enhancing drugs, but the truth is that they don't work. Chemicals such as DHEA, androstenedione, and androstenediol are indeed used by your body to manufacture testosterone. But just because you have elevated amounts of androstenedione in your blood does not mean that your body will automatically convert it all into elevated amounts of testosterone. In fact, your body will convert almost none of the surplus precursor. If testosterone precursor pills actually worked like testosterone doping does, they would be pulled off the shelves and be made just as illegal as testosterone doping. A review article in the Journal of Athletic Training written by Michael E. Powers presents numerous studies which found that taking testosterone precursor pills does not increase long-term testosterone levels. Researchers found that excessive testosterone precursors in the male body are converted to estrogen and not testosterone. Therefore, taking DHEA pills, androstenedione pills, or androstenediol pills leads to elevated estrogen in males, not testosterone. Powers states,

As mentioned previously, ergogenic claims are based on the theory that precursor ingestion will result in increased testosterone levels, which would then stimulate an increase in muscle protein synthesis. However, at this time, there is no scientific support for this theory, as both DHEA and A'dione ingestion have failed to increase protein synthesis in groups of young men. Furthermore, 8 weeks of A'dione supplementation (300 mg/d) and resistance training failed to increase muscle-fiber cross-sectional area when compared with placebo ingestion and training.

Sexual activity does not boost long-term testosterone levels.
While sexual activity, whether visual or physical, does indeed raise testosterone levels for a few hours after the activity, it has no effect on long-term testosterone levels. Therefore sexual activity does not lead to long-term testosterone-induced health benefits such as increased muscle mass or heightened physical energy. In fact, a study by Helena C. Kraemer and her collaborators found that, "Mean testosterone levels were higher for sexually less active individuals."

Exercise does boost long-term testosterone levels.
Consistent exercise has been found to indeed raise long-term testosterone levels. This makes sense since two major roles of testosterone are to build up muscle tissue and to provide higher energy levels, both of which are used when exercising. High-intensity workouts have traditionally been thought to increase testosterone more than moderate-intensity workouts. However, research has found that although this may be true for the hour after the workout, there is no long-term difference in testosterone levels between a man pursuing high-intensity exercise and a man pursuing moderate-intensity exercise, all else being equal. For example, a study by Truls Raastad and his collaborators published in the European Journal of Applied Physiology states, "In conclusion, moderate- and high-intensity strength exercise did not differ with respect to prolonged (1-33 h) hormonal responses."

Adequate sleep does boost long-term testosterone levels.
Just like many other hormones, the release of testosterone follows a daily pattern of highs and lows that is regulated to some extent by the sleep cycle. Therefore, ongoing inadequate sleep, interrupted sleep, and irregular sleep all interfere with the release cycle and lead to lower testosterone levels. While developing good sleep habits will not boost testosterone much beyond the average healthy value, it will keep it from dipping below this value. A research letter by Rachel Leproult and Eve Van Cauter, published in the Journal of the American Medical Association, states, "Daytime testosterone levels were decreased by 10% to 15% in this small convenience sample of young healthy men who underwent 1 week of sleep restriction to 5 hours per night. "

Losing weight and eating a healthy diet does boost long-term testosterone levels.
In addition to a host of other health benefits, losing excess body weight and eating a nutritious, balanced diet indeed increases long-term testosterone levels. Eating too much sugar has been found to reduce testosterone levels, as has obesity in general. A review article by Giovanni Corona and his collaborators, published in the European Journal of Endocrinology, presents their compilation of the results of 24 research studies. The review article concludes that, "Overall, both a low-calorie diet and bariatric surgery are associated with a significant (P<0.0001) increase in plasma sex hormone-binding globulin-bound and -unbound testosterone levels (total testosterone (TT)), with bariatric surgery being more effective in comparison with the low-calorie diet. Androgen rise is greater in those patients who lose more weight. "

Reducing stress does boost long-term testosterone levels.
Ongoing psychological stress has been found to lower testosterone levels. Ongoing stress induces the body to release elevated amounts of the stress hormone cortisol, which signals to the body to make changes allowing it to better cope with the stress. One of these changes is the reduction of testosterone. The body makes this change so that energy and attention can be devoted to surviving the stress instead of building up body mass and enabling reproduction. Therefore, reducing the level of ongoing stress in a man's life can boost long-term testosterone levels. Note that over-exercising is a type of stress.

Taking vitamin D supplements and zinc supplements can boost long-term testosterone levels.
For those who aren't getting enough vitamin D or zinc, returning the amounts of these nutrients in the body to normal levels can indeed increase long-term testosterone levels. A study by Stefan Pilz and his collaborators, as published in the journal Hormone and Metabolic Research states, "In overweight men with deficient vitamin D status a significant increase in testosterone was observed after intake of 83 &mug vitamin D daily for 1 year whereas there was no significant change in men receiving placebo."

The complicated truth about testosterone’s effect on athletic performance

It’s hard to know exactly how much the hormone affects any given body, but what we do know suggests it’s not the end-all be-all.

Caster Semenya, champion South African sprinter, who's still fighting for her right to compete as a woman Jon Connell/Flickr

If you give a person testosterone, society considers it a performance enhancer. If you naturally have lots of the hormone, though, it’s a competitive advantage—if you’re a man. But if you’re a woman, at least according to some of the biggest sports associations in the world, it’s just plain unfair.

Female athletes like champion sprinters Caster Semenya and Dutee Chand have had to fight in recent years for their right to compete as women because their natural testosterone levels are far higher than the average woman’s. Organizations like the International Association of Athletics Federations and the International Olympic Committee have put hard limits on the amount these women are allowed to have in their bloodstream on the grounds that it enhances their performance in a way that’s unfair to their fellow competitors. But every time a new ruling comes up, a debate flares in its wake.

