59 - 3469_0_merged_1469359076.pdf (870.72 kB)
Download file

The effect of α1-adrenergic blockade on post-exercise brachial artery flow-mediated dilatation at sea level and high altitude

Download (870.72 kB)
journal contribution
posted on 2023-01-20, 17:19 authored by Michael Tymko, Joshua C. Tremblay, Alex B. Hansen, Connor A Howe, Chris K. Willie, Michael StembridgeMichael Stembridge, Daniel J. Green, Ryan L. Hoiland, Prajan Subedi, James D. Anholm, Philip N. Ainslie

 We examined the hypotheses that (1) at rest, endothelial function would be impaired at high altitude compared to sea level, (2) endothelial function would be reduced to a greater extent at sea level compared to high altitude after maximal exercise, and (3) reductions in endothelial function following moderate-intensity exercise at both sea level and high altitude are mediated via an α1-adrenergic pathway. In a double-blinded, counterbalanced, randomized and placebo-controlled design, nine healthy participants performed a maximal-exercise test, and two 30 min sessions of semi-recumbent cycling exercise at 50% peak output following either placebo or α1-adrenergic blockade (prazosin; 0.05 mg kg −1). These experiments were completed at both sea-level (344 m) and high altitude (3800 m). Blood pressure (finger photoplethysmography), heart rate (electrocardiogram), oxygen saturation (pulse oximetry), and brachial artery blood flow and shear rate (ultrasound) were recorded before, during and following exercise. Endothelial function assessed by brachial artery flow-mediated dilatation (FMD) was measured before, immediately following and 60 min after exercise. Our findings were: (1) at rest, FMD remained unchanged between sea level and high altitude (placebo P = 0.287; prazosin: P = 0.110); (2) FMD remained unchanged after maximal exercise at sea level and high altitude (P = 0.244); and (3) the 2.9 ± 0.8% (P = 0.043) reduction in FMD immediately after moderate-intensity exercise at sea level was abolished via α1-adrenergic blockade. Conversely, at high altitude, FMD was unaltered following moderate-intensity exercise, and administration of α1-adrenergic blockade elevated FMD (P = 0.032). Our results suggest endothelial function is differentially affected by exercise when exposed to hypobaric hypoxia. These findings have implications for understanding the chronic impacts of hypoxaemia on exercise, and the interactions between the α1-adrenergic pathway and endothelial function. 


This study was supported by the Natural Sciences and Engineering Research Council of Canada (PNA), and the Canadian Foundation for Innovation and a Canada Research Chair (PNA)


Published in

The Journal of Physiology




AM (Accepted Manuscript)


Tymko, M. M., Tremblay, J. C., Hansen, A. B., Howe, C. A., Willie, C. K., Stembridge, M., ... & Ainslie, P. N. (2017). The effect of α1‐adrenergic blockade on post‐exercise brachial artery flow‐mediated dilatation at sea level and high altitude. The Journal of Physiology, 595(5), 1671-1686.

Print ISSN


Electronic ISSN


Cardiff Met Affiliation

  • Cardiff School of Sport and Health Sciences

Cardiff Met Authors

Mike Stembridge

Cardiff Met Research Centre/Group

  • Cardiovascular Physiology

Copyright Holder

© The Publisher