Puberty and upper airway dynamics during sleep.

NORMAL CHILDREN HAVE FEWER OBSTRUCTIVE APNEAS DURING SLEEP THEN DO NORMAL ADULTS.1,2 CONSISTENT WITH THIS CLINICAL FINDING, WE HAVE previously shown that normal children are able to maintain near-constant inspiratory airflow despite the application of increasing subatmospheric nasal pressure loads during sleep, i.e., the pediatric upper airway appears to dynamically regulate airflow.3–5 This compensatory response to upper airway subatmospheric pressure loading declines with age.4,5 However, the upper airway response to subatmospheric pressure loading has not been studied in detail during puberty and adolescence, the transitional period from childhood to adulthood. In children, most community-based studies have shown that the prevalence of obstructive sleep apnea syndrome (OSAS) is similar amongst boys and girls,6–9 although this is somewhat controversial, as 1 study showed a higher prevalence of obstructive apneas in infant boys than girls,10 and some studies have shown more snoring in boys than in girls.11,12 In adults, the prevalence of OSAS in men is about 3 times that of premenopausal women.13 The prevalence of OSAS then increases in women after menopause.14 This epidemiology suggests that sex hormones play a critical role in upper airway function, with male sex hormones associated with increased upper airway collapsibility and female sex hormones having a protective effect. During puberty, sex hormone levels progress from minimally detectable to adult levels, making puberty the ideal natural physiologic model with which to determine the role of sex hormones on upper airway function during sleep. We therefore studied upper airway dynamic function during sleep in males and females at different stages of puberty. Our initial hypothesis was that the upper airway compensatory response to a subatmospheric pressure load declines with increasing pubertal Tanner stage in males but remains stable during puberty in females. For this study, we measured the upper airway pressure-flow relationship during sleep, using techniques similar to those previously used to evaluate the upper airway in children and adults.3–5,15–20 This approach is based on the concept that the upper airway functions as a simple collapsible tube, as predicted by the Starling resistor model.21 According to this model, under conditions of flow limitation, maximal inspiratory airflow is determined by the pressure changes upstream (nasal) to a collapsible locus of the upper airway and is independent of the downstream (hypopharyngeal) pressure generated by the diaphragm. The upper airway can be represented as a tube with a collapsible segment, the resistance of which is 0. The segments upstream and downstream from the collapsible segment have fixed diameters and resistances. Upstream (nasal) resistance (RN) can be determined by calculating the reciprocal of the slope of the pressure-flow curve. In this model of the upper airway, inspiratory pressure at the nares is atmospheric and downstream pressure is equal to hypopharyngeal/tracheal pressure. Collapse would occur when the pressure surrounding the collapsible segment of the upper airway (critical tissue pressure, Pcrit) becomes greater than the pressure within the collapsible segment of the airway. In the normal subject with low upstream resistance or subatmospheric Pcrit, who is breathing at atmospheric pressure, the downstream pressure never drops to Pcrit; thus, airflow is not limited and is largely determined by negative tracheal (inspiratory) pressure. However, if the downstream pressure falls below Pcrit, inspiratory flow (VImax) reaches a maximum (inspiratory airflow limitation) and becomes independent of downstream pressure swings. Under these circumstances, RN and Pcrit determine maximal inspiratory flow, as described by the following equation: VImax = (PN − Pcrit)/RN. The slope of the pressure-flow curve (SPF) represents the conductance of the upper airway (1/RN). Airflow will become 0 (i.e., the airway will occlude) when PN falls below Pcrit. Thus, both Pcrit and SPF can be used to characterize the flow response to changes in PN. This is analogous to using both the slope and X-intercept of the minute ventilation-Pco2 curve in order to characterize the sensitivity of the ventilatory response to hypercapnia. Previous studies in children have found a very flat SPF. This precludes the determination of Pcrit in many subjects, as airway collapse does not occur even at maximal subatmospheric PN.3–5 Therefore, pediatric studies have used the SPF as the primary outcome parameter.