Many researchers agree with the IAAF and IOC, but many also think separating men and women by their testosterone levels alone flies in the face of scientific evidence. Despite all the debate, though, there hasn’t been much of any conclusion about what the science actually says about testosterone’s effect on women’s athletic performance. And that’s for a good reason: there isn’t much conclusive evidence at all.

When it comes to nailing down a link between testosterone and athletic performance, part of the problem is that, to put it simply, human bodies are complicated. We know that among elite athletes, men seem to have a consistent 10 to 12 percent athletic advantage over women. Lots of people chalk that up to testosterone alone, but the truth is there are many other factors, from other hormones to societal conditioning, might boost athletic performance, making it difficult to pinpoint exactly what testosterone does for athletes. But one option to try to isolate testosterone’s effect is to give people extra hormones and look to see what impact that has on the person’s performance.

Dutee Chand, an Indian sprinter with an androgen receptor mutation who won her case against the IAAF Wikimedia Commons

One recent study showed that female runners given topical testosterone cream increased their time to exhaustion, one measure of athletic ability. The study got a lot of traction for supposedly showing how high testosterone would give women a competitive advantage. But studies like these aren’t really that relevant to a discussion of hormones naturally produced by the body. Adding extra testosterone, called exogenous testosterone, is essentially just doping. “In the broadest sense, we’ve always known that doping increases athleticism,” says Katrina Karkazis, a senior research fellow with the Global Health Justice Partnership at Yale University and co-author of Testosterone: An Unauthorized Biography. “While the molecule is the same, it’s not the same to put T in the body as it is to have exogenous T. When you add it, you get more bang for the buck, because the body isn’t used to it.”

So if you can’t study testosterone by giving it to people, you have to look at natural hormone levels and whether those correlate with performance. Men have it in far higher quantities than do most women, and conventional thinking has long held that this is the primary reason that men tend to outperform women athletically. “There are certainly a number of factors that affect athletic performance and testosterone is certainly only one of those factors,” says Joanna Harper, a medical physicist at Loughborough University who focuses on trans athletes. “However, if you’re looking for factors that differentiate male performance from female performance, the majority of biologists feel that testosterone is the primary factor that distinguishes that.”

That idea, Harper explains, is based on the theory that testosterone increases two key attributes: strength and aerobic capacity (i.e. your body’s ability to get oxygen to your muscles). Testosterone is a powerful anabolic hormone—it helps you build lean muscle mass significantly—so it tends to boost your generalized strength, especially in areas like the upper body where your muscles have more receptors for it. It’s also a driver of red blood cell count, and the more red blood cells you have the more oxygen you can carry to your muscles, increasing your aerobic capacity.

It seems to follow logically, then, that testosterone would boost your athletic ability generally. But if that were true, we’d expect to find a strong correlation with performance and testosterone. And we don’t.

“If you start to look at men who are competing across a professional level, you can’t predict their performance based on their testosterone levels,” says Richard Holt, a professor of endocrinology at the University of Southampton. “The male range goes from 10 to 25 nanomoles per liter, and you can’t say that a person with a level of 25 is necessarily going to outperform a man with a level of 10.” The same goes for women, he explains, which suggests that it’s not testosterone alone that’s contributing to men’s athletic advantage.

Michael Phelps, the American swimmer, was lauded for his abnormal physical attributes that helped him become a champion Wikimedia Commons

It’s not clear yet exactly what other factors might be contributing, but Holt notes we can get some clues by looking at women with androgen receptor mutations. Androgens are a group of hormones including testosterone and estrogen that influence sex traits. It’s testosterone that determines whether a developing baby will have male or female genitalia—its presence helps prompt the embryo to go down the male route. But some people are born with mutations in their androgen receptors that makes them non-functional, so even though they’re producing testosterone it can’t actually affect anything. These people mostly develop and live life as women, often not even realizing they have the male XY chromosome pattern. In severe cases they have female external genitalia, though also internal testes, though in more mild cases the genitalia can be mixed.

What’s strange is that women with androgen receptor mutations are extremely overrepresented among elite athletes, even though those with severe cases can’t possibly be getting the benefit of their natural testosterone without receptors to carry out those effects. Holt points out some of these women have even had their testes removed, bringing their testosterone levels to below female levels, and yet they’re still able to compete internationally.

Many researchers now think it’s factors on the Y chromosome that account for some of those differences. Holt’s own research suggests part of it might be growth hormone, which varies between men and women and plays important roles in muscle gain and repair, among other things.

That could help explain why the research on natural testosterone levels has been so erratic.

One study of professional male triathletes found no relationship between testosterone levels and performance. Another, looking at professional cyclists, found the same lack of correlation. Yet another, comparing cyclists, weightlifters, and controls to each other on a cycling test, found a negative correlation between testosterone levels and performance. A study of teenage weightlifters found no relationship between boys’ testosterone levels and their performance, and a negative correlation among the girls—meaning they performed better when their testosterone was lower.

Some studies have even found mixed or opposing results within their own findings. One found that sprinters seem to get an advantage from testosterone, while other runners didn’t. Another came to the conclusion that it helped female track athletes, but not male ones. There’s also differences in results depending on what type of strength you look at—endurance strength seems to decrease with higher testosterone levels, while maximum strength generally only increases.

Complicating all of this is the fact that elite athletes’ testosterone levels vary quite a lot. One analysis found that 25 percent of elite male athletes have testosterone levels below what the International Association of Athletics Federations consider the lower limit for men. What’s more, it wasn’t the athletes in less strength- or speed-oriented sports. Some of the events with the most men below the limit were powerlifting, rowing, track and field, ice hockey, and rowing. Basketball players and alpine skiers had some of the highest levels. That all seems to imply, at least to some researchers, that high testosterone isn’t a universal performance booster.

