What physiological processes occur during male ejaculation?

1. Emission: the “point of no return” for seminal transit

During emission, sympathetic and parasympathetic autonomic signals drive contraction of the distal epididymis and vas deferens and secretions from the seminal vesicles, prostate and bulbourethral glands so that sperm and accessory fluids collect in the prostatic (posterior) urethra; once this posterior urethral reservoir is filled the expulsion phase becomes inevitable—clinically described as the point of no return ^{[1] [5] [6]}.

2. Expulsion: muscular rhythm that ejects semen

Expulsion is a brief, forceful series of rhythmic contractions—primarily of pelvic floor muscles such as the bulbospongiosus (also called bulbocavernosus) and pubococcygeus/ischiocavernosus—that squeeze the urethra and propel semen through the penile urethra and out the meatus; the bladder neck simultaneously closes to prevent retrograde flow into the bladder ^{[2] [7] [8]}.

3. Neural control: spinal reflexes plus higher centers

Ejaculation is organized by spinal circuits (notably at sacral levels S2–S4 and thoracolumbar sympathetic segments) and mediated by the pudendal nerve for somatic pelvic muscle contraction; higher brain centers modulate this reflex, and functional imaging has struggled to isolate a single “ejaculation center” because ejaculation is brief and embedded within a broader sexual response ^{[2] [4] [9]}.

4. Chemical regulators: neurotransmitters and hormones at work

Multiple neurotransmitters and neuropeptides contribute to timing and sensation: sympathetic catecholamines (e.g., norepinephrine) are implicated in emission, while serotonergic and dopaminergic systems influence ejaculatory latency and central control; transient hormonal changes, including rises in prolactin and other factors after orgasm, have been observed but their precise causal roles remain debated in the literature ^{[9] [10]}.

5. Semen composition and physical changes during ejaculation

Semen is a complex, non‑homogeneous fluid containing spermatozoa and secretions from accessory glands plus thousands of proteins, ions, hormones and vesicles; after ejaculation semen normally liquefies over time via proteolytic activity—alterations in viscosity or liquefaction can reflect glandular dysfunction or infection ^[3].

6. Cardiovascular and autonomic signs that accompany climax

Orgasm and ejaculation often coincide with autonomic arousal: transient tachycardia, elevated blood pressure and increased respiratory rate are commonly reported, and heart rate can rise markedly during ejaculation—signs that reflect sympathetic activation accompanying the ejaculatory reflex ^{[10] [6]}.

7. Clinical variations and dysfunctions: what can go wrong

Ejaculatory disorders include premature ejaculation, delayed ejaculation, anejaculation (absent ejaculation), and retrograde ejaculation (where semen flows into the bladder because the bladder neck fails to close). Causes range from neural injury (e.g., spinal cord injury) to medication effects, glandular pathology, or psychological factors; accurate diagnosis requires distinguishing emission failures from expulsion failures because management differs ^{[1] [11] [12]}.

8. Points of consensus and remaining uncertainties

Experts agree on the two‑phase model (emission + expulsion), the role of pelvic muscles and autonomic/somatic innervation, and the multi‑glandular composition of semen ^{[1] [2] [3]}. However, the detailed central neuronal circuitry, precise roles of particular neuropeptides, and the neuroendocrine triggers that set the ejaculatory threshold remain active research areas—functional imaging and mechanistic studies have limited temporal resolution for this brief event ^{[9] [6]}.

Limitations: this summary synthesizes findings from contemporary reviews and teaching sources; available sources do not mention some detailed molecular pathways or newer imaging findings beyond those cited here.