During adolescence, the rise in estrogen levels significantly enhances muscle development and strength. The studies consistently showed that higher estrogen levels during puberty contribute to increased muscle mass and improved metabolic function. Menopause is characterized by a significant decline in estrogen levels, leading to reduced muscle mass and strength, increased muscle fatigue, and impaired metabolic function.

We recently evaluated endocrine parameters in nine female weight lifters using steroids and seven not using these agents. Of the nine anabolic steroid users, seven took multiple anabolic steroids simultaneously. Thirty-fold elevations of serum testosterone were noted in the women injecting testosterone. A significant compensatory decrease in sex hormone-binding globulin and a decrease in thyroid-binding proteins were noted in the women steroid users. [Article does not report a general finding that muscular women have low estrogen; rather, it describes hormonal alterations in female weight lifters specifically using anabolic steroids.]

Accelerated muscle loss, such as that of sarcopenia, has been associated with the menopausal transition and thus linked to declining estrogen levels. There is also some evidence to suggest that hormone therapy (HT), a method of estrogen supplementation, may have beneficial effects on muscle mass in postmenopausal women, although across all studies participants receiving HT lost only 0.06 kg less lean body mass compared with those not receiving HT and this was not statistically significant. Overall, the literature links lower estrogen levels with reduced muscle mass, not with increased or "excessive" muscularity.

Skeletal muscle mass, strength, and regenerative capacity decline with age, with many measures showing a greater deterioration in females around the time estrogen levels decrease at menopause. Estradiol deficiency reduces skeletal muscle mass and force generation in women and female rodents and prevents the recovery of strength following contraction-induced muscle injury. In summary, estradiol is a necessary factor regulating in vivo satellite cell function in female rodents and is supported by similar results in humans, indicating estrogen supports maintenance and recovery of muscle mass.

In human and animals, any reduction in estrogen function leads to a significant increase in visceral adiposity. Surgical ovariectomy or genetic ablation of the estrogen receptor all result in substantial gains in visceral fat mass. Importantly, loss of estrogenic function also contributes to alterations in muscle function that when extrapolated to the human would be predicted to contribute to increased risk of various chronic conditions including sarcopenia, type 2 diabetes, metabolic syndrome and cardiovascular disease.

The athletes demonstrated significantly higher levels of the precursor androgens dehydroepiandrosterone (DHEA) and 5-androstene-3β, 17β-diol (5-DIOL) and the metabolite etiocholanolone glucuronide (Etio-G), significantly lower levels of estrone (p<0.05, respectively), higher bone mineral density (p<0.001) and more lean mass (p<0.001) compared with controls. Serum levels of DHEA, 5-DIOL and Etio-G correlated positively to lean mass variables and physical performance in the athletes. The present data suggest that endogenous androgens are associated with a more anabolic body composition and enhanced performance in women athletes.

Female athletes are therefore at risk of overtraining and/or poor dietary intake, both of which are usually associated with estrogen deficiency and subsequent menstrual disorders. The hormonal profile of these young women engaged in endurance and weight-class sports is characterized by hypoestrogenism linked to dysfunction of the hypothalamic-pituitary-ovarian axis with reduced GnRH pulsatility. Delays in growth and pubertal development are the major consequences, whereas the potential negative effect of reduced estradiol secretion on bone mass acquisition may be partially compensated by the mechanical loading generated by high-impact or weight-bearing exercise.

The results demonstrated reduced intramuscular estradiol, testosterone and dehydroepiandrosterone (DHEA) concentrations after resistance training irrespective of estrogen therapy. Acute exercise had no effect on intramuscular sex hormone levels. Low circulating levels of follicle-stimulating hormone (FSH) and luteinizing hormone (LH) associated with high muscle mass at baseline, and a decline in circulating FSH after the intervention associated with a greater gain in muscle cross-sectional area in response to the resistance training. In conclusion, intramuscular estradiol, testosterone and DHEA were reduced by resistance training and unaffected by changes in circulating estrogen levels induced by estrogen therapy. Serum FSH and LH were superior predictors of muscle mass compared to other circulating and intramuscular sex steroid hormones.

