Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 2014 Jul 1;37(7):1227-36.
doi: 10.5665/sleep.3844.

Obstructive sleep apnea in older adults is a distinctly different physiological phenotype

Affiliations

Obstructive sleep apnea in older adults is a distinctly different physiological phenotype

Bradley A Edwards et al. Sleep. .

Abstract

Study objectives: Current evidence suggests that the pathological mechanisms underlying obstructive sleep apnea (OSA) are altered with age. However, previous studies examining individual physiological traits known to contribute to OSA pathogenesis have been assessed in isolation, primarily in healthy individuals.

Design: We assessed the four physiological traits responsible for OSA in a group of young and old patients with OSA.

Setting: Sleep research laboratory.

Participants: Ten young (20-40 y) and old (60 y and older) patients with OSA matched by body mass index and sex.

Measurements and results: Pharyngeal anatomy/collapsibility, loop gain (LG), upper airway muscle responsiveness/gain (UAG) and the respiratory arousal threshold were determined using multiple 2- to 3-min decreases or drops in continuous positive airway pressure (CPAP). Passive pharyngeal anatomy/collapsibility was quantified as the ventilation at CPAP = 0 cmH2O immediately after the CPAP drop. LG was defined as the ratio of the ventilatory overshoot to the preceding reduction in ventilation. UAG was taken as the ratio of the increase in ventilation to the increase in ventilatory drive across the pressure drop. Arousal threshold was estimated as the ventilatory drive that caused arousal. Veupnea was quantified as the mean ventilation prior to the pressure drop. In comparison with younger patients with OSA, older patients had a more collapsible airway (ventilation at 0 cmH2O = 3.4 ± 0.9 versus 1.5 ± 0.7 L/min; P = 0.05) but lower Veupnea (8.2 ± 0.5 versus 6.1 ± 0.4 L/min; P < 0.01) and a lower LG (5.0 ± 0.7 versus 2.9 ± 0.5; P < 0.05). The remaining traits were similar between groups.

Conclusions: Our data suggest that airway anatomy/collapsibility plays a relatively greater pathogenic role in older adults, whereas a sensitive ventilatory control system is a more prominent trait in younger adults with obstructive sleep apnea.

Citation: Edwards BA, Wellman A, Sands SA, Owens RL, Eckert DJ, White DP, Malhotra A. Obstructive sleep apnea in older adults is a distinctly different physiological phenotype.

Keywords: aging; loop gain; lung; obstructive sleep apnea; sleep disordered breathing; upper airway collapsibility.

