Do Oral Contraceptives Affect Your Gains?

A recent study examined the effects of oral contraceptives on strength gains, hypertrophy, and anabolic signaling. Do female lifters need to worry about hormonal contraceptives affecting their gains? Read on to find out.

A quick note about this article before we dive in:

This article was first published in MASS Research Review and is a review and breakdown of a recent study.  The study reviewed is Molecular Markers of Skeletal Muscle Hypertrophy Following 10 Weeks of Resistance Training in Oral Contraceptive Users and Non-Users. Oxfeldt et al. (2020)

Key Points

  1. Two groups of untrained females participated in a 10-week training study. One group was composed of oral contraceptives users, and the other group was composed of non-users.
  2. Strength gains and hypertrophy were not significantly different between groups. However, the subjects using oral contraceptives tended to have larger increases in lean body mass, along with some molecular indicators of anabolism.
  3. When analyzing these results within the context of the rest of the literature, it doesn’t seem that second- or third-generation oral contraceptives have a meaningful effect on strength or hypertrophy outcomes.

Many female lifters use hormonal contraceptives, but we’ve only discussed them twice in MASS. I previously reviewed a study by Myllyaho and colleagues which found that oral contraceptives didn’t have a significant impact on strength gains or changes in lean body mass (2), and a meta-analysis by Elliott-Sale and colleagues which found that hormonal contraceptives don’t have a particularly notable effect on acute performance measures (3). So, we’ve only reviewed one study that examined longitudinal outcomes, and as we all know, it’s dangerous to put too much faith in the results of a single study.

The presently reviewed study (1) assessed strength, hypertrophy, body composition, and cellular signaling outcomes before and after 10 weeks of training in users and non-users of oral contraceptives. Strength gains and hypertrophy were not significantly different between groups. However, the subjects using oral contraceptives tended to have larger increases in lean body mass, along with some molecular indicators of anabolism. Based on these results, it may initially be tempting to conclude that oral contraceptives might have a small positive effect on hypertrophy, but when examining the rest of the research on the topic, it seems that hormonal contraceptives simply don’t have much of an effect (positive or negative) on strength, hypertrophy, or lean mass outcomes.

Purpose and Hypotheses


The purpose of this study was to investigate whether oral (hormonal) contraceptives influence hypertrophy, molecular signaling markers, and satellite cell responses to resistance training.


The authors hypothesized that oral contraceptives would “potentiate the anabolic response to resistance training.”

Subjects and Methods


38 untrained young women completed this study. 20 used second-generation oral contraceptives (containing 30µg ethinyl estrogen and 0.15mg levonorgestrel, or 35µg ethinyl estrogen and 0.25mg norgestimate), and 18 did not use hormonal contraceptives. All subjects were healthy but untrained and menstruated regularly. You can see more information about the subjects in Table 1.

All graphics and tables in this review are by Kat Whitfield.

Experimental Design

Subjects trained for 10 weeks, and vastus lateralis muscle biopsies were collected before and after the 10-week training period.

The training consisted of three weekly training sessions. During each session, subjects performed leg press, knee extensions, leg curls, back extensions, pull-downs, and incline crunches. The subjects performed each exercise for 3 sets of 12 reps during weeks 1-5, 3 sets of 10 reps during weeks 6-8, and 4 sets of 8 reps during weeks 9 and 10. The subjects were “encouraged to use maximal effort and train near momentary muscle failure,” and “adjusted weights throughout the entire training period to maintain muscle loading as muscle strength increased.” I’d prefer more details about proximity to failure and the process for progressing loads, but it sounds like the training program likely provided an adequate stimulus for untrained subjects. 

From the biopsies, the researchers examined changes in muscle fiber cross-sectional area, myosin heavy chain isoform ratios (the same procedure used in this study), satellite cells per fiber, myonuclei per fiber, mRNA levels for various muscular regulatory factors (Pax7, MYF5, MyoD1, MRF4, and MyoG, which are generally reflective of growth, and FOXO1, FOXO3, FOXO4, TNF-α, Atrogin-1, and MURF-1, which are generally reflective of protein breakdown), and levels of various proteins associated with anabolism (mTOR, alpha estrogen receptor, androgen receptor, Pax7, and MyoD).

