Article From: Asian Journal of Andrology Year : 2014  |  Volume : 16  |  Issue : 2  | Page : 262-265

By: Gary Wittert

Discipline of Medicine and Freemasons Foundation Centre for Men’s Health, University of Adelaide, Adelaide, South Australia, Australia

Abstract

Plasma testosterone levels display circadian variation, peaking during sleep, and reaching a nadir in the late afternoon, with a superimposed ultradian rhythm with pulses every 90 min reflecting the underlying rhythm of pulsatile luteinizing hormone (LH) secretion. The increase in testosterone is sleep, rather than circadian rhythm, dependent and requires at least 3 h of sleep with a normal architecture. Various disorders of sleep including abnormalities of sleep quality, duration, circadian rhythm disruption, and sleep-disordered breathing may result in a reduction in testosterone levels. The evidence, to support a direct effect of sleep restriction or circadian rhythm disruption on testosterone independent of an effect on sex hormone binding globulin (SHBG), or the presence of comorbid conditions, is equivocal and on balance seems tenuous. Obstructive sleep apnea (OSA) appears to have no direct effect on testosterone, after adjusting for age and obesity. However, a possible indirect causal process may exist mediated by the effect of OSA on obesity. Treatment of moderate to severe OSA with continuous positive airway pressure (CPAP) does not reliably increase testosterone levels in most studies. In contrast, a reduction in weight does so predictably and linearly in proportion to the amount of weight lost. Apart from a very transient deleterious effect, testosterone treatment does not adversely affect OSA. The data on the effect of sleep quality on testosterone may depend on whether testosterone is given as replacement, in supratherapeutic doses, or in the context abuse. Experimental data suggest that testosterone may modulate individual vulnerability to subjective symptoms of sleep restriction. Low testosterone may affect overall sleep quality which is improved by replacement doses. Large doses of exogenous testosterone and anabolic/androgenic steroid abuse are associated with abnormalities of sleep duration and architecture.
Keywords: obesity; obstructive sleep apnea; shift work; sleep restriction; testosterone

Introduction

Normal sleep physiology
From a neurophysiological standpoint, there are two types of sleep: nonrapid eye movement (NREM) and rapid eye movement (REM) sleep. The first two phases of NREM sleep (phases 1 and 2) are light and often alternate with brief waking episodes. Two deeper phases of NREM sleep (phases 3 and 4) together known as slow wave sleep (SWS) tend to occur predominantly in the earlier part of the night and become lighter thereafter. Usually four to six cycles of REM sleep occur at intervals of approximately 90 min becoming longer and more frequent over the course of the night. The time between sleep onset and the first REM episode is termed REM latency. The term sleep architecture is used to describe the pattern of sleep that occurs through the night. From approximately middle-aged onwards, less time is spent in the deeper phases of sleep and there is more stage I sleep and more awakenings. The effect of ageing on REM sleep is more variable and it tends to be preserved until quite late in life. [1]

Sleep and the regulation of the hypothalamo-pituitary-gonadal axis

Plasma testosterone levels vary in a circadian manner, higher on waking and decreasing to a low point at the end of the day. Superimposed on this are burst-like increases in testosterone production that occur every 90 min or so. [2] Plasma testosterone levels begin to increase with the onset of sleep, and in young men peak at the first REM sleep episode and remaining at that level until waking; [3] the longer the REM sleep latency the slower the rise in testosterone. >[4]

It was originally thought that there is an endogenous rhythm of testosterone production similar to what occurs for cortisol.[5]More recently it has become clear that the production of testosterone is dependent on sleep generally reaching the peak during the first 3 h of uninterrupted sleep, and at least in young men at about the time of the first REM episode. [4] Total fragmentation of normal sleep architecture throughout the night prevents the increase in testosterone.[4] It has also been shown, at least in young men, that the sleep-dependent increase in testosterone occurs irrespective of whether the sleep occurs at night or for an equivalent duration during the day. The increase in testosterone with sleep time and a decrease during time awake is stable within an individual, but in turn there are large individual differences.[6] It seems likely that there is an effect of ageing, since in healthy older men objectively measured differences in the amount of nighttime sleep are associated with the variability in the morning testosterone levels. [7] Middle-aged men secrete less testosterone at night then healthy young men. [1]

Prevalence and nature of sleep disorders including short sleep, circadian rhythm disruption, and sleep-disordered breathing

Sleep restriction is an increasing problem of an electrified, digitalized, and constantly connected lifestyle. In the USA, average nocturnal sleep time is 6.9 h per night and 20% of adults sleep less than 6.5 h per night as compared to an average optimal sleep time of 8.2 h per night.[8]

They are a number of definitions of shift work. Typically it is defined as at least half of the work shift being outside the standard work time of 08:00-17:00 hours and this may apply to 25%-33% of the workforce. Of these, 5%-7% either work permanent nights or rotating shifts. In night workers or those working rotating shifts, as compared to night sleep, day sleep is associated with a reduction in SWS.[9]

There are a number of syndromes characterized by disordered breathing during sleep. One group of these relates to increased upper airway resistance. Vibration of the upper airways during the passage of air results in snoring. More severe obstruction of the upper airway during sleep results in the obstructive sleep apnea (OSA) or OSA syndrome (OSAS) when there are compatible symptoms present. Apneas are repetitive pauses in breathing lasting 10-40 s despite efforts to breathe. Hypopneas are defined as a 50% decrease in airflow for 10 s or 30% decrease when oxygen saturation falls or sleep arousal occurs.[10] The presence and severity can be classified by a number of indices including the oxygen desaturation index (ODI), arousal index, or apnea hypopnea index (AHI). The AHI describes the number of apneas or hypopneas per hour of sleep. A normal AHI is less than 5.

Although originally considered to affect around 4% of middle-aged men, OSA has been shown to affect 41% of men in an urban Brazilian population where 60% were overweight or obese [11] and 53% of men aged 40 and over from suburban Adelaide, Australia, where 72% were overweight or obese.(Submitted)

The severity of OSA is considerably worse during daytime sleep after night shift as compared to normal nighttime sleep and this may intensify the unfavorable health effects of OSAS. [9]

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