Literature DB >> 19820987

Peripheral chemoreflex regulation of sympathetic vasomotor tone in apnea divers.

Toni Breskovic1, Zoran Valic, Axel Lipp, Karsten Heusser, Vladimir Ivancev, Jens Tank, Gordan Dzamonja, Jens Jordan, J Kevin Shoemaker, Davor Eterovic, Zeljko Dujic.   

Abstract

OBJECTIVES: Involuntary apnea episodes in obstructive sleep apnea patients result in selective potentiation of peripheral chemoreceptor regulation of sympathetic vasomotor tone. Breath-hold diving is associated with repeated "voluntary" apnea episodes and massive arterial oxygen desaturation, which could also perturb chemoreflex function.
METHODS: We measured ventilation, heart rate, blood pressure, cardiac stroke volume, and muscle sympathetic nerve activity (MSNA) during isocapnic hypoxia in 11 breath-hold divers and eleven matched control subjects. The study was carried out at least 1 month after intense apnea training.
RESULTS: Baseline MSNA frequency was 30 +/- 4 bursts/min in control subjects and 31 +/- 7 bursts/min in divers (ns). During hypoxia MSNA frequency and total activity increased similarly in both groups (30 and 66% in controls and 27 and 60% in divers, respectively). MSNA remained increased after termination of hypoxia and approached baseline measurements after 20 min. Hypoxia-induced stimulation of minute ventilation was similar in both groups, although in divers it was maintained by higher tidal volumes and lower breathing frequency compared with control subjects. In both groups, hypoxia-induced tachycardia drove an increase in cardiac output whereas total peripheral resistance decreased. Blood pressure remained unchanged.
INTERPRETATION: We conclude that after the end of intensive training/competition periods, apnea divers show normal peripheral chemoreflex regulation of ventilation and sympathetic vasomotor tone. Although voluntary apnea may not lead to sustained changes in sympathetic nervous system regulation, we cannot exclude the possibility that repeated sympathetic activation elicited by voluntary apnea imposes a burden on the cardiovascular system.

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Year:  2009        PMID: 19820987     DOI: 10.1007/s10286-009-0034-1

Source DB:  PubMed          Journal:  Clin Auton Res        ISSN: 0959-9851            Impact factor:   4.435


  31 in total

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