Unlike the GnRH agonists, which cause an initial stimulation of the hypothalamic-pituitary-gonadal axis (HPGA), leading to a surge in testosterone levels, and under certain circumstances, a flare-up of the tumour, GnRH antagonists do not cause a surge in testosterone or clinical flare.  Clinical flare is a phenomenon that occurs in patients with advanced disease, which can precipitate a range of clinical symptoms such as bone pain , urethral obstruction, and spinal cord compression . Drug agencies have issued boxed warnings regarding this phenomenon in the prescribing information for GnRH agonists. As testosterone surge does not occur with GnRH antagonists, there is no need for patients to receive an antiandrogen as flare protection during prostate cancer treatment. GnRH agonists also induce an increase in testosterone levels after each reinjection of the drug – a phenomenon that does not occur with GnRH antagonists such as degarelix.
Ecdysterone was tested in another study performed in 1986 by Smetanin. For this research, 117 highly trained speed skaters between the ages of 18 and 28 were tested for work capacity, body weight, lung capacity and VO 2 max. The results speak for themselves: all of the said parameters increased as well as an increase in the O 2 pulse max and an increase in the exhalation of CO 2 . Basically, they received more oxygen to their cells! This equates to decreasing recovery time, maximizing performance, permitting optimal muscle anabolism and maximum fat reduction. It also means the athletes using ecdysterone compared to those on a placebo experienced increased stamina, endurance and energy.