A common concern for men considering Testosterone Replacement Therapy (TRT) is whether testosterone injections will cause their testicles to shrink. Testosterone injections introduce external (exogenous) testosterone into the body to treat low levels. The introduction of this external hormone triggers a natural biological response that often leads to a reduction in testicular size. Understanding this mechanism is important for anyone beginning this form of treatment.
The Direct Answer: Why Testicular Size Changes
Testosterone injections frequently lead to a reduction in testicular size, medically known as testicular atrophy. This is a predictable physiological consequence of receiving external testosterone, not a defect in the therapy. The testicles have two primary functions: producing testosterone and producing sperm. When the body receives the hormone via injection, the testicles receive a signal that their job is largely complete.
The shrinkage occurs because the testicles suspend their normal functions, specifically their own hormone production. This suspension decreases the volume of tissue that makes up the testes. For most men, this reduction is typically a 15% to 25% decrease in volume after several months of continuous therapy. The effect is generally reversible if the external testosterone is stopped, allowing the body’s natural signaling processes to resume.
The Underlying Biological Mechanism
The reason for testicular atrophy lies in the body’s hormonal regulation system, known as the Hypothalamic-Pituitary-Testicular (HPT) Axis. This axis involves a three-way communication network between the hypothalamus, the pituitary gland, and the testicles. The entire system operates on a mechanism called a negative feedback loop, which maintains hormone levels within a narrow range.
When the testicles produce adequate testosterone, the high concentration is sensed by the hypothalamus and the pituitary gland. This signals the brain to slow down the production of two messenger hormones: Luteinizing Hormone (LH) and Follicle-Stimulating Hormone (FSH). These hormones are collectively known as gonadotropins, and they are the primary signals that stimulate the testicles to function.
Introducing exogenous testosterone via injection raises the overall hormone level in the bloodstream, strongly activating this negative feedback loop. The brain detects the high concentration and drastically reduces the release of LH and FSH. Without the signal from LH, the Leydig cells stop producing testosterone. Without the signal from FSH, the Sertoli cells stop supporting sperm production. The lack of these gonadotropin signals causes the testicles to decrease in size, similar to how an unused muscle atrophies.
Impact on Fertility and Sperm Production
The suppression of the HPT axis impacts male fertility beyond the physical size of the testicles. The primary fertility concern is the cessation of sperm production, or spermatogenesis. Follicle-Stimulating Hormone (FSH) is the hormone primarily responsible for driving sperm production within the testes.
Since external testosterone suppresses the release of FSH, spermatogenesis is severely impaired or halted. Testosterone injections can be so effective at suppressing sperm production that this mechanism has been studied as a potential form of male contraception. Men undergoing TRT should be aware that they will likely experience a significant reduction in sperm count, often leading to temporary infertility.
The duration of this infertility varies widely among individuals, but it is typically reversible upon discontinuation of TRT. However, men who use the injections for an extended period, or those who are older, may experience a slower recovery of their sperm count. For men who wish to preserve their ability to father children while on TRT, fertility preservation strategies must be discussed with a healthcare provider before beginning treatment.
Strategies for Prevention and Reversal
Medical protocols exist to counteract the suppressive effect of exogenous testosterone and preserve fertility. These strategies involve introducing compounds that mimic or replace the signaling hormones the brain has stopped producing. The most common medication used for this purpose is Human Chorionic Gonadotropin (hCG).
HCG acts as a substitute for Luteinizing Hormone (LH), directly stimulating the Leydig cells in the testes. By mimicking the LH signal, hCG prompts the testicles to continue producing intratesticular testosterone. This helps maintain testicular volume and supports spermatogenesis. HCG is often administered concurrently with testosterone injections to prevent atrophy and maintain function from the outset.
Another class of medications sometimes used are Selective Estrogen Receptor Modulators (SERMs), such as clomiphene citrate. SERMs block estrogen receptors in the hypothalamus, which stimulates the body’s natural production of LH and FSH. These strategies require careful medical supervision to balance the benefits of TRT with the goal of maintaining testicular health and function.