Post-apneic inhalation reverses apnea-induced sympathoexcitation before restoration of blood oxygen levels

Abstract

Sleep apneas acutely increase sympathetic nerve activity (SNA) and thus arterial blood pressure. We hypothesized that after apnea, sympathoexcitation decreases before recovery of blood oxygen levels because of the predominant inhibitory effect respiratory factors exert over sympathetic nervous system activation. Seven healthy subjects were instrumented for arterial oxygen saturation (pulse oximetry, SaO2), leg muscle SNA (microneurography), and arterial pressure (Finapres). Supine subjects breathed 12% oxygen, 3% carbon dioxide, and 85% nitrogen for one rain prior to apnea at the end of a normal tidal expiration. We accounted for circulatory delay in SaO2 measurement (5.4±0.4 s, mean±SE) as the time from the termination of apnea to the midpoint of the nadir of SaO2. SaO2 decreased to average 84±3% over the final 10 seconds of apnea, and recovered only partially to average 87±3% over the 10 seconds immediately following apnea. End-expiratory apnea increased SNA 14-fold from baseline levels of 217±37 units/10 seconds to 3063±442 units/10 seconds. However, SNA decreased to 93±32 units/10 s during the first 10 seconds after apnea. These findings indicate that sympathoinhibitory effects of respiratory signals, either lung inflation receptors or central respiratory inputs, predominate over sympathoexcitatory inputs from chemoreceptors to produce immediate and complete sympathoinhibition at the termination of a voluntary apnea. Arterial baroreflexes probably also contribute to sympathoinhibition after apnea.