In postmenopausal women, the decline in estrogen levels is associated with a decrease in muscle mass and strength (62). Besides, a review discusses estrogen deficiency can lead to decrements in muscle strength from both inadequate preservation of skeletal muscle mass and decrements in the quality of the remaining skeletal muscle (22). Research findings indicate that postmenopausal women with estrogen deficiency have reduced mitochondrial content in their skeletal muscles, while estrogen replacement therapy can increase mitochondrial content (16). [This review describes that low estrogen is linked to *lower* muscle mass and strength, not that high muscle mass causes low estrogen.]

The weight of evidence from human and animal studies demonstrates that estrogen based hormone replacement therapy (HRT) will have significant beneficial effects on skeletal muscle mass, strength and protection from damage in older women. Benefits to skeletal muscle may be most evident in younger post-menopausal females and those who initiate HRT proximal to menopause. These findings imply that higher estrogen levels via HRT are associated with better muscle mass and strength, contradicting the idea that more muscle reflects reduced estrogen.

Ovarian estradiol (E2) deficiency was associated with impaired myofiber growth, myofiber regeneration, and extracellular matrix remodeling during muscle recovery from hindlimb unloading. Importantly, impairments in the recovery of skeletal muscle mass from mechanical unloading can be rescued by E2 treatment, pinpointing E2 as the major ovarian hormone impacting muscle mass. Overall, such studies indicate that in females the regulation of skeletal muscle mass following periods of disuse appears to be affected by ovarian hormone status and that ovarian function is important to recover from disuse-induced muscle atrophy.

The preponderance of recent evidence highlights the important effects of estrogen and hormone therapy on maintenance and regeneration of skeletal muscle mass, which has implications for the health of estrogen-deficient and aging females. Estrogen deficiency has been associated with accelerated loss of muscle mass and strength in postmenopausal women, whereas estrogen replacement may help preserve muscle tissue.

In the study by Eklund et al. (5), significantly higher serum levels of dehydroepiandrosterone (DHEA) were measured in 106 Olympic female athletes than in sedentary control subjects. Based on published data on increasing doses of exogenous testosterone in women and on elevated hemoglobin levels due to increased testosterone concentration in women with differences of sex development, it is estimated that the ergogenic advantage for a female athlete with testosterone levels in the male range is >9%. Overall, hyperandrogenism in female athletes is associated with an anabolic profile, increased lean body mass, and performance advantages, rather than directly characterized by low estrogen.

All together, the existing data suggest that acute treatment with estrogen does not improve basal muscle protein synthesis; however, estrogen increases the anabolic response to exercise and this may result in the increase in muscle mass reported in long term studies. Hansen et al. (2012) surprisingly found that myofibrillar protein synthesis decreased with ERT suggesting that ERT inhibits basal skeletal muscle protein synthesis in the postabsorptive state. [Review summarizes that estrogen modulates muscle protein synthesis and exercise response; it does not state that increasing muscle mass lowers estrogen levels in women.]

Thus, results are insufficient to support the deduction that basal rates of muscle protein degradation are elevated with estrogen deficiency. Collectively, evidence that estrogen deficiency causes dysregulation in muscle protein turnover with the balance tipping away from protein synthesis and toward protein degradation and thus contributing to the loss of muscle mass is weak. There is some evidence for reduced responsiveness of muscle protein synthesis to anabolic stimuli when estrogen is low [26]. [This paper discusses how *loss* of estrogen may contribute to *loss* of muscle mass with aging, rather than excessive muscle mass causing reduced estrogen.]

In summary, muscle weakness ensues with age and in women tends to become more pronounced when the production of estrogens and progesterone declines at menopause. Additional analyses showed that the quantity of muscle was not affected by estradiol status but that the intrinsic quality of muscle was altered. The collective results support the contention that estradiol is beneficial to muscle strength, improving intrinsic muscle quality rather than causing a reduction in estrogen when muscle mass is high.

