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Sympathetic transduction to blood pressure following a three-day sojourn in hypobaric hypoxia: influence of nocturnal periodic breathing
Fisher F, Roche J, Duffy A, Ibrahim A, Turner R, Vinetti G, Cesari M, Furian M,
Rachel Turner, Giovanni Vinetti, Hannes Gatterer, Christoph Siebenmann
The vascular responsiveness to sympathetic nerve activity (i.e., sympathetic transduction) is preserved with acute hypoxia but diminishes with acclimation to chronic hypoxia. However, it is unclear whether such reductions in sympathetic transduction are already present after three days, which would be a typical time for recreational mountaineers to be at high altitude. Furthermore, the mechanisms for the reduced sympathetic transduction with chronic hypoxia are unclear but could relate to the nocturnal periodic breathing (nPB) that characterizes sleep in hypoxia since, at sea level, sleep-disordered breathing is also associated with blunted sympathetic transduction. Using a randomized, placebo-controlled, cross-over protocol, we thus explored whether nPB diminishes sympathetic transduction during a three-day sojourn in hypoxia. In twelve young, healthy males, muscle sympathetic nerve activity (MSNA; microneurography) and beat-to-beat blood pressure (finger photoplethysmography) were measured first in normoxia, and then at the end of two three-day sojourns in hypobaric hypoxia (equivalent to 4,000m altitude), where nPB was either allowed to occur (PB+) or prevented by increased inspiratory carbon dioxide (PB-). Sympathetic transduction was quantified using burst-triggered signal-averaging, where the mean arterial pressure (MAP) response to a MSNA burst was tracked over 15 cardiac cycles. At the end of the nPB+ and nPB- sojourns, MSNA burst frequency was increased by 118±103% and 107±101%, respectively, with no difference between sojourns (p≥0.80). The transient increase in MAP following a sympathetic burst was not different between measurement time points (peak +2.8±2.2, +2.8±2.0 and +3.3±2.3 mmHg, for normoxia, nPB+ and nPB-, respectively; p=0.208). Conversely, the transient decrease in MAP following cardiac cycles without a sympathetic burst tended to be similarly increased at the end of nPB+ and nPB- sojourns compared to normoxia (nadir -1.3±0.6, -2.0±0.9 and -2.3±1.6 mmHg, for normoxia, nPB+ and nPB- respectively; p=0.051). In summary, three days exposure to hypobaric hypoxia did not diminish the pressor response following a spontaneous MSNA burst, regardless of the severity of nPB. The larger drop in MAP following cardiac cycles without a sympathetic burst, however, suggests that hypoxia increases the importance of the sympathetic vasoconstrictor support of beat-to-beat MAP.
DOI: 10.1152/physiol.2025.40.S1.0665
