Effects of hypoxia on sympathetic neural control in humans.

This special issue is principally focused on the time domain of the adaptive mechanisms of ventilatory responses to short-term, long-term and intermittent hypoxia. The purpose of this review is to summarize the limited literature on the sympathetic neural responses to sustained or intermittent hypoxia in humans and attempt to discern the time domain of these responses and potential adaptive processes that are evoked during short and long-term exposures to hypoxia.

Effect of sleep restriction on orthostatic cardiovascular control in humans.

We hypothesized that sleep restriction (4 consecutive nights, 4 h sleep/night) attenuates orthostatic tolerance. The effect of sleep restriction on cardiovascular responses to simulated orthostasis, arterial baroreflex gain, and heart rate variability was evaluated in 10 healthy volunteers. Arterial baroreflex gain was determined from heart rate responses to nitroprusside-phenylephrine injections, and orthostatic tolerance was tested via lower body negative pressure (LBNP). A Finapres device measured finger arterial pressure. No difference in baroreflex function, heart rate variability, or LBNP tolerance was observed with sleep restriction (P > 0.3). Systolic pressure was greater at -60 mmHg LBNP after sleep restriction than before sleep restriction (110 +/- 6 and 124 +/- 3 mmHg before and after sleep restriction, respectively, P = 0.038), whereas heart rate decreased (108 +/- 8 and 99 +/- 8 beats/min before and after sleep restriction, respectively, P = 0.028). These data demonstrate that sleep restriction produces subtle changes in cardiovascular responses to simulated orthostasis, but these changes do not compromise orthostatic tolerance.

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

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 min 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.