Can Excessive Exercise Cause Low Estradiol Levels?
Yes, excessive exercise can cause low estradiol levels in female athletes, primarily through the mechanism of low energy availability (EA) that disrupts the hypothalamic-pituitary-gonadal axis, leading to suppressed GnRH pulsatility, menstrual dysfunction, and systemically reduced estradiol concentrations. 1
Mechanism: Energy Deficit, Not Exercise Per Se
The critical factor is not the exercise itself, but rather insufficient energy intake relative to exercise energy expenditure, creating a state of low energy availability. 1, 2
Low EA (defined as <30 kcal/kg fat-free mass per day) causes disruptions in LH pulsatility, which serves as a surrogate for GnRH pulsatility, ultimately disturbing gonadotropin release and causing menstrual dysfunction manifested as oligo-amenorrhea. 1
Irregular or absent menses, combined with abnormal pituitary signaling, causes systemic reductions in estradiol. 1
This represents functional hypothalamic amenorrhea (FHA), where energy deficit suppresses the hypothalamic-pituitary-gonadal axis, leading to decreased GnRH pulsatility that preferentially reduces LH secretion. 2, 3
Evidence of Hormonal Alterations
Low EA causes the following hormonal changes in exercising women: decreased estradiol, decreased progesterone, decreased leptin, increased ghrelin, increased cortisol, decreased insulin, decreased thyroid hormones (T3, T4), and decreased IGF-1. 1
Even 5 days of reduced EA (10-30 kcal/kg FFM·day⁻¹) demonstrated decreased levels of estradiol in eumenorrheic young women, which may have led to menstrual dysfunction with extended study duration. 1
Research in female long-distance runners with irregular menstrual function showed clear hypoestrogenism (11 ± 1.6 pg/L) compared to runners with regular menstrual function (31 ± 6 pg/L). 4
High-intensity training in endurance runners was associated with decreased estradiol concentrations on specific cycle days, and seriously disturbed folliculogenesis was found in 50% of study cycles in runners versus 9% in controls. 5
Clinical Consequences of Low Estradiol
The health implications prioritize morbidity, mortality, and quality of life:
Bone Health (Critical for Long-Term Morbidity)
Estradiol is an osteoprotective agent that inhibits osteoclast activity. When estrogen levels are aberrantly subphysiologic, osteoclast activity predominates and bone mass is lost. 1
Oligo-amenorrhea decreases trabecular number and cortical thickness, leading to decreased bone mineral density and increased incidence of bone stress injury. 1
Low estradiol is recognized as an independent factor causing poor bone health in athletes with relative energy deficiency in sport (RED-S), separate from the mechanical effects of exercise. 6
Cardiovascular Health
- Hypoestrogenism in oligo-amenorrhea induces a post-menopausal-like physiology: endothelial dysfunction, poor lipid profiles (elevated LDL, total cholesterol, triglycerides), and renin-angiotensin-aldosterone axis changes. 1
Performance Decrements
- Adolescent female swimmers with ovarian suppression (lower estradiol and progesterone) had a 9.8% increase in time (worse performance) versus 8.2% improvement in eumenorrheic swimmers over 12 weeks. 1
Diagnostic Approach
Measure FSH and LH to differentiate primary from central causes:
FHA from low energy availability shows low or low-normal FSH and LH (<5 IU/L) with low estradiol, with LH:FSH ratio typically <1 in approximately 82% of FHA patients. 2, 3
This contrasts with primary ovarian failure (elevated FSH and LH >10-20 IU/L with low estradiol) from chemotherapy, radiation, or surgical causes. 6, 3
Management: Restore Energy Balance
The treatment for exercise-induced low estradiol focuses on restoring energy balance, NOT hormone replacement therapy. 6
Target energy availability of approximately 45 kcal/kg FFM·day⁻¹ is likely ideal for endurance athletes to maintain body mass and fuel high levels of training with fitness and performance improvements. 1
Weight restoration is the primary therapeutic intervention for FHA, with BMI reaching ≥18.5 kg/m² before ovulation induction is offered. 2
Clomiphene citrate is not recommended as first-line treatment for FHA due to uncertain efficacy and lack of randomized trials. 2
Common Pitfalls to Avoid
Do not confuse FHA with PCOS: PCOS shows LH:FSH ratio >2, higher testosterone, lower SHBG, and insulin resistance, while FHA shows ratio <1 and lacks these features. 2, 3
Hormonal contraceptive use fundamentally alters hormone assessment: ovarian function cannot be reliably assessed during use, and withdrawal bleeding on oral contraceptives is pharmacologic, not evidence of ovarian function. 3
The problem in FHA is central (hypothalamic), not ovarian: pulsatile GnRH administration can restore ovulation, proving the ovaries are functional. 2
Nuance: Habitual vs. Acute Exercise Effects
Habitual physical activity shows a dose-response relationship with estradiol suppression in regularly menstruating women (mean estradiol: 21.1 pmol/L in low activity, 17.9 pmol/L in moderate, 16.6 pmol/L in high activity groups). 7
Acute heavy exercise in untrained subjects provokes significant increments in ovarian hormones (37.6% increase in progesterone, 13.5% increase in estradiol), whereas no such increments are observed in trained subjects exercising at the same absolute workload. 8
This suggests chronic training adaptations alter the acute hormonal response to exercise. 8