The second problem is the clearly more relevant and probably the more decisive factor for the potentially considerable performance loss of the athletes. As we know, steroids have a highly anticatabolic effect by reducing the catabolic effect of the body's own hormone, cortisone. When taking steroids, the steroid molecules block the cortisone receptors so that the cortisone produced by the adrenal gland cannot attach to the receptors, thus remaining for the most part deactivated. The body reacts by producing additional cortisone receptors so that, in the meantime, the unusually high amount of cortisone receptors in the blood can finally do their job. This again is not very serious as long as the athlete continues to take the steroids as planned. However, when the steroid regime is terminated the cortisone receptors are suddenly freed and the large quantity of free cortisone molecules in the blood now know exactly what to do. They rush to the cortisone receptors to form a molecule/receptor complex and transmit to the muscle cell the following message which is so unpleasant for the athlete: break down amino acids. These leave the muscle cell and enter the blood where they are transformed into glucose or blood sugar. The consequence of this process has already been described in another chapter. The athlete's second problem, in addition to increasing the endogenous testosterone production, is to lower the cortisone level to an acceptable level. As the reader knows, this goal is achievable to a high extent. In the following we will describe a sensible, step-by-step approach to interrupt the steroid regime, and the time after. Particular attention will be paid to the two problematic factors described in detail. We want to, however, explicitly emphasize that this information is no guarantee to protect the athlete from a loss of performance.