Validation of Fitbit Charge 2 Sleep and Heart Rate Estimates Against Polysomnographic Measures in Shift Workers: Naturalistic Study

Background Multisensor fitness trackers offer the ability to longitudinally estimate sleep quality in a home environment with the potential to outperform traditional actigraphy. To benefit from these new tools for objectively assessing sleep for clinical and research purposes, multisensor wearable devices require careful validation against the gold standard of sleep polysomnography (PSG). Naturalistic studies favor validation. Objective This study aims to validate the Fitbit Charge 2 against portable home PSG in a shift-work population composed of 59 first responder police officers and paramedics undergoing shift work. Methods A reliable comparison between the two measurements was ensured through the data-driven alignment of a PSG and Fitbit time series that was recorded at night. Epoch-by-epoch analyses and Bland-Altman plots were used to assess sensitivity, specificity, accuracy, the Matthews correlation coefficient, bias, and limits of agreement. Results Sleep onset and offset, total sleep time, and the durations of rapid eye movement (REM) sleep and non–rapid-eye movement sleep stages N1+N2 and N3 displayed unbiased estimates with nonnegligible limits of agreement. In contrast, the proprietary Fitbit algorithm overestimated REM sleep latency by 29.4 minutes and wakefulness after sleep onset (WASO) by 37.1 minutes. Epoch-by-epoch analyses indicated better specificity than sensitivity, with higher accuracies for WASO (0.82) and REM sleep (0.86) than those for N1+N2 (0.55) and N3 (0.78) sleep. Fitbit heart rate (HR) displayed a small underestimation of 0.9 beats per minute (bpm) and a limited capability to capture sudden HR changes because of the lower time resolution compared to that of PSG. The underestimation was smaller in N2, N3, and REM sleep (0.6-0.7 bpm) than in N1 sleep (1.2 bpm) and wakefulness (1.9 bpm), indicating a state-specific bias. Finally, Fitbit suggested a distribution of all sleep episode durations that was different from that derived from PSG and showed nonbiological discontinuities, indicating the potential limitations of the staging algorithm. Conclusions We conclude that by following careful data processing processes, the Fitbit Charge 2 can provide reasonably accurate mean values of sleep and HR estimates in shift workers under naturalistic conditions. Nevertheless, the generally wide limits of agreement hamper the precision of quantifying individual sleep episodes. The value of this consumer-grade multisensor wearable in terms of tackling clinical and research questions could be enhanced with open-source algorithms, raw data access, and the ability to blind participants to their own sleep data.

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Validation of Fitbit Charge 2 Sleep and Heart Rate Estimates Against Polysomnographic Measures in Shift Workers: Naturalistic Study (Preprint)

10.2196/preprints.26476 ◽

2020 ◽

Author(s):

Benjamin Stucky ◽

Ian Clark ◽

Yasmine Azza ◽

Walter Karlen ◽

Peter Achermann ◽

...

Keyword(s):