Accelerated muscle loss, such as that of sarcopenia, has been associated with the menopausal transition and thus linked to declining estrogen levels. Therefore, hormone therapy has been suggested as a potential intervention. In this systematic review and meta-analysis of 12 studies comprising 4474 postmenopausal women, those who received estrogen-based hormone therapy lost less lean body mass compared with women who received no hormone therapy and women who received placebo, but this finding was not statistically significant.

In the absence of high-quality evidence to indicate that cyclical hormonal fluctuations substantially influence acute strength performance or RET-induced muscular adaptations, it is, in our view, premature to assume that it is essential to control for the menstrual cycle phase in which women are tested. Current evidence shows no influence of women’s menstrual cycle phase on retail-induced muscular adaptations. [Authors conclude that across available studies, menstrual estrogen fluctuations do not meaningfully alter strength or hypertrophy adaptations, which argues against a simple direct link between estrogen level and muscle gain.]

In competitive athletes, the benefits of normal cycling can be seen by contrasting them with those athletes who experience relative energy deficiency in sport (RED-S), formerly known as the female athlete triad. With a chronic energy deficiency, women stop normal cycling, and estrogen levels drop to very low levels, resulting in amenorrhea, loss of bone mass, and increased risk of musculoskeletal injury. Thus, low estrogen in female athletes is primarily linked to relative energy deficiency and menstrual dysfunction, not simply to high muscle mass per se.

Circulating levels of testosterone, dehydroepiandrosterone, dehydroepiandrosterone sulphate, estradiol, growth hormone and cortisol have been shown to increase in response to an acute bout of endurance exercise in women. With the notable exception of growth hormone, the anabolic hormones reviewed here appear to decline with endurance training. [The study shows complex changes in sex steroids with training; it does not report that women who develop high muscle mass have chronically reduced estrogen compared to less muscular women.]

Twelve weeks of aerobic and anaerobic exercise program based on ACSM protocol has beneficial effect on estradiol level and lean mass, whereas it is inversely correlated with fat mass of postmenopausal osteoporotic female. Our results suggest that exercise intervention based on aerobic and anaerobic exercise does improve the level of circulating estrogen in overweight postmenopausal osteoporotic women. The findings indicate that despite decreasing fat mass, physical exercises increase the estradiol level significantly when a 12-week exercise protocol is incorporated, showing that higher lean mass with training can coincide with higher estrogen levels.

Circulating levels of testosterone, dehydroepiandrosterone, dehydroepiandrosterone sulphate, estradiol, growth hormone and cortisol have been shown to increase in response to an acute bout of endurance exercise in women. With the notable exception of growth hormone, the anabolic hormones reviewed here appear to decline with endurance training. [Original study elaborates on hormone changes with endurance vs resistance exercise in women; it does not claim that ‘excessive muscle mass’ in women is associated with reduced estrogen levels.]

High estrogen levels may increase muscle mass and strength, while at the same time the mechanical properties of tendons and ligaments may be compromised. This editorial summarizes evidence that female hormones, particularly estrogens, modulate musculoskeletal adaptation, with estradiol generally exerting anabolic effects on muscle tissue. It does not report that high muscle mass in women is associated with reduced estrogen; instead it emphasizes estrogen’s positive role in muscle.

The lean mass decline lines up with estrogen dropping — the timing overlaps. But replacing estrogen through HRT does not reverse it. And changing estrogen through the pill does not affect muscle growth either. Across 32 studies, estrogen was not directly associated with muscle mass or function in postmenopausal women. Supplementing estrogen through HRT preserved 0.06 kilograms of lean mass across 4,474 women — the weight of one egg. [This synthesis of 78 studies concludes that estrogen level is only weakly and indirectly related to muscle mass, and does not present evidence that high muscle mass in women causes low estrogen.]

