The effects of testosterone in humans and other vertebrates occur by way of two main mechanisms: by activation of the androgen receptor (directly or as DHT), and by conversion to estradiol and activation of certain estrogen receptors. Free testosterone (T) is transported into the cytoplasm of target tissue cells, where it can bind to the androgen receptor, or can be reduced to 5α-dihydrotestosterone (DHT) by the cytoplasmic enzyme 5α-reductase. DHT binds to the same androgen receptor even more strongly than T, so that its androgenic potency is about times that of T. The T-receptor or DHT-receptor complex undergoes a structural change that allows it to move into the cell nucleus and bind directly to specific nucleotide sequences of the chromosomal DNA. The areas of binding are called hormone response elements (HREs), and influence transcriptional activity of certain genes, producing the androgen effects.
Due to stimulation of the Androgen Receptors (either directly or as DHT ), accelerated muscle gain, fat loss, increased muscle repair and growth was experienced (5),(6). Testosterone binds to the . on fat cells; therefore, adipose (fat) tissue can be broken down more readily while new fat formation is prevented (7). Since the body is building muscle at an accelerated rate, more ingested food is shuttled directly to the muscle tissue (this is known as nutrient portioning) and away from fat. This is another indirect effect of testosterone on fat loss. Testosterone also promotes glycogen synthesis, which is activated by insulin in response to high glucose levels (8). Glycogen provides fuel to the muscle; therefore endurance and strength increases were reported during severe muscle breakdown in intense training and workouts.