Combined hypoxia and hypercapnia evokes long-lasting sympathetic activation in humans

Abstract

We studied ventilatory and neurocirculatory responses to combined hypoxia (arterial O2 saturation 80%) and hypercapnia (end-tidal CO2 + 5 Torr) in awake humans. This asphyxic stimulus produced a substantial increase in minute ventilation (6.9 +/- 0.4 to 20.0 +/- 1.5 l/min) that promptly subsided on return to room air breathing. During asphyxia, muscle sympathetic nerve activity (intraneural microelectrodes) increased to 220 +/- 28% of the room air baseline. Approximately two-thirds of this sympathetic activation persisted after return to room air breathing for the duration of our measurements (20 min in 8 subjects, 1 h in 2 subjects). In contrast, neither ventilation nor sympathetic outflow changed during time control experiments. A 20-min exposure to hyperoxic hypercapnia also caused a sustained increase in sympathetic activity, but, unlike the aftereffect of asphyxia, this effect was short lived and coincident with continued hyperpnea. In summary, relatively brief periods of asphyxic stimulation cause substantial increases in sympathetic vasomotor outflow that outlast the chemical stimuli. These findings provide a potential explanation for the chronically elevated sympathetic nervous system activity that accompanies sleep apnea syndrome.

Spontanous periodic breathing is associated with sympathetic hyperreactivity and baroreceptor dysfunction in hypertension

“…[4,5] Morgan et al demonstrated in healthy volunteers that hypoxic hypercapnia leads to a protracted increase in MSA, whereas hyperoxic hypercapnia only transiently increases sympathetic activity indicating that hypoxemia is responsible for the effect. [40] Chronic intermittent hypoxia has thus clinically relevant prolonged effects on blood pressure in animal models.…”

Effect of facial cooling and cold air inhalation on sympathetic nerve activity in men

“…Alterations of ventilation or blood gases may also have caused modulations in MSNA during the different cold stimuli (Hardy et al, 1994;Morgan et al, 1995). In our study, respiratory movements were monitored with a strain gauge strapped around the chest with a rubber band to control the inadvertent apneas and irregular breathing.…”

Sympathovagal balance changes in sleep breathing disorders

“…The mechanisms implicated in this phenomenon are still unclear. Firstly, it has been hypothesized that the effect of sympathetic excitation induced by hypoxia might persist for a long time, also during normo-oxygenation conditions (28,29). Secondly, a potentiation of peripheral chemo-reflex responses has been detected in OSA subjects, possibly contributing to maintain a tonic sympathetic excitation during wakefulness (27,30).…”