Notably, the present study (1) is the second paper published from a single investigation. The first paper (4) also tested 5RM leg press strength, maximal knee extension and knee flexion torque, quadriceps cross-sectional area, countermovement jump height, Wingate test average power, and body composition (via DEXA) pre- and post-training. I’ll report those findings as well.


Quadriceps cross-sectional area at three different sites along the quadriceps increased significantly in both groups, without significant differences between groups.

Fat-free mass also increased significantly in both groups. It tended to increase to a greater extent in the subjects using oral contraceptives (3.7 ± 3.8% vs. 2.7 ± 3.5%; p = 0.08), but the difference between groups wasn’t statistically significant.

Muscle fiber cross-sectional area significantly increased in both groups for both major fiber types, with no significant differences between groups.

Fat mass decreased to a significantly greater extent in the subjects not using hormonal contraceptives, but the raw changes were tiny in both groups (-0.1kg vs. -0.8kg).

Knee flexion torque, knee extension torque, leg press strength, countermovement jump height, and Wingate test average power increased significantly in both groups, without significant differences between groups.

From pre- to post-training, the oral contraceptive users had a significantly larger increase in type IIa myosin heavy chain isoform proportion (+6.9% vs. -0.1%; p < 0.01), probably due to the fact that they had a larger proportion of type IIx myosin heavy chain protein pre-training (7.5% vs. 3.8%).

Myonuclei per fiber changed to a similar degree in both groups, as did satellite cells per fiber. When expressed as satellite cells per unit of fiber cross-sectional area (basically the inverse of myonuclear domain), the increase in the subjects using hormonal contraceptives tended to be larger than the change in the controls, but the difference didn’t quite reach statistical significance (p = 0.055).

The only significant difference between groups for changes in mRNA levels of generally anabolic regulatory factors was for MRF4, which increased to a significantly greater extent in the oral contraceptive users. For generally catabolic regulatory factors, TNF-α mRNA significantly increased in the oral contraceptive users but not the non-users (though the difference between groups wasn’t significant). Furthermore, both groups experienced a significant increase in MURF-1 mRNA, with no significant differences between groups. There were no other significant within-group or between group changes for the various mRNAs examined (Pax-7, MYF5, MyoD1, MyoG, FOXO1, FOXO3, FOXO4, and Atrogin-1).

There was only one significant change in protein levels. Androgen receptor protein levels significantly increased in the oral contraceptive users, but not the non-users; however, there wasn’t a significant difference between groups. No other protein examined significantly changed in either group, or significantly differed between groups.


In previous issues of MASS, we’ve reviewed another study examining the effects of oral contraceptives on strength and body composition outcomes (2), and a meta-analysis investigating the effects of oral contraceptives on exercise performance (3). The study investigating body composition and performance outcomes failed to find any significant differences between users and non-users, and the meta-analysis found that non-users may perform slightly better, but any mean difference is likely to be trivial, if one exists at all.

In that light, the results of the present studies are unsurprising (14). Hormonal contraceptives didn’t seem to affect hypertrophy or strength gains, their effect on body composition seemed to be trivial, and most molecular markers were unaffected. Thus, especially in light of the studies we’ve previously reviewed on the topic, the conservative interpretation of these results is that hormonal contraceptives are unlikely to have much of an impact (either positive or negative) on strength gains or hypertrophy.

