Do Women’s Testosterone Levels Increase During Period?

Unpack the science of female testosterone fluctuations across the menstrual cycle. Discover the true timing of peaks and drops, and their effect on mood.

Testosterone in women follows a subtle but measurable pattern across the menstrual cycle, and the period itself is actually when levels tend to be at their lowest. The early follicular phase, which begins with menstruation, represents a nadir for testosterone, with concentrations climbing modestly toward a small peak around ovulation at mid-cycle. That said, the shift is far less dramatic than many wellness sources imply, and what any individual woman experiences can look quite different from the population average.

The General Pattern Across the Cycle

A large study of women with natural menstrual cycles found that testosterone and androstenedione levels followed a pattern similar to estrogen, with statistically significant lows in the early follicular phase compared to mid-cycle and the luteal phase. The median early follicular testosterone was about 0.32 nmol/L, rising to roughly 0.35 nmol/L at mid-cycle and in the luteal phase. Those numbers are close together, and that closeness matters: the fluctuation exists, but it is modest in absolute terms.

Daily blood sampling using highly sensitive measurement techniques has confirmed this overall shape: testosterone concentrations are higher around mid-cycle, though a clear peak is not discernible in every individual woman. So the honest answer is that testosterone does not increase during the period. It rises slightly after the period ends, usually reaching its highest point near ovulation, and the magnitude of that rise is small enough that it can be hard to detect in any single person.

Why Testosterone Peaks Around Ovulation

The mid-cycle bump in testosterone traces back to what the ovaries are doing in the days leading up to egg release. Theca cells in the ovary produce androgens, including testosterone and its precursor androstenedione, in response to luteinizing hormone (LH). When LH surges to trigger ovulation, it also ramps up androgen production in those theca cells. Much of the androstenedione produced gets converted into estrogen by neighboring granulosa cells, but some testosterone escapes into the bloodstream, creating the modest mid-cycle rise.

The ovaries are not the only source. Roughly a quarter to a third of circulating testosterone in women comes from ovarian production, with the adrenal glands contributing substantially as well. Because adrenal output does not follow the menstrual cycle in the same way, the cycle-related swing in total testosterone is dampened. It is essentially one source (the ovary) pulsing while the other (the adrenals) hums along at its own rhythm, governed more by daily cortisol cycles and stress than by reproductive phase.

Total Testosterone Versus What Your Body Actually Uses

Knowing that total testosterone nudges upward at mid-cycle does not tell you the whole story, because most circulating testosterone is bound to a protein called sex hormone-binding globulin (SHBG) and is biologically inactive in that state. SHBG levels themselves change across the cycle: they are significantly higher in the luteal phase, the roughly two-week stretch after ovulation and before the next period. When SHBG rises, it soaks up more testosterone, leaving less in the free, active form.

One study found that while total testosterone stayed roughly the same between the follicular and luteal phases, the higher luteal SHBG redistributed testosterone so that the free androgen index actually dropped. Older research on free testosterone concentrations tells a similar story: total testosterone fell progressively across the cycle, but the percentage that was free increased from the follicular to the luteal phase, partially offsetting the decline, until it dropped more sharply in the late luteal phase just before menstruation.

The practical upshot is that mid-cycle may be when total testosterone is at its highest, but the free, bioavailable fraction does not necessarily track in lockstep. The interplay between testosterone production and SHBG means the actual androgenic signal your tissues receive is harder to predict from a single blood draw than you might think.

Individual Variation Is Enormous

Population averages mask something important: not every woman follows the textbook pattern. A 2024 study of 339 women with confirmed ovulation measured salivary testosterone multiple times across the cycle and found that, while the group average showed a small mid-cycle peak and a luteal dip, individual women varied hugely in both the direction and size of their testosterone swings. Some women showed a clear ovulatory spike; others showed a flat line or even the opposite pattern. This is not measurement noise. The variability was real and substantial.

This finding matters because it means generalizations like “your testosterone peaks at ovulation” may not apply to you personally. Your age, body composition, stress levels, sleep, adrenal function, and genetics all shape your particular testosterone profile. Anyone tracking symptoms and trying to map them onto a generic hormone chart should treat the chart as a rough guide, not a timetable.

What This Means for Libido

The idea that testosterone drives sexual desire in women is popular, and there is some truth to it, but the relationship is weaker and messier than the simple narrative suggests. A review of studies on menstrual cycle hormones and libido found that estradiol had a moderate positive correlation with sexual desire, while testosterone showed a weak modulatory effect, with a positive link in only about 40% of the studies examined. Progesterone, meanwhile, was associated with lower sexual motivation, which helps explain why desire often wanes in the luteal phase even though testosterone has not dropped dramatically yet.

Older research adds nuance. One study found that women not using hormonal contraception reported a peak in sexual interest in the premenstrual phase, while those on the pill peaked around ovulation, suggesting that the hormonal context shapes when desire surfaces. Another study found that sexual feelings and pleasant sexual thoughts cycled consistently regardless of whether androgen levels were high or low, hinting that the psychological rhythm of desire has some independence from the hormonal rhythm. In short, testosterone contributes to desire in women, but it is not the sole conductor.

