scholarly journals Age and time-of-day differences in the hypothalamo–pituitary–testicular, and adrenal, response to total overnight sleep deprivation

SLEEP ◽  
2020 ◽  
Vol 43 (7) ◽  
Author(s):  
Peter Y Liu ◽  
Paul Y Takahashi ◽  
Rebecca J Yang ◽  
Ali Iranmanesh ◽  
Johannes D Veldhuis
Keyword(s):  
Sleep Deprivation ◽  
Older Men ◽  
Pulse Frequency ◽  
Time Of Day ◽  
Regulatory Control ◽  
Sleep Restriction ◽  
Older Individuals ◽  
Deconvolution Analysis ◽  
Age Related ◽  
Adrenal Response

Abstract Study Objectives In young men, sleep restriction decreases testosterone (Te) and increases afternoon cortisol (F), leading to anabolic–catabolic imbalance, insulin resistance, and other andrological health consequences. Age-related differences in the hypothalamo–pituitary–testicular/adrenal response to sleep restriction could expose older individuals to greater or lesser risk. We aimed to evaluate and compare the 24-h and time-of-day effect of sleep restriction on F, luteinizing hormone (LH), and Te in young and older men. Methods Thirty-five healthy men, aged 18–30 (n = 17) and 60–80 (n =18) years, underwent overnight sleep deprivation (complete nighttime wakefulness) or nighttime sleep (10 pm to 6 am) with concurrent 10-min blood sampling in a prospectively randomized crossover study. F, LH, and Te secretion were calculated by deconvolution analysis. Results Sleep deprivation had multiple effects on 24-h Te secretion with significant reductions in mean concentrations, basal, total and pulsatile secretion, and pulse frequency (each p < 0.05), in the absence of detectable changes in LH. These effects were most apparent in older men and differed according to age for some parameters: pulsatile Te secretion (p = 0.03) and Te pulse frequency (p = 0.02). Time-of-day analyses revealed that sleep restriction significantly reduced Te in the morning and afternoon, reduced LH in the morning in both age groups, and increased F in the afternoon in older men. Conclusions These data suggest a time-of-day dependent uncoupling of the regulatory control of the testicular axis and of F secretion. Future studies will need to directly verify these regulatory possibilities specifically and separately in young and older men. Clinical Trial Not applicable.

scholarly journals OR02-02 Possible Age and Time-Of-Day Differences in the Hypothalamo-Pituitary-Testicular, and Adrenal, Response to Total Overnight Sleep Restriction

2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Peter Y Liu ◽  
Paul Takahashi ◽  
Rebecca Yang ◽  
Ali Iranmanesh ◽  
Johannes D Veldhuis
Keyword(s):  
Repeated Measures ◽  
Statistical Significance ◽  
Approximate Entropy ◽  
Older Men ◽  
Pulse Frequency ◽  
Time Of Day ◽  
Regulatory Control ◽  
Sleep Restriction ◽  
Adrenal Response ◽  
Entropy Statistics