Heart Rate ◽

Eye Movement ◽

Shift Work ◽

Rem Sleep ◽

Sleep Onset ◽

Data Access ◽

Sleep Stages ◽

Rapid Eye Movement ◽

Limits Of Agreement ◽

Shift Workers

BACKGROUND Multisensor fitness trackers offer the ability to longitudinally estimate sleep quality in a home environment with the potential to outperform traditional actigraphy. To benefit from these new tools for objectively assessing sleep for clinical and research purposes, multisensor wearable devices require careful validation against the gold standard of sleep polysomnography (PSG). Naturalistic studies favor validation. OBJECTIVE This study aims to validate the Fitbit Charge 2 against portable home PSG in a shift-work population composed of 59 first responder police officers and paramedics undergoing shift work. METHODS A reliable comparison between the two measurements was ensured through the data-driven alignment of a PSG and Fitbit time series that was recorded at night. Epoch-by-epoch analyses and Bland-Altman plots were used to assess sensitivity, specificity, accuracy, the Matthews correlation coefficient, bias, and limits of agreement. RESULTS Sleep onset and offset, total sleep time, and the durations of rapid eye movement (REM) sleep and non–rapid-eye movement sleep stages N1+N2 and N3 displayed unbiased estimates with nonnegligible limits of agreement. In contrast, the proprietary Fitbit algorithm overestimated REM sleep latency by 29.4 minutes and wakefulness after sleep onset (WASO) by 37.1 minutes. Epoch-by-epoch analyses indicated better specificity than sensitivity, with higher accuracies for WASO (0.82) and REM sleep (0.86) than those for N1+N2 (0.55) and N3 (0.78) sleep. Fitbit heart rate (HR) displayed a small underestimation of 0.9 beats per minute (bpm) and a limited capability to capture sudden HR changes because of the lower time resolution compared to that of PSG. The underestimation was smaller in N2, N3, and REM sleep (0.6-0.7 bpm) than in N1 sleep (1.2 bpm) and wakefulness (1.9 bpm), indicating a state-specific bias. Finally, Fitbit suggested a distribution of all sleep episode durations that was different from that derived from PSG and showed nonbiological discontinuities, indicating the potential limitations of the staging algorithm. CONCLUSIONS We conclude that by following careful data processing processes, the Fitbit Charge 2 can provide reasonably accurate mean values of sleep and HR estimates in shift workers under naturalistic conditions. Nevertheless, the generally wide limits of agreement hamper the precision of quantifying individual sleep episodes. The value of this consumer-grade multisensor wearable in terms of tackling clinical and research questions could be enhanced with open-source algorithms, raw data access, and the ability to blind participants to their own sleep data.

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Altered heart rate variability during sleep in mild cognitive impairment

SLEEP ◽

10.1093/sleep/zsaa232 ◽

2020 ◽

Author(s):

Shawn D X Kong ◽

Camilla M Hoyos ◽

Craig L Phillips ◽

Andrew C McKinnon ◽

Pinghsiu Lin ◽

...

Keyword(s):

Older Adults ◽

Heart Rate ◽

Heart Rate Variability ◽

Cognitive Impairment ◽

Mild Cognitive Impairment ◽

Eye Movement ◽

Rem Sleep ◽

Nrem Sleep ◽

Sleep Stages ◽

Rapid Eye Movement

Abstract Study Objectives Cardiovascular autonomic dysfunction, as measured by short-term diurnal heart rate variability (HRV), has been reported in older adults with mild cognitive impairment (MCI). However, it is unclear whether this impairment also exists during sleep in this group. We, therefore, compared overnight HRV during sleep in older adults with MCI and those with subjective cognitive impairment (SCI). Methods Older adults (n = 210) underwent overnight polysomnography. Eligible participants were characterized as multi-domain MCI or SCI. The multi-domain MCI group was comprised of amnestic and non-amnestic subtypes. Power spectral analysis of HRV was conducted on the overnight electrocardiogram during non-rapid eye movement (NREM), rapid eye movement (REM), N1, N2, N3 sleep stages, and wake periods. High-frequency HRV (HF-HRV) was employed as the primary measure to estimate parasympathetic function. Results The MCI group showed reduced HF-HRV during NREM sleep (p = 0.018), but not during wake or REM sleep (p > 0.05) compared to the SCI group. Participants with aMCI compared to SCI had the most pronounced reduction in HF-HRV across all NREM sleep stages—N1, N2, and N3, but not during wake or REM sleep. The naMCI sub-group did not show any significant differences in HF-HRV during any sleep stage compared to SCI. Conclusions Our study showed that amnestic MCI participants had greater reductions in HF-HRV during NREM sleep, relative to those with SCI, suggesting potential vulnerability to sleep-related parasympathetic dysfunction. HF-HRV, especially during NREM sleep, may be an early biomarker for dementia detection.