However, if you squint just right, you could possibly make the case that oral contraceptives may be a weak ergogenic. In the present studies, direct measures of hypertrophy (type I and type II fiber cross-sectional area and quadriceps cross-sectional area) all leaned in favor of the oral contraceptives group, though the differences weren’t statistically significant. The subjects using oral contraceptives also tended to gain more lean mass (p = 0.08). Furthermore, in type II fibers, satellite cells per unit of cross-sectional area tended to increase more in the subjects using oral contraceptives (p = 0.055); increases in satellite cells suggest that muscle fibers are “setting the stage” to future growth. The subjects using oral contraceptives also had a significantly greater increase in mRNA levels for a pro-anabolic regulatory factor (MRF4), and non-significant differences in mRNA levels for all other pro-anabolic regulatory factors tended to favor the subjects using oral contraceptives. The oral contraceptive group also significantly increased androgen receptor protein levels; previous research has found that androgen receptor density is a positive predictor of hypertrophy (albeit in males; 5). The authors of the present study also argue that the significant increase in TNF-α mRNA levels in the subjects using oral contraceptives may reflect an increase in adaptive protein remodeling (1).

On the other hand, the non-users may have been slightly more “trained” at baseline (all of the subjects were untrained, but not all untrained subjects are equally untrained). They had lower proportions of type IIx myosin (which decreases as training status increases). Furthermore, body composition changes reveal that the oral contraceptive users were in a slight caloric surplus, on average (+1.5kg of body mass; -0.1kg decrease in fat mass), while the non-users were in a slight deficit (+0.3kg of body mass, -0.8kg of fat mass), which may be sufficient to explain the non-significant differences in hypertrophy. Thus, while some of the findings regarding molecular markers are certainly interesting, I wouldn’t read too much into them yet.

Let’s now look beyond the presently reviewed studies. When I last wrote about a study examining the effects of oral contraceptives on performance and body composition outcomes, there weren’t many other longitudinal studies to analyze. There are a few more now, so I think we’re ready for a preliminary summary of the literature.

Graphics in this review are by Kat Whitfield.

I was able to find 10 papers from 8 distinct studies (two studies were responsible for two papers apiece) that investigated the effects of oral contraceptives on strength, lean mass, or hypertrophy outcomes (1246789101112). You can see a summary of their results in Table 5. It’s not really worth breaking down every study in depth, because the overall pattern is clear: oral contraceptives don’t seem to have a consistent, notable impact on the sorts of outcomes most SBS or MASS readers care about. The strength outcomes are clearly a wash, as are the lean body mass outcomes. For hypertrophy outcomes, only two studies (spanning three papers) have directly investigated the effects of oral contraceptives on direct measures of muscle growth (1411), and they’re both chock full of non-significant results favoring the use of hormonal contraceptives. In fact, the difference in type I fiber CSA in Dalgaard’s 2019 study was actually statistically significant, favoring the subjects using oral contraceptives (11). Personally, I’m not incredibly impressed by one significant difference out of eight outcome measures, especially when all we have to go on is a pair of relatively small studies, and especially when the entire body of research doesn’t suggest that there are meaningful differences in strength gains or lean mass accretion.

With that being said, there are two little nuggets in the “notes” column of Table 5 that are worth dwelling on for a moment. A study by Lee and colleagues found a significant difference in lean mass accretion between people taking oral contraceptives with weakly androgenic progestins, compared to people taking oral contraceptives with more strongly androgenic progestins (6). Furthermore, a study by Dalgaard (11) found that subjects taking oral contraceptives with a higher estrogen dose (30µg) experienced more vastus lateralis hypertrophy than subjects taking oral contraceptives with a lower estrogen dose (20µg). When discussing these findings, I’ll reverse the orders of “good cop” and “bad cop” for a change.

