A mini-review of the effects of taking oral contraceptives (both combined and progesterone-only) on athletic performance in women.
Written by Helena Humphries
I have recently seen a few posts on social media and on various other blogs which claim that taking oral contraceptives reduced strength, primarily through reduction of available testosterone. I wanted to check the research myself to see if these claims were supported by the scientific literature, or if these bloggers had just over-dramatized this. Of the blogs/posts I saw, there were no or insufficient links to articles. It is very easy for us to read an abstract from one valid study which demonstrates testosterone reduction, and assume that overall muscle strength and athletic performance must be reduced. In this blog, I’ll be sharing my review of the literature and linking the evidence for what I find. At this point, I also like to mention I have only referred to the most up-to-date and relevant research, from the past 20 years.
Estrogen, androgenicity & testosterone
At first, I set out to find evidence of the effects of the progesterone-only pill (POP) on performance, as this is the pill I am currently taking. Then I realized that most research has been carried out on women taking combined oral contraceptives (COC). Just to clarify – COCs are a mixture of estrogen and progestins (synthetic progesterone). Both of these are sex hormones involved in preparing the female body for pregnancy and secondary sexual characteristics. All contraception works to reduce variation in cycle length and ultimately reduce the chances of pregnancy. COCs reduce natural production of estrogens and progestins by inhibiting pituitary secretion of gonadotrophins (hormones which stimulate the ovary to produce estrogen and progesterone). Perhaps the first mistake people make is to assume that there are only 2 types of contraception and that each works the same. There are so many variations of progestins in the available medication, all of which act differently pharmacokinetically, that few studies take this variation into account. Below is a table (1) of just some of the available contraceptive medication. It is important to note, that this research is from 2005, and not all currently-available contraceptives were indicated in this table. The table also includes information about the androgenicity of each variant. Androgenicity, simply put, is the ability to stimulate masculine characteristics. The potency refers to the power of progestin to produce its desired effects.
It is interesting to note that for most of these variants, there is a level of androgenicity. But where does this ‘level of androgenicity’ come from, and how was this measured. This article seemed to show this rather ambiguously, so I began digging for the original article that this came from. In this article by Greer et al (2), androgenicity is described as – calculated by measuring the progestin’s affinity for and binding to the androgen receptor, and it’s effect on the sex hormone binding globulin (SHBG). SHBG is important in this story as it is this globulin which binds testosterone and estrogen making the sex hormones unavailable for use at the receptors. Greer et al then go on to discuss two of the most androgenic progestins -levonorgestrel and dl-norgestrel ‘They have a high affinity for sex hormone binding globulin and decrease free sex hormone binding globulin levels by binding it and displacing testosterone, consequently increasing free testosterone levels.’ (2)
As they explain, the reason for these progestin’s ability to produce androgenic effects is because they bind to SHBG, which therefore prevents the binding of SHBG to testosterone, thereby increasing free testosterone. From this, one might assume that contraceptives containing levonorgestrel and dl-norgestrel, would, therefore, increase free testosterone, thereby helping to promote strength increases. However, there is also evidence to suggest that some COCs may be anti-androgenic. Wright et al, (11) found that ‘progesterone competitively inhibits the action of androgen, as it is a preferred substrate to the enzyme 5α-reductase, hence preventing the conversion of testosterone into its active metabolite dihydrotestosterone’. From the source, it is not clear which progestins Wright et al studied. Note article from 1983, modern-day progestins were not researched. In the table above, there is one variant whereby the potency and androgenicity are not available/this variant may have anti-androgenic effects. In a review of COCs by Zimmerman et al (3), they refer to studies which find decreases free testosterone and total testosterone and increasing concentrations of SBHG. In this review, they show that this is varied depending on which pill is taken. Thorneycroft et al (4) looked at the effects of 2 specific progestins levonorgestrel (LNG, 100 μg), and norethindrone acetate (NETA, 1000 μg) on testosterone levels. Both significantly reduced bioavailable testosterone, despite a 2.2 fold increase of SHBG with NETA than LNG (4). With this increase in SHBG with NETA, you might expect the testosterone to be further reduced, but it isn’t. This suggests there are other mechanisms at play that aren’t fully understood. According to Stanczyk (5), there is a misconception about the androgenicity of progestins due to extrapolation of data between rat to humans, and progestins differ greatly in chemical structures, metabolism, and pharmacokinetics. Indeed, both Greer et al and Thorneycroft et al looked into the same progestins LNG and found contradictory results.
