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Effects Of Acute Suppression Of Slow-Wave Sleep On Young Men’s Androgen Levels

Sleep restriction and sleep disturbances are increasingly common in modern industrialized societies, due to, for instance, work-related stress and atypical working hours. In addition, our sleep often becomes worse as we age.

Among the consequences of insufficient and poor-quality sleep are direct effects on health and bodily systems. It has also been shown that disturbed sleep is associated with erectile dysfunction. However, how sleep disturbances affect the androgen level, but which sleep stages are most important for their secretion and release is largely unknown.

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Increasing physiological evidence regarding the deepest stage of non-REM sleep, slow-wave sleep (SWS), has positioned it as a major actor in metabolism regulation, hormone release, and immunity. And it is this stage that is greatly reduced in aging and in sleep disorders. That’s why the core experimental question of our study was simple: does the acute suppression of SWS trigger a decrease in androgen level in young healthy men?

In a within-subject, counterbalanced design, we directly suppressed SWS during one night, then compared next-morning salivary androgen measures to those after a night of sleep without any perturbation (control). For SWS suppression, we continuously monitored the polysomnogram, and every time a participant entered SWS, we delivered an acoustic tone with gradually rising sound intensity until the occurrence in polysomnogram signs of lighter sleep stages. The aim of this intervention was to substitute SWS with shallow non-REM sleep, i.e., stage 2, without awakening the subject.

Across the experimental night of sleep, the auditory tone perturbation reduced overall SWS duration by 54.2%. Participants spent less time in SWS and proportionally more time in light sleep stages (in stages 1 and 2), so despite a major decrease in the quantity of SWS, the total sleep time was not greatly changed. Consistent with the hypothesis, there was a decrease in saliva levels of testosterone and its precursor 17α-hydroxyprogesterone the following day. Thus, we can conclude that the observed alterations in the release of hormones were not caused by general sleep insufficiency but were associated mainly with the time spent in SWS. 

Considering that such changes in sleep quality might be the age-related and begin early in midlife, they may increase the risk for the development of androgen deficiency in the long term. Besides regulation of the development and maintenance of male characteristics, androgens exert a variety of physiological effects on our body, in particular on the carbohydrate and lipid metabolism.

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In addition, testosterone, 17α-hydroxyprogesterone, their precursors, and their metabolites have neurogenic and neuroprotective properties, regulating the stress response, mood, and cognition. That is, poor sleep quality, whether through voluntary sleep restriction, age, or due to medical illness, has the potential to contribute to the development of metabolic and psychiatric disorders even in healthy adults.

These findings are described in the article entitled Slow-wave sleep and androgens: selective slow-wave sleep suppression affects testosterone and 17α-hydroxyprogesterone secretion, recently published in the journal Sleep Medicine. This work was conducted by Yu. V. Ukraintseva from the Russian Academy of Sciences and ITMO University, K.M. Liaukovich and О.V. Martynova from the Russian Academy of Sciences and the National Research University Higher School of Economics, А.A. Polishchuk from the Russian Academy of Sciences and the Lomonosov Moscow State University, D.A. Belov, E.S. Simenel, and А.N. Nizhnik from the ArhiMed Clinique for New Medical Technologies, and М. Meira e Cruz from the University of Lisbon.

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