These findings deserve some degree of skepticism because they appear to be the result of exploratory analyses; in other words, it’s unlikely that they’re comparisons the researchers had in mind when designing their studies. The reason I think these were exploratory analyses is that the dominant subject recruitment paradigm revolves around developing a research question, predicting the magnitude of the effect you’ll find (or assuming whatever magnitude of effect you think will be “meaningful”), and recruiting enough subjects to be able to reliably detect an effect of your predicted magnitude. If you can’t recruit enough people or you overestimate the actual effect size, your study is underpowered. If you underestimate the actual effect size, and recruit way more people than you need, your study is overpowered. In both of these studies, the primary comparisons were between people using versus not using oral contraceptives; thus, the studies would be powered to detect differences between those two groups. In other words, in the Dalgaard study, there were 14 subjects per group meaning the researchers were likely anticipating that 14 subjects per group would provide adequate statistical power to detect differences between users and non-users of oral contraceptives (11). But then, the comparison between high-estrogen and low-estrogen oral contraceptive users compared groups of just seven subjects apiece. That would only make sense as an a priori decision if the researchers had reason to believe that the difference between high- and low-estrogen oral contraceptive users would be considerably larger than the difference between users and non-users. Furthermore, for the low- versus high-estrogen comparison to be a planned analysis, the researchers would have needed to make an effort to recruit similar numbers of subjects who used low- and high-estrogen oral contraceptives; they wound up with 7 and 7, but they could have easily wound up with 3 and 11, which would make traditional significance testing basically impossible. The authors don’t state that they went out of their way to recruit similar numbers of high- and low-estrogen oral contraceptive users.

So, what does that mean? Well, for starters, I’m certainly not claiming the authors did anything wrong. Running exploratory analyses is a perfectly normal part of science. However, we inherently need to be more skeptical of findings that are a result of exploratory analyses. Why? Because there are an almost infinite amount of analyses you can run and comparisons you can make when you’re working with data. There are a huge number of statistically significant “findings” lurking in every dataset, and a non-negligible proportion of them are bound to be illusory and spurious. If you pre-specify a data analysis plan, you run a study correctly, you stick to your pre-specified data analysis plan, and you get a statistically significant result, there’s a low probability that your significant result is spurious. However, once you start running exploratory analyses, you’re almost guaranteed to stumble upon some statistically significant “discoveries” that are completely spurious. As one example, in my thesis study, I found that soreness 24 hours post-training was significantly positively associated with hours of sleep the night following the training session (p = 0.017). I was dealing with a rich dataset, which would lend itself to literally thousands of comparisons, and examining the relationship between sleep and soreness was not part of my pre-specified data analysis plan. So what’s more likely? Sleeping more is predictive of greater soreness following training? Or I stumbled across one of the (likely hundreds of) spurious findings lurking in my dataset? My money’s on option 2. Now, don’t get me wrong. I’m certainly not claiming that all significant results that result from exploratory analyses are spurious. I’m not even claiming that a majority of them are. I’m simply stating that the probability of a “false positive” is greater when you see a significant finding resulting from an exploratory analysis, than when you see a significant finding resulting from researchers’ primary analyses.

The value of exploratory analyses is that they help you generate hypotheses for future research. If you see that, in subgroups of seven subjects apiece, people who use high-estrogen oral contraceptives experience more hypertrophy than people who use low-estrogen oral contraceptives, you might want to design a study to test that preliminary finding more rigorously. If you get similar results in a study specifically designed to make that comparison, then you can start having considerably more confidence in the finding. If a study designed to test that comparison fails to find significant or meaningful differences, then you know there’s a decent chance that your exploratory analysis found a false positive and sent you on a wild goose chase.

In a roundabout way, all I’m saying is that you always need to be cautious of findings that are only supported by one study, and you need to be doubly cautious of findings that are only supported by exploratory analysis in one study.

So, now that I’m done with the bad cop routine, let’s discuss why you should maybe have a little confidence in these exploratory findings, suggesting that hormonal contraceptives with higher levels of estrogen and less androgenic progestins might be beneficial for hypertrophy.

