Exercise intolerance in Type 2 diabetes: is there a cardiovascular contribution?Synthesis
Physical activity is critically important for Type 2 diabetes management, yet adherence levels are poor. This might be partly due to disproportionate exercise intolerance. Submaximal exercise tolerance is highly sensitive to muscle oxygenation; impairments in exercising muscle oxygen delivery may co...
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Veröffentlicht in: | Journal of applied physiology (1985) 2018-05, Vol.124 (5), p.1117 |
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description | Physical activity is critically important for Type 2 diabetes management, yet adherence levels are poor. This might be partly due to disproportionate exercise intolerance. Submaximal exercise tolerance is highly sensitive to muscle oxygenation; impairments in exercising muscle oxygen delivery may contribute to exercise intolerance in Type 2 diabetes since there is considerable evidence for the existence of both cardiac and peripheral vascular dysfunction. While uncompromised cardiac output during submaximal exercise is consistently observed in Type 2 diabetes, it remains to be determined whether an elevated cardiac sympathetic afferent reflex could sympathetically restrain exercising muscle blood flow. Furthermore, while deficits in endothelial function are common in Type 2 diabetes and are often cited as impairing exercising muscle oxygen delivery, no direct evidence in exercise exists, and there are several other vasoregulatory mechanisms whose dysfunction could contribute. Finally, while there are findings of impaired oxygen delivery, conflicting evidence also exists. A definitive conclusion that Type 2 diabetes compromises exercising muscle oxygen delivery remains premature. We review these potentially dysfunctional mechanisms in terms of how they could impair oxygen delivery in exercise, evaluate the current literature on whether an oxygen delivery deficit is actually manifest, and correspondingly identify key directions for future research. |
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This might be partly due to disproportionate exercise intolerance. Submaximal exercise tolerance is highly sensitive to muscle oxygenation; impairments in exercising muscle oxygen delivery may contribute to exercise intolerance in Type 2 diabetes since there is considerable evidence for the existence of both cardiac and peripheral vascular dysfunction. While uncompromised cardiac output during submaximal exercise is consistently observed in Type 2 diabetes, it remains to be determined whether an elevated cardiac sympathetic afferent reflex could sympathetically restrain exercising muscle blood flow. Furthermore, while deficits in endothelial function are common in Type 2 diabetes and are often cited as impairing exercising muscle oxygen delivery, no direct evidence in exercise exists, and there are several other vasoregulatory mechanisms whose dysfunction could contribute. Finally, while there are findings of impaired oxygen delivery, conflicting evidence also exists. A definitive conclusion that Type 2 diabetes compromises exercising muscle oxygen delivery remains premature. We review these potentially dysfunctional mechanisms in terms of how they could impair oxygen delivery in exercise, evaluate the current literature on whether an oxygen delivery deficit is actually manifest, and correspondingly identify key directions for future research.</description><identifier>ISSN: 8750-7587</identifier><identifier>EISSN: 1522-1601</identifier><language>eng</language><publisher>Bethesda: American Physiological Society</publisher><subject>Blood ; Blood flow ; Cardiac output ; Cardiovascular system ; Diabetes ; Diabetes mellitus ; Diabetes mellitus (non-insulin dependent) ; Exercise ; Intolerance ; Muscles ; Muscular system ; Oxygen ; Oxygenation ; Physical activity ; Physical training ; Sensory neurons</subject><ispartof>Journal of applied physiology (1985), 2018-05, Vol.124 (5), p.1117</ispartof><rights>Copyright American Physiological Society May 2018</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784</link.rule.ids></links><search><creatorcontrib>Poitras, Veronica J</creatorcontrib><creatorcontrib>Hudson, Robert W</creatorcontrib><creatorcontrib>Tschakovsky, Michael E</creatorcontrib><title>Exercise intolerance in Type 2 diabetes: is there a cardiovascular contribution?Synthesis</title><title>Journal of applied physiology (1985)</title><description>Physical activity is critically important for Type 2 diabetes management, yet adherence levels are poor. This might be partly due to disproportionate exercise intolerance. Submaximal exercise tolerance is highly sensitive to muscle oxygenation; impairments in exercising muscle oxygen