Eero Mäntyranta, the Finnish skiier with an erythropoietin receptor mutation that increases his red blood cell count

This is all in line with what Karkazis notes is a pattern of studies which claim to find broad links between testosterone and athletic performance, but have really only found minor correlations with very specific measures of athleticism.

The mixed results might explain why even broad review articles find opposing results. Reviews have suggested both that there’s not enough evidence to enforce any upper testosterone limit in women, and that there’s reason to apply a very specific one.

There’s simply not a lot of great research out there. As a result, Karkazis explains, researchers are forced to cobble together a picture of testosterone’s role based on studies in men, women with differences of sexual development (called DSDs, which includes androgen receptor mutations), and anyone given exogenous testosterone. Peter Sonksen, a now-retired professor of endocrinology at St. Thomas’ Hospital and King’s College, London, has written extensively about testosterone’s relative unimportance with regard to athletic performance in women without androgen receptor mutations. But he says when it comes to how the hormone might play a role in women with DSDs, “the answer is that there is little or no credible science to answer the question.”

But none of this really addresses the issue at the heart of all of this: when it comes to formulating rules for who can and can’t compete, what’s fair?

Some researchers, like Harper, argue that there needs to be a specific limit on women’s testosterone. Above that, and you’d need to go compete with the men. But many others say this idea of fairness is fundamentally flawed. Eric Vilain, director of the Center for Genetic Medicine Research at Children’s National Hospital, says that even if testosterone does give certain women a performance boost, they can and should still compete with their fellow women. “Sports relies on abilities that are fundamentally unfair,” Vilain says. Just as tiny gymnasts do better than tall ones, he explains, there are myriad factors that give some athletes advantages over others. For that reason, he says, “within the female category, testosterone should be ‘de-gendered.’ It is a hormone present in both genders, which is why continuity of gender should trump levels of testosterone.”

Holt agrees. “It strikes me as far too simplistic to say that the only difference between men and women is their testosterone levels.” If you’re going to look at performance differences, he says, you also have to look at sociological ones. There are almost certainly biological differences that mean men will always outperform women to some degree, but he points out that teenage girls are much less likely to compete in sports at school than boys and are given generally worse facilities. Male athletes are paid much better than female ones on the whole. Holt says these and other factors mean “there are a whole load of sociological reasons that may also drive men to coach and be driven to achieve at a high level beyond testosterone.”

Besides, the idea that a naturally occurring variation in some women’s bodies is somehow unfair doesn’t mesh with how much we exalt male athletes with unusual abilities. Michael Phelps’ muscles produce half the lactic acid of a normal person, enabling him to push himself for much longer without fatigue. Finnish cross-country skier Eero Mäntyranta has an inherited mutation that increases his red blood cells’ oxygen-carrying capacity by 25 to 50 percent, which is the genetic equivalent of doping. Those men were celebrated, not pillaried.

Sports are inherently unfair, and while there have to be some regulations to account for true cheating, it seems like a double standard to demonize women for the same kind of natural advantages that we appreciate in men. And to simplify the entire debate down to a single (albeit important) hormone ignores a great deal of biology and sociology, says Holt. “We should celebrate those biological differences.”

Sara Chodoshis an associate editor at PopSci where she writes about everything from vaccine hesitancy to extreme animal sex. She got her master's degree in science journalism at NYU's Science Health and Environmental Reporting Program, and is getting a second master's in data visualization from the University of Girona. Contact the author here.

Testosterone Reduces Body Fat in Male Mice by Stimulation of Physical Activity Via Extrahypothalamic ERα Signaling

Testosterone (T) reduces male fat mass, but the underlying mechanisms remain elusive, limiting its clinical relevance in hypogonadism-associated obesity. Here, we subjected chemically castrated high-fat diet-induced adult obese male mice to supplementation with T or the nonaromatizable androgen dihydrotestosterone (DHT) for 20 weeks. Both hormones increased lean mass, thereby indirectly increasing oxygen consumption and energy expenditure. In addition, T but not DHT decreased fat mass and increased ambulatory activity, indicating a role for aromatization into estrogens. Investigation of the pattern of aromatase expression in various murine tissues revealed the absence of Cyp19a1 expression in adipose tissue while high levels were observed in brain and gonads. In obese hypogonadal male mice with extrahypothalamic neuronal estrogen receptor alpha deletion (N-ERαKO), T still increased lean mass but was unable to decrease fat mass. The stimulatory effect of T on ambulatory activity was also abolished in N-ERαKO males. In conclusion, our work demonstrates that the fat-burning action of T is dependent on aromatization into estrogens and is at least partially mediated by the stimulation of physical activity via extrahypothalamic ERα signaling. In contrast, the increase in lean mass upon T supplementation is mediated through the androgen receptor and indirectly leads to an increase in energy expenditure, which might also contribute to the fat-burning effects of T.

Keywords: estradiol fat mass hypogonadism physical activity sex steroids testosterone.

© The Author(s) 2021. Published by Oxford University Press on behalf of the Endocrine Society.


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18 Best Foods to Boost Testosterone Levels

Egg yolk

The yolk of the egg in particular is noted for being a rich source of various nutrients. Particularly, it has a high content of vitamin D. This helps in triggering the vitamin D receptors located in the testes. As such, the testes participate in an enhanced synthesis of testosterone. In addition, the nutrients in egg yolk also help to aid in the free flow of this androgenic hormone throughout the body.


Tuna is often noted as one of the healthiest seafood along with salmon and sardine. Among these, tuna has a particularly high content of vitamin D and Omega 3 fatty acids. Add the fact that it is rich in proteins, and you have got one of the best foods to boost testosterone levels, burn fat and gain massive muscle gains.

