Bloat makes a lot of guys lose sight of the fact that testosterone not only builds muscle, but also burns fat. Guys that are at a higher bodyfat percentage get shafted with regard to bloat from test. From what I understand old school bodybuilders didn't have aromatase inhibitors available like today so the "test is dirty" mentality is understandable for them. If you keep your bodyfat and estrogen in check you shouldn't turn into a water buffalo.
Test is not dirty. Your genetics makes it dirty or not. Any anabolics will increase fat free mass and reduce body fat to some extent depend on the diet. And AI doesn't reduce water retention one bit for me. And I stay around 10-12% 9fold calipers tested year round so I'm not contest lean but I'm not "FAT" either.
This is quoted from patrick arnold blog:
People familiar with the use of anabolic steroids know that water retention and hypertension (high blood pressure) are potential side effects. This is due to the fact that all androgenic hormones have the capacity to cause some sodium retention (and hence water retention) through direct action via androgen receptors in the kidneys.
Furthermore, anabolic steroids that are estrogenic or can convert to estrogens can cause even more sodium retention via additional interaction with renal (kidney) estrogen receptors. So it’s often thought that an anabolic steroids propensity for water retention is related to its potency both as an androgen and as an estrogen (manifested via aromatization to estrogenic metabolites).
Confusion has often arisen however when people have noticed that some steroids – which traditional thinking tells us should not result in extraordinary water retention – end up doing just that. Steroids that should not aromatize to estrogens such as oxymetholone (anadrol) and methyl-1-testosterone are known to result in extreme water retention in some individuals. A recent paper* suggests a heretofore unmentioned explanation for this.
There is an enzyme that is localized primarily in the kidneys whose function is to protect the kidneys from circulating cortisol. The kidneys have receptors called mineralcorticoid receptors (MR’s) which are meant to bind to specific adrenal hormones (called mineralcorticoids) in the body such as aldosterone. The result of this binding is a signal to increase sodium and water retention in the body, while stimulating the excretion of potassium. This is an important mechanism to maintain fluid and electrolyte balance in the body.
A problem exists though in that cortisol can also bind activate these receptors. Cortisol is a widely circulating hormone and serves a multitude of functions throughout the body. However its intended biological functions do not include mineralcorticoid action in the kidneys, so to prevent this from happening the kidneys are rich in the enzyme 11b-hydroxysteroid dehydrogenase 2 (11b-HSD2). This enzyme deactivates cortisol by converting it into cortisone before it can bind to the renal MRs.
Certain substances can block 11b-HSD2, and that can lead to problems. One example is a constituent of black licorice known as glycyrrhetinic acid. This enzyme inhibition potential is precisely why people that consume a lot of black licorice are known to retain water and experience high blood pressure and electrolyte disturbances. Interestingly, legend has it that Genghis Khan had his armies ingest licorice while on the march to prevent thirst and dehydration. Of course Genghis Khan had no idea that 11b-HSD2 inhibition was responsible for these effects, and today many have been similarly unaware that this property might be responsible for some of the salt/water effects of anabolic steroids.