Muscle fibre‐type dependence of neuronal nitric oxide synthase‐mediated vascular control in the rat during high speed treadmill running
Key points • Neuronal nitric oxide (NO) synthase (nNOS) inhibition does not impact skeletal muscle blood flow or vascular conductance (VC) during low‐speed (20 m min−1) treadmill running. • This may be due to the fact that low exercise intensities recruit primarily oxidative muscle and that nNOS‐d...
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| Veröffentlicht in: | The Journal of physiology 2013-06, Vol.591 (11), p.2885-2896 |
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| creator | Copp, Steven W. Holdsworth, Clark T. Ferguson, Scott K. Hirai, Daniel M. Poole, David C. Musch, Timothy I. |
| description | Key points
•
Neuronal nitric oxide (NO) synthase (nNOS) inhibition does not impact skeletal muscle blood flow or vascular conductance (VC) during low‐speed (20 m min−1) treadmill running.
•
This may be due to the fact that low exercise intensities recruit primarily oxidative muscle and that nNOS‐derived NO contributes to vascular control primarily within glycolytic muscle.
•
Rats ran in the severe‐intensity domain at 15% above critical speed (an important glycolytic fast‐twitch fibre recruitment boundary in the rat) before and after selective nNOS inhibition with S‐methyl‐l‐thiocitrulline (SMTC).
•
SMTC reduced blood flow and VC during supra‐critical speed treadmill running (52.5 ± 1.3 m min−1) with the greatest proportional reductions observed in glycolytic fast‐twitch compared to oxidative slow‐ and fast‐twitch muscle. There were no effects of SMTC on muscle blood flow or VC during low‐speed running (20 m min−1).
•
The present data reveal important fibre‐type‐ and exercise intensity‐dependent peripheral vascular effects of nNOS‐derived NO during whole‐body exercise.
We have recently shown that nitric oxide (NO) derived from neuronal NO synthase (nNOS) does not contribute to the hyperaemic response within rat hindlimb skeletal muscle during low‐speed treadmill running. This may be attributed to low exercise intensities recruiting primarily oxidative muscle and that vascular effects of nNOS‐derived NO are manifest principally within glycolytic muscle. We tested the hypothesis that selective nNOS inhibition via S‐methyl‐l‐thiocitrulline (SMTC) would reduce rat hindlimb skeletal muscle blood flow and vascular conductance (VC) during high‐speed treadmill running above critical speed (asymptote of the hyperbolic speed versus time‐to‐exhaustion relationship for high‐speed running and an important glycolytic fast‐twitch fibre recruitment boundary in the rat) principally within glycolytic fast‐twitch muscle. Six rats performed three high‐speed treadmill runs to exhaustion to determine critical speed. Subsequently, hindlimb skeletal muscle blood flow (radiolabelled microspheres) and VC (blood flow/mean arterial pressure) were determined during supra‐critical speed treadmill running (critical speed + 15%, 52.5 ± 1.3 m min−1) before (control) and after selective nNOS inhibition with 0.56 mg kg−1 SMTC. SMTC reduced total hindlimb skeletal muscle blood flow (control: 241 ± 23, SMTC: 204 ± 13 ml min−1 (100 g)−1, P < 0.05) and VC (control: 1.88 ± 0.20, SMTC: 1.48 |
