Editor's Note: Commentary based on Dawn simulation light: a potential cardiac events protector. Viola AU, Gabel V, Chellappa SL, Schmidt C, Hommes V, Tobaldini E, Montano N, Cajochen C. Sleep Med. 2015 Apr;16(4):457-61.

Background:

Cardiovascular events have a bimodal distribution primarily occurring between 0600-1200 and 1801-0000. An abrupt change in sympatho-vagal cardiac control as part of the transition from sleep to wakefulness may be responsible for this circadian variability. The authors hypothesized that a more "naturalistic" (gradual) exposure to light, simulating sunrise, during sleep to wake transition could optimizing sympatho-vagal tone decreasing abrupt changes in heart rate and heart rate variability.

Methods:

Seventeen healthy men between the ages of 20-33 had a baseline sleep study to rule out sleep disorders and were asked to keep a fixed schedule, minimize alcohol and caffeine intake and sleep 8 hours, which was confirmed with a wrist activity monitor. Subjects were then kept in dark bedrooms without any information as to time of day for 48 hours. All participants were exposed to dim light (8 lux) for the two hours after waking up and then to slightly brighter, but still dim light (40 lux) until bedtime. Subjects were restricted to sleep 6 hours overnight and in a counter balanced within subject design, either woken up by the technician's voice (control condition) or dawn light simulation (DSL) (intervention condition). DSL involved gradually increasing the light from 0 to 250 lux for the 30 minutes prior to waking up. Light then remained at that brightness for 20 minutes after waking up. Subjects had blood pressures measured on waking up along with salivary cortisol. Heart rate variability was measured using a two-derivation ECG system in accordance with guidelines by the Task Force on HRV Interpretation.

Results:

DSL led to a significant gradient reduction in heart rate during transition from sleep to wakefulness as compared to the control condition. In the control condition subjects had an increase in heart rate from 63.6±2.5 to 89.7±3.7 while DSL resulted in an increase from 65.5±4.8 to 78.4±5 (p <0.05). Comparing baseline data, 30 minutes prior to scheduled awakening and post awakening, heart rate increased in the DSL group 30 minutes prior to scheduled awakening. After awakening the increase in heart rate with DSL was significantly lower than during the control condition. Cardiac sympatho-vagal modulation increased more smoothly under DSL as compared to control conditions. Sympathetic cardiac tone remained stable under both conditions, however parasympathetic tone only remained stable when the subjects were under DSL conditions.

Conclusion:

The authors concluded that DSL, or more naturalistic, light exposure might be cardio protective in healthy young men who underwent mild sleep restriction as awakening with DSL led to a flatter slope for heart rate increase and more stable sympatho-vagal control which may decrease cardiovascular events at sleep wake transition. The authors suggest that this study could trigger further research on gradual exposure to light as a non-invasive tool to decrease cardiovascular events in the early morning hours.

Commentary:

Risk of sudden death from cardiac causes is significantly greater during the morning hours after waking up then during other times of the day.^1-4 This circadian variability has also been demonstrated with cerebrovascular accidents and in prospective observational hospital based studies.^5,6 Similarly the TRIMM study found that the incidence of myocardial ischemia was highest in the 3 hours after awakening, when adjusted for awakening time.⁷ It has been proposed that a dysfunction of the circadian clock may contribute to increases in heart rate and heart rate variability and may be a factor in the predisposition to cardiovascular events in the early morning.

Heart rate variability is a widely used tool to investigate autonomic cardiovascular function and changes in sympatho-vagal balance manifested by altered responsiveness to an excitatory stimulus or changes in oscillatory patterns noted in many disease states.⁸ The DSL study investigated if a naturalistic light stimulating sunrise would result in a smoother increase in heart rate and decrease heart rate variability during transition from sleep to wakefulness.⁹ Subjects were in a similar state before DSL, heart rate significantly increased in the first 30 minutes of exposure to DSL and then the rate was increase was lower immediately after wake up. The researchers found that during sleep wake transition, sympathetic cardiac predominance was stable in both experimental settings while parasympathetic cardiac activity was stable only when subjects were exposed to DSL suggesting that sunrise simulation may minimize the sharp decrease is in parasympathetic cardiac control, minimizing abrupt cardiovascular events. Authors also noted that under DSL salivary cortisol levels were higher following wake-up time perhaps due to phase advancement which may prepare the body for waking up.

This is a small study of the effects of sunrise simulation during sleep wake transition in young healthy subjects without underlying medical issues during two nights of mild sleep restriction. While the study shows some promising effects on heart rate variability, it is difficult to translate this data to clinical use in middle-aged or older individuals with multiple cardiovascular risk factors and underlying illnesses. This study does provide an avenue of exploration of this noninvasive and relatively inexpensive tool in trials of risk factor reduction for cardiovascular illnesses.

References

1. Cohen MC, Rohtla KM, Lavery CE, Muller JE, Mittleman MA. Meta-analysis of the morning excess of acute myocardial infarction and sudden cardiac death. Am J Cardiol 1997;79:1512-6.
2. Atkinson G. Circadian variation in the circulatory responses to exercise: relevance to the morning peaks in strokes and cardiac events. Eur J Appl Physiol 2010;108:15-29.
3. Muller JE. Circadian variation in the frequency of sudden cardiac death. Circulation 1987;75:131-8.
4. Pasqualetti P, Colantonio D, Casale R, Acitelli P, Natali G. The chronobiology of sudden cardiac death. The evidence for a circadian, circaseptimanal and circannual periodicity in its incidence. Minerva medica 1990;81:391-398.
5. Turin TC, Kita Y, Rumana N et al. Morning surge in circadian periodicity of ischaemic stroke is independent of conventional risk factor status: findings from the Takashima Stroke Registry 1990-2003. Eur J Neurol 2009;16:843-851.
6. Gupta A, Shetty H. Circadian variation in stroke - a prospective hospital-based study. Int J Clin Practice 2005;59:1272-1275.
7. Willich SN, Lowel H, Lewis M et al. Association of wake time and the onset of myocardial infarction. Triggers and mechanisms of myocardial infarction (TRIMM) pilot study. TRIMM Study Group. Circulation 1991;84:VI62-7.
8. Montano N, Porta A, Cogliati C et al. Heart rate variability explored in the frequency domain: a tool to investigate the link between heart and behavior. Neurosci Biobehav Rev 2009;33:71-80.
9. Viola AU, Gabel V, Chellappa SL et al. Dawn simulation light: a potential cardiac events protector. Sleep Med 2015;16:457-61.

Keywords: Adult, Alcohols, Blood Pressure, Caffeine, Cardiovascular Diseases, Death, Sudden, Electrocardiography, Heart Rate, Hydrocortisone, Incidence, Middle Aged, Myocardial Ischemia, Polysomnography, Prospective Studies, Research Personnel, Risk Factors, Sleep, Sleep Wake Disorders, Stroke, Tachycardia, Wakefulness, Young Adult

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