"In addition to the ovaries, steroidogenic enzymes are present in skeletal muscle, enabling the local synthesis of myogenic estrogen." "Myogenic estrogen can regulate muscle function and metabolism in an autocrine or paracrine manner within skeletal muscle tissue." "Exercise, as a safe and effective non-pharmacological intervention, has been shown to regulate estrogen levels in skeletal muscle." The review describes local synthesis and metabolism of estrogen within skeletal muscle, not systemic estrogen clearance by muscle mass.

The main source of circulating estrogens in postmenopausal women are derived from androgen aromatization in the peripheral tissues such as notably adipose tissue (Feigelson et al., 2004). A decline in estrogen levels in menopausal women is associated with the loss of muscle mass and function; therefore, it has been suggested that menopause can accelerate sarcopenia (Messier et al., 2011).

In postmenopausal women, estrogens are formed mainly in adipose tissue from the aromatization of androstenedione to estrone. The amount of adipose tissue and the activity of aromatase within it are therefore important determinants of circulating estrogen levels in postmenopausal women.

The main source of circulating estrogens in postmenopausal women is the aromatization of androgens in peripheral tissues, especially adipose tissue. Higher amounts of adipose tissue are associated with higher circulating estrogen levels in postmenopausal women. Lean tissue (including muscle) contributes far less to systemic estrogen production than adipose tissue.

In young women the role of estrogen on muscle anabolism is still uncertain; however, it is clear that OCs with high progesterone have a negative impact on muscle. Importantly, serum estrogen levels were 5-fold higher in the twins on HRT, regardless of whether the product the women were taking contained only estrogen or estrogen and progesterone together (Ronkainen et al., 2009). Together, these data suggest that HRT is beneficial for postmenopausal muscle mass and function, but that HRT together with exercise improves muscle mass and function more than either HRT or exercise alone.

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. Overall, HT users lost 0.06 kg (−0.05 to 0.18) less lean body mass compared with participants not receiving HT. This finding was not statistically significant and is unlikely to be clinically relevant for the average postmenopausal woman.

Some studies suggest a beneficial effect of estrogen therapy on muscle size and strength, but evidence is largely conflicting and inconclusive. Overall, current evidence does not support a strong or consistent effect of estrogen therapy on skeletal muscle size in women, although estrogen may modulate muscle quality and function.

Evidence is accumulating that estrogen deficiency induces apoptosis in skeletal muscle contributing to loss of mass and thus strength. Current evidence indicates that estrogens have a role in maintaining muscle mass. These data, based on sex differences, suggest that estrogen may be protective against skeletal muscle apoptosis in women.

"As estrogen may be involved in muscle metabolism, it has been suggested that estrogen-based HT has potential benefits on muscle mass." "Although use of hormone therapy (HT) can have some protective effect on muscle mass in postmenopausal women, the benefit is small in the general population and likely does not outweigh the potential risks of prolonged HT." The meta-analysis evaluates how estrogen-based hormone therapy affects lean body mass; it does not report that greater muscle mass in turn increases estrogen clearance or elimination.

Estrogens are metabolized mainly in the liver through hydroxylation and conjugation, leading to metabolites that are excreted in urine and bile. Enterohepatic recirculation of estrogens involves biliary excretion into the intestine, deconjugation by gut bacteria, and reabsorption, constituting a major route of estrogen clearance. The review highlights hepatic enzymes and intestinal processes as central to estrogen elimination; skeletal muscle mass is not listed among primary determinants of estrogen metabolism or excretion.

"In addition to the ovaries, steroidogenic enzymes are present in skeletal muscle, enabling the local synthesis of myogenic estrogen." "Exercise may promote the synthesis of myogenic estrogen by enhancing the expression of estrogen precursor substances and steroidogenic enzymes in skeletal muscle, thereby improving skeletal muscle function and metabolism." This summary reiterates that skeletal muscle can **synthesize and metabolize estrogen locally**, and that exercise affects **local estrogen levels**, rather than describing systemic estrogen clearance linked to total muscle mass.