| doi_str_mv | 10.1113/jphysiol.2013.251082 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_3690692</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>1365053938</sourcerecordid><originalsourceid>FETCH-LOGICAL-c5192-d11a12c19792020c0a585bd29cb8ee1fdfe8f92ce493290552d9bff163db70283</originalsourceid><addsrcrecordid>eNqNks1u1DAUhS0EokPhDRCyxIZNBv-Mk3iDhCp-WhXBoqwtx76ZeOSxg50UsmPPhmfkSZp02grYwOou7neOzr06CD2lZE0p5S93fTdlF_2aEcrXTFBSs3toRTelLKpK8vtoRQhjBa8EPUKPct6RGSRSPkRHjAtS1ZVcoR8fxmw84NY1CX59_zlMPWALPQQLwQCOLQ4wphi0x8ENyRkcvzkLOE9h6HReNHuwTg9g8aXOZvQ6YRPDkKLHLuChA5z0gO2YXNjizm07nHuY6SGBtnvnPU5jCPPyMXrQap_hyc08Rp_fvrk4eV-cf3x3evL6vDCCSlZYSjVlhspKMsKIIVrUorFMmqYGoK1toW4lM7CRnEkiBLOyaVtacttUhNX8GL06-PZjM2c3MIfVXvXJ7XWaVNRO_bkJrlPbeKl4KUkp2Wzw4sYgxS8j5EHtXTbgvQ4Qx6zohkpekbqi_0Z5KYjgki-xnv-F7uKY5scvlCjrWvJranOgTIo5J2jvclOilmKo22KopRjqUIxZ9uz3m-9Et02YAXkAvjoP03-ZqouzT6IUjF8Bm8_N6g</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1356889338</pqid></control><display><type>article</type><title>Muscle fibre‐type dependence of neuronal nitric oxide synthase‐mediated vascular control in the rat during high speed treadmill running</title><source>MEDLINE</source><source>Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals</source><source>Access via Wiley Online Library</source><source>IngentaConnect Free/Open Access Journals</source><source>Wiley Online Library (Open Access Collection)</source><source>PubMed Central</source><creator>Copp, Steven W. ; Holdsworth, Clark T. ; Ferguson, Scott K. ; Hirai, Daniel M. ; Poole, David C. ; Musch, Timothy I.</creator><creatorcontrib>Copp, Steven W. ; Holdsworth, Clark T. ; Ferguson, Scott K. ; Hirai, Daniel M. ; Poole, David C. ; Musch, Timothy I.</creatorcontrib><description>Key points
•
Neuronal nitric oxide (NO) synthase (nNOS) inhibition does not impact skeletal muscle blood flow or vascular conductance (VC) during low‐speed (20 m min−1) treadmill running.
•
This may be due to the fact that low exercise intensities recruit primarily oxidative muscle and that nNOS‐derived NO contributes to vascular control primarily within glycolytic muscle.
•
Rats ran in the severe‐intensity domain at 15% above critical speed (an important glycolytic fast‐twitch fibre recruitment boundary in the rat) before and after selective nNOS inhibition with S‐methyl‐l‐thiocitrulline (SMTC).
•
SMTC reduced blood flow and VC during supra‐critical speed treadmill running (52.5 ± 1.3 m min−1) with the greatest proportional reductions observed in glycolytic fast‐twitch compared to oxidative slow‐ and fast‐twitch muscle. There were no effects of SMTC on muscle blood flow or VC during low‐speed running (20 m min−1).
•
The present data reveal important fibre‐type‐ and exercise intensity‐dependent peripheral vascular effects of nNOS‐derived NO during whole‐body exercise.
