The prevalence of snoring clearly increases with age at least up to age 70 (1). Snoring is an inspiratory noise caused by vibration of the soft palate and posterior faucial pillars (2). Snoring corresponds to a partial obstruction of the upper airways. Complete obstruction of upper airways is followed by an apnea. Snoring is practically always present in the obstructive sleep apnea syndrome (OSAS). In a clinical case series, the occurrence of breathing abnormalities during sleep increases with age, at least up to age 60 (3). In non-clinical elderly populations, a number of studies have shown a relatively high age-associated prevalence of sleep apnea (4, 5). The results suggest that tens of millions people older than 65 years incur some form of disturbed respiration during sleep (6). Most studies examining sleep apnea in community-based elderly populations show that obstructive, rather than central, events predominate (7, 8), and OSAS continues to be modestly male predominant (6, 8).
Upper airway obstruction during sleep occurs when the activation of dilator muscles is unable to overcome the negative pharyngeal pressure (9). The genioglossus muscles (GG), which pull the tongue forward, function as muscles of inspiration opposing pharyngeal collapse due to negative pressure (10). It was proposed that hypoxia preferentially activates the genioglossus muscle relative to the diaphragm (10). Our previous studies demonstrated a reduced reflex increase in GG activity and impaired ventilatory response to hypoxic stimulation in OSAS patients (11, 12, 13).
In the present study, we investigated the possible role of the process of biological aging in the development of OSAS, as a consequence of the age-dependent reduction of the GG muscle reactivity. Is the biological aging a risk factor for OSAS?
MATERIAL AND METHODS
A group of 10 subjects aged 20-40 (G-I, mean 29.1 ±1.8 years old) and another
of 10 subjects aged 41-60 (G-II, mean 53.2 ±2.3 years old) were investigated.
All volunteers of both groups studied were healthy, normotensive, non-smokers
and weight-matched (Fig. 1
GG-EMG activity and hypoxic response
An electromyogram from the genioglossus muscle (GG-EMG) was recorded from gold cup surface electrodes (10). The electrodes were attached to the skin using double-sided adhesive disks and collodion. They were positioned in the midline 1 cm apart and halfway between the chin and the hyoid bone (14). The raw EMG signal was amplified 100 to 1000 times with 30 and 1000 Hz low- and high-frequency filters and integrated with a RC circuit. The integrator band was 70 to 1500 Hz.
In order to activate the arterial chemoreceptors, the progressive isocapnic
hypoxia test was used. Progressive hypoxia was induced by a rebreathing method
(15), using an MES-Lungtest-System (Cracow, Poland). A mask covering the nose
and mouth was connected to the instrument setup. End-tidal CO2
was continuously monitored, as was arterial O2
) with a finger oximeter.
All measurements were done in awake subjects in the sitting position. They were
allowed to breathe quietly through the apparatus until the end-tidal CO2
stabilized. Measurements were obtained during a 1-min baseline period and during
progressive normocapnic hypoxia. During the rebreathing test, end-tidal CO2
remained within 0.2% of the baseline value. During baseline time and hypoxia
test, breath-by-breath values of SaO2
in inspiratory drive, and in GG-EMG-activity were determined and analyzed for
the groups G-I and G-II. The inspiratory drive was estimated from the continuous
determination of minute ventilation (MV) and tidal volume/inspiratory time (VT/TI)
ratio. Slopes of the regression curves MV/SaO2
(l/s/%), and GG-EMG-activity/SaO2
(% of baseline/%) were compared in both groups. Values are expressed as means
±SE. Student’s t-test was used for the statistical analysis.
RESULTS AND DISCUSSION
Values of both MV and VT/TI were not different in both investigated groups during
the baseline control time (1 min before the rebreathing test). All subjects
showed a linear increase in MV, VT/TI, and GG-EMG-activity in response to progressive
isocapnic hypoxia, but the increases in these variables were significantly reduced
in the older group (G-II), as compared with the younger group (G-I) (Fig.
and Fig. 2
). The slopes of the regression curves, shown in Fig.
, were for MV/SaO2
-1.90 ±0.12 and -1.44
±0.07 and for VT/TI/SaO2
-0.049 ±0.004 and –0.029
±0.002 in G-1 and G-II groups, respectively.
Demographics (age and body mass index), systolic and diastolic pressures, and the slopes representing the inspiratory drive during progressive hypoxia in both age groups studied.
Increases in inspiratory drive, represented by VT/TI, during progressive hypoxia in G-I (*) and G-II (o) subjects. The increases differed significantly in the two groups (P<0.01).
Attenuation of the ventilatory and heart responses to hypoxia with aging in normal men has been described (16). The mechanisms underlying diminished carotid chemoreceptor reactivity remain unclear. The following factors should be taken into consideration. Aging seems to involve a modest thickening of all wall elements in both arterioles and small arteries (17, 18). Animal studies showed age-dependent morphological changes in the position, shape and size of carotid bodies (19). Thus, morphological changes in the structure of vascular wall (in older individuals the vessels are more rigid) and in the carotid body, may lead to the impairment of carotid body function. Several studies indicated functional changes in the autonomic nervous system with age, such as decreased baroreceptor sensitivity, decreased beta- and alpha-adrenergic responsiveness, reduced parasympathetic input and vagal tone (20), suggesting impairment of central and peripheral interaction between baroreceptor and chemoreceptor control.
Another element of the age-dependent impaired chemoreceptor function, shown
in the present study, is reduced hypoxic control of the GG-activity and thereby
of upper airways (Fig. 3
). This fact is in accordance with our previous
observations, indicating a linear decrease in upper airway resistance with decreasing
. These changes seem to be related to an
increase in the activity of upper airway dilator muscles – GG-EMG-activity (10).
Increases in GG-EMG-activity during progressive hypoxia in G-I (*) and G-II (o) subjects. The increases differed significantly in the two groups (P<0.01).
The present results show that in healthy subjects the defense abilities against hypoxia, considered as a dilating forces by the upper airway muscles, decrease in the course of aging. Thus, biological aging might be considered as a risk factor for increased collapsibility of upper airways.
This study was supported by KBN grant Nr 4P05B07010.
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