The decline in male sperm motility is a concerning issue that significantly impacts the future development of many men. Numerous factors contribute to this decline, including male diseases, individuals with generally healthy lifestyles, those residing in unfavorable environments, and work-related stress.

One primary cause of reduced sperm motility is the occurrence of acute and chronic inflammation in reproductive tracts and glands such as the epididymis, vas deferens, seminal vesicle, and prostate.

When orchitis, inflammation of the testicles, remains untreated, it can negatively affect sperm motility. The testicles play a crucial role in hormone secretion and sperm production. Therefore, inflammation in the testicles can compromise the quality of sperm, especially in cases of orchitis resulting from viral infections. This type of orchitis can significantly impact male testicular spermatogenic function.

If orchitis is caused by mumps virus infection, it may lead to atrophy of testis, decline of spermatogenic function, or even spermatogenic dysfunction without proper treatment, leading to male infertility.
The epididymis is a place to store sperm. Normal men have a large number of sperm stored in the epididymis. When the epididymis is inflamed, it can lead to inflammatory exudate or purulent secretion in the epididymis. At this time, inflammatory exudate or purulent secretion will cause protein denaturation in sperm, thus affecting sperm activity, or even dead sperm, causing sperm quality to decline.

Seminal vesiculitis, to a certain extent, can affect sperm mobility. Seminal vesiculitis caused by pathogenic microbial infection will change the composition of sperm, leading to the mixing of bacteria with seminal plasma, and bacteria will consume the nutrients in seminal plasma and produce some metabolic waste. These waste and toxins will lead to the viability of sperm decline. 
Seminal vesiculitis reduces the pH of seminal plasma and increases acidity, which can cause sperm motility to decline. Seminal vesiculitis will improve the viscosity of sperm, resulting in sperm not being easy to liquefy.
Prostatitis can also affect sperm mobility. Normal sperm is liquid, but prostatitis will reduce the proteolytic enzymes in the prostatic fluid of patients, resulting in non-liquefaction for an extended period, resulting in jelly-like sperm. 
Patients with abnormal sperm liquefaction also have low sperm motility. Elongated fibrin can be seen in the seminal plasma of sperm without liquefaction, and the mesh between each other reduces the space for sperm activity, and the sperm is restrained. At the same time, the coarse fibers were also seen to be connected by many fine fibers into a network, which may be the cause of the mechanical restriction of sperm forward movement. This leads to low sperm motility.
Secondly, the direct effect of microorganisms on sperm can lead to low sperm motility. For example, mycoplasma can adhere to the head, middle, and tail of sperm so that when sperm moves forward, the fluid dynamic resistance is increased, the movement speed is slowed down, and the sperm motility and the ability to penetrate the egg cell are affected. Escherichia coli can reduce sperm motility by binding to spermatogenesis through its receptors.
Thirdly, varicocele can lead to male infertility in various ways. It affects the production of sperm and also causes sperm motility. The mechanism may cause blood retention in varicose veins, microcirculation disturbance, lack of nutrient supply and oxygen partial pressure reduction, insufficient energy production, and endocrine dysfunction.
It may also be related to the autoimmunity problems caused by varicocele, such as the production of anti-sperm antibodies and infections with mycoplasma, which indirectly lead to decreased sperm motility.

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