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Esler, Murray; Lambert, Gavin W.; Kaye, David M.; Rumantir, Magdalena S.; Hastings, Jacqueline; Seals, Douglas R.

doi:10.1023/a:1015203328878

Cited by 34 publications

(11 citation statements)

References 13 publications

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“…and in the lack of appropriate compensatory increase in AIRg. Indeed, overactivity of the sympathetic nervous system results in insulin resistance (21), and pancreatic insulin release is inhibited by increased sympathetic vs. parasympathetic tone (22). Individuals with low SWS at baseline had the lowest amounts of SWS after our intervention and experienced the largest decrements in S.I.…”

Section: Discussionmentioning

confidence: 99%

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Slow-wave sleep and the risk of type 2 diabetes in humans

Tasali

Leproult²,

Ehrmann³

et al. 2008

Proc. Natl. Acad. Sci. U.S.A.

807

617

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There is convincing evidence that, in humans, discrete sleep stages are important for daytime brain function, but whether any particular sleep stage has functional significance for the rest of the body is not known. Deep non-rapid eye movement (NREM) sleep, also known as slow-wave sleep (SWS), is thought to be the most ''restorative'' sleep stage, but beneficial effects of SWS for physical well being have not been demonstrated. The initiation of SWS coincides with hormonal changes that affect glucose regulation, suggesting that SWS may be important for normal glucose tolerance. If this were so, selective suppression of SWS should adversely affect glucose homeostasis and increase the risk of type 2 diabetes. Here we show that, in young healthy adults, all-night selective suppression of SWS, without any change in total sleep time, results in marked decreases in insulin sensitivity without adequate compensatory increase in insulin release, leading to reduced glucose tolerance and increased diabetes risk. SWS suppression reduced delta spectral power, the dominant EEG frequency range in SWS, and left other EEG frequency bands unchanged. Importantly, the magnitude of the decrease in insulin sensitivity was strongly correlated with the magnitude of the reduction in SWS. These findings demonstrate a clear role for SWS in the maintenance of normal glucose homeostasis. Furthermore, our data suggest that reduced sleep quality with low levels of SWS, as occurs in aging and in many obese individuals, may contribute to increase the risk of type 2 diabetes.aging ͉ sleep quality ͉ sleep disordered breathing ͉ delta waves ͉ insulin resistance H uman sleep is composed of rapid-eye-movement (REM) sleep and stages 1, 2, 3, and 4 of non-REM (NREM) sleep. The deeper stages of NREM sleep, i.e., stages 3 and 4, also known as slow-wave sleep (SWS), are thought to be the most ''restorative.'' There is indeed evidence that SWS plays a role in waking neurobehavioral function (1), particularly in memory consolidation (2, 3), but whether SWS is also important for peripheral physiological function is not known. The initiation of SWS is temporally associated with transient metabolic, hormonal, and neurophysiologic changes, all of which could potentially affect glucose homeostasis. These include decreased brain glucose utilization, stimulation of growth hormone release, inhibition of corticotropic activity, decreased sympathetic nervous activity, and increased vagal tone. We therefore hypothesized that SWS plays a role in glucose regulation and that suppression of SWS may adversely affect glucose homeostasis.To test this hypothesis, we developed an experimental model in young healthy lean individuals that was designed to selectively suppress SWS and assessed the impact of this intervention on glucose homeostasis. The EEG was continuously monitored, and SWS was suppressed by delivering acoustic stimuli of varying frequencies and intensities. The intervention was designed to substitute deep NREM sleep, i.e., stages 3 and 4, with shallow NREM slee...

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Section: Discussionmentioning

confidence: 99%

“…bolus. Blood samples were then taken at times 2,3,4,5,6,8,10,12,15,19,21,22,24,26,28,30,40,50,60,70,90, 100, 120, 140, 180, 210, and 240 min. At time 20 min, i.v.…”

Section: (A) Baseline Night (B1) (B) First Night Of Sws Suppression mentioning

confidence: 99%

Slow-wave sleep and the risk of type 2 diabetes in humans

Tasali

Leproult²,

Ehrmann³

et al. 2008

Proc. Natl. Acad. Sci. U.S.A.

807

617

View full text Add to dashboard Cite

show abstract

“…As a result, age-associated peripheral sympathetic nervous system activation that initiates as a consequence of accumulating adiposity with the intent of preventing further fat storage, ironically, may in time evolve into a potential mechanism contributing to the development of obesity with aging (110). With aging, sympathetic activation was evident in the heart, and the gut and liver at rest (111). The mechanism appears to be mediated via activation of sympathoexcitatory noradrenergic suprabulbar projections from brainstem resulting augmented sympathetic nervous responses (111).…”

Section: Senescence Difference In Neuroregulatory System Of the Heartmentioning

confidence: 99%

“…The mechanism appears to be mediated via activation of sympathoexcitatory noradrenergic suprabulbar projections from brainstem resulting augmented sympathetic nervous responses (111). Conversely, adrenal medullary release of epinephrine is subnormal in the elderly, at rest and during exercise stress (111). A disparate sympathetic nervous activation is also present in older men (101).…”

Section: Senescence Difference In Neuroregulatory System Of the Heartmentioning

confidence: 99%

Views From Within and Beyond: Narratives of Cardiac Contractile Dysfunction Under Senescence

Yang

Nair

Ren

2005

ENDO

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Senesecence is associated with enhanced risk of cardiovascular diseases. It is generally considered that decline in growth hormones (such as insulin-like growth factor I), intrinsic myocardial and endothelial functions, as well as accumuation of reactive oxygen species with increased age may contribute to cardiovascular senescence. It is believed that heart function, especially cardiac reserve declines with advanced age. However, most experimental and clinical investigations on ventricluar function only included young or adult subjects and failed to address this important age issue in heart pathophysiology. Although senescent but otherwise healthy hearts may possess normal pumping function at the resting or non-stressed state, some aging-associated factors such as accumulation of reactive oxygen species and activation of selective stress signaling pathways may interact with certain risk factors and compromise overall cardiac function. The precise cause and progression of compromised cardiac function in the elderly remain controversial. This review will focus on senescene-related alterations in cardiac contractile function with a special emphasis on oxidative stress and activation of stress signaling.

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“…In a study of older males, the peripheral plasma norepinephrine concentration was approximately 66% higher than that observed in younger men. This finding is explained by the reduction in the rate of clearance of norepinephrine from plasma and 29% higher whole-body norepinephrine spillover to plasma The cardiac spillover of catecholamines is higher in older than in younger men [2, 3]. Different factors can play a role in determining the rate of spillover of norepinephrine from sympathetic nerve terminals to plasma including nerve traffic, pre-junctional modulation, and the rate of catecholamine reuptake, principally via neuronal uptake.…”

Section: Introductionmentioning

confidence: 99%

Adrenergic signaling in heart failure and cardiovascular aging

Santulli

Iaccarino

2016

Maturitas

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Both cardiovascular disease and aging are associated with changes in the sympathetic nervous system. Indeed, mounting evidence indicates that adrenergic receptors are functionally involved in numerous processes underlying both aging and cardiovascular disorders, in particular heart failure. This article will review the pathophysiological role of the sympathetic nervous system in heart failure and cardiovascular aging.

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Cited by 34 publications

References 13 publications

Slow-wave sleep and the risk of type 2 diabetes in humans

Slow-wave sleep and the risk of type 2 diabetes in humans

Views From Within and Beyond: Narratives of Cardiac Contractile Dysfunction Under Senescence

Adrenergic signaling in heart failure and cardiovascular aging

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