Athletic Performance and Testosterone Reactivity

For women interested in how cycle-related testosterone shifts affect physical performance, the evidence is intriguing but complicated. A study of female athletes found that menstrual cycle changes in salivary testosterone were more pronounced in elite performers who already had higher baseline testosterone levels. In these women, the mid-cycle testosterone peak coincided with greater training motivation, a stronger testosterone response to physical stress, and higher neuromuscular power output. For less elite athletes, the cycle-related differences were smaller and less consistent.

Exercise itself transiently raises testosterone regardless of cycle phase. Research on prolonged aerobic exercise found that post-exercise testosterone was significantly higher than resting levels in both high-estrogen and low-estrogen phases, with no significant difference between the two phases in how much testosterone rose. So while your baseline testosterone may nudge higher at mid-cycle, the acute spike from a hard workout seems to happen whenever you train.

Where cycle phase may make a more meaningful difference is in the stress response. Athletic women tested on cycle day 14 (near ovulation) showed a roughly 14% testosterone response to both physical and psychological stressors, compared with about 7% on days 7 and 21. Interestingly, cortisol showed the opposite pattern, being less responsive at mid-cycle. This suggests the hormonal environment around ovulation may tilt the body’s stress response toward testosterone and away from cortisol, which could subtly favor certain kinds of explosive or competitive performance.

PCOS Changes the Entire Equation

Everything discussed above applies to women with regular ovulatory cycles. Polycystic ovary syndrome (PCOS) rewrites the rules. In PCOS, the ovaries tend to produce higher levels of androgens at baseline, and the degree of menstrual irregularity correlates with the severity of hormonal disruption. Women with increasingly irregular cycles show progressively higher testosterone, higher LH, and altered free androgen indices compared with regularly cycling women.

Even in adolescents, polycystic ovaries are associated with significantly higher LH and androgen levels compared with girls who have normal ovaries. If you have PCOS, your testosterone may be elevated throughout the cycle rather than following the gentle mid-cycle wave. This is one reason irregular periods paired with symptoms like acne, excess body hair, or hair thinning prompt clinicians to check androgen levels.

How Hormonal Contraception Flattens the Pattern

Combined oral contraceptives dramatically suppress the cycle-linked testosterone pattern. A systematic review and meta-analysis confirmed that combined pills reduce testosterone by inhibiting both ovarian and adrenal androgen production and by raising SHBG levels. The result is a steady, low testosterone state with no meaningful mid-cycle peak.

The degree of suppression depends on the formulation. One trial comparing two pill types found that free testosterone dropped by roughly two-thirds to three-quarters across both formulations, with the specific progestin making a notable difference in total testosterone suppression. If you are on hormonal contraception and wondering whether your testosterone follows a cycle, it almost certainly does not, at least not in the way it would without the pill. This partly explains reports of lower libido on certain contraceptives, since the testosterone dip is persistent rather than transient.

When Testosterone Testing Is Done and Why Timing Matters

Clinicians who want an accurate picture of a woman’s testosterone typically draw blood in the early follicular phase, usually within the first few days of menstruation. This is precisely because it is the low point: a baseline reading taken at the nadir is the most reproducible and easiest to compare against reference ranges. Measuring at random points in the cycle introduces variability that can make interpretation unreliable.

Accurate measurement in women is tricky in general. Testosterone levels in women are far lower than in men, and many older assay methods struggled with the precision needed to distinguish normal from abnormal at these concentrations. Newer techniques using liquid chromatography–tandem mass spectrometry have improved the picture, but even with better tools, the clinical significance of small changes across the cycle has remained a subject of debate. If you are getting testosterone levels checked, asking your provider whether the draw was timed to your cycle phase is a reasonable question.

The Perimenopause Question

As women approach menopause, the ovarian contribution to testosterone shifts. Interestingly, one study looking directly at testosterone in the ovarian vein during perimenopause found no difference in levels between cycle phases, suggesting that the ovary’s testosterone output becomes less responsive to the rhythmic LH fluctuations that drive the mid-cycle bump in younger women. The cycle-related variation, modest to begin with, may flatten further as cycles become irregular and ovulation becomes sporadic.

After menopause, the ovary does not shut off testosterone production entirely, but the cyclical pattern disappears because there is no cycle. For perimenopausal women experiencing symptoms they attribute to testosterone shifts, the reality may be that estrogen and progesterone changes are doing the heavier lifting and testosterone is relatively stable in the background.

Testosterone, Immunity, and an Unexpected Twist

A small but provocative study examined how testosterone interacts with immune markers across the cycle, and found something unexpected: the relationship depended on sexual activity. In sexually abstinent women, higher testosterone at ovulation was associated with higher levels of the inflammatory marker IL-6. In sexually active women, the pattern reversed: at ovulation, higher testosterone was linked to lower IL-6. The researchers framed this as a potential reproductive tradeoff: the body may adjust immune surveillance around ovulation depending on whether conception is a realistic possibility.

This is a single small study and far from settled science, but it illustrates how testosterone’s role across the menstrual cycle extends beyond the obvious domains of desire and performance into immune regulation and metabolic signaling. The interplay between hormones and immunity remains one of the less-explored frontiers of cycle research, and findings like this suggest testosterone is not just along for the ride.