PubMed Disclaimer

Figures

Figure 1
Figure 1
Technique for determining the physiological traits using continuous positive airway pressure (CPAP) drops. A representative example of a CPAP drop to demonstrate how all the changes in ventilation was used to assess the physiological traits. The top panel shows CPAP being dropped from the therapeutic level of 9 cmH2O to a sub-therapeutic level of 3.5 cmH2O. The effect that the CPAP reduction has on flow, tidal volume and minute ventilation is also shown. Resting ventilation (Veupnea) is determined from the 60-sec average of ventilation preceding the CPAP drop. When CPAP is dropped there is an immediate reduction in flow (due to airway narrowing) that is reflected in the measured tidal volume and calculated minute ventilation. The reduction in ventilation leads to an increase in respiratory drive (labeled Vr). We measure how much ventilatory drive accumulates by rapidly restoring CPAP to the therapeutic level and measuring the overshoot in ventilation (Vr). The ratio of this ventilatory response or overshoot (Vr) to the net reduction in ventilation during the drop period (Vd) provides a measure of loop gain (Vr/Vd). A delay and time constant are also estimated from the dynamics of the ventilatory overshoot. In response to the increase in drive (Vr), the subject activates his or her upper airway muscles and partially reopens the airway, allowing for ventilation to recover slightly (Vuag: determined by subtracting the mean ventilation on the last three breaths [open circles] of the drop from the mean ventilation of breaths two and three of the drop [circled]). The ratio of the compensatory increase in ventilation (Vuag) to the increase in ventilatory drive (Vr) across the drop provides a measure of neuromuscular compensation (Vuag/Vr), which we refer to as the upper airway gain (UAG). The breaths (two to three) following the reduction in CPAP were used to calculate the pharyngeal collapsibility or (see text for details) – the inset shows how the breaths from the current drop [circled] are placed on a graph of ventilation vs. mask pressure in order to calculate. Finally, if an arousal occurs during a drop, we quantify the arousal threshold as the level of ventilatory drive immediately preceding the arousal. However, in the example shown, there was no EEG arousal and thus this drop could not be used to determine arousal threshold.
Figure 2
Figure 2
Effect of aging on loop gain and its components, controller and plant gain. The loop gain magnitude was approximately 50% (43% reduction) lower in the older subjects compared to the young subjects with OSA (A). The reduction in loop gain was driven by reductions in controller gain (B) with aging, as plant gain (C) remained unchanged. * P < 0.05.
Figure 3
Figure 3
Relationship between respiratory event length and respiratory control indices. Pooling the average respiratory event duration data from all young (black circles) and old (white circles) subjects, we found that loop gain magnitude (A) was inversely associated with NREM respiratory event duration (i.e., the lower the loop gain magnitude the longer the respiratory event), a relationship driven by controller gain (B).
Figure 4
Figure 4
Effect of aging on the other pathophysiological obstructive sleep apnea traits. Aging was associated with a worsening of the passive airway collapsibility as measured by 0 (A); however, there was no difference in the arousal threshold (B) or the upper airway gain (C) between the two groups. * P = 0.05.
Figure 5
Figure 5
Differences in obstructive sleep apnea (OSA) pathogenesis between young and old subjects. Mean data of resting ventilation and the four physiological traits in young (A) and older subjects (B). Aging significantly reduced resting ventilation (P < 0.05) and the passive anatomy or 0 (P = 0.05) by approximately 2 L/min during stable NREM sleep. Loop gain (LG) was reduced with age (P < 0.05); however, the arousal threshold and the upper airway gain remained unchanged. Note that both young subjects and older subjects have OSA for different reasons: young people primarily have a disorder of high ventilatory drive and LG, whereas in older individuals OSA primarily occurs due to a poor upper airway anatomy/collapsibility. If young people had a ventilatory drive and LG similar to older adults, our model predicts that the new steady-state ventilation (i.e., where the LG line and upper airway response line intersect) would lie in the stable region (i.e., to the left of the arousal threshold line) and that they would not have OSA (C). Similarly, if older adults improved their poor passive anatomy, our model would also predict OSA resolution (D).

Comment in

Similar articles

Cited by

References

    1. Young T, Palta M, Dempsey J, Skatrud J, Weber S, Badr S. The occurrence of sleep-disordered breathing among middle-aged adults. N Engl J Med. 1993;328:1230–5. - PubMed
    1. Roth T, Roehrs T, Rosenthal L. Hypersomnolence and neurocognitive performance in sleep apnea. Curr Opin Pulm Med. 1995;1:488–90. - PubMed
    1. Peppard PE, Young T, Palta M, Skatrud J. Prospective study of the association between sleep-disordered breathing and hypertension. N Engl J Med. 2000;342:1378–84. - PubMed
    1. Shahar E, Whitney CW, Redline S, et al. Sleep-disordered breathing and cardiovascular disease: cross-sectional results of the Sleep Heart Health Study. Am J Respir Crit Care Med. 2001;163:19–25. - PubMed
    1. Young T, Shahar E, Nieto FJ, et al. Predictors of sleep-disordered breathing in community-dwelling adults: the Sleep Heart Health Study. Arch Intern Med. 2002;162:893–900. - PubMed

Publication types

-