Abstract Erectile function is a complex neurovascular process influenced by multiple physiological systems, including autonomic regulation, vascular integrity, and endocrine balance. Sleep-related erections (SRE), which occurs predominantly during rapid eye movement sleep (REM), plays a critical role in maintaining erectile physiology by ensuring periodic oxygenation of penile tissue and preventing fibrosis. Sleep fragmentation, particularly disruption of REM sleep, has been increasingly recognized as a contributing factor to erectile dysfunction (ED), with mechanisms involving heightened sympathetic activity, impaired parasympathetic vasodilation, and neuroendocrine dysregulation. Sleep disorders, such as obstructive sleep apnea and chronic sleep deprivation are associated with reduced SRE frequency, increased oxidative stress, and decreased nitric oxide bioavailability, all of which contribute to endothelial dysfunction and erectile impairment. Ageing exacerbates these issues by further reducing SRE occurrence and increasing the prevalence of sleep disturbances. Therapeutic strategies aimed at optimizing sleep architecture and its quality, including pharmacological, hormonal, and neuromodulatory interventions, may provide promising avenues for mitigating ED and promoting healthy ageing. This review highlights the interplay between sleep physiology, erectile function, and therapeutic implications, underscoring the importance of sleep optimization in ED management.
Andersen et al. (2026) studied this question.