Although steroids and training are a bit outside of the lab's research interests, they appear to be a topic of great general interest. We've put together these few pages to serve that interest and hopefully provide some objective information and a starting point for your own investigation (meaning we probably won't answer steroid questions).

Structure

All anabolic steroids are chemical derivatives of the male sex hormone, testosterone. Due to testosterone's short biological half-life, pharmacological use requires the steroid be modified to slow metabolism by the liver. Typically, oral steroids are modified primarily by alkylation (replacing an H with a CH₃ group), while injectable steroids are modified by esterification of the hydroxyl group.

Function

Anabolic steroids work by binding with the cytoplasmic (free within the cell) androgen receptor. Like all steroids, the steroid-receptor complex has a strong affinity for the nucleus. The complex is translocated into the nucleus and binds to DNA. It is also possible that the steroid and receptor dissociate in the nucleus and act on DNA separately. The rate limiting factor in this process appears to be the cytoplasmic concentration of the receptor, rather than the concentration of the steroid or translocation of the complex. Testosterone also appears to inhibit the catabolic (protein degrading) pathway associated with glucocorticoids, but it is unclear whether this is related to an interaction between testosterone and glucocorticoid or the nuclear behavior of the steroid-receptor complex.

Once in the nucleus, the steroid appears to enhance transcription of specific genes. The resulting mRNA is processed and sent out of the nucleus, resulting in increased protein synthesis.

Catabolic inhibition may also occur in the nucleus if the complex inhibits the transcription of catabolic enzymes.

The presence of the androgen receptor indicates a tissue is androgen sensitive, and it's concentration gives an indication of how sensitive. The receptor is present in a number of organs, including skeletal muscle. Skeletal muscle typically contains 0.5-3 femto (1E-12) moles per milligram of protein, while other androgen sensitive organs, like the prostate gland, may have up to 25 times more receptors.

A final observation about feedback in biological systems: in a perfect example of biological control, a byproduct of testosterone metabolism is estradiol, which enhances catabolism. Thus, overadministration of testosterone-analog steroids can feed-back and minimize results.

Effects

Testosterone's effects are generally broken into two classes: anabolic and androgenic. Both appear to result from the same signalling pathway as there are no proteins with anabolic effects independent of androgenic effects.

References

These should provide a good beginning for a more detailed investigation of anabolic steroid behavior. If you are considering them as part of a training program, please consult a physician.

• Hickson, R.C. and Kurowski, T.G. (1986) Anabolic steroids and training. Clinics in Sports Medicine 5(3):461-469.
• Alén, M. and Komi, P.V. (1984) Changes in neuromuscular performance and muscle fiber characteristics of elite power athletes self-administering androgenin and anabolic steroids. Acta Physiologica Scandanavia 122:535-544.
• Wilson, J.D. and Griffin, J.E. (1980) The use and misuse of androgens. Metabolism 29(12):1278-1295.
• Martinez J.A., Buttery, P.J. and Pearson, J.T. (1984) The mode of action of anabolic agents: the effect of testosterone on muscle protein metabolism in the female rat. British Journal of Nutrition 52:515-521.
• Yesalis C.E. and Bahrke M.S. (1995) Anabolic-androgenic steroids: current issues. Sports Medicine 19(5):326-40.