Abstract Introduction: In young men, sleep restriction decreases testosterone and increases afternoon cortisol, leading to anabolic-catabolic imbalance, insulin resistance and metabolic, neurocognitive, reproductive, and other adverse effects. Age-related differences in the hypothalamo-pituitary-testicular/adrenal response to sleep restriction could expose older individuals to greater or lesser risk, but this possibility has not been previously studied. Subjects and Methods: Thirty-five healthy young and older men aged 18-30y (n=17) and 60-80y (n=18), underwent blood sampling in the Mayo Clinic Center for Clinical and Translational Science every 10 minutes for 24 hours from 6PM-6PM under two conditions in random order spaced at least 3 weeks apart: awake (no sleep) or sleep (from 10PM to 6AM). Blood was assayed for LH, testosterone (T) and cortisol (F), and then analyzed by automated mathematical deconvolution and with cross approximate entropy statistics to determine hormone secretion and hormone synchrony, respectively. Statistical significance was construed by repeated measures ANOVA using a full factorial model that included age, sleep and the interaction. Results: Sleep deprivation had multiple effects on 24-hour (6PM-6PM) Te secretion with significant reductions in mean concentrations, basal, total and pulsatile secretion, and pulse frequency (each P<0.05), in the absence of detectable changes in LH. These effects were most apparent in older men and differed according to age for some parameters: pulsatile Te secretion (P=0.03) and T pulse frequency (P=0.02). Time-of-day analyses revealed that sleep restriction significantly reduced Te in the morning (6AM-9AM) and afternoon (3PM-6PM), reduced LH in the morning, and increased F in the afternoon, particularly in older men. Cross-approximate entropy statistics showed that sleep restriction enforced greater LH-Te and Te-LH joint synchrony in the morning (P<0.05 for each), but not in the afternoon. Conclusion: Sleep restriction decreases morning LH secretion, morning and afternoon Te secretion, and increases afternoon F secretion, especially in older men. This combination of findings could plausibly cause metabolic and reproductive ill-health when accumulated over decades of life, and may explain how chronic sleep loss contributes to metabolic and reproductive diseases that are more prevalent in older men. These preliminary data also suggest a time-of-day dependent uncoupling of the regulatory control of the testicular axis, and of cortisol secretion. Direct verification by interventions that manipulate hormones during the morning and late afternoon in appropriately matched cohorts of young and older men are now required.

scholarly journals Contribution of Body Fatness and Adipose Tissue Distribution to the Age Variation in Plasma Steroid Hormone Concentrations in Men: The HERITAGE Family Study*

2000 ◽  
Vol 85 (3) ◽  
pp. 1026-1031 ◽  
Author(s):  
Charles Couillard ◽  
Jacques Gagnon ◽  
Jean Bergeron ◽  
Arthur S. Leon ◽  
D. C. Rao ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Steroid Hormone ◽  
Older Men ◽  
Sex Hormone ◽  
Sex Hormone Binding Globulin ◽  
Older Individuals ◽  
Hormone Binding ◽  
Body Fatness ◽  
Hormone Profile ◽  
Age Related

Abstract Obesity has been associated with alterations in plasma steroid hormone concentrations in men. Older men present an altered steroid hormone profile compared to younger individuals, and an increase in body fatness and changes in adipose tissue (AT) distribution are noted with advancing age. Thus, there is a need to examine the relative importance of increased body fatness and changes in AT distribution with advancing age to plasma steroid hormone and sex hormone-binding globulin levels in men. We, therefore, investigated the relationships among age, body fatness, AT distribution, and the plasma steroid hormone profile in a group of 217 Caucasian men (mean age ± sd, 36.2± 14.9 yr) who covered a wide age range (17–64 yr). Compared to young adult men, older men were characterized by increased adiposity (P < 0.0001) expressed either as body mass index or total body fat mass assessed by underwater weighing. Differences in AT distribution were also noted with a preferential accumulation of abdominal fat as indicated by a larger waist girth (P < 0.0001) and higher visceral AT accumulation (P < 0.0001), measured by computed tomography, in older subjects. Age was associated with decreases (P < 0.0001) in C19 adrenal steroid levels, namely reduced dehydroepiandrosterone (DHEA), DHEA fatty acid ester, DHEA sulfate, as well as androstenedione levels. Androgens, i.e. dihydrotestosterone and testosterone, were also affected by age, with lower levels of both steroids being found in older individuals (P < 0.0005). When statistical adjustment for body fatness and AT distribution was performed, differences in C19 adrenal steroids between the age groups remained significant, whereas differences in androgens and sex hormone-binding globulin concentrations were no longer significant. The present study suggests that age-related differences in plasma steroid hormone levels, especially androgens, are partly mediated by concomitant variation in adiposity in men.

scholarly journals Age-related abnormalities of thalamic shape and dynamic functional connectivity after three hours of sleep restriction

