Sex differences in the coronary vascular response to combined chemoreflex and metaboreflex stimulation in healthy humans
New Findings What is the central question of this study? Coronary blood flow in healthy humans is controlled by both local metabolic signalling and adrenergic activity: does the integration of these signals during acute hypoxia and adrenergic activation differ between sexes? What are the main findin...
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Veröffentlicht in: | Experimental physiology 2022-01, Vol.107 (1), p.16-28 |
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description | New Findings
What is the central question of this study?
Coronary blood flow in healthy humans is controlled by both local metabolic signalling and adrenergic activity: does the integration of these signals during acute hypoxia and adrenergic activation differ between sexes?
What are the main findings and its importance?
Both males and females exhibit an increase in coronary blood velocity in response to acute hypoxia, a response that is constrained by adrenergic stimulation in males but not females. These findings suggest that coronary blood flow control differs between males and females.
Coronary hyperaemia is mediated through multiple signalling pathways, including local metabolic messengers and adrenergic stimulation. This study aimed to determine whether the coronary vascular response to adrenergic stressors is different between sexes in normoxia and hypoxia. Young, healthy participants (n = 32; 16F) underwent three randomized trials of isometric handgrip exercise followed by post‐exercise circulatory occlusion (PECO) to activate the muscle metaboreflex. End‐tidal PO2 was controlled at (1) normoxic levels throughout the trial, (2) 50 mmHg for the duration of the trial (hypoxia trial), or (3) 50 mmHg only during PECO (mixed trial). Mean left anterior descending coronary artery velocity (LADVmean; transthoracic Doppler echocardiography), heart rate and blood pressure were assessed at baseline and during PECO. In normoxia, there was no change in LADVmean or cardiac workload induced by PECO in males and females. Acute hypoxia increased baseline LADVmean to a greater extent in males compared with females (P |
doi_str_mv | 10.1113/EP090034 |
format | Article |
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What is the central question of this study?
Coronary blood flow in healthy humans is controlled by both local metabolic signalling and adrenergic activity: does the integration of these signals during acute hypoxia and adrenergic activation differ between sexes?
What are the main findings and its importance?
Both males and females exhibit an increase in coronary blood velocity in response to acute hypoxia, a response that is constrained by adrenergic stimulation in males but not females. These findings suggest that coronary blood flow control differs between males and females.
Coronary hyperaemia is mediated through multiple signalling pathways, including local metabolic messengers and adrenergic stimulation. This study aimed to determine whether the coronary vascular response to adrenergic stressors is different between sexes in normoxia and hypoxia. Young, healthy participants (n = 32; 16F) underwent three randomized trials of isometric handgrip exercise followed by post‐exercise circulatory occlusion (PECO) to activate the muscle metaboreflex. End‐tidal PO2 was controlled at (1) normoxic levels throughout the trial, (2) 50 mmHg for the duration of the trial (hypoxia trial), or (3) 50 mmHg only during PECO (mixed trial). Mean left anterior descending coronary artery velocity (LADVmean; transthoracic Doppler echocardiography), heart rate and blood pressure were assessed at baseline and during PECO. In normoxia, there was no change in LADVmean or cardiac workload induced by PECO in males and females. Acute hypoxia increased baseline LADVmean to a greater extent in males compared with females (P < 0.05), despite a similar increase in cardiac workload. The change in LADVmean induced by PECO was similar between sexes in normoxia (P = 0.31), greater in males during the mixed trial (male: 12.8 (7.7) cm/s vs. female: 8.1 (6.3) cm/s; P = 0.02) and reduced in males but not females in acute hypoxia (male: −4.8 (4.5) cm/s vs. female: 0.8 (6.2) cm/s; P = 0.006). In summary, sex differences in the coronary vasodilatory response to hypoxia were observed, and metaboreflex activation during hypoxia caused a paradoxical reduction in coronary blood velocity in males but not females.