Toned milk fortified with vitamin D

Milk is any day recognised as a glass of goodness and high nutrition. Apart from having proteins and multiple essential minerals, the milk fortified with vitamin D is a great source of food to boost your testosterone levels and gain muscular strength. Moreover, milk’s calcium content make it excellent for promoting bone health.


Zinc is one of the most important essential macronutrients and oyster is the best source of zinc among foods. There is absolutely nothing that contains as much zinc as oyster. This makes it an amazing aphrodisiac and T booster. It is an ideal sex food.

Pumpkin seeds

These humble seeds are an excellent source of both zinc and magnesium. We have already mentioned how potent zinc is when it comes to enhancing your testosterone levels and sexual performance. Magnesium plays a vital role by promoting the functionality of zinc. In addition, magnesium in itself is responsible for hundreds of biochemical reactions in the body. As such, it acts as a catalyst to help govern the biochemical generation of testosterone in the testicles.


Yoghurt is a great source of protein. This helps in the anabolic gains that testosterone achieved in itself. In addition, yoghurt is also full of probiotic bacteria. This assists in the biochemical reactions that give rise to the synthesis of testosterone in the testicles and adrenal gland.

Tender coconut

Both coconut water and coconut meat are known for their rich content of various important minerals. It is also known to be a rich source of various saturated fats. This form of fats come with various health benefits. They boost testosterone levels, help in managing the blood cholesterol levels and also boost your body’s rate of metabolism.

Minced red meat

Consuming meat in minced form has various benefits. This form of processing has various useful fats and proteins which effectively boost testosterone and contribute in muscle growth.


The active chemical compound found in parsley is apigenin. This potent organic compound is supremely effective in triggering the testicles to produce testosterone. In addition, it also helps to manage blood pressure. As such, it also facilitates the flow of testosterone throughout the body.


Coffee is known to be a powerful stimulant which promotes your physical and mental energy. It also aids in the shedding of fat and though debatable, has been established as a testosterone boosting food source.


This is one of the most powerful foods for boosting testosterone in the body as it causes a pretty high amount of increase. In addition, it promotes high sex drive and good sperm count.


Raisins are high in boron content. Additionally, they contain a strong antioxidant known as resveratol. Both boron and resveratol are associated with high levels of testosterone generation and lowering of estrogen in men.


Shrimp is great for lean protein content and vitamin D, which is super effective in boosting testosterone levels. In addition, it also promotes blood health, thereby improving sexual characteristics in men.


Not really a favourite among foods, but cabbage contains a chemical known as indole 3-carbinol (IC3), which is a powerful testosterone booster. It also reduces estrogen levels in men and helps in maintaining food brain health with age.


It works very similar to cabbage as it is rich in IC3, and as such, boosts testosterone and lowers estrogen. Furthermore, it contains many vital nutrients and is great for the heart.


An excellent anti-inflammatory agent, ginger helps to treat muscle soreness, and reduces blood sugar and lower. It is also an amazing testosterone boosting food.

Extra virgin olive oil

This oil is one of the best foods to improve testosterone levels in your body. It is often classified as a super food due to its many health benefits.


A known aphrodisiac, it boosts your sex drive and also helps in purifying your blood. This leads to better erections. In addition, it provides a huge boost to your testosterone levels.


Over the past 15 years it has become evident that in men estradiol is responsible for a number of effects originally attributed to testosterone. Estradiol has an important role in gaining and maintaining bone mass, closing of the epiphyses and the feedback on gonadotropin secretion. This fact became particularly evident in men with aromatase deficiency. Aromatase is the enzyme responsible for conversion of androgens to estrogens. Men with estrogen deficiency caused by a mutation in the CYP19 gene suffer from low bone mineral density (BMD) and unfused epiphyses, and have high gonadotropin and testosterone levels [1]. Estrogen excess in turn has been associated with premature closure of the epiphyses, gynecomastia and low gonadotropin and testosterone levels. Lowering estrogen levels in men has emerged, consequently, as a potential treatment for a number of disorders including pubertas praecox, the andropause (also referred to as late-onset hypogonadism) and gynecomastia. Aromatase inhibitors were proven to be safe, convenient and effective for the treatment of hormone sensitive breast cancer in women although their use is associated with a modest increase in bone resorption [2,3]. This review will discuss the potential targets and the evidence for the use of aromatase inhibitors in men and adds more recent data to the text of an earlier review on this subject [4].

Metabolism of estrogens in men

Aromatase, also known as estrogen synthetase, is the key enzyme in estrogen biosynthesis. The enzyme, localized in the endoplasmic reticulum of the estrogen-producing cell, is encoded by the CYP19A1 gene. This gene is a member of the CYP gene family, encoding a class of enzymes active in the hydroxylation of endogenous and exogenous substances. The CYP19A1 gene is localized on chromosome 15 and comprises nine exons the start codon for translation is located on exon 2. Transcription of the aromatase gene is regulated by several tissue-specific promoters. These promoters are under the influence of different hormones and growth factors such as gonadotropins (gonadal promoter II) and interleukin-6, interleukin-11 and tumor necrosis factor-a (adipose/bone promoter I.4 for review see [5]). Aromatase activity has not only been demonstrated in gonads and placenta but also in brain [6], fat tissue [7,8], muscle [9], hair [10], bone [11] and vascular tissue [12].

Estradiol is the most potent estrogen produced in the body. It is synthesized from testosterone or estrone via aromatase or 17β-hydroxysteroid dehydrogenase, respectively. The total estradiol production rate in the human male has been estimated to be 35-45 μg (0.130-0.165 μmol) per day, of which approximately 20% is directly produced by the testes [13,14]. Roughly 60% of circulating estradiol is derived from direct testicular secretion or from conversion of testicular androgens. The remaining fraction is derived from peripheral conversion of adrenal androgens [15]. The mean estradiol plasma concentration in men is only about 1/200 of the mean plasma testosterone concentration [16] and is comparable to estradiol levels found in women in the early follicular phase of the menstrual cycle.

