Estradiol is known to attenuate the rate of inflammatory processes following damaging exercise (also seen in ischemia/reperfusion) 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 with similar effects in male rats and is thought to explain the higher than average rates of sarcopenia observed in menopausal women relative to premenopausal women which is alleviated with hormone replacement therapy. This anti-inflammatory response does not appear to be mediated by either estrogen receptor.
Treatment of male and female rats with estradiol results in increased muscle cell recruitment following damaging exercise by an estrogen receptor dependent mean and particularly satellite cell recruitment is mediated through the alpha subset (ERα).
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; Activation of ERβ appears to enhance IGF-1 related anabolic pathways.
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