</description><identifier>ISSN: 0958-0670</identifier><identifier>EISSN: 1469-445X</identifier><identifier>DOI: 10.1113/EP090034</identifier><identifier>PMID: 34788486</identifier><language>eng</language><publisher>England: John Wiley & Sons, Inc</publisher><subject>Blood pressure ; Blood Pressure - physiology ; Chemoreception (internal) ; Coronary artery ; coronary blood flow ; Coronary Vessels ; Doppler effect ; Echocardiography ; Exercise - physiology ; Female ; Females ; Gender differences ; Hand Strength - physiology ; Heart ; Heart rate ; Humans ; Hyperemia ; Hypoxia ; Male ; Males ; Muscle contraction ; Muscle, Skeletal - physiology ; Occlusion ; Physical training ; Sex differences ; Sex Factors ; Sexes ; Signal transduction ; Velocity ; Workloads</subject><ispartof>Experimental physiology, 2022-01, Vol.107 (1), p.16-28</ispartof><rights>2021 The Authors. Experimental Physiology © 2021 The Physiological Society</rights><rights>2021 The Authors. Experimental Physiology © 2021 The Physiological Society.</rights><rights>2022 The Physiological Society</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3840-6571bba8ef019d3c6a4713240d937da55a1bac6e675564097b95335b41a7c1513</citedby><cites>FETCH-LOGICAL-c3840-6571bba8ef019d3c6a4713240d937da55a1bac6e675564097b95335b41a7c1513</cites><orcidid>0000-0002-5776-0460 ; 0000-0003-0477-6511 ; 0000-0003-4110-9574 ; 0000-0001-7102-4235</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1113%2FEP090034$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1113%2FEP090034$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,776,780,1411,1427,27901,27902,45550,45551,46384,46808</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/34788486$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Boulet, Lindsey M.</creatorcontrib><creatorcontrib>Atwater, Taylor L.</creatorcontrib><creatorcontrib>Brown, Courtney V.</creatorcontrib><creatorcontrib>Shafer, Brooke M.</creatorcontrib><creatorcontrib>Vermeulen, Tyler D.</creatorcontrib><creatorcontrib>Cotton, Paul C.</creatorcontrib><creatorcontrib>Day, Trevor A.</creatorcontrib><creatorcontrib>Foster, Glen E.</creatorcontrib><title>Sex differences in the coronary vascular response to combined chemoreflex and metaboreflex stimulation in healthy humans</title><title>Experimental physiology</title><addtitle>Exp Physiol</addtitle><description>New Findings
What is the central question of this study?
Coronary blood flow in healthy humans is controlled by both local metabolic signalling and adrenergic activity: does the integration of these signals during acute hypoxia and adrenergic activation differ between sexes?
What are the main findings and its importance?
Both males and females exhibit an increase in coronary blood velocity in response to acute hypoxia, a response that is constrained by adrenergic stimulation in males but not females. These findings suggest that coronary blood flow control differs between males and females.
Coronary hyperaemia is mediated through multiple signalling pathways, including local metabolic messengers and adrenergic stimulation. This study aimed to determine whether the coronary vascular response to adrenergic stressors is different between sexes in normoxia and hypoxia. Young, healthy participants (n = 32; 16F) underwent three randomized trials of isometric handgrip exercise followed by post‐exercise circulatory occlusion (PECO) to activate the muscle metaboreflex. End‐tidal PO2 was controlled at (1) normoxic levels throughout the trial, (2) 50 mmHg for the duration of the trial (hypoxia trial), or (3) 50 mmHg only during PECO (mixed trial). Mean left anterior descending coronary artery velocity (LADVmean; transthoracic Doppler echocardiography), heart rate and blood pressure were assessed at baseline and during PECO. In normoxia, there was no change in LADVmean or cardiac workload induced by PECO in males and females. Acute hypoxia increased baseline LADVmean to a greater extent in males compared with females (P < 0.05), despite a similar increase in cardiac workload. The change in LADVmean induced by PECO was similar between sexes in normoxia (P = 0.31), greater in males during the mixed trial (male: 12.8 (7.7) cm/s vs. female: 8.1 (6.3) cm/s; P = 0.02) and reduced in males but not females in acute hypoxia (male: −4.8 (4.5) cm/s vs. female: 0.8 (6.2) cm/s; P = 0.006). In summary, sex differences in the coronary vasodilatory response to hypoxia were observed, and metaboreflex activation during hypoxia caused a paradoxical reduction in coronary blood velocity in males but not females.