Testosterone replacement therapy (TRT) restores testosterone levels in men diagnosed with low testosterone (hypogonadism) by administering exogenous testosterone. Men often wonder about the effects of TRT on reproductive fluids, specifically ejaculate volume. The common effect of TRT is a reduction in ejaculate volume, which is a direct consequence of how the body regulates hormone production.
Understanding Ejaculate Composition
Ejaculate is a complex fluid composed of secretions from various male reproductive organs; sperm makes up only a small fraction of the total volume. The largest component (50 to 80 percent) comes from the seminal vesicles, which contribute a yellowish, viscous fluid rich in fructose to nourish the sperm. This fluid is alkaline and helps neutralize the acidic environment of the vagina, promoting sperm survival.
The prostate gland contributes the next largest portion (15 to 30 percent). Prostatic fluid is a thin, whitish secretion containing enzymes like prostate-specific antigen (PSA) and citric acid. The smallest contribution comes from the testicles and epididymis, which is the source of spermatozoa (sperm), accounting for only 2 to 5 percent of the total volume. A typical ejaculate volume ranges between 2 to 5 milliliters.
How TRT Affects Ejaculate Volume: The Negative Feedback Loop
The administration of exogenous testosterone in TRT directly influences the body’s natural hormone regulation system, known as the Hypothalamic-Pituitary-Testicular Axis (HPTA). This axis operates via a negative feedback loop, which is the mechanism that ensures hormone levels remain within a tight range. When testosterone levels are high in the bloodstream, the brain signals the pituitary gland to reduce the release of Luteinizing Hormone (LH) and Follicle-Stimulating Hormone (FSH).
Exogenous testosterone tricks the brain into thinking the body is producing sufficient testosterone, leading to the suppression of LH and FSH. LH stimulates the Leydig cells in the testes to produce testosterone, while FSH stimulates the Sertoli cells necessary for supporting sperm development (spermatogenesis). When TRT suppresses LH and FSH, the testes receive fewer signals to perform their functions.
This lack of stimulation causes the testes to significantly reduce or stop sperm production, which can lead to testicular atrophy (shrinkage). Although sperm makes up a small percentage of the total volume, the testes and epididymis also contribute fluid. The suppression of testicular function and subsequent atrophy results in a measurable, though often slight, decrease in the overall ejaculate volume.
The Connection Between Volume Reduction and Fertility
While the physical reduction in ejaculate volume may be noticeable for some men on TRT, the most significant consequence of HPTA suppression is the impact on fertility. Reduced FSH levels and suppressed spermatogenesis mean the ejaculate contains significantly fewer sperm, a condition known as oligospermia, or in many cases, no sperm at all, which is called azoospermia. Studies indicate that a large percentage of men on TRT experience azoospermia within months of starting the therapy.
The ejaculate may not appear dramatically different because the bulk of the fluid comes from the seminal vesicles and prostate, which are generally not as directly affected by HPTA suppression as the testes. However, the reproductive quality of the ejaculate is severely compromised due to the lack of sperm. The effect on sperm production is typically reversible once TRT is discontinued, although the time required for sperm count to return to normal can vary widely, ranging from several months to a year or more.
Strategies for Maintaining Reproductive Function While on TRT
Men who require TRT but wish to preserve reproductive function have several medical strategies available to mitigate the suppression of the HPTA. A common co-treatment involves Human Chorionic Gonadotropin (HCG), a hormone that mimics Luteinizing Hormone (LH). HCG directly stimulates the Leydig cells in the testes, promoting local testosterone production and helping maintain testicular size and function, thereby preserving spermatogenesis.
Low-dose HCG co-administered with TRT maintains sperm parameters and prevents the azoospermia common with testosterone therapy alone. Another approach involves Selective Estrogen Receptor Modulators (SERMs), such as clomiphene citrate. These medications block the negative feedback of estrogen on the pituitary gland, encouraging the release of LH and FSH, which stimulates the testes and promotes sperm production.
In cases where fertility is an immediate goal, a physician may recommend cycling off TRT and using high-dose HCG, sometimes combined with a SERM, to recover sperm production. For men starting TRT who anticipate wanting children in the future, cryopreservation (sperm banking) remains a reliable option to secure reproductive material before treatment begins.