We have recently shown that nitric oxide (NO) derived from neuronal NO synthase (nNOS) does not contribute to the hyperaemic response within rat hindlimb skeletal muscle during low‐speed treadmill running. This may be attributed to low exercise intensities recruiting primarily oxidative muscle and that vascular effects of nNOS‐derived NO are manifest principally within glycolytic muscle. We tested the hypothesis that selective nNOS inhibition via S‐methyl‐l‐thiocitrulline (SMTC) would reduce rat hindlimb skeletal muscle blood flow and vascular conductance (VC) during high‐speed treadmill running above critical speed (asymptote of the hyperbolic speed versus time‐to‐exhaustion relationship for high‐speed running and an important glycolytic fast‐twitch fibre recruitment boundary in the rat) principally within glycolytic fast‐twitch muscle. Six rats performed three high‐speed treadmill runs to exhaustion to determine critical speed. Subsequently, hindlimb skeletal muscle blood flow (radiolabelled microspheres) and VC (blood flow/mean arterial pressure) were determined during supra‐critical speed treadmill running (critical speed + 15%, 52.5 ± 1.3 m min−1) before (control) and after selective nNOS inhibition with 0.56 mg kg−1 SMTC. SMTC reduced total hindlimb skeletal muscle blood flow (control: 241 ± 23, SMTC: 204 ± 13 ml min−1 (100 g)−1, P < 0.05) and VC (control: 1.88 ± 0.20, SMTC: 1.48 ± 0.13 ml min−1 (100 g)−1 mmHg−1, P < 0.05) during high‐speed running. The relative reductions in blood flow and VC were greater in the highly glycolytic muscles and muscle parts consisting of 100% type IIb+d/x fibres compared to the highly oxidative muscles and muscle parts consisting of ≤35% type IIb+d/x muscle fibres (P < 0.05). These results extend our understanding of vascular control during exercise by identifying fibre‐type‐selective peripheral vascular effects of nNOS‐derived NO during high‐speed treadmill running.</description><identifier>ISSN: 0022-3751</identifier><identifier>EISSN: 1469-7793</identifier><identifier>DOI: 10.1113/jphysiol.2013.251082</identifier><identifier>PMID: 23507879</identifier><identifier>CODEN: JPHYA7</identifier><language>eng</language><publisher>Oxford, UK: Blackwell Publishing Ltd</publisher><subject>Animals ; Arterial Pressure ; Blood pressure ; Dependence ; Fitness equipment ; Glycolysis ; High speed ; Hindlimb - blood supply ; Male ; Muscle Fibers, Fast-Twitch - classification ; Muscle Fibers, Fast-Twitch - metabolism ; Muscle Fibers, Fast-Twitch - physiology ; Muscle, Skeletal - blood supply ; Musculoskeletal system ; Nitric oxide ; Nitric Oxide - metabolism ; Nitric Oxide Synthase Type I - metabolism ; Oxidative Phosphorylation ; Physical Exertion ; Rats ; Rats, Sprague-Dawley ; Regional Blood Flow ; Rodents ; Running ; Skeletal Muscle and Exercise</subject><ispartof>The Journal of physiology, 2013-06, Vol.591 (11), p.2885-2896</ispartof><rights>2013 The Authors. The Journal of Physiology © 2013 The Physiological Society</rights><rights>2013 The Authors. The Journal of Physiology © 2013 The Physiological Society 2013</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5192-d11a12c19792020c0a585bd29cb8ee1fdfe8f92ce493290552d9bff163db70283</citedby><cites>FETCH-LOGICAL-c5192-d11a12c19792020c0a585bd29cb8ee1fdfe8f92ce493290552d9bff163db70283</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3690692/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3690692/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,315,729,782,786,887,1419,1435,27931,27932,45581,45582,46416,46840,53798,53800</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23507879$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Copp, Steven W.</creatorcontrib><creatorcontrib>Holdsworth, Clark T.</creatorcontrib><creatorcontrib>Ferguson, Scott K.</creatorcontrib><creatorcontrib>Hirai, Daniel M.</creatorcontrib><creatorcontrib>Poole, David C.</creatorcontrib><creatorcontrib>Musch, Timothy I.</creatorcontrib><title>Muscle fibre‐type dependence of neuronal nitric oxide synthase‐mediated vascular control in the rat during high speed treadmill running</title><title>The Journal of physiology</title><addtitle>J Physiol</addtitle><description>Key points
•
Neuronal nitric oxide (NO) synthase (nNOS) inhibition does not impact skeletal muscle blood flow or vascular conductance (VC) during low‐speed (20 m min−1) treadmill running.
•
This may be due to the fact that low exercise intensities recruit primarily oxidative muscle and that nNOS‐derived NO contributes to vascular control primarily within glycolytic muscle.
•
Rats ran in the severe‐intensity domain at 15% above critical speed (an important glycolytic fast‐twitch fibre recruitment boundary in the rat) before and after selective nNOS inhibition with S‐methyl‐l‐thiocitrulline (SMTC).