</description><subject>Blood pressure</subject><subject>Blood Pressure - physiology</subject><subject>Chemoreception (internal)</subject><subject>Coronary artery</subject><subject>coronary blood flow</subject><subject>Coronary Vessels</subject><subject>Doppler effect</subject><subject>Echocardiography</subject><subject>Exercise - physiology</subject><subject>Female</subject><subject>Females</subject><subject>Gender differences</subject><subject>Hand Strength - physiology</subject><subject>Heart</subject><subject>Heart rate</subject><subject>Humans</subject><subject>Hyperemia</subject><subject>Hypoxia</subject><subject>Male</subject><subject>Males</subject><subject>Muscle contraction</subject><subject>Muscle, Skeletal - physiology</subject><subject>Occlusion</subject><subject>Physical training</subject><subject>Sex differences</subject><subject>Sex Factors</subject><subject>Sexes</subject><subject>Signal transduction</subject><subject>Velocity</subject><subject>Workloads</subject><issn>0958-0670</issn><issn>1469-445X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2022</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kV2L1TAQhoMo7nEV_AUS8MabrjPNV3Mpy-oKCwoqeFfSdEq7tMkxaXXPvzeH3aMgeDVh8uRh8g5jLxEuEFG8vfoMFkDIR2yHUttKSvX9MduBVU0F2sAZe5bzLQAKaORTdiakaRrZ6B27-0J3vJ-GgRIFT5lPga8jcR9TDC4d-E-X_Ta7xBPlfQyZ-BrL7dJNgXruR1piomEuFhd6vtDqulMjr9NSnq5TDEftSG5exwMft8WF_Jw9Gdyc6cVDPWff3l99vbyubj59-Hj57qbyopFQaWWw61xDA6DthddOGhS1hN4K0zulHHbOa9JGKS3Bms4qIVQn0RmPCsU5e3Pv3af4Y6O8tsuUPc2zCxS33NbKWtBW10f09T_obdxSKNO1tUYljFbS_hX6FHMuX233aVpKVC1Ce9xGe9pGQV89CLduof4PeIq_ABf3wK9ppsN_ReVwjQJrEL8BGIeSqg</recordid><startdate>202201</startdate><enddate>202201</enddate><creator>Boulet, Lindsey M.</creator><creator>Atwater, Taylor L.</creator><creator>Brown, Courtney V.</creator><creator>Shafer, Brooke M.</creator><creator>Vermeulen, Tyler D.</creator><creator>Cotton, Paul C.</creator><creator>Day, Trevor A.</creator><creator>Foster, Glen E.</creator><general>John Wiley & Sons, Inc</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QP</scope><scope>7TK</scope><scope>7TS</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0002-5776-0460</orcidid><orcidid>https://orcid.org/0000-0003-0477-6511</orcidid><orcidid>https://orcid.org/0000-0003-4110-9574</orcidid><orcidid>https://orcid.org/0000-0001-7102-4235</orcidid></search><sort><creationdate>202201</creationdate><title>Sex differences in the coronary vascular response to combined chemoreflex and metaboreflex stimulation in healthy humans</title><author>Boulet, Lindsey M. ; Atwater, Taylor L. ; Brown, Courtney V. ; Shafer, Brooke M. ; Vermeulen, Tyler D. ; Cotton, Paul C. ; Day, Trevor A. ; Foster, Glen E.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3840-6571bba8ef019d3c6a4713240d937da55a1bac6e675564097b95335b41a7c1513</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2022</creationdate><topic>Blood pressure</topic><topic>Blood Pressure - physiology</topic><topic>Chemoreception (internal)</topic><topic>Coronary artery</topic><topic>coronary blood flow</topic><topic>Coronary Vessels</topic><topic>Doppler effect</topic><topic>Echocardiography</topic><topic>Exercise - physiology</topic><topic>Female</topic><topic>Females</topic><topic>Gender differences</topic><topic>Hand Strength - physiology</topic><topic>Heart</topic><topic>Heart rate</topic><topic>Humans</topic><topic>Hyperemia</topic><topic>Hypoxia</topic><topic>Male</topic><topic>Males</topic><topic>Muscle contraction</topic><topic>Muscle, Skeletal - physiology</topic><topic>Occlusion</topic><topic>Physical training</topic><topic>Sex differences</topic><topic>Sex Factors</topic><topic>Sexes</topic><topic>Signal transduction</topic><topic>Velocity</topic><topic>Workloads</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Boulet, Lindsey M.</creatorcontrib><creatorcontrib>Atwater, Taylor L.</creatorcontrib><creatorcontrib>Brown, Courtney V.</creatorcontrib><creatorcontrib>Shafer, Brooke M.</creatorcontrib><creatorcontrib>Vermeulen, Tyler D.</creatorcontrib><creatorcontrib>Cotton, Paul C.</creatorcontrib><creatorcontrib>Day, Trevor A.</creatorcontrib><creatorcontrib>Foster, Glen E.</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Physical Education Index</collection><collection>MEDLINE - Academic</collection><jtitle>Experimental physiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Boulet, Lindsey M.</au><au>Atwater, Taylor L.</au><au>Brown, Courtney V.</au><au>Shafer, Brooke M.</au><au>Vermeulen, Tyler D.</au><au>Cotton, Paul C.</au><au>Day, Trevor A.</au><au>Foster, Glen E.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Sex differences in the coronary vascular response to combined chemoreflex and metaboreflex stimulation in healthy humans</atitle><jtitle>Experimental physiology</jtitle><addtitle>Exp Physiol</addtitle><date>2022-01</date><risdate>2022</risdate><volume>107</volume><issue>1</issue><spage>16</spage><epage>28</epage><pages>16-28</pages><issn>0958-0670</issn><eissn>1469-445X</eissn><abstract>New Findings
What is the central question of this study?