Sitruk-Ware et al, (12) mention that most current progestins, according to their chemical structure, could interact with the androgen and estrogen receptor, among others and elicit both androgenic and antiandrogenic effects. In this article, they also take a look into more newly developed progestins on the market drospirenone (DRSP), dienogest (DNG) – so-called fourth-generation progestins and find that these bind very specifically to the progesterone receptor, with less interaction of other steroid receptors. Despite this, they also report that these ‘new progestins’ have antiandrogenic effects and are 30-40% less potent than cyproterone acetate (CPA) the most potent antiandrogenic progestin (13).
As most people focus on testosterone when they talk about strength/performance, I thought it right to shed some light on the role of estrogen, which is often overlooked. Estrogen is hugely important in both females and males and performs a wide array of tasks. These include promoting sex drive, accelerating metabolism, protein synthesis, lipid metabolism, the name just a few. Given its role in so many body functions, it makes sense that this hormone would also be important for athletic performance. Lowe et al, demonstrate the positive effects of estrogen on quality of skeletal muscle and improvement of myosin function (molecule required for muscle contraction). There are in fact, many examples of positive associations of estrogen and strength. Another article from Pöllänen et al (7), showed in a study of explosive lower body muscle in females, that the muscular composition of pre-menopausal women was greater than that of post-menopausal women, and that estrogen, testosterone, and DHEAS (dehydroepiandrosterone sulfate) were involved in muscle performance.
Links with contraceptives to other factors affecting athletic performance
There are many elements to athletic performance - it could be postulated that oral contraceptives may cause strength limiting effects in some areas, but have more positive effects in other areas. Indeed this is what I found in the literature. Lebrun (8), noted that musculoskeletal injuries have been shown to be reduced in women taking oral contraceptives. This ties in with research from Herzberg et al (9), that reviewed 21 studies including 68,000 participants that showed that hormonal contraceptives offered protection against ACL (anterior cruciate ligament) injury.
The table below reviews numerous studies in which an aspect of athletic performance is tested on women taking various contraceptive pills (1).
These studies show a variety of results, that in some there was a decrease in performance, in others an increase. The difficulty is that there are so many different types of contraceptive, with varying amounts and differing progestins, it is hard to compare one against another, and draw solid conclusions.
Focusing in on the element of recovery. Thompson et al, (10) found that there was no difference between contraceptive users and non-users with respect to muscle damage, but that women A taking contraceptives perceived less muscle soreness following exercise. This led to the conclusion that users may have a higher pain threshold due to the exogenous progesterone and estrogen, and this may influence the maximal force they can produce. (10)
Like I mentioned previously, my reasons for wanting to find out about specifically the effects of the POP pill on athletic performance were first because I find this an interesting topic, and with my scientific background, I thought I could do a reasonable and unbiased review. But secondly, because I am currently competing as an athlete and want to know what is best for my performance. I know there are many women out there who also would like a conclusion on this, but one that is backed up by substantial scientific evidence. In addition to this, many of the reviews I found online, by non-scientists attempting to answer this question, didn’t seem to be backed-up. I found online blogs which convincingly put forward that Progesterone is an antagonist (works against) of testosterone and therefore, a conclusion made, one shouldn’t take the pill if they want to help their athletic performance. I wondered if this was conclusive, but the papers they linked either were unavailable or were from 1971 and extrapolated data from chicken, rats, and mice (14). Having looked into this myself it would seem that from the progesterone component of the combined pills tested, many of these can bind the androgen receptor and decrease circulating testosterone. Although once bound to the androgen receptor it is still unclear the whether an androgenic or antiandrogenic effect will be seen. Of course, the testosterone-side to this question is important and should be considered. With the introduction of even more, and new, progestins more research should be conducted to find the effects at the androgen receptor, and also on strength as a whole with these fourth gen progestins. As I also pointed out, there are so many pills on the market, with slightly different pharmacokinetic effects, and most research focusing on the combined pill, it is not easy to draw conclusions. From what I have found, I would conclude that there is more evidence to suggest oral contraception can lower available testosterone, but the effects of this with regards to overall strength have been insufficiently studied. There are certainly positive effects to taking oral contraception on elements of athletic performance which have been noted in the various articles I linked in this mini-review. If pharmaceutical companies would decrease the available contraceptives and would regulate the formulations more tightly, more effective studies could be conducted to draw more conclusions. In short – I wouldn’t come off the pill in order to amplify my athletic performance because it is likely that differences would be negligible, and further research must be conducted.
(11) Wright F, Giacomini M, Riahi M and Mowszowicz I (1983) Antihormone activity of progesterone and progestins. In Bardin CW, Milgröm E and Mauvais-Jarvis P (eds), Progesterone and Progestins. Raven Press, New York, pp. 121–134