Cardiac autonomic activity during sleep deprivation with and without caffeine administration

Crooks, Elena; Hansen, Devon; Satterfield, Brieann C.; Layton, Matthew E.; Dongen, Hans P A Van

doi:10.1016/j.physbeh.2019.112643

Cited by 16 publications

(14 citation statements)

References 47 publications

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“…In agreement with the study by Crooks et al (2019) that demonstrated no significant result between sleep quality and IL-6 levels, this study approved that there was no significant result between the levels of proinflammatory cytokines, IL-6, with various sleep deprivation stress models (p = 0.658). Conversely, a study by Siregar (2017) showed a significant result between sleep quality and IL-6 levels.…”

Section: Results S and Discussionsupporting

confidence: 91%

“…On the other hand, some studies indicated that people with sleep disorders showed an alteration in circulating levels of TNF-α and IL-6. However, other studies failed to demonstrate the change in TNF-α and IL-6 levels between normal and sleep-deprived subjects (Crooks et al, 2019;Irwin et al, 2006;Shearer et al, 2001;Siregar, 2017). Although this study showed insignificant results, sleep deprivation also has a potency to increase the pro-inflammatory cytokine expression that is associated with inflammatory reaction-related diseases such as cancer, neurodegeneration, and cardiovascular disease (Garbarino et al, 2021).…”

Section: Results S and Discussionmentioning

confidence: 98%

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Levels of Cortisol and Inflammatory Cytokines after The Induction of Various Sleep Deprivation Stress Models in Male Wistar Rats

Arjadi

Wisesa²,

Inayani³

et al. 2022

molekul

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Sleep deprivation (SD) can modulate the production of various cytokines, including pro-inflammatory cytokines such as IL-6, TNF-α, and IFN-γ, and anti-inflammatory cytokines such as IL-10. Paradoxical sleep deprivation (PSD) increases the risk of inflammation but can be relieved by sleep recovery (SR). This study aimed to determine the differences in levels of cortisol and inflammatory cytokines (IL-6, IL-10, TNF-α, dan IFN-γ) in male Wistar rats (Rattus norvegicus) after induction of various sleep deprivation stress models. Twenty-five of male Wistar rats were randomly divided into five groups: control, PSD (20 hours of SD/day for five days), Total Sleep Deprivation or TSD (24 hours of SD/day for five days), PSD+SR (PSD followed by SR), and TSD+SR (TSD followed by SR). The plasma cortisol levels were measured with ELISA, and inflammatory cytokine levels were measured with immunoassay and calculated with fold change. Mean cortisol levels were significantly increased in treatment groups compared to the control group (p=0.029). Multivariate analysis showed no statistically significant difference in inflammatory cytokine levels of IL-6 (p=0.658), IL-10 (p=0.065), TNF-α (p=0.399), and IFN-γ (p=0.283) in all groups. In conclusion, various sleep deprivation stress models affect cortisol levels but not inflammatory cytokine levels of IL-6, IL-10, TNF-α, and IFN-γ among male Wistar rats.

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Section: Results S and Discussionsupporting

confidence: 91%

Section: Results S and Discussionmentioning

confidence: 98%

Levels of Cortisol and Inflammatory Cytokines after The Induction of Various Sleep Deprivation Stress Models in Male Wistar Rats

Arjadi

Wisesa²,

Inayani³

et al. 2022

molekul

View full text Add to dashboard Cite

show abstract

“…Although not necessarily the main goal for mitigating the effects of fatigue, changes in physiology are inevitable. For instance, an increase in HRV, decrease in heart rate, an unchanged pre Ejection period (PEP), and an overall increase in parasympathetic activity were observed following caffeine administration (Kohler et al, 2006;Crooks et al, 2019). Furthermore, it was found that caffeine resulted in an increase in skin conductivity, EEG alpha frequency, and a decrease in EEG alpha power (Barry et al, 2005).…”

Section: Mitigating Physiological Effectsmentioning

confidence: 99%

“…Drug Caffeine Penetar et al, 1993;Lieberman et al, 2002;Barry et al, 2005;Wesensten et al, 2005;Kohler et al, 2006;Killgore et al, 2011;McIntire et al, 2014;Paech et al, 2016;McIntire et al, 2017;Crooks et al, 2019;Killgore andKamimori, 2020a Modafinil Pigeau et al, 1995;Caldwell et al, 2000, Caldwell et al, 2004bWesensten et al, 2005D-amphetamine Newhouse et al, 1989Pigeau et al, 1995;Wesensten et al, 2005Donepezil Dodds et al, 2011 CX717 (AMPAKINE compound) Boyle et al, 2012 Non-invasive stimulation Transcranial direct current stimulation (tDCS) Nitsche and Paulus, 2001;McIntire et al, 2014McIntire et al, , 2017Cheng et al, 2021 Transcutaneous vagal nerve stimulation (tVNS) Rizzo et al, 2003;McIntire et al, 2021 Other Break period Pigeau et al, 1995 have found that it only takes 1 h for caffeine to have its greatest effects and lasts for 8 h (Lieberman et al, 2002). Additionally, caffeine has prevented an increase in the number of risks taken when compared to placebo during sleep deprivation (Killgore et al, 2011).…”

Section: Mitigation Category Mitigation Type Representative Citationmentioning

confidence: 99%

Predicting and mitigating fatigue effects due to sleep deprivation: A review

Kayser¹,

Puig²,

Estepp

2022

Front. Neurosci.