Starting with estrogen, we’ve previously discussed the beneficial effects of estrogen for muscle remodeling. However, it appears that most of the popular oral contraceptives on the market induce less total estrogenic activity on a monthly basis than females would naturally be exposed to (13). Ethinyl estrogen is the form of estrogen used in the vast majority of hormonal contraceptives, and the typical monthly dose of ethinyl estrogen contained in oral contraceptives is a little less than half the amount of estradiol (the primary estrogen humans produce) naturally menstruating women produce on a monthly basis, on average. However, ethinyl estrogen’s affinity for the estrogen receptor is approximately 90% greater than estradiol’s, so the total estrogenic activity of the ethinyl estrogen in a month’s supply of oral contraceptives is probably around 10-12% lower than the total estrogenic activity of the estradiol that naturally menstruating women produce. There’s a pretty broad range, though, with some oral contraceptives providing more than 50% less monthly estrogenic activity than would be present in an average natural menstrual cycle, and others providing almost 50% more (13). Given the positive effects of estrogen on skeletal muscle and the wide range of estrogen doses one could possibly derive from oral contraceptives, I do think it’s plausible that formulations with higher estrogen content could be meaningfully ergogenic. Though, to reiterate, I’d want to see future research confirm Dalgaard’s exploratory findings.

Now, let’s move on to the matter of progestins. How much stock should we place in Lee et al’s finding that oral contraceptives with less androgenic progestins could be beneficial for hypertrophy? Quite a bit, actually.


Bad cop’s back, baby.

First off, I need to eat some crow. I’ve previously made the claim that progestins with greater androgenicity were a negative for hypertrophy, because the progestins with a high affinity for the androgen receptors would essentially “clog up” the receptors without actually causing downstream androgenic signalling, and thus keep androgens from being able to do their job (competitive antagonism, if you prefer the fancy biochem jargon). In my defense, I vividly remember learning this in my undergraduate exercise physiology class, and that is how progesterone functions (though progesterone has a relatively low affinity for the androgen receptor). However, that’s not how most of the progestins present in oral contraceptives function. First-, second-, and third-generation progestins (second- and third-generation progestins are present in most oral contraceptives currently on the market) are truly androgenic, binding to the androgen receptor and functioning like an androgen when bound to the receptor. Fourth-generation progestins, on the other hand, do function more like progesterone, functioning as androgen receptor antagonists (14).

So, with that in mind, I suspect Lee et al’s finding (smaller gains in lean mass with less androgenic progestins; 6) is likely spurious, for three reasons. First, androgenic signaling is generally a positive thing for hypertrophy, and one would assume that it would be especially positive for people using oral contraceptives: oral contraceptives tend to decrease free testosterone levels, so getting an androgenic signalling boost from a highly androgenic progestin seems like it would be a good thing. Second, it’s hard to square Lee et al’s findings with the results of the present study (1): 17 of the 20 oral contraceptive users in the present study used formulations featuring the progestin levonorgestrel, which is either the most androgenic progestin commonly used in oral contraceptives, or one of the most androgenic progestins commonly used in oral contraceptives (depending on the measure of androgenicity you look at; 14). As previously mentioned, the hormonal contraceptive users in the present study grew just fine (1), and basically all (mostly non-significant) hypertrophy differences between the users and non-users leaned in favor of the users. At minimum, if more androgenic progestins blunt hypertrophy, the Lee study likely overestimates the effect (the mean increase in lean body mass was 3.5% in non-users and 0.3% in hormonal contraceptive users whose pills included moderately-to-highly androgenic progestins). Lastly, in re-examining Lee’s results, I think the exploratory analysis comparing the low- versus moderate-to-highly androgenic progestins was inappropriate in the first place. The average increase in lean body mass for the group of hormonal contraceptive users was 2.1% (n = 34). The sub-group using progestins with low androgenicity had an average increase of 2.5%, while the sub-group using progestins with moderate-to-high androgenicity had an average increase of 0.3%. What should jump out at you (and what should have jumped out at me sooner) is the fact that 2.1% is nowhere near the midpoint of 2.5% and 0.3%. That’s relevant, because you’d expect the group average to be the midpoint of the two subgroup averages if the subgroups were the same size. So, I did a little algebra, and calculated how large the two subgroups were. As it turns out, there were 28 subjects using progestins that were deemed to have low androgenicity, and just 6 subjects using progestins that were deemed to have moderate-to-high androgenicity (15). The authors don’t state what statistical test they used to compare the two groups (though, in their defense, the only published results from this study are in the from of a conference abstract, and abstracts don’t generally have sprawling statistics sections), but most parametric tests assume that the number of datapoints are roughly similar between groups. That’s arguably less important with large sample sizes, but it seems pretty darn important when you’re dealing with relatively small groups that differ in size by more than four-fold. And, on a more basic level, I don’t really see the point in using inferential statistics on a group of six subjects in the first place. With a group that small, one or two new subjects that differ substantially from the mean can completely change your results.

