Acute intermittent hypercapnic hypoxia and sympathetic neurovascular transduction in men Stuckless, Troy J.R.; Vermeulen, Tyler D.; Brown, Courtney V.; Boulet, Lindsey M.; Shafer, Brooke M.; Wakeham, Denis J.; Steinback, Craig D.; Ayas, Najib T.; Floras, John S.; Foster, Glen E.
Acute intermittent hypercapnic hypoxia (IH) induces long-lasting elevations in sympathetic vasomotor outflow and blood pressure in healthy humans. It is unknown whether IH alters sympathetic neurovascular transduction (sNVT), measured as the relationship between sympathetic vasomotor outflow and either forearm vascular conductance (FVC; regional sNVT) or diastolic blood pressure (DBP; systemic sNVT). We tested the hypothesis that IH augments sNVT by exposing healthy males to 40 consecutive 1-minute breathing cycles, each comprising 40-seconds of hypercapnic hypoxia (PETCO₂: +4±3 mm Hg above baseline; PETO₂: 48±3 mm Hg) and 20-seconds of normoxia (n=9), or a 40-minute air-breathing control (n=7). Before and after the intervention, lower body negative pressure (LBNP; 3 minutes at -15, -30, and -45 mmHg) was applied to elicit reflex increases in muscle sympathetic nerve activity (MSNA, fibular microneurography) while clamping end-tidal gases at baseline levels. Ventilation, arterial pressure (SBP, DBP, MAP), brachial artery blood flow (Q̇ BA), FVC (Q̇ BA/MAP), and MSNA burst frequency were measured continuously. Following IH, but not control, ventilation (5 l/min; 95% CI: 1 - 9), and MAP (5 mmHg; 95% CI: 1 - 9) were increased, while FVC (-0.2 ml/min/mm Hg; 95% CI: -0.0 - -0.4) and mean shear rate (SR; -21.9 /s; 95% CI: -5.8 - -38.0; all P
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