I pin 2 iu daily the first week and could feel something but chalked it up to placebo. Bumped it to 3iu on MWF and 4 on Tuesday/Thursday and that when typical sides kicked in. My hands are already weighing me down but now they are like bricks sometimes. I have slight carpel, but the good outweighs the bad. Skin has improved hair no longer being considered a total loss, nails look prime for biting, and my favorite, the sleep. My sleep is great. Taking addiction meds makes difficult to fall asleep, but that hasn't been case since week 3. I'm in my 6th week now and feel great as the fat starts to come off for my transformation. For GH I am mainly concerned with overall well being than fat loss. I may lower the Tues/Thursday dose to 3iu. I've taken Humatrope throughout my usage, and while this isnt exactly equal, for the money it's my new go to.
The mechanism that caffeine increases activity by is via antagonizing adenosine A2 A receptors (the standard mechanism of caffeine). Adenosine normally suppresses the effects of dopamine on locomotion (via working in opposition on neuronal excitation  ) in the striatum where A2 A and dopaminergic neurons co-exist, and preventing this suppression with an antagonist increases the effects of dopamine on D2, of which include spontaneous activity and (in rats) rotational behaviour when unilateral lesions are induced in the striatum.   Non-caffeine adenosine antagonists also share this effect on locomotion, further implicating A2A antagonism and dopamine as the cause rather than a separate, unseen effect of caffeine.  As for why A2 A is mentioned more frequently than A1 in this section, it is since A2 A receptors appear to co-exist with dopamine receptors in many parts of the brain (nuclear accumbens, striatum, tuberculum olfactorium) whereas although A1 are heterogeneously expressed in the brain, there is no pattern with dopamine receptors.  Interactions with motor control appear to be highly relevant to the striatum, where A2 A predominates.