# Tracking androgens in female elite athletes: menstrual cycle and hormonal contraceptive effects

**Authors:** Jana Nolte, Sven C. Voss, Annekathrin Martina Keiler, Emily Büthe, Kirsten Legerlotz, Petra Platen

PMC · DOI: 10.1186/s12905-026-04344-y · BMC Women's Health · 2026-03-13

## TL;DR

This study tracks androgen levels in elite female athletes to understand how menstrual cycles and hormonal contraceptives affect hormone availability and training strategies.

## Contribution

The study provides detailed longitudinal data on androgen fluctuations in elite female athletes under different hormonal conditions.

## Key findings

- Athletes using hormonal contraceptives show significantly lower androgen levels compared to naturally cycling athletes.
- Natural menstrual cycles show peak androgen levels in the late follicular phase before ovulation.
- Menstrual disturbances and contraceptive use alter androgen profiles, requiring individualized hormone monitoring for performance optimization.

## Abstract

Understanding variations in the androgen profile is crucial for interpreting hormone data and developing cycle-based training strategies tailored to individual athlete needs. Therefore, this study investigates the androgen concentrations of elite female track and field athletes across various hormonal conditions, including natural eumenorrheic cycles, cycles under hormonal contraception, and cycles with menstrual disturbances.

Using a prospective, longitudinal observational cohort design, 22 athletes (15 naturally cycling, 7 using hormonal contraception) were monitored for up to three consecutive cycles. The study utilised daily or near-daily urine sampling to analyse urinary steroid hormones (including testosterone and its metabolites) via gas chromatography-coupled mass spectrometry (GC-MS/MS).

Results demonstrated that in athletes with ovulatory menstrual cycles, urinary androgen concentrations, particularly testosterone, varied significantly by phase, peaking around the late follicular phase (lateFP: 7.35 ± 6.25 ng/mL). In contrast, athletes using combined oral contraceptives exhibited significantly suppressed androgen concentrations throughout the cycle compared to the natural cycle group, with mean urinary testosterone levels being notably lower (2.55 ± 2.91 ng/mL vs. 5.45 ± 4.31 ng/mL; p<0.001). These pill users also showed elevated concentrations of the inactive 5β-reductase metabolites (5β-androstanedione and 5β-androstanediol). Cycles with menstrual disturbances, such as luteal phase deficiency, also displayed altered and often lower concentrations of all urinary androgens.

These findings highlight the significant influence of both endogenous menstrual cycle dynamics and exogenous hormone interventions on androgen availability, underscoring the necessity of considering the individual hormone status for performance optimization and athlete health management.

The online version contains supplementary material available at 10.1186/s12905-026-04344-y.

• Androgen suppression by contraception: Androgen concentrations, particularly urinary testosterone, are significantly suppressed and remain consistently low throughout the cycle in elite female athletes using combined oral contraceptives compared to naturally cycling athletes.

• Cyclical fluctuation in natural cycles: During the natural, ovulatory menstrual cycle, urinary androgen concentrations show systematic fluctuations, with testosterone and its metabolites peaking in the late follicular phase, immediately prior to ovulation.

• Need for individualised interpretation: Both menstrual disturbances and hormonal contraceptive use fundamentally change the androgen profile, emphasising that understanding individual androgen availability and considering contraceptive type and dosage is essential for performance strategies and accurate interpretation of hormonal data in elite female athletes.

The online version contains supplementary material available at 10.1186/s12905-026-04344-y.

## Linked entities

- **Chemicals:** testosterone (PubChem CID 6013), 5β-androstanedione (PubChem CID 440114)

## Full-text entities

- **Genes:** ESR2 (estrogen receptor 2) [NCBI Gene 2100] {aka ER-BETA, ESR-BETA, ESRB, ESTRB, Erb, NR3A2}, CLDN11 (claudin 11) [NCBI Gene 5010] {aka HLD22, OSP, OTM}, AR (androgen receptor) [NCBI Gene 367] {aka AIS, AR8, DHTR, HPCX3, HUMARA, HYSP1}, UGT2B17 (UDP glucuronosyltransferase family 2 member B17) [NCBI Gene 7367] {aka BMND12, UDPGT2B17}, ESR1 (estrogen receptor 1) [NCBI Gene 2099] {aka ER, ESR, ESRA, ESTRR, Era, NR3A1}, SHBG (sex hormone binding globulin) [NCBI Gene 6462] {aka ABP, SBP, TEBG}, INS (insulin) [NCBI Gene 3630] {aka IDDM, IDDM1, IDDM2, ILPR, IRDN, MODY10}
- **Diseases:** Luteal phase deficiency (MESH:D000210), Oligomenorrhea (MESH:D009839), bleeding (MESH:D006470), IUD (MESH:D058736), Menstrual disturbances (MESH:D004412), alcohol (MESH:D000437), amenorrhea (MESH:D000568), luteal phase insufficiency (MESH:D000309), anovulation (MESH:D000858), hyperandrogenism (MESH:D017588), polycystic ovary syndrome (MESH:D011085)
- **Chemicals:** ethyl glucuronide (MESH:C093924), 5alpha-reduced (-), cholesterol (MESH:D002784), LH (MESH:D007986), 5alpha-dihydrotestosterone (MESH:D013196), EDTA (MESH:D004492), etiocholanolone (MESH:D005043), progesterone (MESH:D011374), DHEA (MESH:D003687), alcohol (MESH:D000438), Testosterone (MESH:D013739), androstenedione (MESH:D000735), pregnenolone (MESH:D011284), copper (MESH:D003300), 5alpha-androstanedione (MESH:C006576), levonorgestrel (MESH:D016912), ethinylestradiol (MESH:D004997), Androsterone (MESH:D000738), steroid (MESH:D013256)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

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## Figures

7 figures with captions in the complete paper: https://tomesphere.com/paper/PMC13001183/full.md

## References

6 references — full list in the complete paper: https://tomesphere.com/paper/PMC13001183/full.md

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Source: https://tomesphere.com/paper/PMC13001183