The menopausal transition is associated not only with a decline in estradiol levels, but also with an increased visceral adiposity and decreased bone density, muscle mass, and muscle strength. This muscle dysfunction, caused by decreased proliferation of muscle satellite cells, increased levels of inflammatory markers, and altered levels of sex hormones, exposes women to a raised incidence of sarcopenia.

Our results demonstrated an inverted U-shaped curve relationship between serum E2 levels and ALMI in middle-aged postmenopausal women, suggesting that low serum E2 levels play an important role in the loss of muscle mass in middle-aged postmenopausal women. Overall, this study showed an inverted U-shaped curve relationship between serum E2 levels and ALMI in middle-aged postmenopausal women, suggesting that low serum E2 levels play a crucial role in the loss of muscle mass in middle-aged postmenopausal women.

Cross‐sectionally, serum estradiol (E2) and free estradiol index (FEI) were positively associated with relative appendicular lean mass (ALM) and thigh muscle percentage in females across the lifespan, independent of age. The study highlighted "a positive cross‐sectional association between serum E2 levels (total and FEI) and measures of muscle mass (relative ALM and thigh muscle percentage) in females across the lifespan, independent of age." Additionally, total serum E2 was negatively associated with total body fat percentage and thigh subcutaneous fat, "suggesting a potential role for E2 in maintaining the proportion of muscle mass throughout ageing."

Skeletal muscle weakness occurs with aging and in females this is compounded by the loss of estrogen with ovarian failure. Evidence is accumulating that estrogen deficiency induces apoptosis in skeletal muscle contributing to loss of mass and thus strength. When estrogen is deficient, as occurs with advanced age in females, muscle atrophy ensues and contributes to muscle weakness.

Estrogen levels are not associated with muscle mass or function after the menopause. Overall, postmenopausal females had lower muscle mass and CSA than premenopausal females. However, in postmenopausal females, the association between estrogen status and muscle mass was unclear in ET users and non-users. This suggests that reductions in E2 may influence menopause-induced loss of muscle mass, but that its role may diminish after menopause.

Recent evidence from human and animal studies provides compelling evidence for the role of estrogen based hormone replacement therapy (HRT) in maintaining and enhancing muscle mass and strength and protecting against muscle damage. The weight of evidence from human and animal studies demonstrates that estrogen based 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.

In postmenopausal women, the decline in estrogen levels is associated with a decrease in muscle mass and strength. Studies suggest that there is an accelerated loss of muscle mass associated with the onset of menopause. E2 deficiency is relevant for younger women as well, as it can be a consequence of eating disorders, energy imbalances due to high-load exercise training, chemotherapy, or hysterectomy.

This preprint reports that "serum E2 and FEI were positively associated with relative ALM and thigh muscle percentage in females across the lifespan." It further notes that changes in serum E2 and FEI over a 5-year follow-up were positively associated with changes in absolute ALM, "suggesting females with a larger decline in serum E2 and FEI have a greater decline in muscle mass." These data indicate that lower estrogen is linked to lower muscle mass rather than low muscle mass causing excess estrogen.

In this cross-sectional study of middle-aged postmenopausal women, "There was a positive association between serum E2 level and appendicular lean mass index (ALMI). Compared to individuals in quartile 1 group, those in other quartiles had higher ALMI levels." The authors found "an inverted U-shaped curve relationship between serum E2 level and ALMI" with an inflection point at 85 pg/mL, and concluded: "Our results demonstrated an inverted U-shaped curve relationship between serum E2 levels and ALMI in middle-aged postmenopausal women, suggesting that low serum E2 levels play an important [role] in the loss of muscle mass."

It has been proposed that this greater decline in strength and muscle mass in postmenopausal women is directly due to estrogen deficiency, and this proposal has been supported by data showing that strength was preserved in postmenopausal women who were taking an estrogen-based HT. The preponderance of recent evidence highlights the important effects of estrogen and HT on maintenance and regeneration of skeletal muscle mass, which has implications for the health of estrogen-deficient and aging females.

There is considerable confusion in the literature related to direct estrogen effects on muscle mass and strength, but it can be reasonably concluded that estrogen does influence muscle mass in younger women and loss of estrogen negatively impacts contractile function. These findings strongly suggest that women with low estrogen levels are more susceptible to inactivity-related declines in muscle mass and strength. All of these factors predispose women in a low estrogen state to muscle atrophy, losses in muscle strength, and functional decline.

Our working hypothesis is that estrogens do benefit muscle strength, and that the underlying mechanism involves estrogen receptors to improve muscle quality more so than quantity. 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, instead, that the intrinsic quality of muscle was altered.

Estrogen deficiency is known to reduce the bulk of skeletal muscle and the maximum muscular force in women. These results showed that human satellite cell number fluctuated significantly in relation to variations in the serum estrogen levels. When estrogen levels fell after menopause, the number of muscle satellite cells decreased, suggesting a mechanism for estrogen-related muscle loss.

This review from NIH notes: "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." It adds that "There is a growing body of evidence describing the beneficial effects and mechanisms behind estrogen and HT effects on muscle mass, strength, and related muscle connective tissue" and that these effects "can have important implications for offsetting or delaying age-related loss of muscle mass and function, particularly in postmenopausal women."

