Our other area of focus will be the hypothalamus-pituitary-testicular axis (HPTA). An 8-10 week, 24-7 cycle will almost certainly cause full suppression despite any strategies we might undertake, so it's a mute point in that situation, but with the 2 week mini-cycles that are becoming increasingly popular, it's likely that we can still have significant testicular function when our cycle is stopped.
There are two mechanisms by which negative feedback inhibition of the HPTA occurs, estrogen binding to the estrogen receptors (ER) and androgens binding to the androgen receptors(AR), both of which occur in the hypothalamus. We could prevent binding to the AR by using a receptor antagonist, but it would also antagonize the AR in the muscle, thus defeating the purpose of taking steroids -- unless, that is, significant non-AR mediated anabolism occurs, as has been suggested by some.
Another option here is to be "on" only during the mornings, using either orals or intranasal (or possibly a fast acting topical when/if an effective one becomes available), leaving us with normal systemic androgen levels at night when LH release occurs. This has been found to avoid significant alterations of the HPTA, even with as high as 100mg d-bol/day.
The final option is to decrease estrogen binding in the hypothalamus. This can be accomplished by lowering systemic estrogen with an aromatase inhibitor (and/or choosing anabolics that do not readily convert to estrogen) such as Arimadex, Cytadren, and perhaps high delivered doses of chrysin (whose in vivo potency equals that of Cytadren, but whose oral bioavailabilty is extremely poor, making sufficient delivery by that route basically unattainable for all practical purposes). We can also block access to the ER with an antagonist such as Clomid, Proviron, or Nolvadex (which, unfortunately, also interferes with a couple of enzymes involved in steroid production in the testes, thus canceling out its benefits on the AR, making it inferior to Clomid in that regard). Or, we could use a combination of aromatase inhibition and receptor antagonism. This strategy should prevent negative feedback to some extent, perhaps leaving us with testosterone levels of 400 instead of 200 (again, being rather arbitrary).
We have done all we can during the cycle, and now we have stopped and must do all we can to preserve our gains. If steps have not been taken to reduce estrogen binding in the hypothalamus, that should begin immediately. Clomid is the preferred choice in this area at 50-100mg/day, but an aromatase inhibitor should be just as effective, but its use should begin a few days earlier as it won't do anything for estrogen that's already present. Ideally, both methods should probably be used.
We must also now decide if we want to completely stop cold or use a morning only system in an attempt to maximize anabolism for as long as possible while still allowing HPTA recovery. If we choose the latter, it would probably not be a bad idea to time workouts to occur during this period - both for CNS effects and for anabolic effects. In deciding which is the best choice, the basic questions to be answered are: Does this method even provide significant anabolic benefit?? How much, if any, does it inhibit natural testosterone production?? And most importantly, do the positives of the first outweigh the possible negatives of the second?? My guess based on the available data and anecdotal reports is that is does. I would recommend this strategy for 2-3 weeks. At that point either go off completely or start a new "on" cycle.