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Hemodynamic changes associated with obstructive sleep apnea followed by arousal in a porcine model

Journal of Applied Physiology ◽

10.1152/jappl.1993.75.4.1439 ◽

1993 ◽

Vol 75 (4) ◽

pp. 1439-1443 ◽

Cited By ~ 36

Author(s):

J. M. Pinto ◽

E. Garpestad ◽

J. W. Weiss ◽

D. M. Bergau ◽

D. A. Kirby

Keyword(s):

Heart Rate ◽

Blood Flow ◽

Eye Movement ◽

Coronary Blood Flow ◽

Rem Sleep ◽

Resistance Index ◽

Nrem Sleep ◽

Sleep Stages ◽

Rapid Eye Movement ◽

Obstructive Sleep

To study the effects of airway obstruction (AWO) and arousal on coronary blood flow, mean arterial pressure (MAP), and heart rate, pigs were chronically instrumented with arterial catheters, Doppler flow probes on the left circumflex coronary artery, and electrodes for determination of sleep stages. A modified tracheostomy tube was placed in the trachea to obstruct the upper airway during sleep sessions. In control studies, during non-rapid-eye-movement (NREM) sleep, MAP was 84 +/- 2 mmHg before AWO and increased by 5 +/- 2 mmHg on arousal. MAP was lower during rapid-eye-movement (REM) sleep (62 +/- 2 mmHg), and the increase on arousal was fourfold greater (22 +/- 2 mmHg). Heart rate was similar in both sleep stages (NREM: 120 +/- 4 beats/min; REM: 124 +/- 5 beats/min) and increased significantly on arousal (NREM: 12 +/- 2 beats/min; REM: 18 +/- 1 beats/min). Coronary blood flow was similar during both stages (NREM: 43 +/- 4 ml/min; REM: 46 +/- 8 ml/min) and increased by 12–15% on arousal. Coronary vascular resistance index increased significantly by 24% on arousal from AWO during REM sleep. All increases and decreases were significant at P < 0.05. Receptor blockade studies were performed to assess alpha-adrenergic receptor involvement.

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Abstract P417: Relationship Between Blood Pressure Variability and Sleep Architecture

Circulation ◽

10.1161/circ.141.suppl_1.p417 ◽

2020 ◽

Vol 141 (Suppl_1) ◽

Author(s):

Xiaoyue Liu ◽

Jeongok G Logan ◽

Younghoon Kwon ◽

Jennifer Lobo ◽

Hyojung Kang ◽

...

Keyword(s):

Blood Pressure ◽

Eye Movement ◽

Rem Sleep ◽

Sleep Time ◽

Sleep Architecture ◽

Sleep Stages ◽

Apnea Hypopnea Index ◽

Rapid Eye Movement ◽

Sleep Studies ◽

The Relationship

Introduction: Blood pressure (BP) variability (BPV) is a novel marker for cardiovascular disease (CVD) independent of high BP. Sleep architecture represents the structured pattern of sleep stages consisting of rapid eye movement (REM) and non-rapid eye movement (NREM), and it is an important element in the homeostatic regulation of sleep. Currently, little is known regarding whether BPV is linked to sleep stages. Our study aimed to examine the relationship between sleep architecture and BPV. Methods: We analyzed in-lab polysomnographic studies collected from individuals who underwent diagnostic sleep studies at a university hospital from 2010 to 2017. BP measures obtained during one year prior to the sleep studies were included. BPV was computed using the coefficient of variation for all individuals who had three or more systolic and diastolic BP data. We conducted linear regression analysis to assess the relationship of systolic BPV (SBPV) and diastolic BPV (DBPV) with the sleep stage distribution (REM and NREM sleep time), respectively. Covariates that can potentially confound the relationships were adjusted in the models, including age, sex, race/ethnicity, body mass index, total sleep time, apnea-hypopnea index, mean BP, and history of medication use (antipsychotics, antidepressants, and antihypertensives) during the past two years before the sleep studies. Results: Our sample (N=3,565; male = 1,353) was racially and ethnically diverse, with a mean age 54 ± 15 years and a mean BP of 131/76 ± 13.9/8.4 mmHg. Among the sleep architecture measures examined, SBPV showed an inverse relationship with REM sleep time after controlling for all covariates ( p = .033). We subsequently categorized SBPV into four quartiles and found that the 3 rd quartile (mean SBP SD = 14.9 ± 2.1 mmHg) had 3.3 fewer minutes in REM sleep compared to the 1 st quartile ( p = .02). However, we did not observe any relationship between DBPV and sleep architecture. Conclusion: Greater SBPV was associated with lower REM sleep time. This finding suggests a possible interplay between BPV and sleep architecture. Future investigation is warranted to clarify the directionality, mechanism, and therapeutic implications.