So, just to wrap this sucker up, I don’t think you need to be too concerned about how oral contraceptives will affect your strength or hypertrophy goals. Now that the body of evidence is growing, you could possibly make a very tentative case that hormonal contraceptives potentially improve hypertrophy results, but I’d want to see stronger evidence before stating that confidently. There’s also some (quite weak) evidence suggesting that formulations with higher estrogen doses may be beneficial for hypertrophy, so if you use oral contraceptives and you’re willing to do anything for a slight edge, you could consider asking your doctor about oral contraceptives with higher estrogen doses (though, as someone with no skin in the game, the risks seem to outweigh the rewards; if estrogen levels get too high, they can cause headaches, nausea, and lethargy. At minimum, those are symptoms worth monitoring if you and your doctor decide to change to a new oral contraceptive). Ultimately, no matter what you do, you shouldn’t expect a night-and-day difference. Based on the current state of the research, the most commonly discussed reasons for using or not using oral contraceptives (contraception, more control over your period, managing menstrual symptoms, etc.) seem like the most justifiable reasons. Future research may tip the balance of evidence toward oral contraceptives being meaningfully ergogenic or ergolytic, or research on fourth-generation oral contraceptives may have results that differ substantially from the research on primarily second- and third-generation oral contraceptives (which dominate the literature currently). But for now, the research suggests that you probably don’t need to think about your gains when you’re deciding whether to start, stop, or change oral contraceptives.

As always, you should talk to your doctor about drugs, and nothing in this article should be construed as medical advice. 

Next Steps

There are a lot of forms of hormonal contraception that haven’t yet been studied in a resistance training context. We don’t know how the minipill (progestin-only oral contraception), fourth-generation combination pills, hormonal IUDs, intravaginal inserts, or progestin injections affect strength and hypertrophy. A straightforward training study with any of the un-researched forms of hormonal contraception would fill a significant hole in the literature. 

Application and Takeaways

To this point, it doesn’t seem like second- or third-generation oral contraceptives have much of an effect on strength or hypertrophy outcomes following resistance training. If you choose to use hormonal contraceptives, you probably don’t need to worry about your gains.