PeerJ ◽  
2021 ◽  
Vol 9 ◽  
pp. e10751
Author(s):  
Zhiliang Long ◽  
Jia Zhao ◽  
Danni Chen ◽  
Xu Lei
Keyword(s):  
Young Adults ◽  
Functional Connectivity ◽  
Sleep Deprivation ◽  
Parietal Cortex ◽  
Shape Analysis ◽  
Sleep Restriction ◽  
Dynamic Functional Connectivity ◽  
Age Related ◽  
Superior Parietal Cortex ◽  
Left Thalamus

Background Previous neuroimaging studies have detected abnormal activation and intrinsic functional connectivity of the thalamus after total sleep deprivation. However, very few studies have investigated age-related changes in the dynamic functional connectivity of the thalamus and the abnormalities in the thalamic shape following partial sleep deprivation. Methods Fifty-five participants consisting of 23 old adults (mean age: 68.8 years) and 32 young adults (mean age: 23.5 years) were included in current study. A vertex-based shape analysis and a dynamic functional connectivity analysis were used to evaluate the age-dependent structural and functional abnormalities after three hours of sleep restriction. Results Shape analysis revealed the significant main effect of deprivation with local atrophy in the left thalamus. In addition, we observed a significant age deprivation interaction effect with reduced variability of functional connectivity between the left thalamus and the left superior parietal cortex following sleep restriction. This reduction was found only in young adults. Moreover, a significantly negative linear correlation was observed between the insomnia severity index and the changes of variability (post-deprivation minus pre-deprivation) in the functional connectivity of the left thalamus with the left superior parietal cortex. Conclusions The results indicated that three hours of sleep restriction could affect both the thalamic structure and its functional dynamics. They also highlighted the role of age in studies of sleep deprivation.

scholarly journals Joint Basal and Pulsatile Hypersecretory Mechanisms Drive the Monotropic Follicle-Stimulating Hormone (FSH) Elevation in Healthy Older Men: Concurrent Preservation of the Orderliness of the FSH Release Process: A General Clinical Research Center Study*

1999 ◽  
Vol 84 (10) ◽  
pp. 3506-3514
Author(s):  
J. D. Veldhuis ◽  
A. Iranmanesh ◽  
L. M. Demers ◽  
T. Mulligan
Keyword(s):  
High Sensitivity ◽  
Approximate Entropy ◽  
Fold Increase ◽  
Older Men ◽  
Older Individuals ◽  
Release Process ◽  
Deconvolution Analysis ◽  
Clinical Research Center ◽  
Lower Amplitude ◽  
Neuroendocrine Mechanisms

Abstract To appraise the neuroendocrine mechanisms that underlie a selective (monotropic) elevation of serum FSH concentrations in healthy older men, we sampled blood in 11 young (ages 21–34) and 8 older men (ages 62–72) men every 2.5 min overnight. Serum FSH concentrations were quantitated in an automated, high-sensitivity, chemiluminescence-based assay. Rates of basal and pulsatile FSH secretion were estimated by deconvolution analysis, and the orderliness of the FSH release process via quantitated the approximate entropy statistic. Statistical analysis revealed that healthy older men manifest dual neuroendocrine hypersecretory mechanisims; specifically, a 2-fold increase in the basel (nonpulsatile) FSH secretion rate, and a concurrent 50% amplification of FSH secretory burst mass (and amplitude). The regularity or orderliness of ad seriatim FSH release is preserved in older individuals. We postulate that higher basel FSH secretion in older men is a consequence of reduced testosterone negative feedback, whereas amplified FSH secretory burst mass reflects net enhanced stimulation of gonadotrope cells by endogenous FSH secretagogues (e.g. GnRH and/or activin). The foregoing specific mechanisms driving heightened FSH secretion in older men contrast with the lower-amplitude pulsatility and more disorderly patterns of LH release in the same individuals. Thus, the present data illuminate an age-dependent disparity in the disruption of FSH neuroregulation in the aging male.