Phenotype of aromatase deficiency and excess

To date, eight males with aromatase deficiency have been described: seven adults [17-23] and one newborn [24]. Estradiol levels in these males were extremely low. All adult aromatase-deficient men demonstrated a remarkably low bone mass and unfused epiphyses leading to linear growth into adulthood and above-average body length. Testicular size in these men ranged from micro- to macroorchidism and the plasma testosterone levels varied roughly in accordance with testis size. Levels of luteinizing hormone (LH) were either normal or elevated. Four men were infertile, in one younger male fertility was not described. Two aromatase-deficient men had a brother who also suffered from infertility despite a normal aromatase genotype, suggesting an unrelated second condition. Once treated with estradiol, epiphyses closed, BMD increased and disturbances in the lipid profile improved in most of these patients.

On the other hand, several, mostly familial cases of aromatase excess have been reported. The clinical picture consists of gynecomastia, accelerated growth and premature bone maturation due to excessive peripheral estrogen synthesis. Stratakis et al. [25] described a family with aromatase excess syndrome in which the syndrome appeared to be caused by inappropriately high expression of an alternative first exon. Shozu et al. [26] described a father and his son and one unrelated patient with aromatase excess caused by a chromosomal rearrangement, which placed the aromatase gene adjacent to cryptic promoters. As a result an inappropriate amount of aromatase was expressed in adipose tissue of the affected subjects.

These case reports illustrate the important contribution of estrogens to male health and identify the possible indications and risks of aromatase-inhibitor treatment in men. Aromatase inhibitors may be used to treat or prevent gynecomastia. They may be used to increase gonadotropin secretion and thereby stimulate Leydig and Sertoli cell function. Aromatase inhibitors may be used to prevent or delay epiphysial closure and thereby increase adult height. A major concern of aromatase inhibition is the possible detrimental effect on bone mineralization.

Aromatase inhibitors

Aromatase inhibitors are classified as either steroidal or nonsteroidal, or as first, second or third generation. Steroidal inhibitors such as formestane and exemestane inhibit aromatase activity by mimicking the substrate androstenedione. Nonsteroidal enzyme inhibitors such as anastrozole and letrozole inhibit enzyme activity by binding with the heme iron of the enzyme. First-generation aromatase inhibitors such as aminoglutethimide are relatively weak and nonspecific they can also block other steroidogenic enzymes necessitating adrenal steroid supplementation. Third-generation inhibitors such as letrozole and anastrozole are potent and do not inhibit related enzymes. They are well tolerated and apart from their effects on estrogen metabolism their use does not appear to be associated with important side effects in postmenopausal women [27]. Although aromatase inhibition by anastrozole and letrozole is reported to be close to 100%, administration of these inhibitors to men will not suppress plasma estradiol levels completely. In men third-generation aromatase inhibitors will decrease the mean plasma estradiol/testosterone ratio by 77% [28,29]. This finding probably relates to the high plasma concentrations of testosterone, a major precursor for estradiol synthesis in adult men. As aromatase inhibition is dose dependent it has been suggested that aromatase is less suppressed in the testis compared to adipose and muscle tissue, explaining the incomplete efficacy of aromatase inhibition in men. Aromatase activity is high in the testes and the molar ratio of testosterone to letrozole is much higher in the testes compared with adipose and muscle tissue. When testicular testosterone and estradiol synthesis are suppressed and testosterone is administered exogenously in combination with letrozole, however, the estradiol/testosterone ratio is suppressed by 81% [30], which is only marginally different from the suppression of this ratio in intact men after treatment with letrozole. This incomplete suppression may be regarded as advantageous for it prevents excessive reduction of estrogen levels in men and the possible associated adverse effects. In postmenopausal women with breast carcinoma, long-term use of potent aromatase inhibitors reduces circulating estradiol levels by 88% [31] and is associated with adverse effects on bone [2,3]. Due to the much higher estrogen levels in treated men it remains to be determined whether this also holds true for men.

Effects of aromatase inhibition on luteinizing hormone release and testosterone production

It is well known from experimental evidence and from clinical observations that estradiol has powerful effects on gonadotropin release in men. Modulation of plasma estradiol levels within the male physiological range is associated with strong effects on plasma levels of LH through an effect at the level of the pituitary gland [32]. Lowering estradiol levels, by administering an aromatase inhibitor, is associated with an increase in levels of LH, follicle-stimulating hormone (FSH) and testosterone [28,29]. Aromatase inhibitors, therefore, have been suggested as a tool to increase testosterone levels in men with low testosterone levels. Due to their mode of action the use of aromatase inhibitors is limited to men with at least some residual function of the hypothalamo-pituitary-gonadal axis. Therefore aromatase inhibitors have been tested in older men suffering from so-called late-onset hypogonadism or partial androgen deficiency. Aging in men is associated with a gradual decline of total and free testosterone levels [33] as a result of combined testicular and hypothalamic dysfunction. The decline of testosterone levels has been implicated in the pathogenesis of physical frailty in older men. Androgen treatment, therefore, has been advocated for older men with signs and symptoms of androgen deficiency and unequivocally low plasma testosterone levels [34,35].