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Primary vagally mediated decelerations in heart rate during tonic rapid eye movement sleep in cats

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.1998.274.4.r1136 ◽

1998 ◽

Vol 274 (4) ◽

pp. R1136-R1141 ◽

Cited By ~ 4

Author(s):

Richard L. Verrier ◽

T. Rern Lau ◽

Umesha Wallooppillai ◽

James Quattrochi ◽

Bruce D. Nearing ◽

...

Keyword(s):

Blood Pressure ◽

Heart Rate ◽

Eye Movement ◽

Arterial Blood Pressure ◽

Rem Sleep ◽

Blocking Agent ◽

Rapid Eye Movement ◽

Arterial Blood ◽

State Dependent ◽

Hippocampal Theta

Rapid eye movement (REM) sleep results in profound state-dependent alterations in heart rate. The present study describes a novel phenomenon of a primary deceleration in heart rate that is not preceded or followed by increases in heart rate or arterial blood pressure and occurs primarily during tonic REM sleep. The goals were to characterize the primary decelerations and to provide insights on the underlying central and peripheral autonomic mechanisms. Cats were chronically implanted with electrodes to record electroencephalogram, pontogeniculooccipital wave activity in lateral geniculate nucleus, hippocampal theta rhythm, electromyogram, electrooculogram, respiration (diaphragm), and electrocardiogram. Arterial blood pressure was monitored from a carotid artery catheter. R-R interval fluctuations were continuously tracked using customized software. The muscarinic blocking agent glycopyrrolate (0.1 mg/kg iv) and the β-adrenergic blocking agent atenolol (0.3 mg/kg iv) were administered in alternating sequence with a 90- to 120-min interval. Glycopyrrolate immediately eliminated the decelerations during REM sleep. Atenolol alone had no effect on their frequency. These findings suggest that a change in the centrally induced pattern of autonomic activity to the heart is responsible for the primary decelerations, namely, a bursting of cardiac vagal efferent fiber activity.

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Effects of sleep on the cardiovascular and thermoregulatory systems: a possible role for hypocretins

Journal of Applied Physiology ◽

10.1152/japplphysiol.00516.2010 ◽

2010 ◽

Vol 109 (4) ◽

pp. 1053-1063 ◽

Cited By ~ 34

Author(s):

H. Schwimmer ◽

H. M. Stauss ◽

F. Abboud ◽

S. Nishino ◽

E. Mignot ◽

...

Keyword(s):

Blood Pressure ◽

Heart Rate ◽

Eye Movement ◽

Time Of Day ◽

Male Rats ◽

State Transitions ◽

Sleep Stages ◽

Electromyographic Activity ◽

Rapid Eye Movement ◽

Hypocretin Neuron

Sleep influences the cardiovascular, endocrine, and thermoregulatory systems. Each of these systems may be affected by the activity of hypocretin (orexin)-producing neurons, which are involved in the etiology of narcolepsy. We examined sleep in male rats, either hypocretin neuron-ablated orexin/ataxin-3 transgenic (narcoleptic) rats or their wild-type littermates. We simultaneously monitored electroencephalographic and electromyographic activity, core body temperature, tail temperature, blood pressure, electrocardiographic activity, and locomotion. We analyzed the daily patterns of these variables, parsing sleep and circadian components and changes between states of sleep. We also analyzed the baroreceptor reflex. Our results show that while core temperature and heart rate are affected by both sleep and time of day, blood pressure is mostly affected by sleep. As expected, we found that both blood pressure and heart rate were acutely affected by sleep state transitions in both genotypes. Interestingly, hypocretin neuron-ablated rats have significantly lower systolic and diastolic blood pressure during all sleep stages (non-rapid eye movement, rapid eye movement) and while awake (quiet, active). Thus, while hypocretins are critical for the normal temporal structure of sleep and wakefulness, they also appear to be important in regulating baseline blood pressure and possibly in modulating the effects of sleep on blood pressure.

