Skeletal Muscle and Hypertrophy
Mechanisms
Both the alpha subset (ERα) and beta subset (ERβ) of the estrogen receptor are present in the skeletal muscle tissue of rats[1][2] and humans[3][4][5] of both sexes.
Estradiol is known to attenuate the rate of inflammatory processes following damaging exercise[6] (also seen in ischemia/reperfusion[7]) by reducing neutrophil accumulation, which is thought to explain the reduce rates of muscle tissue regeneration in ovarectomized rats (model of menopause) relative to those given estrogen[8][9] with similar effects in male rats[10] and is thought to explain the higher than average rates of sarcopenia observed in menopausal women relative to premenopausal women[11] which is alleviated with hormone replacement therapy.[12] This anti-inflammatory response does not appear to be mediated by either estrogen receptor.[13]
Treatment of male[14] and female[15] rats with estradiol results in increased muscle cell recruitment following damaging exercise by an estrogen receptor dependent mean[13] and particularly satellite cell recruitment is mediated through the alpha subset (ERα).[16]
Selective activation of the β subset (ERβ) results in muscle protein synthesis, as ablation of the receptor exacerbates damage from exercise while treatment with agonists causes satellite cell activation and proliferation;[17] Activation of ERβ appears to enhance IGF-1 related anabolic pathways.[17]
Both estrogen receptors and injections of estrogen (to reach a higher circulating level) are associated with increased recovery rates of skeletal muscle secondary to anti-inflammatory effects and increased satellite cell activation