Aromatase inhibitors may be an attractive alternative for traditional testosterone substitution in elderly men because these compounds can be administered orally once daily and may result in physiological 24 h testosterone profiles. Additionally, misuse of aromatase inhibitors is unlikely since testosterone levels will not be stimulated to vastly supraphysiological levels. A small, controlled study demonstrated that anastrozole in a dose of 1 mg daily during 12 weeks will result in doubling of the mean bioavailable testosterone level in older men [36]. A more recent study also showed a moderate but significant effect of aromatase inhibition on estradiol and testosterone levels in older men [37]. Treatment with atamestane 100 mg once daily resulted in a 40% increase in total testosterone levels after 36 weeks. However, no beneficial effects were seen on muscle strength, body composition or quality-of-life scores. A similar increase of testosterone levels in the absence of effects on body composition and strength was reported in a study, in which elderly men with borderline low levels of serum testosterone were treated with anastrozole during 1 year [38]. There is a number of possible explanations for the lack of a clear treatment effect. First of all, the numbers of studied subjects were relatively small. Moreover, the mean baseline testosterone levels in the treated groups were in, or only slightly below, the normal range for young adult men and the relative increase in testosterone levels may have been too small. It has been suggested that men with the lowest baseline testosterone levels benefit most from testosterone substitution [39]. Finally, the decreased levels of estradiol may have affected the expected rise in lean body mass [38]. These observations outline a serious limitation of the use of aromatase inhibitors in older men the stimulating effect on testosterone levels may be too weak, especially in the men with the lowest baseline testosterone levels who would potentially benefit most.

Effects of aromatase inhibition in obese men

Peripheral androgen aromatization is enhanced in subjects with increased body mass index [40]. Massively obese men show markedly increased plasma estradiol concentrations and low testosterone concentrations [41]. In three small studies, letrozole or testolactone has been administered to morbidly obese men to improve their testosterone levels [42-44]. Treatment resulted in normalization of testosterone levels in all subjects, with a concomitant suppression of the originally increased levels of estradiol. This normalization of the estradiol/testosterone ratio might be of advantage, because of the suppressive effects of testosterone on the expression of the estrogen receptor β, which in itself, in the presence of high levels of estradiol, can suppress the expression of GLUT-4, leading to insulin insensitivity [45]. A case study describes a morbidly obese infertile man, who after a similar treatment with anastrozole showed a normalized pituitary-testis axis, spermatogenesis and fertility [46]. However, testosterone levels will also improve on weight loss [47], which is the intervention of choice for obese men with or without low testosterone levels.

Effects of aromatase inhibition on release of follicle-stimulating hormone and spermatogenesis

Although FSH release is primarily under the control of inhibin, circulating estradiol has a substantial effect on FSH levels in men [28]. Aromatase inhibition results in a three-fold increase in levels of FSH [28,29] in eugonadal men and may potentially stimulate sperm production. Earlier studies using tamoxifen or clomifene to increase FSH levels did not show unequivocal evidence for the efficacy of this approach [48]. Uncontrolled studies using anastrozole, testolactone or letrozole have shown some evidence for a positive effect on sperm concentration and motility [49-51]. However, one double-blind crossover trial using testolactone did not show a significant improvement of sperm quality in men with oligospermia [52]. More recently, a study in which anastrozole was added to the treatment with tamoxifen in men with idiopathic oligoasthenoteratozoospermia and a decreased testosterone over estradiol ratio after treatment with tamoxifen alone indicated an increased pregnancy rate compared with the group without the addition of the aromatase inhibitor [53]. Finally, pretreatment with aromatase inhibitors was described to lead to positive results of testicular sperm extraction in Klinefelter's syndrome patients with low pretreatment testosterone concentrations: men from whose testes spermatozoa were retrieved showed higher posttreatment testosterone levels and testosterone over estradiol ratios compared to men in whom no spermatozoa could be obtained, whereas pretreatment levels of testosterone, LH and FSH did not predict the result of treatment outcome [54].

Effects of aromatase inhibition on bone metabolism and epiphysial closure

Estrogens are essential for epiphysial maturation in boys. Aromatase inhibitors, therefore, may be used to lower estradiol levels and thereby slow down epiphysial maturation. This approach proved successful in rare conditions such as the aromatase-excess syndrome [25] and high estrogen levels due to Sertoli cell tumors in boys with Peutz-Jeghers syndrome [55]. In boys with familial male precocious puberty due to activating mutations of the LH receptor, also known as testotoxicosis, treatment with an antiandrogen in combination with an aromatase inhibitor to prevent effects on bone is the treatment of choice. In an earlier study a combination of spironolactone and testolactone proved effective [56], whereas in later studies the combination of bicalutamide and anastrozole was used [57-59].

Aromatase inhibition has also been studied in boys with idiopathic short stature. Boys with a mean age of 11 years at the start of the study were treated with letrozole 2.5 mg once daily or placebo for 2 years [60]. Letrozole treatment was associated with higher plasma levels of gonadotropins and testosterone in boys who entered puberty during the study. In spite of this fact, plasma estradiol levels were mostly lower in the letrozole-treated group. Both groups showed similar growth velocity but bone age progressed significantly slower in the letrozole group resulting in a gain of 5.9 cm in predicted adult height. The fact that growth velocity was not affected is remarkable in the light of the observation, that in adult men treated with a combination of testosterone and anastrozole the responses to GH secretagogues were smaller than in men treated with a combination of testosterone and a placebo the GH and IGF-1 concentrations were positively correlated with estradiol levels [61]. Also in letrozole-treated boys in whom treatment started at the beginning of puberty, IGF-I levels were lower than in placebo-treated controls [62]. As expected, GH-deficient boys treated with GH and anastrozole showed a larger increase in height than their GH only-treated controls [63].