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The deleterious effects of insufficient sleep have been well-established in the literature and can lead to a wide range of adverse health outcomes. Some of the most replicated findings demonstrate significant declines in cognitive functions such as vigilance and executive attention, psychomotor and cognitive speed, and working memory. Consequently, these decrements often lead individuals who are in a fatigued state to engage in substandard performance on everyday tasks. In the interest of curtailing these effects, prior work has attempted to identify mechanisms that predict fatigue onset and develop techniques to mitigate its negative consequences. Nonetheless, these results are often confounded by variables such as an individual’s resistance to fatigue, sleep history, and unclear distinctions about whether certain performance decrements are present due to fatigue or due to other confounding factors. Similar areas of research have provided approaches to produce models for the prediction of cognitive performance decrements due to fatigue through the use of multi-modal recording and analysis of fatigue-related responses. Namely, gathering and combining response information from multiple sources (i.e., physiological and behavioral) at multiple timescales may provide a more comprehensive representation of what constitutes fatigue onset in the individual. Therefore, the purpose of this review is to discuss the relevant literature on the topic of fatigue-related performance effects with a special emphasis on a variety of physiological and behavioral response variables that have shown to be sensitive to changes in fatigue. Furthermore, an increasing reliance on sleep loss, meant to assist in meeting the demands of modern society, has led to an upsurge in the relevance of identifying dependable countermeasures for fatigued states. As such, we will also review methods for the mitigation of performance effects due to fatigue and discuss their usefulness in regulating these effects. In sum, this review aims to inspire future work that will create opportunities to detect fatigue and mitigate its effects prior to the onset of cognitive impairments.

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“…In humans, several clinical observational studies with small sample size have witnessed the alterations of circadian sleep-wake ( Landolt et al, 1995a ; Landolt et al, 1995b ; McHill et al, 2014 ; Weibel et al, 2021 ), body temperature ( Wright et al, 1997 ; Wright et al, 2000 ; McHill et al, 2014 ), blood pressure ( Green and Suls, 1996 ; Guessous et al, 2014 ), heart rates ( Green and Suls, 1996 ; Kohler et al, 2006 ; Crooks et al, 2019 ), melatonin ( Wright et al, 1997 ; Wright et al, 2000 ; Burke et al, 2015 ), and cortisol rhythms ( Lovallo et al, 2005 ; Rieth et al, 2016 ) in adults who consumed caffeine by comparison with placebo controls.…”

Section: The Effects and Mechanisms Of Caffeine On Circadian Rhythmsmentioning

confidence: 99%

Precision caffeine therapy for apnea of prematurity and circadian rhythms: New possibilities open up

Dai

Guo

et al. 2022

Front. Pharmacol.

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Caffeine is the globally consumed psychoactive substance and the drug of choice for the treatment of apnea of prematurity (AOP), but its therapeutic effects are highly variable among preterm infants. Many of the molecular underpinnings of the marked individual response have remained elusive yet. Interestingly, the significant association between Clock gene polymorphisms and the response to caffeine therapy offers an opportunity to advance our understanding of potential mechanistic pathways. In this review, we delineate the functions and mechanisms of human circadian rhythms. An up-to-date advance of the formation and ontogeny of human circadian rhythms during the perinatal period are concisely discussed. Specially, we summarize and discuss the characteristics of circadian rhythms in preterm infants. Second, we discuss the role of caffeine consumption on the circadian rhythms in animal models and human, especially in neonates and preterm infants. Finally, we postulate how circadian-based therapeutic initiatives could open new possibilities to promote precision caffeine therapy for the AOP management in preterm infants.

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Cardiac autonomic activity during sleep deprivation with and without caffeine administration

Cited by 16 publications

References 47 publications

Levels of Cortisol and Inflammatory Cytokines after The Induction of Various Sleep Deprivation Stress Models in Male Wistar Rats

Levels of Cortisol and Inflammatory Cytokines after The Induction of Various Sleep Deprivation Stress Models in Male Wistar Rats

Predicting and mitigating fatigue effects due to sleep deprivation: A review

Precision caffeine therapy for apnea of prematurity and circadian rhythms: New possibilities open up

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