Short-term intermittent hypoxia enhances sympathetic responses to continuous hypoxia in humans.

Autor: Leuenberger, Urs A., Cynthia S. Hogeman, Sadeq Quraishi, Latoya Linton-Frazier, And Kristen S. Gray
Předmět:
Zdroj: Journal of Applied Physiology; Sep2007, Vol. 103 Issue 3, p835-842, 8p, 1 Diagram, 3 Charts, 3 Graphs
Abstrakt: Short-term intermittent hypoxia leads to sustained sympathetic activation and a small increase in blood pressure in healthy humans. Because obstructive sleep apnea, a condition associated with intermittent hypoxia, is accompanied by elevated sympathetic activity and enhanced sympathetic chemoreflex responses to acute hypoxia, we sought to determine whether intermit- tent hypoxia also enhances chemoreflex activity in healthy humans. To this end, we measured the responses of muscle sympathetic nerve activity (MSNA, peroneal microneurography) to arterial chemoreflex stimulation and deactivation before and following exposure to a paradigm of repetitive hypoxic apnea (20 s/min for 30 mon; O2 saturation nadir 81.4 ± 0.9%). Compared with baseline, repetitive hypoxic apnea increased MSNA from 113 ± 11 to 159 ± 21 units/min (P = 0.001) and mean blood pressure from 92.1 ± 2.9 to 95.5 ± 2.9 mmHg (P = 0.01; n = 19). Furthermore, compared with before, following intermittent hypoxia the MSNA (units/mm) responses to acute hypoxia [fraction of inspired O2 (FIO2) 0.1, for 5 min] were enhanced (pre- vs. post-intermittent hypoxia: + 16 ± 4 vs. +49 ± 10%; P = 0.02; n = 11), whereas the responses to hyperoxia (Fl02 0.5, for 5 mm) were not changed significantly (P = NS; n = 8). Thus 30 mm of intermittent hypoxia is capable of increasing sympathetic activity and sensitizing the sympathetic reflex responses to hypoxia in normal humans. Enhanced sympathetic chemoreflex activity induced by intermittent hypoxia may contribute to altered neuro- circulatory control and adverse cardiovascular consequences in sleep apnea. [ABSTRACT FROM AUTHOR]
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