As alluded to above, one very important thing to acknowledge when using AAS (whether taking one hormone, stacking or cycling) is the risk of harmful side effects. Within a steroid cycle, the users will often stack other non-anabolic hormones into their program to maximize specific cycle objectives for example: the addition of drugs like Clenbuterol and/or Cytomel /T3 augment cutting/definition cycles; others called aromatase inhibitors (estrogen reducing drugs) like Letrozole . Letro and Anastrozole Arimidex are often included to inhibit the conversion of excess testosterone to negatively cycle impacting estrogen and; incorporating post-cycle therapy (PCT) drugs such as the synthetic estrogens Tamoxifen . Nolvadex , or Clomiphene Citrate . Clomid (which act as anti-estrogens in the male body), can be used alone, together, or in conjunction with those like Mesterolone . Proviron and Human Chorionic Gonadotropin ( HCG ) during PCT to bridge the gap between the end of a steroid cycle (synthetic testosterone usage) and the restoration of the bodys natural testosterone production. These drugs too must be researched, and controlled in similar fashion to AAS. Thus, steroid cycles can be as simple or complex as the users individualized goals, cycle histories and levels of understanding. Below are three samples of AAS stacked cycles of varying complexity along with a beginning PCT sample, and an explanation of goal intention & rationale for the selected compounds, dosages & durations. These illustrations and commentaries will provide a better understanding of what stacking and cycling are along with the many nuances they require.
Add more substrate; it will outcompete the inhibitor and increase the reaction rate.
Competitive inhibition can be overcome by adding more substrate to outcompete the inhibitor. Many drugs used to treat different medical conditions, including hypertension, are competitive inhibitors. It is fairly easy to make a molecule that is similar in structure to a particular substrate because the known enzyme’s shape can be used as a model of what the molecule needs to look like. It is more difficult to make a noncompetitive inhibitor because it is less obvious what the noncompetitive inhibitor’s shape and structure should be.