Acute hypoxia elicits lasting reductions in the sympathetic action potential transduction of arterial blood pressure in males.

: 47 (2) mmHg) and 30-min recovery. Multi-unit microneurography (muscle sympathetic nerve activity; MSNA) and continuous wavelet transform with matched mother wavelet was used to detect sympathetic APs during baseline, hypoxia, early (first 7-min), and late recovery (last 7-min). AP groups were classified as synchronous APs, asynchronous APs (occurring outside a MSNA burst), and no AP activity. Sympathetic transduction of MAP was quantified using signal-averaging, with ΔMAP tracked following AP group cardiac cycles. Following synchronous APs, ΔMAP was reduced in hypoxia (+1.8 (0.9) mmHg) and early recovery (+1.5 (0.7) mmHg) compared to baseline (+3.1 (2.2) mmHg). AP group-by-condition interactions show that at rest asynchronous APs attenuate MAP reductions compared to no AP activity (-0.4 (1.1) vs. -2.2 (1.2) mmHg, respectively), with no difference between AP groups in hypoxia, early, or late recovery. Sympathetic transduction of MAP is blunted in hypoxia and early recovery. At rest, asynchronous sympathetic APs contributes to neural regulation of MAP by attenuating nadir pressure responses. Abstract figure legend Seven healthy men underwent 20-min isocapnic hypoxia and 30-min recovery. The study tested the hypotheses that hypoxia would blunt the sympathetic transduction of mean arterial pressure (MAP) following synchronous AP activity and that asynchronous APs would elicit smaller ΔMAP compared to synchronous APs. All sympathetic APs were detected and extracted from the filtered MSNA neurogram using a continuous wavelet transform with matched mother wavelet. AP groups were classified as synchronous (with MSNA burst), asynchronous (outside MSNA burst), and no AP activity. An effect of condition showed that following synchronous APs, ΔMAP was reduced in hypoxia and early recovery compared to baseline. AP group-by-condition interactions revealed that asynchronous APs attenuate MAP reductions compared to no AP activity under resting conditions. Our findings demonstrate that sympathetic transduction of MAP is blunted in hypoxia and remains diminished into early recovery. At rest, asynchronous AP activity contributes to MAP regulation by attenuating pressure reductions. This article is protected by copyright. All rights reserved.