•
SMTC reduced blood flow and VC during supra‐critical speed treadmill running (52.5 ± 1.3 m min−1) with the greatest proportional reductions observed in glycolytic fast‐twitch compared to oxidative slow‐ and fast‐twitch muscle. There were no effects of SMTC on muscle blood flow or VC during low‐speed running (20 m min−1).
•
The present data reveal important fibre‐type‐ and exercise intensity‐dependent peripheral vascular effects of nNOS‐derived NO during whole‐body exercise.
We have recently shown that nitric oxide (NO) derived from neuronal NO synthase (nNOS) does not contribute to the hyperaemic response within rat hindlimb skeletal muscle during low‐speed treadmill running. This may be attributed to low exercise intensities recruiting primarily oxidative muscle and that vascular effects of nNOS‐derived NO are manifest principally within glycolytic muscle. We tested the hypothesis that selective nNOS inhibition via S‐methyl‐l‐thiocitrulline (SMTC) would reduce rat hindlimb skeletal muscle blood flow and vascular conductance (VC) during high‐speed treadmill running above critical speed (asymptote of the hyperbolic speed versus time‐to‐exhaustion relationship for high‐speed running and an important glycolytic fast‐twitch fibre recruitment boundary in the rat) principally within glycolytic fast‐twitch muscle. Six rats performed three high‐speed treadmill runs to exhaustion to determine critical speed. Subsequently, hindlimb skeletal muscle blood flow (radiolabelled microspheres) and VC (blood flow/mean arterial pressure) were determined during supra‐critical speed treadmill running (critical speed + 15%, 52.5 ± 1.3 m min−1) before (control) and after selective nNOS inhibition with 0.56 mg kg−1 SMTC. SMTC reduced total hindlimb skeletal muscle blood flow (control: 241 ± 23, SMTC: 204 ± 13 ml min−1 (100 g)−1, P < 0.05) and VC (control: 1.88 ± 0.20, SMTC: 1.48 ± 0.13 ml min−1 (100 g)−1 mmHg−1, P < 0.05) during high‐speed running. The relative reductions in blood flow and VC were greater in the highly glycolytic muscles and muscle parts consisting of 100% type IIb+d/x fibres compared to the highly oxidative muscles and muscle parts consisting of ≤35% type IIb+d/x muscle fibres (P < 0.05). These results extend our understanding of vascular control during exercise by identifying fibre‐type‐selective peripheral vascular effects of nNOS‐derived NO during high‐speed treadmill running.</description><subject>Animals</subject><subject>Arterial Pressure</subject><subject>Blood pressure</subject><subject>Dependence</subject><subject>Fitness equipment</subject><subject>Glycolysis</subject><subject>High speed</subject><subject>Hindlimb - blood supply</subject><subject>Male</subject><subject>Muscle Fibers, Fast-Twitch - classification</subject><subject>Muscle Fibers, Fast-Twitch - metabolism</subject><subject>Muscle Fibers, Fast-Twitch - physiology</subject><subject>Muscle, Skeletal - blood supply</subject><subject>Musculoskeletal system</subject><subject>Nitric oxide</subject><subject>Nitric Oxide - metabolism</subject><subject>Nitric Oxide Synthase Type I - metabolism</subject><subject>Oxidative Phosphorylation</subject><subject>Physical Exertion</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Regional Blood Flow</subject><subject>Rodents</subject><subject>Running</subject><subject>Skeletal Muscle and Exercise</subject><issn>0022-3751</issn><issn>1469-7793</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNks1u1DAUhS0EokPhDRCyxIZNBv-Mk3iDhCp-WhXBoqwtx76ZeOSxg50UsmPPhmfkSZp02grYwOou7neOzr06CD2lZE0p5S93fTdlF_2aEcrXTFBSs3toRTelLKpK8vtoRQhjBa8EPUKPct6RGSRSPkRHjAtS1ZVcoR8fxmw84NY1CX59_zlMPWALPQQLwQCOLQ4wphi0x8ENyRkcvzkLOE9h6HReNHuwTg9g8aXOZvQ6YRPDkKLHLuChA5z0gO2YXNjizm07nHuY6SGBtnvnPU5jCPPyMXrQap_hyc08Rp_fvrk4eV-cf3x3evL6vDCCSlZYSjVlhspKMsKIIVrUorFMmqYGoK1toW4lM7CRnEkiBLOyaVtacttUhNX8GL06-PZjM2c3MIfVXvXJ7XWaVNRO_bkJrlPbeKl4KUkp2Wzw4sYgxS8j5EHtXTbgvQ4Qx6zohkpekbqi_0Z5KYjgki-xnv-F7uKY5scvlCjrWvJranOgTIo5J2jvclOilmKo22KopRjqUIxZ9uz3m-9Et02YAXkAvjoP03-ZqouzT6IUjF8Bm8_N6g</recordid><startdate>201306</startdate><enddate>201306</enddate><creator>Copp, Steven W.