@article{5b6849a7f0654f0793584a776e4a5f6a,
title = "Esmolol acutely alters oxygen supply-demand balance in exercising muscles of healthy humans",
abstract = "Beta-adrenoreceptor antagonists (β blockers) reduce systemic O2 delivery and blood pressure (BP) during exercise, but the subsequent effects on O2 extraction within the active limb muscles are unknown. In this study, we examined the effects of the fast-acting, β1 selective blocker esmolol on systemic hemodynamics and leg muscle O2 saturation (near infrared spectroscopy, NIRS) during submaximal leg ergometry. Our main hypothesis was that esmolol would augment exercise-induced reductions in leg muscle O2 saturation. Eight healthy adults (6 men, 2 women; 23–67 year) performed light and moderate intensity bouts of recumbent leg cycling before (PRE), during (β1-blocked), and 45 min following (POST) intravenous infusion of esmolol. Oxygen uptake, heart rate (HR), BP, and O2 saturation (SmO2) of the vastus lateralis (VL) and medial gastrocnemius (MG) muscles were measured continuously. Esmolol attenuated the increases in HR and systolic BP during light (−12 ± 9 bpm and −26 ± 12 mmHg vs. PRE) and moderate intensity (−20 ± 10 bpm and −40 ± 18 mmHg vs. PRE) cycling (all P < 0.01). Exercise-induced reductions in SmO2 occurred to a greater extent during the β1-blockade trial in both the VL (P = 0.001 vs. PRE) and MG muscles (P = 0.022 vs. PRE). HR, SBP and SmO2 were restored during POST (all P < 0.01 vs. β1-blocked). In conclusion, esmolol rapidly and reversibly increases O2 extraction within exercising muscles of healthy humans.",
author = "Proctor, {David N.} and Luck, {J. Carter} and Maman, {Stephan R.} and Leuenberger, {Urs A.} and Muller, {Matthew D.}",
note = "Funding Information: Funding Information This project was supported by a grant from the Association of Faculty and Friends of the Penn State Milton S. Hershey Medical Center (Dr. Muller). This project was also supported, in part, by NIH Grants UL1 TR000127 and KL2 TR000126 from the National Center for Advancing Translational Sciences (NCATS) and also under a grant with the Pennsylvania Department of Health using Tobacco CURE funds (Dr. Muller). The Pennsylvania Department of Health and the NIH specifically disclaim responsibility for any analyses, interpretations, or conclusions. The authors thank Cheryl Blaha and Aimee Cauffman for nursing assistance, Jen Stoner and Kris Gray for administrative support, and Anne Muller for the graphic design assistance. We also appreciate the constructive comments of Dr. James Pawelczyk. Funding Information: This project was supported by a grant from the Association of Faculty and Friends of the Penn State Milton S. Hershey Medical Center (Dr. Muller). This project was also supported, in part, by NIH Grants UL1 TR000127 and KL2 TR000126 from the National Center for Advancing Translational Sciences (NCATS) and also under a grant with the Pennsylvania Department of Health using Tobacco CURE funds (Dr. Muller). The Pennsylvania Department of Health and the NIH specifically disclaim responsibility for any analyses, interpretations, or conclusions. Publisher Copyright: {\textcopyright} 2018 The Authors. Physiological Reports published by Wiley Periodicals, Inc. on behalf of The Physiological Society and the American Physiological Society.",
year = "2018",
month = apr,
doi = "10.14814/phy2.13673",
language = "English (US)",
volume = "6",
journal = "Physiological reports",
issn = "2051-817X",
publisher = "John Wiley and Sons Inc.",
number = "8",
}