The Impact of Male Diseases on Sperm Motility: Exploring Factors and Potential Solutions

The decrease in male sperm motility is a significant concern for many men, as it can profoundly influence their future health and reproductive potential. Numerous factors contribute to the decline in sperm motility among males, including underlying male diseases, individuals with otherwise healthy lifestyles, those residing in unfavorable environments, and those grappling with high levels of occupational stress.

Primarily, the presence of acute and chronic inflammation within the reproductive tracts or glands, such as the epididymis, vas deferens, seminal vesicle, and prostate, has the capacity to adversely impact sperm motility. Orchitis, an inflammatory condition affecting the testicles, warrants special attention. Given the testicles' pivotal role in androgen secretion and sperm production, inflammation in this crucial organ can indeed compromise sperm quality. Particularly concerning is orchitis caused by viral infections, which can exert a pronounced influence on testicular spermatogenic function.

In cases where orchitis stems from mumps virus infection, the consequences can be even more dire, leading to testicular atrophy, diminished spermatogenic function, or even spermatogenic dysfunction when left untreated, ultimately culminating in male infertility.

The epididymis, a reservoir for sperm storage, is another noteworthy element in this context. Inflammation of the epididymis can result in the accumulation of inflammatory exudate or purulent secretion, contributing to protein denaturation in sperm. This, in turn, compromises sperm activity, potentially leading to sperm incapacitation and a decline in sperm quality.

Seminal vesiculitis, a condition marked by inflammation of the seminal vesicles, can also exert a discernible impact on sperm mobility. Microbial infection-induced seminal vesiculitis can alter sperm composition, leading to bacterial mingling with seminal plasma. Bacteria's nutrient consumption and waste production within seminal plasma subsequently culminate in sperm viability reduction.

Additionally, seminal vesiculitis can disrupt the pH balance of seminal plasma, augmenting its acidity and thereby negatively influencing sperm motility. This condition also impairs sperm liquefaction, further contributing to diminished sperm mobility.

Prostatitis, characterized by inflammation of the prostate, adds another layer of complexity to the discussion. While normal sperm exhibits a liquid state, prostatitis can lead to reduced proteolytic enzymes within patients' prostatic fluid. This, in turn, results in prolonged non-liquefaction, leading to the formation of jelly-like sperm.

Furthermore, abnormal sperm liquefaction is correlated with reduced sperm motility. Seminal plasma of non-liquefied sperm often contains elongated fibrin, forming a mesh-like structure that limits the space available for sperm movement and subsequently restrains sperm mobility. Coarse fibers interwoven with fine fibers also form a network that mechanically impedes forward sperm motion, resulting in decreased sperm motility.

Microorganisms can also directly impact sperm motility. For instance, mycoplasma can adhere to various parts of sperm, elevating fluid dynamic resistance during forward movement, thus decelerating sperm speed and compromising motility and egg cell penetration capability. Escherichia coli, on the other hand, reduces sperm motility by binding to spermatogenesis receptors.

Furthermore, varicocele, a condition characterized by the enlargement of veins in the scrotum, can contribute to male infertility through multiple pathways, including its impact on sperm production and motility. Varicocele-related mechanisms may involve blood retention within varicose veins, disturbances in microcirculation, compromised nutrient supply, reduced oxygen partial pressure, inadequate energy production, and endocrine dysfunction.

Varicocele's ramifications may also extend to autoimmune issues, such as the production of anti-sperm antibodies and susceptibility to mycoplasma infections, indirectly culminating in decreased sperm motility.