Total lean mass and leg lean mass were significantly correlated with free, but not total, testosterone; arm lean mass was not correlated with either measure of testosterone. Serum estradiol was significantly correlated with sex hormone-binding globulin and free testosterone. These observations imply that, by reducing the concentration of bioavailable testosterone, oral estrogen therapy may accelerate or augment lean mass loss among postmenopausal women.

We therefore measured in 21 non-menstruating contraceptive (NMC) anaerobically trained female athletes: 12 highly trained (HT) and nine recreationally trained (RT) during low estradiol and high estradiol phases. While no group difference was detected in hormone concentrations, HT versus RT subjects presented higher muscle mass and positive affects and lower free androgen index. In conclusion, testosterone and androstenedione were modulated across the menstrual cycle, probably resulting from a variable ovarian contribution, but without inducing any change in the anabolic/catabolic balance, regardless of the physical training level; high anaerobic training may enhance testosterone sensitivity without necessarily lowering estrogen.

Having significantly lower levels of natural testosterone, females may be more susceptible to side effects and toxicity associated with AAS abuse. Its abuse among cis-gender women is uncommon and further research is needed to evaluate its toxicity among this group. [Abstract on anabolic androgenic steroid abuse in cisgender women notes potential endocrine side effects but does not assert that muscularity per se lowers estrogen; the main concern is supraphysiologic androgen exposure.]

In muscle biopsies taken shortly before and after the transition to menopause, numbers of satellite cells correlated strongly with changing serum estradiol levels. The team shows that muscle stem cells start to disappear when estrogen levels decline; these satellite cells require estrogen to function optimally in females. This research links declining estrogen with reduced muscle repair and maintenance capacity, supporting the view that lower estrogen is associated with muscle loss rather than with increased muscle mass.

Estrogen deficiency accelerates age-related sarcopenia via mitochondrial dysfunction. Although there have been conflicting results regarding the effects of exercise training on the skeletal muscle induced by estrogen deficiency, many studies have shown that aerobic and resistance exercise training has positive effects on skeletal muscle mass, strength, and estrogen levels in menopausal women and ovariectomized rodents.

Women who train intensively may produce abnormally low levels of estrogen, which may lead to weakened bones. Regular vigorous exercise is associated with decreased estrogen levels in the blood. In one study, healthy women who began training for a marathon reduced their estrogen levels by over 50%, and amenorrheic/oligomenorrheic athletes have 8–31% lower bone density than normally menstruating athletes, indicating that low estrogen in some highly trained women is linked to energy imbalance and menstrual disturbances rather than to muscle mass alone.

Still, there is some evidence to suggest that at least slightly elevated estrogen levels are necessary for maximizing all of these benefits. Although science has yet to reveal the amount of estrogen required to maximize muscle hypertrophy, bodybuilders should be cautioned against the over-suppression of estrogen, as the evidence suggests that the current trend of maintaining estrogen levels within the low-normal range is unlikely to provide full muscle building benefits. [Article aimed at bodybuilders argues that excessively *low* estrogen may impair muscle-related benefits, implying that reduced estrogen is not a typical or desirable consequence of muscle gain.]

The study did not record significant differences in estrogen and testosterone levels between the two groups. This indicates a biological similarity in hormonal balance among female athletes in high-impact sports, regardless of the type of sport. Despite differences in training load and physical demands, female athletes showed comparable sex hormone levels, suggesting that high-impact or strength-focused sports do not inherently cause reduced estrogen.

Across the literature, estrogen is generally described as an anabolic hormone in women, supporting muscle protein synthesis, satellite cell activation, and protection against muscle damage. Conditions with low estrogen, such as menopause or hypothalamic amenorrhea in athletes, are associated with decreased muscle mass and impaired recovery. There is no established consensus that women with high muscle mass have reduced estrogen; instead, low estrogen is typically linked to energy deficiency, menstrual dysfunction, or aging, while normal-to-high estrogen supports muscle development.