This is thought to be because very high local levels of testosterone in the testes (concentrations in the seminiferous tubules are 20- to 100-fold greater than circulating levels) are required to mediate spermatogenesis, and exogenous testosterone therapy (which is administered systemically) cannot achieve these required high local concentrations (at least not without extremely supraphysiological dosages). Moreover, exogenous androgen therapy can actually impair or abolish male fertility by suppressing gonadotropin secretion from the pituitary gland, as seen in users of androgens/anabolic steroids (who often have partially or completely suppressed sperm production). This is because suppression of gonadotropin levels results in decreased testicular androgen production (causing diminished local concentrations in the testes) and because FSH is independently critical for spermatogenesis. In contrast to FSH, LH has little role in male fertility outside of inducing gonadal testosterone production.Estrogen, at some concentration, has been found to be essential for male fertility/spermatogenesis. However, estrogen levels that are too high can impair male fertility by suppressing gonadotropin secretion and thereby diminishing intratesticular androgen levels. As such, clomiphene citrate (an antiestrogen) and aromatase inhibitors such as testolactone or anastrozole have shown effectiveness in benefiting spermatogenesis.Low-dose estrogen and testosterone combination therapy may improve sperm count and motility in some men, including in men with severe oligospermia. Research
Researchers at Münster University developed in vitro culture conditions using a three-dimensional agar culture system which induces mouse testicular germ cells to reach the final stages of spermatogenesis, including spermatozoa generation.
The sample should never be obtained through coitus interruptus for several reasons:

Some part of ejaculation could be lost. Bacterial contamination could happen. The acid vaginal pH could be deleterious for sperm motility.Also is very important to label the sample correctly the recipient with patient identification, date, hour, abstinence days, among other data required to be known. The volume of the semen sample (must be more than 1.5 ml), approximate number of total sperm cells, sperm motility/forward progression, and % of sperm with normal morphology are measured. It is possible to have hyperspermia (high volume more than 6 ml) or Hypospermia (low volume less than 0.5 ml). This is the most common type of fertility testing. Semen deficiencies are often labeled as follows:

Oligospermia or oligozoospermia – decreased number of spermatozoa in semen
Aspermia – complete lack of semen
Hypospermia – reduced seminal volume
Azoospermia – absence of sperm cells in semen
Teratospermia – increase in sperm with abnormal morphology
Asthenozoospermia – reduced sperm motility
Necrozoospermia – all sperm in the ejaculate are dead
Leucospermia – a high level of white blood cells in semen
Normozoospermia or normospermia – It is a result of semen analysis that shows normal values of all ejaculate parameters by WHO but still there are chances of being infertile. This is also called as unexplained InfertilityThere are various combinations of these as well, e.g. Teratoasthenozoospermia, which is reduced sperm morphology and motility. Low sperm counts are often associated with decreased sperm motility and increased abnormal morphology, thus the terms "oligoasthenoteratozoospermia" or "oligospermia" can be used as a catch-all.