In a synapse , action potentials are conducted along motor nerves to their terminals where they initiate a Ca 2+ influx and the release of acetylcholine (ACh). The ACh diffuses across the synaptic cleft and binds to receptors on the post synaptic membrane, causing an influx of Na + , resulting in depolarization. If large enough, this depolarization results in an action potential. To prevent constant stimulation once the ACh is released, an enzyme called acetylcholinesterase is present in the endplate membrane close to the receptors on the post synaptic membrane, and quickly hydrolyses ACh.

Because the ultimate goal of a steroid cycle is to increase strength and muscle size, the associated spike in estrogen which accompanies steroids such as Testosterone is considered undesirable. In order to disassociate the two effects, two classes of drug are used. Medications such as Nolvadex or Clomid target the estrogen receptors. They make it more difficult for the estrogen to exert it’s influence within the body thus allowing the testosterone to act more freely. The second class is aromatase inhibitors such as Femara. They target the aromatase enzyme itself in order to prevent the production of estrogen in the first place. Sometimes, it’s not always clear which option you should go with or even what the differences are between the two. Lets clear that up a little.