Aging and sleep: physiology and pathophysiology

Abstract

Aging effects on sleep are important to consider for the practicing pulmonologist due to the increase in prevalence of major respiratory disorders as well as the normal changes that occur in sleep patterns with aging. Typically, aging is associated with decreases in the amount of slow wave sleep and increases in stage 1 and 2 non-rapid eye movement sleep, often attributed to an increased number of spontaneous arousals that occur in the elderly. Elderly individuals tend to go to sleep earlier in the evening and wake earlier due to a phase advance in their normal circadian sleep cycle. Furthermore the development of sleep-related respiratory disorders such as obstructive sleep apnea (OSA) and central sleep apnea or Cheyne-Stokes respiration (CSA-CSR) associated with congestive heart failure (CHF) occur with increasing prevalence in the elderly. The development of such disorders is often of major concern because they are associated with systemic hypertension and cardiovascular disease, metabolic disorders such as diabetes, and impaired neurocognition. The present review reflects the current understanding of the normal changes in sleep patterns and sleep needs with advancing age, in addition to the effect that aging has on the predisposition to and consequences of OSA and CSA-CSR associated with CHF.

Figure 1

Effect of aging on the architecture of sleep. The top panel depicts the different stages of sleep and their associated characteristics. The bottom panel is an example of a typical hypnogram from a healthy young adult aged 24 years and a healthy elderly individual aged 72 years. It demonstrates the cycling between non–rapid eye movement (NREM) and rapid eye movement (REM) (black bars) throughout the night, with more stage 3 and 4 NREM sleep or slow wave sleep (SWS) during the early part of the night and the increased proportion of REM in the early hours. Note that elderly individuals have a reduction in SWS and REM as well as the frequent arousals/awakenings. N1–N4, non–rapid eye movement sleep stages 1 through 4.

Figure 2

An example of obstructive sleep apnea (OSA). Polysomnographic example from a clinical study in a patient with severe OSA (apnea/hypopnea index = 55.5 events per hour). Note that despite the repeated respiratory efforts to breathe (thoracic and abdomen), there is no nasal airflow, indicating the airway has become obstructed. Such obstructions are often associated with repeated oxygen desaturations and arousals (gray boxes) from sleep. EKG, electrocardiogram; EEG, electroencephalogram (C3-A2); SaO₂, arterial blood oxygen saturation.

Figure 3

Summary of the potential aging effects on the pathogenesis of obstructive sleep apnea (OSA). Schematic of the various phenotypical traits or factors that contribute to OSA and how aging may affect them to increase the incidence of OSA in the elderly. Furthermore both the intermediate effects of OSA and the long-term consequences are also depicted. Refer to the text for further detail.

Figure 4

An example of Cheyne-Stokes respiration associated with congestive heart failure. Polysomnographic example from a clinical study in a patient with congestive heart failure and central sleep apnea (CHF-CSA). Note the waxing and waning that occur in respiration and presence of repeated central apneas. Like OSA, the repeated apneas are often associated with repeated oxygen desaturations, arousals, and fluctuations in blood pressure and heart rate. EKG, electrocardiogram; BP, blood pressure; EEG, electroencephalogram (C4-A1, O2-A1); SaO₂, arterial blood oxygen saturation; TcCO₂, transcutaneous carbon dioxide.