Aging alters feed-forward and feedback linkages between LH and testosterone in healthy men

1997 ◽  
Vol 273 (4) ◽  
pp. R1407-R1413 ◽  
Author(s):  
Thomas Mulligan ◽  
Ali Iranmanesh ◽  
Michael L. Johnson ◽  
Martin Straume ◽  
Johannes D. Veldhuis
Keyword(s):  
Feedback Inhibition ◽  
Serum Testosterone ◽  
Older Men ◽  
Older Individuals ◽  
Deconvolution Analysis ◽  
Feed Forward ◽  
Testosterone Secretion ◽  
Serum Lh ◽  
Lh Secretion ◽  
Secretion Rates

To discern the effect of aging on coordinate luteinizing hormone (LH) and testosterone secretion, we sampled healthy older men (age 62–74 yr, n = 11) and young controls (age 21–34 yr, n = 13) every 2.5 min overnight. Deconvolution analysis and cross-correlation were used to relate serum LH concentrations to calculated testosterone secretion rates (feed-forward stimulation), as well as serum testosterone concentrations to computed LH secretion rates (feedback inhibition). Despite statistically similar mean serum LH and testosterone concentrations in the young and older men, older individuals had diminished feed-forward stimulation of LH concentrations on calculated testosterone secretion rates, as well as delayed feedback inhibition of testosterone concentrations on computed LH secretion rates.

Disruption of the hypothalamic luteinizing hormone pulsing mechanism in aging men

2001 ◽  
Vol 281 (6) ◽  
pp. R1917-R1924 ◽  
Author(s):  
Daniel M. Keenan ◽  
Johannes D. Veldhuis
Keyword(s):  
Luteinizing Hormone ◽  
Older Men ◽  
Interpulse Interval ◽  
Deconvolution Analysis ◽  
Age Related ◽  
Aging Men ◽  
Gamma Density ◽  
Lower Amplitude ◽  
Interval Lengths ◽  
Lh Secretion

The incremental nature of neuroendocrine aging suggests that subtle system dysregulation may precede overt axis failure. The present analyses unmask threefold disruption of pulsatile gonadotropin-releasing hormone (GnRH)-luteinizing hormone (LH) secretion in the aging male. First, by way of random effects-based deconvolution analysis, we document an elevated daily GnRH-LH pulse frequency in healthy older men [namely, mean (±SE) 23 ± 1 (older) vs. 15 ± 1 (young) LH secretory bursts/24 h, P < 0.001] and lower mean LH pulse mass [3.73 ± 0.58 (older) vs. 5.46 ± 0.66 (young) IU/l, P = 0.038]. However, total LH secretion rates and two-compartment LH elimination kinetics were comparable in the two age cohorts. Second, using the approximate entropy statistic, we show an equivalently random order-dependent succession of LH interpulse-interval lengths in young and older men, but a marked age-related deterioration of the ad seriatim regularity of LH pulse mass series in older individuals (P = 0.0057). Third, by modeling GnRH pulse-generator output as a Weibull renewal process (generalized Gamma density) to emulate loosely coupled GnRH neuronal oscillators, we identify an age-related reduction in the frequency-independent and order-independent variability of GnRH-LH interpulse-interval sets (P = 0.08). These findings indicate that the GnRH-LH pulsing mechanism in healthy older men maintains an increased mean frequency and lower amplitude of bursting activity, a reduced uniformity of serial LH pulse-mass values, and an impaired variability among interpulse-interval lengths. Thereby, the foregoing order-dependent and order-independent alterations in GnRH-LH signal generation in the aging human suggest a general framework for exploring subtle disruption of time-sensitive regulation of other neurointegrative systems.

scholarly journals Residual, differential neurobehavioral deficits linger after multiple recovery nights following chronic sleep restriction or acute total sleep deprivation

SLEEP ◽  
2020 ◽  
Author(s):  
Erika M Yamazaki ◽  
Caroline A Antler ◽  
Charlotte R Lasek ◽  
Namni Goel
Keyword(s):  
Sleep Deprivation ◽  
Response Speed ◽  
Sleep Loss ◽  
Sleep Restriction ◽  
Total Sleep Deprivation ◽  
Psychomotor Vigilance Test ◽  
Recovery Sleep ◽  
Time In Bed ◽  
Neurobehavioral Deficits ◽  
Chronic Sleep