Accelerated muscle loss, such as that of sarcopenia, has been associated with the menopausal transition and thus linked to declining estrogen levels. Overall, HT users lost 0.06 kg 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.

In summary, there is considerable confusion in the literature related to direct estrogen effects on muscle mass and strength, but it can be reasonably concluded that estrogen does influence muscle mass in younger women and loss of estrogen negatively impacts contractile function. All of these factors predispose women in a low estrogen state to muscle atrophy, losses in muscle strength, and functional decline. The review discusses that sex steroids like estrogen affect both bone and muscle with aging.

This can result in women spending approximately one-third of their lives in a postmenopausal, E2-deficient state, and studies suggest that there is an accelerated loss of muscle mass associated with the onset of menopause. E2 deficiency is relevant for younger women as well as it can be a consequence of eating disorders, energy imbalances due to high-load exercise training, chemotherapy, or hysterectomy. Overall, such studies indicate that across nonclinical models and in humans, the regulation of skeletal muscle mass in females following periods of disuse appears to be affected by ovarian hormone status and that ovarian function is important to recover from disuse that induces muscle atrophy.

The free fractions of testosterone and progesterone in serum were consistently associated with the regulation of muscle mass, while estrogens may be primarily involved in mediating the muscle contractile function in conjunction with other sex hormones. Highlights: Free testosterone, but not total testosterone, is associated with lean mass but not strength in pre- and post-menopausal females. Progesterone and estrogens may regulate muscle mass and strength, respectively, in females.

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. Estrogen appears to play a role in musculoskeletal performance, including muscle strength and injury risk, particularly in women. The review notes that low estrogen is associated with increased muscle damage and reduced repair capacity.

In a paper published in the journal Cell Reports, the team shows that muscle stem cells start to disappear when estrogen levels decline. 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. In muscle biopsies taken shortly before and after the transition to menopause, numbers of satellite cells correlated strongly with changing serum estradiol levels.

In this randomized trial of resistance training plus transdermal estrogen therapy in postmenopausal women, the authors report that "our findings suggest that adaptations to an anabolic stimulus such as resistance training are amplified when circulating 17β-estradiol is enhanced by [estrogen therapy]." Women receiving transdermal estradiol showed greater gains in skeletal muscle following training compared with controls, indicating that higher estrogen can improve training-induced muscle adaptation. The study does not support a causal pathway where low muscle mass increases estrogen; instead, estrogen availability modifies muscle response.

We hypothesize that decreased estrogen levels lead to the deterioration of skeletal muscle, and exercise training ameliorates estrogen deficiency-induced sarcopenia. Maltais et al. (2009) demonstrated that low levels of estrogen seem to be associated with a decline in muscle mass and strength; however, the conflicting results of these studies make it difficult to confirm this relationship. 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 OVX rodents.

This review of estrogen’s effects on musculoskeletal performance summarizes data on estrogen therapy and muscle: in a cross-sectional analysis, "muscle cross-sectional area (CSA) and grip strength were greater in [estrogen replacement therapy] users than in non-users." The authors state that "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." The paper frames estrogen as modulating muscle proteostasis and adaptation, not muscle mass as a driver of estrogen excess.

This narrative review on estrogen and muscle summarizes: "In postmenopausal women, the decline in estrogen levels is associated with a decrease in muscle mass and strength." It notes that significant correlations have been observed between skeletal muscle mass and several factors, but in one study "no correlation was found with estradiol levels." A cited meta-analysis found that women who received estrogen-based hormone therapy lost less lean body mass than non-users or placebo, though this was not statistically significant. The review concludes that "Estrogen plays a crucial role in preserving muscle mass, particularly through its influence on mitochondrial metabolism and synergistic effects with testosterone on muscle strength," again describing estrogen’s role in maintaining muscle rather than low muscle mass causing excess estrogen.

Women also undergo menopause, during which estrogen levels fall. Research indicates that muscle mass in women is lower in postmenopausal women than in premenopausal women. Lower muscle mass is discussed as a consequence of hormonal changes, not as a cause of excess estrogen.

These are sex hormones that influence muscle tone in women. Estrogen promotes muscle repair and growth, while progesterone can have a mild muscle-relaxing effect. When estrogen levels drop, women may notice a decrease in lean muscle mass and strength, along with an increase in body fat, particularly around the abdomen. Strength training and hormone balance both play roles in maintaining muscle tone.

Higher estrogen levels (such as during the first half of your cycle) often correlate with better muscle performance, while lower levels (like after ovulation or during perimenopause and menopause) can contribute to muscle fatigue and weakness. The article explains that estrogen supports muscle repair and performance, and that reduced estrogen is linked to decreased muscle function, but it does not describe low muscle mass as a driver of excess estrogen levels.

M and that's why when we have lower estrogen levels, we see the degradation or lower amounts of muscle mass over time because estrogen actually plays a huge role in muscle repair, regeneration, and metabolism. So estrogen is essential for maintaining our muscle stem cells which are called satellite cells which are absolutely vital for muscle repair and regeneration after exercise. So having low estrogen means those satellite cells are either diminished in number or not doing as strong of a job. Post-menopausal women often experience a decrease in lean muscle mass and studies have shown that estrogen deficiency contributes to that muscle atrophy and increased fat infiltration in the muscle tissue.