  1. Oxfeldt M, Dalgaard LB, Jørgensen EB, Johansen FT, Dalgaard EB, Ørtenblad N, Hansen M. Molecular markers of skeletal muscle hypertrophy following 10 weeks of resistance training in oral contraceptive users and non-users. J Appl Physiol (1985). 2020 Oct 15. doi: 10.1152/japplphysiol.00562.2020. Epub ahead of print. PMID: 33054662.
  2. Myllyaho MM, Ihalainen JK, Hackney AC, Valtonen M, Nummela A, Vaara E, Häkkinen K, Kyröläinen H, Taipale RS. Hormonal Contraceptive Use Does Not Affect Strength, Endurance, or Body Composition Adaptations to Combined Strength and Endurance Training in Women. J Strength Cond Res. 2018 Jun 20. doi: 10.1519/JSC.0000000000002713. Epub ahead of print. PMID: 29927884.
  3. Elliott-Sale KJ, McNulty KL, Ansdell P, Goodall S, Hicks KM, Thomas K, Swinton PA, Dolan E. The Effects of Oral Contraceptives on Exercise Performance in Women: A Systematic Review and Meta-analysis. Sports Med. 2020 Oct;50(10):1785-1812. doi: 10.1007/s40279-020-01317-5. PMID: 32666247; PMCID: PMC7497464.
  4. Dalgaard LB, Jørgensen EB, Oxfeldt M, Dalgaard EB, Johansen FT, Karlsson M, Ringgaard S, Hansen M. Influence of Second Generation Oral Contraceptive Use on Adaptations to Resistance Training in Young Untrained Women. J Strength Cond Res. 2020 Jul 20. doi: 10.1519/JSC.0000000000003735. Epub ahead of print. PMID: 32694286.
  5. Morton RW, Sato K, Gallaugher MPB, Oikawa SY, McNicholas PD, Fujita S, Phillips SM. Muscle Androgen Receptor Content but Not Systemic Hormones Is Associated With Resistance Training-Induced Skeletal Muscle Hypertrophy in Healthy, Young Men. Front Physiol. 2018 Oct 9;9:1373. doi: 10.3389/fphys.2018.01373. PMID: 30356739; PMCID: PMC6189473.
  6. Lee CW, Newman MA, Riechman SE. Oral Contraceptive Use Impairs Muscle Gains in Young Women. FASEB. 2009 Apr;23:51. doi: 10.1096/fasebj.23.1_supplement.955.25.
  7. Ihalainen JK, Hackney AC, Taipale RS. Changes in inflammation markers after a 10-week high-intensity combined strength and endurance training block in women: The effect of hormonal contraceptive use. J Sci Med Sport. 2019 Sep;22(9):1044-1048. doi: 10.1016/j.jsams.2019.04.002. Epub 2019 May 30. PMID: 31186194.
  8. Nichols AW, Hetzler RK, Villanueva RJ, Stickley CD, Kimura IF. Effects of combination oral contraceptives on strength development in women athletes. J Strength Cond Res. 2008 Sep;22(5):1625-32. doi: 10.1519/JSC.0b013e31817ae1f3. PMID: 18714222.
  9. Romance R, Vargas S, Espinar S, Petro JL, Bonilla DA, Schöenfeld BJ, Kreider RB, Benítez-Porres J. Oral Contraceptive Use does not Negatively Affect Body Composition and Strength Adaptations in Trained Women. Int J Sports Med. 2019 Dec;40(13):842-849. doi: 10.1055/a-0985-4373. Epub 2019 Sep 6. PMID: 31491790.
  10. Ruzić L, Matković BR, Leko G. Antiandrogens in hormonal contraception limit muscle strength gain in strength training: comparison study. Croat Med J. 2003 Feb;44(1):65-8. PMID: 12590431.
  11. Dalgaard LB, Dalgas U, Andersen JL, Rossen NB, Møller AB, Stødkilde-Jørgensen H, Jørgensen JO, Kovanen V, Couppé C, Langberg H, Kjær M, Hansen M. Influence of Oral Contraceptive Use on Adaptations to Resistance Training. Front Physiol. 2019 Jul 2;10:824. doi: 10.3389/fphys.2019.00824. PMID: 31312144; PMCID: PMC6614284.
  12. Wikström-Frisén L, Boraxbekk CJ, Henriksson-Larsén K. Effects on power, strength and lean body mass of menstrual/oral contraceptive cycle based resistance training. J Sports Med Phys Fitness. 2017 Jan-Feb;57(1-2):43-52. doi: 10.23736/S0022-4707.16.05848-5. Epub 2015 Nov 11. PMID: 26558833.
  13. Lovett JL, Chima MA, Wexler JK, Arslanian KJ, Friedman AB, Yousif CB, Strassmann BI. Oral contraceptives cause evolutionarily novel increases in hormone exposure: A risk factor for breast cancer. Evol Med Public Health. 2017 Jun 5;2017(1):97-108. doi: 10.1093/emph/eox009. PMID: 28685096; PMCID: PMC5494186.
  14. Louw-du Toit R, Perkins MS, Hapgood JP, Africander D. Comparing the androgenic and estrogenic properties of progestins used in contraception and hormone therapy. Biochem Biophys Res Commun. 2017 Sep 9;491(1):140-146. doi: 10.1016/j.bbrc.2017.07.063. Epub 2017 Jul 12. PMID: 28711501; PMCID: PMC5740213.
  15. [(0.3 × 6) + (2.5 × 28)] ÷ 34 ≅ 2.1
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