HCG -can- increase the speed in which you recover from a cycle, but your hypothalamic-pituitary-testicular axis is still the boss.
Keeping your testicles at their normal size simply means that when the cycle is finished and the pituitary starts secreting LH again, your testicles have enough functional tissue to output the desired amount of testosterone. If your testicles have atrophied from lack of stimulation, when they begin receiving the message for T output, they do their best but must first grow larger to meet demands.
None of this matters if your HPTT axis is shutdown. It must decide if it wants to revert back to making equivocal levels of LH and therefore testosterone once the cycle is finished. This is where traditional PCT with tamoxifen and clomiphene citrate come into play, by blocking the ability of estrogen to exert its effect on the pituitary estrogen receptor, the homeostatic mechanisms of the body encourage LH secretion to raise the levels of estrogen (since the axis has been tricked into thinking there is less circulating than there actually is).
HCG does not solve the problem of HPTT shutdown. In fact, HCG contributes to shutting down the HPTT axis as it serves to raise testosterone independent of pituitary-derived LH, albeit not as severely as a respectable dose of exogenous testosterone does.