Abstract Study Objectives The amount of recovery sleep needed to fully restore well-established neurobehavioral deficits from sleep loss remains unknown, as does whether the recovery pattern differs across measures after total sleep deprivation (TSD) and chronic sleep restriction (SR). Methods In total, 83 adults received two baseline nights (10–12-hour time in bed [TIB]) followed by five 4-hour TIB SR nights or 36-hour TSD and four recovery nights (R1–R4; 12-hour TIB). Neurobehavioral tests were completed every 2 hours during wakefulness and a Maintenance of Wakefulness Test measured physiological sleepiness. Polysomnography was collected on B2, R1, and R4 nights. Results TSD and SR produced significant deficits in cognitive performance, increases in self-reported sleepiness and fatigue, decreases in vigor, and increases in physiological sleepiness. Neurobehavioral recovery from SR occurred after R1 and was maintained for all measures except Psychomotor Vigilance Test (PVT) lapses and response speed, which failed to completely recover. Neurobehavioral recovery from TSD occurred after R1 and was maintained for all cognitive and self-reported measures, except for vigor. After TSD and SR, R1 recovery sleep was longer and of higher efficiency and better quality than R4 recovery sleep. Conclusions PVT impairments from SR failed to reverse completely; by contrast, vigor did not recover after TSD; all other deficits were reversed after sleep loss. These results suggest that TSD and SR induce sustained, differential biological, physiological, and/or neural changes, which remarkably are not reversed with chronic, long-duration recovery sleep. Our findings have critical implications for the population at large and for military and health professionals.

scholarly journals Sleep in Normal Aging, Homeostatic and Circadian Regulation and Vulnerability to Sleep Deprivation

2021 ◽  
Vol 11 (8) ◽  
pp. 1003
Author(s):  
Jacques Taillard ◽  
Claude Gronfier ◽  
Stéphanie Bioulac ◽  
Pierre Philip ◽  
Patricia Sagaspe
Keyword(s):  
Older Adults ◽  
Sleep Deprivation ◽  
Health Management ◽  
Nrem Sleep ◽  
Early Morning ◽  
Subcortical Structures ◽  
Wake Time ◽  
Adverse Health Outcomes ◽  
Neurobehavioral Function ◽  
Age Related

In the context of geriatric research, a growing body of evidence links normal age-related changes in sleep with many adverse health outcomes, especially a decline in cognition in older adults. The most important sleep alterations that continue to worsen after 60 years involve sleep timing, (especially early wake time, phase advance), sleep maintenance (continuity of sleep interrupted by numerous awakenings) and reduced amount of sigma activity (during non-rapid eye movement (NREM) sleep) associated with modifications of sleep spindle characteristics (density, amplitude, frequency) and spindle–Slow Wave coupling. After 60 years, there is a very clear gender-dependent deterioration in sleep. Even if there are degradations of sleep after 60 years, daytime wake level and especially daytime sleepiness is not modified with age. On the other hand, under sleep deprivation condition, older adults show smaller cognitive impairments than younger adults, suggesting an age-related lower vulnerability to extended wakefulness. These sleep and cognitive age-related modifications would be due to a reduced homeostatic drive and consequently a reduced sleep need, an attenuation of circadian drive (reduction of sleep forbidden zone in late afternoon and wake forbidden zone in early morning), a modification of the interaction of the circadian and homeostatic processes and/or an alteration of subcortical structures involved in generation of circadian and homeostatic drive, or connections to the cerebral cortex with age. The modifications and interactions of these two processes with age are still uncertain, and still require further investigation. The understanding of the respective contribution of circadian and homeostatic processes in the regulation of neurobehavioral function with aging present a challenge for improving health, management of cognitive decline and potential early chronobiological or sleep-wake interventions.

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