Body composition, particularly adipose tissue, is closely linked to circulating estrogen levels. Adipose tissue is an active endocrine organ expressing aromatase, which converts androgens to estrogens. Higher levels of body fat are associated with higher levels of estrogens, especially in postmenopausal women, whereas weight loss and reduced adiposity lower estrogen levels.

Regular physical activity helps regulate hormone levels, including estrogen, through several mechanisms. One key mechanism is **reduction of body fat**, as excessive adipose tissue can both produce and store estrogen. Physical activity also improves metabolism and supports liver function, which is essential for breaking down and excreting excess estrogen. The article recommends combining aerobic exercise with strength training but describes exercise effects in terms of fat reduction and liver support, not in terms of muscle mass directly enhancing estrogen elimination.

"In addition to its potential role as an antioxidant, estrogen may also protect muscle from secondary damage through its influence on various regulators of muscle catabolism and apoptosis." "Taken together, the data suggest that some of the protective potential of estrogen on skeletal muscle from injury may be due to its membrane-stabilizing properties." This older review discusses how estrogen affects skeletal muscle damage, repair and catabolism; it does not indicate that having more muscle mass facilitates systemic estrogen elimination.

"Aging is associated with a decline in sex hormone production. Therefore, elucidating the effects of sex hormone substitution on skeletal muscle homeostasis and regeneration in older individuals is imperative." The article (overview) highlights how sex hormones, including estrogen, regulate skeletal muscle homeostasis and regeneration; it does not describe skeletal muscle mass as a determinant of estrogen elimination or clearance from circulation.

In adipose tissue, aromatase converts androgens into estrogens, contributing to circulating estrogen levels, particularly in postmenopausal women. Obesity is associated with higher estrogen levels because increased adipose mass enhances estrogen production and storage. The review states that weight loss and reduction of fat mass lower circulating estrogen concentrations, thereby reducing risk of estrogen‑dependent cancers; it does not identify increased muscle mass as an independent mechanism for enhancing estrogen clearance, beyond its role in improving body composition and metabolic health.

The studies consistently showed that higher estrogen levels during puberty contribute to increased muscle mass and improved metabolic function. Estrogen appears to support muscle growth and maintenance, but its effects on muscle mass are complex and may differ across the lifespan and hormonal states.

After oral administration, estradiol undergoes extensive first‑pass metabolism in the liver, resulting in estrone and estrone sulfate, which are then excreted renally and via bile. The pharmacokinetic review notes that hepatic metabolism and subsequent renal and biliary excretion are the main routes of estrogen elimination. Body composition parameters such as body weight and fat mass can affect estrogen pharmacokinetics, but the paper does not report skeletal muscle mass as an independent factor facilitating estrogen clearance.

Physical activity is associated with lower circulating estrogen levels in observational studies of women. Mechanisms proposed include reduced adipose tissue mass, changes in sex hormone–binding globulin, and alterations in hepatic metabolism. The authors emphasize that exercise‑related reductions in estrogens appear to be mediated largely by decreases in fat mass rather than increases in lean (muscle) mass per se.

In muscle biopsies taken shortly before and after the transition to menopause, numbers of satellite cells correlated strongly with changing serum estradiol levels. The repair and rebuilding of skeletal muscles depends on a specific population of stem cells—called satellite cells—found in muscle tissue, and the researchers show these cells require estrogen to function optimally in females.

Estrogen deficiency leads to a decrease in muscle mass and energy expenditure, aggravating obesity‑related complications in an ovariectomized rat model. The study investigates how a herbal mixture affects lipid metabolism in estrogen‑deficient rats, noting changes in muscle LPL expression and body weight. While the paper links estrogen status to muscle mass and lipid metabolism, it focuses on fat metabolism and does not identify greater muscle mass as enhancing estrogen elimination from the body.