</creator><creator>Holdsworth, Clark T.</creator><creator>Ferguson, Scott K.</creator><creator>Hirai, Daniel M.</creator><creator>Poole, David C.</creator><creator>Musch, Timothy I.</creator><general>Blackwell Publishing Ltd</general><general>Wiley Subscription Services, Inc</general><general>Blackwell Science 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>7QR</scope><scope>7TK</scope><scope>7TS</scope><scope>8FD</scope><scope>FR3</scope><scope>P64</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>201306</creationdate><title>Muscle fibre‐type dependence of neuronal nitric oxide synthase‐mediated vascular control in the rat during high speed treadmill running</title><author>Copp, Steven W. ; Holdsworth, Clark T. ; Ferguson, Scott K. ; Hirai, Daniel M. ; Poole, David C. ; Musch, Timothy I.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5192-d11a12c19792020c0a585bd29cb8ee1fdfe8f92ce493290552d9bff163db70283</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>Animals</topic><topic>Arterial Pressure</topic><topic>Blood pressure</topic><topic>Dependence</topic><topic>Fitness equipment</topic><topic>Glycolysis</topic><topic>High speed</topic><topic>Hindlimb - blood supply</topic><topic>Male</topic><topic>Muscle Fibers, Fast-Twitch - classification</topic><topic>Muscle Fibers, Fast-Twitch - metabolism</topic><topic>Muscle Fibers, Fast-Twitch - physiology</topic><topic>Muscle, Skeletal - blood supply</topic><topic>Musculoskeletal system</topic><topic>Nitric oxide</topic><topic>Nitric Oxide - metabolism</topic><topic>Nitric Oxide Synthase Type I - metabolism</topic><topic>Oxidative Phosphorylation</topic><topic>Physical Exertion</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Regional Blood Flow</topic><topic>Rodents</topic><topic>Running</topic><topic>Skeletal Muscle and Exercise</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Copp, Steven W.</creatorcontrib><creatorcontrib>Holdsworth, Clark T.</creatorcontrib><creatorcontrib>Ferguson, Scott K.</creatorcontrib><creatorcontrib>Hirai, Daniel M.</creatorcontrib><creatorcontrib>Poole, David C.</creatorcontrib><creatorcontrib>Musch, Timothy I.</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>Chemoreception Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Physical Education Index</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>The Journal of physiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Copp, Steven W.</au><au>Holdsworth, Clark T.</au><au>Ferguson, Scott K.</au><au>Hirai, Daniel M.</au><au>Poole, David C.</au><au>Musch, Timothy I.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Muscle fibre‐type dependence of neuronal nitric oxide synthase‐mediated vascular control in the rat during high speed treadmill running</atitle><jtitle>The Journal of physiology</jtitle><addtitle>J Physiol</addtitle><date>2013-06</date><risdate>2013</risdate><volume>591</volume><issue>11</issue><spage>2885</spage><epage>2896</epage><pages>2885-2896</pages><issn>0022-3751</issn><eissn>1469-7793</eissn><coden>JPHYA7</coden><abstract>Key points
•
Neuronal nitric oxide (NO) synthase (nNOS) inhibition does not impact skeletal muscle blood flow or vascular conductance (VC) during low‐speed (20 m min−1) treadmill running.
