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There's also a 2006 study that showed no effect in humans and a couple from the late 1980s that I can't find but which were described this way in the 2006 study that contradicted the results.   The most often cited scientific study on ecdysterone was published in Scientific Sports Bulletin by Simakin. This study sought to determine the effect of ecdysterone on muscle tissue mass and fat mass, while testing for hormonal changes in the subjects. Seventy-eight highly trained male and female athletes served as subjects in one of three experimental groups: protein, protein and ecdysterone, and placebo. Those consuming just protein, showed only a slight increase in muscle mass for the 10 day period of time, while the placebo group experienced a slight reduction in lean muscle. The addition of ecdysterone in conjunction with protein intake resulted in a 6–7% increase in lean muscle tissue with nearly a 10% reduction in fat. Finally, Gadzhieva and colleagues reported that 3-weeks of Ekdisten, leveton, and Prime Plus (combination of Ekdisten and pure protein) supplementation during training increased skinfold determined muscle mass, decreased fat mass, and increased total work during training. Additionally, Ekdisten and Prime Plus supplementation appeared to promote the greatest gains during training. These studies found that ecdysterone might increase work capacity, decrease fat mass, and increase lean muscle mass.

Yes. Second study in the first post is n=46 human clinical trial.  

Any evidence in humans? I am going to look around as this is interesting. 

Mol Nutr Food Res. 2014 Sep;58(9):1861-72. doi: 10.1002/mnfr.201300806. Epub 2014 Jun 27. Estrogen receptor beta is involved in skeletal muscle hypertrophy induced by the phytoecdysteroid ecdysterone Maria Kristina Parr 1, Piwen Zhao, Oliver Haupt, Sandrine Tchoukouegno Ngueu, Jonas Hengevoss, Karl Heinrich Fritzemeier, Marion Piechotta, Nils Schlörer, Peter Muhn, Wen-Ya Zheng, Ming-Yong Xie, Patrick Diel PMID: 24974955 DOI: 10.1002/mnfr.201300806   Abstract Scope: The phytoectysteroid ecdysterone (Ecdy) was reported to stimulate protein synthesis and enhance physical performance. The aim of this study was to investigate underlying molecular mechanisms particularly the role of ER beta (ERβ).   Results: In male rats, Ecdy treatment increased muscle fiber size, serum IGF-1 increased, and corticosteron and 17β-estradiol (E2) decreased. In differentiated C2C12 myoblastoma cells, treatment with Ecdy, dihydrotestosterone, IGF-1 but also E2 results in hypertrophy. Hypertrophy induced by E2 and Ecdy could be antagonized with an antiestrogen but not by an antiandrogen. In HEK293 cells transfected with ER alpha (ERα) or ERβ, Ecdy treatment transactivated a reporter gene. To elucidate the role of ERβ in Ecdy-mediated muscle hypertrophy, C2C12 myotubes were treated with ERα (ALPHA) and ERβ (BETA) selective ligands. Ecdy and BETA treatment but not ALPHA induced hypertrophy. The effect of Ecdy, E2, and BETA could be antagonized by an ERβ-selective antagonist (ANTIBETA). In summary, our results indicate that ERβ is involved in the mediation of the anabolic activity of the Ecdy.   Conclusion: These findings provide new therapeutic perspectives for the treatment of muscle injuries, sarcopenia, and cachectic disease, but also imply that such a substance could be abused for doping purposes.   Keywords: Dietary supplement; Ecdysterone; Estrogen receptor beta; Skeletal muscle; Traditional Chinese medicine.       Related study, not on ecdy specifically     FASEB J. 2012 May;26(5):1909-20. doi: 10.1096/fj.11-194779. Epub 2012 Jan 25. Selective estrogen receptor-β activation stimulates skeletal muscle growth and regeneration Martina Velders 1, Burkhardt Schleipen, Karl H Fritzemeier, Oliver Zierau, Patrick Diel Affiliations expand PMID: 22278942 DOI: 10.1096/fj.11-194779 There is increasing evidence suggesting that estrogens augment skeletal muscle regeneration processes after injury. To study the contribution of estrogen receptors α and β (ERα and ERβ) during muscle regeneration, skeletal muscles of ovariectomized (OVX) rats, as well as ERα- and ERβ-knockout (αErko and βErko) mice, were injured with a myotoxin (notexin). OVX rats were simultaneously treated with the ER-selective ligands genistein, ERα agonist 16α-LE2 (alpha), ERβ agonist 8β-VE2 (beta), or 17β-estradiol (E(2)). OVX rats showed significantly elevated serum creatine kinase (CK) activity after muscle injury compared to intact sham-treated animals. Treatment with ER ligands significantly reduced CK activity. TNF-α, IL-10, and MCP-1 expression served to characterize immune responses. Treatment with all ER ligands, but particularly E(2) and beta, reduced TNF-α, but elevated MCP-1 and IL-10 expression. PCNA and MyoD expression served to define satellite cell activation and proliferation and were found to be up-regulated by beta and E(2). To further study muscle regeneration responses, expression of the embryonic myosin heavy chain (MHC) was analyzed. Beta and E(2) but not alpha increased embryonic MHC expression compared to OVX. The absence of ERβ in βErko mice negatively affected CK activity levels and expression of satellite cell and muscle regeneration markers (MHC embryonic, MyoD, Pax7) compared with αErko and wild-type mice. In a classic Hershberger assay using male rats, beta stimulated muscle growth, accompanied by a strong induction of IGF-1 expression. Our data provide evidence that ERβ signaling is involved in the regulation of skeletal muscle growth and regeneration by stimulating anabolic pathways, activating satellite cells and modulating immune responses.

So I have added a couple of sets of DB snatch to my other workouts....really gets the blood pumping.   I started ecdysterone about 10 days ago and feel like my strength has taken an unexpected positive jump....maybe related?