Short naps don’t mitigate the effects of a night of sleep deprivation


A nap during the day won’t restore a sleepless night, says the latest study from Michigan State University’s Sleep and Learning Lab.

“We are interested in understanding cognitive deficits associated with sleep deprivation. In this study, we wanted to know if a short nap during the deprivation period would mitigate these deficits,” said Kimberly Fenn, associate professor of MSU, study author and director of MSU’s Sleep and Learning Lab. “We found that short naps of 30 or 60 minutes did not show any measurable effects.”

The study was published in the journal Sleep and is among the first to measure the effectiveness of shorter naps — which are often all people have time to fit into their busy schedules.

“While short naps didn’t show measurable effects on relieving the effects of sleep deprivation, we found that the amount of slow-wave sleep that participants obtained during the nap was related to reduced impairments associated with sleep deprivation,” Fenn said.

Slow-wave sleep, or SWS, is the deepest and most restorative stage of sleep. It is marked by high amplitude, low frequency brain waves and is the sleep stage when your body is most relaxed; your muscles are at ease, and your heart rate and respiration are at their slowest.

“SWS is the most important stage of sleep,” Fenn said. “When someone goes without sleep for a period of time, even just during the day, they build up a need for sleep; in particular, they build up a need for SWS. When individuals go to sleep each night, they will soon enter into SWS and spend a substantial amount of time in this stage.”

Fenn’s research team – including MSU colleague Erik Altmann, professor of psychology, and Michelle Stepan, a recent MSU alumna currently working at the University of Pittsburgh – recruited 275 college-aged participants for the study.

The participants completed cognitive tasks when arriving at MSU’s Sleep and Learning Lab in the evening and were then randomly assigned to three groups: The first was sent home to sleep; the second stayed at the lab overnight and had the opportunity to take either a 30 or a 60 minute nap; and the third did not nap at all in the deprivation condition.

The next morning, participants reconvened in the lab to repeat the cognitive tasks, which measured attention and placekeeping, or the ability to complete a series of steps in a specific order without skipping or repeating them — even after being interrupted.

“The group that stayed overnight and took short naps still suffered from the effects of sleep deprivation and made significantly more errors on the tasks than their counterparts who went home and obtained a full night of sleep,” Fenn said. “However, every 10-minute increase in SWS reduced errors after interruptions by about 4%.”

These numbers may seem small but when considering the types of errors that are likely to occur in sleep-deprived operators — like those of surgeons, police officers or truck drivers — a 4% decrease in errors could potentially save lives, Fenn said.

“Individuals who obtained more SWS tended to show reduced errors on both tasks. However, they still showed worse performance than the participants who slept,” she said.

Fenn hopes that the findings underscore the importance of prioritizing sleep and that naps — even if they include SWS — cannot replace a full night of sleep.

Acute and chronic sleep loss are linked with a range of negative physiological and psychological outcomes (Kecklund & Axelsson, 2016). While complete sleep deprivation rapidly impedes simple and complex cognitive functions, sleep restriction impairs whole‐body homeostasis, leading to undesirable metabolic consequences in the short‐ and longer‐term (Reutrakul & Van Cauter, 2018). Most metabolic tissues including liver (Shigiyama et al., 2018), adipose tissue (Wilms et al., 2019), and skeletal muscle are at risk of developing sleep loss‐associated adverse outcomes.

Skeletal muscle is a primary regulator of human metabolism. Sleep deprivation (Cedernaes et al., 2015, 2018) and restriction (Harfmann et al., 2015) have the potential to profoundly affect muscle health by altering gene regulation and substrate metabolism. Even relatively short periods of sleep restriction (less than a week) can compromise glucose metabolism, reduce insulin sensitivity, and impair muscle function (Bescos et al., 2018; Buxton et al., 2010).

Skeletal muscle is made up of 80% proteins and maintaining optimal muscle protein metabolism is equally critical for muscle health. In situations where skeletal muscle protein synthesis chronically lags protein degradation, a loss of muscle mass is inevitable. Low muscle mass is a hallmark of and precursor to a range of chronic health conditions, including neuromuscular disease, sarcopenia and frailty, obesity, and type II diabetes (Russell, 2010).

Population‐based studies report that the risk of developing these conditions is 15%–30% higher in individuals who regularly experience sleep deprivation, sleep restriction, and inverted sleep–wake cycles (Kowall et al., 2016; Lucassen et al., 2017; Wu et al., 2014). To this end, a growing body of evidence suggests that a lack of sleep may directly affect muscle protein metabolism (Aisbett et al., 2017; Monico‐Neto et al., 2013; Saner et al., 2020).

Rodent studies first demonstrated a possible causal link between complete sleep deprivation and disrupted muscle protein metabolism. Rats subjected to 96 hr of paradoxical sleep deprivation, where rapid eye movement sleep is restricted, experienced a decrease in muscle mass (Dattilo et al., 2012) and muscle fiber cross‐sectional area (de Sa et al., 2016). In this model, sleep deprivation negatively impacted the pathways regulating protein synthesis and increased muscle proteolytic activity (de Sa et al., 2016).

These findings were paralleled by a human study reporting a catabolic gene signature in skeletal muscle following one night of total sleep deprivation in healthy young males (Cedernaes et al., 2018). To expand on this acute model, investigators recently demonstrated that five consecutive nights of sleep restriction (4 hr per night) reduced myofibrillar protein synthesis in healthy young males when compared to normal sleep patterns (Saner et al., 2020). The possible mechanisms underlying these effects might involve the hormonal environment.

Factors that regulate skeletal muscle protein metabolism at the molecular level are influenced by mechanical (muscle contraction), nutritional (dietary protein intake), and hormonal inputs (Russell, 2010). Testosterone and IGF‐1 positively regulate muscle protein anabolism by promoting muscle protein synthesis (Sheffield‐Moore et al., 1999; Urban et al., 1995), while repressing the genes that activate muscle protein degradation (Zhao et al., 2008).

Testosterone binds its specific nuclear receptor, the androgen receptor (AR), at the surface of the muscle fiber and triggers the non‐DNA binding‐dependent activation of the Akt/MTOR pathway (Urban et al., 1995), while IGF‐1 directly upregulates skeletal muscle protein synthesis by activating PI3k/Akt/mTOR (Velloso, 2008). In contrast, cortisol drives catabolism by activating key muscle protein degradation pathways (Kayali et al., 1987).

Experimental evidence suggests that acute and chronic sleep loss alter anabolic (Leproult & Van Cauter, 2011; Reynolds et al., 2012) and catabolic (Cedernaes et al., 2018; Dáttilo et al., 2020) hormone secretion patterns in humans. On this basis, we hypothesized that one night of sleep deprivation would decrease muscle protein synthesis and that the hormonal environment may provide a possible mechanism for impaired muscle protein metabolism.

While our understanding of the health consequences of sleep deprivation continues to improve, important gaps and opportunities remain. This includes linking acute mechanistic changes with clinically observable outcomes and moving toward a more prescriptive, individualized understanding of sleep deprivation by examining sex‐based differences. In this study, we sought to determine if one night of complete sleep deprivation promotes a catabolic hormonal environment and compromises postprandial muscle protein synthesis and markers of muscle protein degradation in young, healthy male and female participants.

reference link:

Original Research:
“Slow-wave sleep during a brief nap is related to reduced cognitive deficits during sleep deprivation” by Kimberly Fenn et al. Sleep


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