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1250 Agrypnia Excitata in a Patient with Paraneoplastic Autoimmune Encephalitis

SLEEP ◽

10.1093/sleep/zsaa056.1244 ◽

2020 ◽

Vol 43 (Supplement_1) ◽

pp. A476-A476

Author(s):

J L Sanchez ◽

S Saeed ◽

H Battistini

Keyword(s):

Eye Movement ◽

Rem Sleep ◽

Sleep Latency ◽

Delirium Tremens ◽

Sleep Onset ◽

Autoimmune Encephalitis ◽

Cystic Teratoma ◽

Low Grade ◽

Rapid Eye Movement ◽

Stage 1

Abstract Introduction Agrypnia Excitata (AE) is a syndrome characterized by loss of sleep with permanent motor and autonomic hyper activation. This case describes this peculiar syndrome in a patient with paraneoplastic autoimmune encephalitis. Report of Case DG is a 35 yr old male with a history of anti-Ma2 limbic encephalitis secondary to cystic teratoma of the left testis diagnosed 6 months prior to presenting in Sleep Clinic. His parents described significant sleep disturbances including short sleep and wake periods throughout the day and night with no apparent pattern, acting out dreams, motor activity during sleep including pulling at his clothes or using his hands to manipulate invisible objects. Additionally they described low-grade fevers, and severe hyperphagia. Polysomnogram showed absence of slow-wave sleep and what appeared to be an admixture of stage 1 non-rapid eye movement (NREM) with rapid-eye movement (REM) sleep. Multiple sleep-latency testing (MSLT) demonstrated a mean sleep latency of 5.2 minutes and four sleep-onset REM periods (SOREMPs). Magnetic resonance imaging of the brain revealed persistent inflammation of the mesial temporal lobes and hippocampal region. Cerebral spinal fluid testing showed persistent anti-Ma2 antibodies. Based on this clinical presentation we made a diagnosis of Agrypnia Excitata. Conclusion Agrypnia Excitata is a syndrome characterized by loss of the normal sleep-wake rhythm. Sleep consists of the disappearance of spindle-delta activities, and persistent stage 1 NREM sleep mixed with recurrent episodes of REM sleep. The second hallmark of AE is persistent motor and autonomic hyperactivity observed during wake and sleep. AE has been described in three distinct clinical syndromes: Morvan Syndrome (autoimmune encephalitis), Fatal Familial Insomnia, and Delirium tremens. The pathogenesis of AE consists of intra-limbic disconnection releasing the hypothalamus and brainstem reticular formation from cortico-limbic inhibitory control. In autoimmune encephalitis, antibodies that act on voltage-gated potassium channels within the limbic system have been implicated in the pathophysiology.

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Why Are Seizures Rare in Rapid Eye Movement Sleep? Review of the Frequency of Seizures in Different Sleep Stages

Epilepsy Research and Treatment ◽

10.1155/2013/932790 ◽

2013 ◽

Vol 2013 ◽

pp. 1-10 ◽

Cited By ~ 22

Author(s):

Marcus Ng ◽

Milena Pavlova

Keyword(s):

Eye Movement ◽

Rem Sleep ◽

Low Voltage ◽

Sleep Stage ◽

Sleep Stages ◽

Seizure Freedom ◽

Rapid Eye Movement ◽

Focal Seizures ◽

Generalized Seizures ◽

Interictal Discharges

Since the formal characterization of sleep stages, there have been reports that seizures may preferentially occur in certain phases of sleep. Through ascending cholinergic connections from the brainstem, rapid eye movement (REM) sleep is physiologically characterized by low voltage fast activity on the electroencephalogram, REMs, and muscle atonia. Multiple independent studies confirm that, in REM sleep, there is a strikingly low proportion of seizures (~1% or less). We review a total of 42 distinct conventional and intracranial studies in the literature which comprised a net of 1458 patients. Indexed to duration, we found that REM sleep was the most protective stage of sleep against focal seizures, generalized seizures, focal interictal discharges, and two particular epilepsy syndromes. REM sleep had an additional protective effect compared to wakefulness with an average 7.83 times fewer focal seizures, 3.25 times fewer generalized seizures, and 1.11 times fewer focal interictal discharges. In further studies REM sleep has also demonstrated utility in localizing epileptogenic foci with potential translation into postsurgical seizure freedom. Based on emerging connectivity data in sleep, we hypothesize that the influence of REM sleep on seizures is due to a desynchronized EEG pattern which reflects important connectivity differences unique to this sleep stage.