Boys with constitutional delay of puberty are typically small for their age and final adult height is often in the low-normal range. These boys may be treated with androgens to induce puberty. Although testosterone induces growth velocity, the estrogens aromatized from testosterone will accelerate epiphysial maturation and for that reason reduce adult height further. The combination of testosterone and letrozole, therefore, was tested in boys with constitutional delay of puberty. This combination treatment effectively increased growth velocity but epiphysial maturation was slower in the letrozole-treated group, leading to a significant increase in predicted adult height [64,65].

Effects of aromatase inhibition on male breast

Aromatase inhibitors are widely prescribed for hormone-responsive breast carcinoma in postmenopausal women. It is well known that aromatase inhibition results in a dramatic reduction of tumor estrogen concentrations [66]. As gynecomastia in men presumably results from an imbalance between androgen and estrogen action, aromatase inhibition was tested as a treatment for gynecomastia in boys. Treatment with anastrozole daily for 6 months, however, did not result in a significant improvement compared with placebo [67]. This is in accordance with the data summarized in a recent review [68], describing similar responses to placebo, tamoxifen and anastrozole in a number of observational studies. Anastrozole was also studied in a group of prostate cancer patients treated with bicalutamide, an androgen antagonist. A dose of 1 mg daily appeared to be mildly effective against the appearance of gynecomastia. Tamoxifen was much more effective, however, in the prevention of gynecomastia in these men [69,70]. Due to these disappointing results, aromatase inhibitors are not recommended as a first-line treatment for gynecomastia in men.

Data on treatment of male mammary tumors with aromatase inhibitors are scarce and indicate that this treatment modality is unlikely to be successful because of the unwanted effect of increased levels of testosterone, making it impossible to reach the low estradiol levels obtained in postmenopausal women after this treatment [71]. The combination with a GnRH analog in order to prevent this increase did not yield beneficial results either [72].

Safety and concerns for aromatase inhibitors in men

Extensive experience with third-generation aromatase inhibitors in postmenopausal women did not reveal major side effects related to their use. Long-term use in postmenopausal women is associated with a moderate increase in bone resorption and a modest decrease in BMD compared with placebo [2,3]. As outlined above, low BMD is a characteristic sign of aromatase deficiency but also in normal men most cross-sectional studies showed that bioavailable or total estradiol levels are associated with BMD [73-77]. The primary concern, therefore, associated with aromatase inhibition in men is the negative effect it may have on bone metabolism. In most studies utilizing aromatase inhibitors in men estradiol levels decreased only moderately. Additionally, the suppression of plasma estradiol levels in men is associated with an increase in gonadotropin levels, which stimulate the production of testosterone, the main precursor for estradiol synthesis. Khosla et al. [76,78] proposed a threshold for bioavailable estradiol of 30 pM, below which BMD appeared to be strongly and negatively associated with the plasma bioavailable estradiol concentration in men. Thresholds should be interpreted with great caution because they rely heavily on the methods used to measure total or bioavailable estradiol levels. These authors used ammonium sulfate precipitation to measure bioavailable estradiol levels whereas if they had calculated bioavailable estradiol levels using the popular Sodergard equation [79,80] their proposed threshold may have been as high as 75 pM. In experimental settings, selective withdrawal of estradiol in men was associated with an increase in markers of bone resorption [30,81]. In the studies published so far aromatase inhibition in men did not appear to be associated with adverse effects on bone in a number of studies [37,59,82,83], but in a more recent study a decrease of spine BMD was observed after one year of treatment of elderly men with anastrozole [84]. Additionally, one short-term study did not show adverse effects of aromatase inhibition in older men on cardiovascular markers. However, it is not clear that this conclusion also holds for boys: vertebral deformities were observed in boys treated for delayed onset of puberty [85]. Furthermore, hyperandrogenism induced by treatment with aromatase inhibitors may result in decreased HDL-cholesterol and increased hemoglobin levels [86], indicating the need for follow-up during treatment. The same group of investigators concluded that there were no effects of letrozole on cognitive performance could be detected in a group of prepubertal boys [87]. In a group of elderly men who obtained exogenous testosterone enenthate, the addition of anastrozole to the injected androgen prevented the androgen induced improvement of verbal memory, but did not affect special memory [88].


78.1 Introduction

Testosterone is the principal circulating androgen in men, secreted almost entirely by the testes. The effects of testosterone on bone in men are therefore best observed when they are deficient in testosterone and then replaced with testosterone. The effects of physiologic concentrations of testosterone in men, as observed in these situations, are substantial.

Testosterone is also the principal circulating androgen, in potency, in women. It is secreted by the ovaries and the adrenal glands and derived also by peripheral conversion of the weak adrenal androgens, androstenedione, and dehydroepiandrosterone (DHEA). The normal serum concentration of testosterone in women, however, is only approximately 10% of that in men, and the effect of testosterone on bone in women is therefore much less clear than in men.

Female Hormones

The stages of the ovarian cycle in the female are regulated by hormones secreted by the hypothalamus, pituitary, and the ovaries.

Learning Objectives

Explain the function of female hormones in reproduction

Key Takeaways

Key Points

  • As in males, GnRH secreted by the hypothalamus triggers the release of FSH and LH from the pituitary however, in females, this signals the ovaries to produce estradiol and progesterone.
  • FSH stimulates the growth and maturation of follicles on the ovaries, which house and nourish the developing eggs the follicle, in turn, releases inhibin, which inhibits the production of FSH.
  • Progesterone stimulates the growth of the endometrial lining of the uterus in order to prepare it for pregnancy a strong surge of LH at around day 14 of the cycle triggers ovulation of an egg from the most mature follicle.
  • After ovulation, the ruptured follicle becomes a corpus luteum, which secretes progesterone to either regrow the uterine lining or to support the pregnancy if it occurs.
  • During middle age, a woman’s ovaries become less sensitive to FSH and LH and, therefore, cease to mature follicles and undergo ovulation this is known as menopause.