Coronary blood flow in healthy humans is controlled by both local metabolic signalling and adrenergic activity: does the integration of these signals during acute hypoxia and adrenergic activation differ between sexes?
What are the main findings and its importance?
Both males and females exhibit an increase in coronary blood velocity in response to acute hypoxia, a response that is constrained by adrenergic stimulation in males but not females. These findings suggest that coronary blood flow control differs between males and females.
Coronary hyperaemia is mediated through multiple signalling pathways, including local metabolic messengers and adrenergic stimulation. This study aimed to determine whether the coronary vascular response to adrenergic stressors is different between sexes in normoxia and hypoxia. Young, healthy participants (n = 32; 16F) underwent three randomized trials of isometric handgrip exercise followed by post‐exercise circulatory occlusion (PECO) to activate the muscle metaboreflex. End‐tidal PO2 was controlled at (1) normoxic levels throughout the trial, (2) 50 mmHg for the duration of the trial (hypoxia trial), or (3) 50 mmHg only during PECO (mixed trial). Mean left anterior descending coronary artery velocity (LADVmean; transthoracic Doppler echocardiography), heart rate and blood pressure were assessed at baseline and during PECO. In normoxia, there was no change in LADVmean or cardiac workload induced by PECO in males and females. Acute hypoxia increased baseline LADVmean to a greater extent in males compared with females (P < 0.05), despite a similar increase in cardiac workload. The change in LADVmean induced by PECO was similar between sexes in normoxia (P = 0.31), greater in males during the mixed trial (male: 12.8 (7.7) cm/s vs. female: 8.1 (6.3) cm/s; P = 0.02) and reduced in males but not females in acute hypoxia (male: −4.8 (4.5) cm/s vs. female: 0.8 (6.2) cm/s; P = 0.006). In summary, sex differences in the coronary vasodilatory response to hypoxia were observed, and metaboreflex activation during hypoxia caused a paradoxical reduction in coronary blood velocity in males but not females.</abstract><cop>England</cop><pub>John Wiley & Sons, Inc</pub><pmid>34788486</pmid><doi>10.1113/EP090034</doi><tpages>13</tpages><orcidid>https://orcid.org/0000-0002-5776-0460</orcidid><orcidid>https://orcid.org/0000-0003-0477-6511</orcidid><orcidid>https://orcid.org/0000-0003-4110-9574</orcidid><orcidid>https://orcid.org/0000-0001-7102-4235</orcidid><oa>free_for_read</oa></addata></record> |
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subjects | Blood pressure Blood Pressure - physiology Chemoreception (internal) Coronary artery coronary blood flow Coronary Vessels Doppler effect Echocardiography Exercise - physiology Female Females Gender differences Hand Strength - physiology Heart Heart rate Humans Hyperemia Hypoxia Male Males Muscle contraction Muscle, Skeletal - physiology Occlusion Physical training Sex differences Sex Factors Sexes Signal transduction Velocity Workloads |
title | Sex differences in the coronary vascular response to combined chemoreflex and metaboreflex stimulation in healthy humans |
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