•
This may be due to the fact that low exercise intensities recruit primarily oxidative muscle and that nNOS‐derived NO contributes to vascular control primarily within glycolytic muscle.
•
Rats ran in the severe‐intensity domain at 15% above critical speed (an important glycolytic fast‐twitch fibre recruitment boundary in the rat) before and after selective nNOS inhibition with S‐methyl‐l‐thiocitrulline (SMTC).
•
SMTC reduced blood flow and VC during supra‐critical speed treadmill running (52.5 ± 1.3 m min−1) with the greatest proportional reductions observed in glycolytic fast‐twitch compared to oxidative slow‐ and fast‐twitch muscle. There were no effects of SMTC on muscle blood flow or VC during low‐speed running (20 m min−1).
•
The present data reveal important fibre‐type‐ and exercise intensity‐dependent peripheral vascular effects of nNOS‐derived NO during whole‐body exercise.
We have recently shown that nitric oxide (NO) derived from neuronal NO synthase (nNOS) does not contribute to the hyperaemic response within rat hindlimb skeletal muscle during low‐speed treadmill running. This may be attributed to low exercise intensities recruiting primarily oxidative muscle and that vascular effects of nNOS‐derived NO are manifest principally within glycolytic muscle. We tested the hypothesis that selective nNOS inhibition via S‐methyl‐l‐thiocitrulline (SMTC) would reduce rat hindlimb skeletal muscle blood flow and vascular conductance (VC) during high‐speed treadmill running above critical speed (asymptote of the hyperbolic speed versus time‐to‐exhaustion relationship for high‐speed running and an important glycolytic fast‐twitch fibre recruitment boundary in the rat) principally within glycolytic fast‐twitch muscle. Six rats performed three high‐speed treadmill runs to exhaustion to determine critical speed. Subsequently, hindlimb skeletal muscle blood flow (radiolabelled microspheres) and VC (blood flow/mean arterial pressure) were determined during supra‐critical speed treadmill running (critical speed + 15%, 52.5 ± 1.3 m min−1) before (control) and after selective nNOS inhibition with 0.56 mg kg−1 SMTC. SMTC reduced total hindlimb skeletal muscle blood flow (control: 241 ± 23, SMTC: 204 ± 13 ml min−1 (100 g)−1, P < 0.05) and VC (control: 1.88 ± 0.20, SMTC: 1.48 ± 0.13 ml min−1 (100 g)−1 mmHg−1, P < 0.05) during high‐speed running. The relative reductions in blood flow and VC were greater in the highly glycolytic muscles and muscle parts consisting of 100% type IIb+d/x fibres compared to the highly oxidative muscles and muscle parts consisting of ≤35% type IIb+d/x muscle fibres (P < 0.05). These results extend our understanding of vascular control during exercise by identifying fibre‐type‐selective peripheral vascular effects of nNOS‐derived NO during high‐speed treadmill running.</abstract><cop>Oxford, UK</cop><pub>Blackwell Publishing Ltd</pub><pmid>23507879</pmid><doi>10.1113/jphysiol.2013.251082</doi><tpages>12</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Animals Arterial Pressure Blood pressure Dependence Fitness equipment Glycolysis High speed Hindlimb - blood supply Male Muscle Fibers, Fast-Twitch - classification Muscle Fibers, Fast-Twitch - metabolism Muscle Fibers, Fast-Twitch - physiology Muscle, Skeletal - blood supply Musculoskeletal system Nitric oxide Nitric Oxide - metabolism Nitric Oxide Synthase Type I - metabolism Oxidative Phosphorylation Physical Exertion Rats Rats, Sprague-Dawley Regional Blood Flow Rodents Running Skeletal Muscle and Exercise |
| title | Muscle fibre‐type dependence of neuronal nitric oxide synthase‐mediated vascular control in the rat during high speed treadmill running |
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