Key Terms

  • corpus luteum: a yellow mass of cells that forms from an ovarian follicle during the luteal phase of the menstrual cycle in mammals it secretes steroid hormones
  • menopause: the ending of menstruation the time in a woman’s life when this happens
  • endometrium: the mucous membrane that lines the uterus in mammals and in which fertilized eggs are implanted
  • estradiol: a potent estrogenic hormone produced in the ovaries of all vertebrates the synthetic compound is used medicinally to treat estrogen deficiency and breast cancer
  • menstruation: the periodic discharging of the menses, the flow of blood and cells from the lining of the uterus in females of humans and other primates

Female Hormones

The control of reproduction in females is more complex than that of the male. As with the male, the hypothalamic hormone GnRH (gonadotropin-releasing hormone) causes the release of the hormones FSH (follicle stimulating hormone) and LH (luteinizing hormone) from the anterior pituitary. In addition, estrogens and progesterone are released from the developing follicles, which are structures on the ovaries that contain the maturing eggs.

In females, FSH stimulates the development of egg cells, called ova, which develop in structures called follicles. Follicle cells produce the hormone inhibin, which inhibits FSH production. LH also plays a role in the development of ova, as well as in the induction of ovulation and stimulation of estradiol and progesterone production by the ovaries. Estradiol and progesterone are steroid hormones that prepare the body for pregnancy. Estradiol is the reproductive hormone in females that assists in endometrial regrowth, ovulation, and calcium absorption it is also responsible for the secondary sexual characteristics of females. These include breast development, flaring of the hips, and a shorter period necessary for bone maturation. Progesterone assists in endometrial re-growth and inhibition of FSH and LH release.

Hormonal control of the female reproductive cycle: The ovarian and menstrual cycles of female reproduction are regulated by hormones produced by the hypothalamus, pituitary, and ovaries. The pattern of activation and inhibition of these hormones varies between phases of the reproductive cycle.

The Ovarian Cycle and the Menstrual Cycle

The ovarian cycle governs the preparation of endocrine tissues and release of eggs, while the menstrual cycle governs the preparation and maintenance of the uterine lining. These cycles occur concurrently and are coordinated over a 22–32 day cycle, with an average length of 28 days.

The first half of the ovarian cycle is the follicular phase. Slowly-rising levels of FSH and LH cause the growth of follicles on the surface of the ovary, which prepares the egg for ovulation. As the follicles grow, they begin releasing estrogens and a low level of progesterone. Progesterone maintains the endometrium, the lining of the uterus, to help ensure pregnancy. Just prior to the middle of the cycle (approximately day 14), the high level of estrogen causes FSH and, especially, LH to rise rapidly and then fall. The spike in LH causes ovulation: the most mature follicle ruptures and releases its egg. The follicles that did not rupture degenerate and their eggs are lost. The level of estrogen decreases when the extra follicles degenerate.

Follicle: This mature egg follicle may rupture and release an egg in response to a surge of LH.

If pregnancy implantation does not occur, the lining of the uterus is sloughed off, a process known as menstruation. After about five days, estrogen levels rise and the menstrual cycle enters the proliferative phase. The endometrium begins to regrow, replacing the blood vessels and glands that deteriorated during the end of the last cycle.

Following ovulation, the ovarian cycle enters its luteal phase and the menstrual cycle enters its secretory phase, both of which run from about day 15 to 28. The luteal and secretory phases refer to changes in the ruptured follicle. The cells in the follicle undergo physical changes, producing a structure called a corpus luteum, which produces estrogen and progesterone. The progesterone facilitates the regrowth of the uterine lining and inhibits the release of further FSH and LH. The uterus is again being prepared to accept a fertilized egg, should it occur during this cycle. The inhibition of FSH and LH prevents any further eggs and follicles from developing. The level of estrogen produced by the corpus luteum increases to a steady level for the next few days.

If no fertilized egg is implanted into the uterus, the corpus luteum degenerates and the levels of estrogen and progesterone decrease. The endometrium begins to degenerate as the progesterone levels drop, initiating the next menstrual cycle. The decrease in progesterone also allows the hypothalamus to send GnRH to the anterior pituitary, releasing FSH and LH to start the cycles again.

Stages of the menstrual cycle: Rising and falling hormone levels result in progression of the ovarian and menstrual cycles.


As women approach their mid-40s to mid-50s, their ovaries begin to lose their sensitivity to FSH and LH. Menstrual periods become less frequent and finally cease this process is known as menopause. There are still eggs and potential follicles on the ovaries, but without the stimulation of FSH and LH, they will not produce a viable egg to be released. The outcome of this is the inability to have children.

Various symptoms are associated with menopause, including hot flashes, heavy sweating, headaches, some hair loss, muscle pain, vaginal dryness, insomnia, depression, weight gain, and mood swings. Estrogen is involved in calcium metabolism and, without it, blood levels of calcium decrease. To replenish the blood, calcium is lost from bone, which may decrease the bone density and lead to osteoporosis. Supplementation of estrogen in the form of hormone replacement therapy (HRT) can prevent bone loss, but the therapy can have negative side effects, such as an increased risk of stroke or heart attack, blood clots, breast cancer, ovarian cancer, endometrial cancer, gall bladder disease, and, possibly, dementia.

Exercise Supports Healthy Testosterone Levels — TRT Overcomes Low T

If you’re struggling to put in the fitness work to meet your goals due to chronic fatigue, you might consider the possibility that you’re suffering from low testosterone.

If you’re having an unusually difficult time losing excess weight or you’re having trouble maintaining your weight despite proper eating and exercise, hormone imbalances like Low T might be the culprit.

We recommend taking the first step towards looking and feeling better by getting a thorough examination that focuses on finding the actual source of your symptoms.