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Vesicular GABA-transporter neurons in the zona incerta are maximally active during non rapid-eye movement (NREM) and rapid-eye movement (REM) sleep

10.1101/2020.04.15.043372 ◽

2020 ◽

Author(s):

Carlos Blanco-Centurion ◽

SiWei Luo ◽

Aurelio Vidal-Ortiz ◽

Priyattam J. Shiromani

Keyword(s):

Eye Movement ◽

Lateral Hypothalamus ◽

Rem Sleep ◽

Sleep Onset ◽

Nrem Sleep ◽

Zona Incerta ◽

Imaging Method ◽

Rapid Eye Movement ◽

Gaba Transporter

AbstractSleep and wake are opposing behavioral states controlled by the activity of specific neurons. The neurons responsible for sleep/wake control have not been fully identifed due to the lack of in-vivo high throughput technology. We use the deep-brain calcium (Ca2+) imaging method to identify activity of hypothalamic neurons expressing the vesicular GABA transporter (vGAT), a marker of GABAergic neurons. vGAT-cre mice (n=5) were microinjected with rAAV-FLEX-GCaMP6M into the lateral hypothalamus and 21d later the Ca2+ influx in vGAT neurons (n=372) was recorded in freely-behaving mice during waking (W), NREM and REM sleep. Post-mortem analysis revealed the lens tip located in the zona incerta/lateral hypothalamus (ZI-LH) and the change in fluorescence of neurons in the field of view was as follows: 54.9% of the vGAT neurons had peak fluorescence during REM sleep (REM-max), 17.2% were NREM-max, 22.8% were wake-max while 5.1% were both wake+REM max. Thus, three quarters of the recorded vGAT neurons in the ZI-LH were most active during sleep. In the NREM-max group Ca2+ fluorescence anticipated the initiation of NREM sleep onset and remained high throughout sleep (NREM and REM sleep). In the REM-max neurons Ca2+fluorescence increased before the onset of REM sleep and stayed elevated during the episode. Activation of the vGAT NREM-max neurons in the zona incerta and dorsal lateral hypothalamus would inhibit the arousal neurons to initiate and maintain sleep.

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Regulation of REM Sleep by Inhibitory Neurons in the Dorsomedial Medulla

10.1101/2020.11.30.405530 ◽

2020 ◽

Author(s):

Joseph A. Stucynski ◽

Amanda L. Schott ◽

Justin Baik ◽

Shinjae Chung ◽

Franz Weber

Keyword(s):

Eye Movement ◽

Rem Sleep ◽

Gabaergic Neurons ◽

Inhibitory Neurons ◽

Sleep Stages ◽

Rapid Eye Movement ◽

Rapid Eye Movement Sleep ◽

Brain Rhythms ◽

Slow Activity ◽

Raphé Nuclei

ABSTRACTThe two major stages of mammalian sleep – rapid eye movement sleep (REMs) and non-REM sleep (NREMs) – are characterized by distinct brain rhythms ranging from millisecond to minute-long (infraslow) oscillations. The mechanisms controlling transitions between sleep stages and how they are synchronized with infraslow rhythms remain poorly understood. Using opto- and chemogenetic manipulation, we show that GABAergic neurons in the dorsomedial medulla (dmM) promote the initiation and maintenance of REMs, in part through their projections to the dorsal and median raphe nuclei. Fiber photometry revealed that dmM GABAergic neurons are strongly activated during REMs. During NREMs, their activity fluctuated in close synchrony with infraslow oscillations in the spindle band of the electroencephalogram, and the phase of this rhythm modulated the latency of optogenetically induced REMs episodes. Thus, dmM inhibitory neurons powerfully promote REMs, and their slow activity fluctuations may coordinate transitions from NREMs to REMs with infraslow brain rhythms.

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