delivery may contribute to exercise intolerance in Type 2 diabetes since there is considerable evidence for the existence of both cardiac and peripheral vascular dysfunction. While uncompromised cardiac output during submaximal exercise is consistently observed in Type 2 diabetes, it remains to be determined whether an elevated cardiac sympathetic afferent reflex could sympathetically restrain exercising muscle blood flow. Furthermore, while deficits in endothelial function are common in Type 2 diabetes and are often cited as impairing exercising muscle oxygen delivery, no direct evidence in exercise exists, and there are several other vasoregulatory mechanisms whose dysfunction could contribute. Finally, while there are findings of impaired oxygen delivery, conflicting evidence also exists. A definitive conclusion that Type 2 diabetes compromises exercising muscle oxygen delivery remains premature. We review these potentially dysfunctional mechanisms in terms of how they could impair oxygen delivery in exercise, evaluate the current literature on whether an oxygen delivery deficit is actually manifest, and correspondingly identify key directions for future research.</description><subject>Blood</subject><subject>Blood flow</subject><subject>Cardiac output</subject><subject>Cardiovascular system</subject><subject>Diabetes</subject><subject>Diabetes mellitus</subject><subject>Diabetes mellitus (non-insulin dependent)</subject><subject>Exercise</subject><subject>Intolerance</subject><subject>Muscles</subject><subject>Muscular system</subject><subject>Oxygen</subject><subject>Oxygenation</subject><subject>Physical activity</subject><subject>Physical training</subject><subject>Sensory neurons</subject><issn>8750-7587</issn><issn>1522-1601</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><recordid>eNqNiksKwjAUAIMoWD93eOC6kNSmKW5ciOJeN64kxidGSlLzErG3t4IHcDUDMwOWCVkUuai4GLKsVpLnStZqzCZED85FWUqRsdP2jcFYQrAu-gaDdubrcOxahAKuVl8wIq3AEsQ7BgQNRoer9S9NJjU6gPEuBntJ0Xq3PnSu38jSjI1uuiGc_zhli932uNnnbfDPhBTPD5-C69O54ErxuiqFWv53fQAK_EP1</recordid><startdate>20180501</startdate><enddate>20180501</enddate><creator>Poitras, Veronica J</creator><creator>Hudson, Robert W</creator><creator>Tschakovsky, Michael E</creator><general>American Physiological Society</general><scope>7QP</scope><scope>7QR</scope><scope>7TK</scope><scope>7TS</scope><scope>7U7</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>P64</scope></search><sort><creationdate>20180501</creationdate><title>Exercise intolerance in Type 2 diabetes: is there a cardiovascular contribution?Synthesis</title><author>Poitras, Veronica J ; Hudson, Robert W ; Tschakovsky, Michael E</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-proquest_journals_20770864173</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>Blood</topic><topic>Blood flow</topic><topic>Cardiac output</topic><topic>Cardiovascular system</topic><topic>Diabetes</topic><topic>Diabetes mellitus</topic><topic>Diabetes mellitus (non-insulin dependent)</topic><topic>Exercise</topic><topic>Intolerance</topic><topic>Muscles</topic><topic>Muscular system</topic><topic>Oxygen</topic><topic>Oxygenation</topic><topic>Physical activity</topic><topic>Physical training</topic><topic>Sensory neurons</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Poitras, Veronica J</creatorcontrib><creatorcontrib>Hudson, Robert W</creatorcontrib><creatorcontrib>Tschakovsky, Michael E</creatorcontrib><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Physical Education Index</collection><collection>Toxicology Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><jtitle>Journal of applied physiology (1985)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Poitras, Veronica J</au><au>Hudson, Robert W</au><au>Tschakovsky, Michael E</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Exercise intolerance in Type 2 diabetes: is there a cardiovascular contribution?Synthesis</atitle><jtitle>Journal of applied physiology (1985)</jtitle><date>2018-05-01</date><risdate>2018</risdate><volume>124</volume><issue>5</issue><spage>1117</spage><pages>1117-</pages><issn>8750-7587</issn><eissn>1522-1601</eissn><abstract>Physical activity is critically important for Type 2 diabetes management, yet adherence levels are poor. This might be partly due to disproportionate exercise intolerance. Submaximal exercise tolerance is highly sensitive to muscle oxygenation; impairments in exercising muscle oxygen delivery may contribute to exercise intolerance in Type 2 diabetes since there is considerable evidence for the existence of both cardiac and peripheral vascular dysfunction. While uncompromised cardiac output during submaximal exercise is consistently observed in Type 2 diabetes, it remains to be determined whether an elevated cardiac sympathetic afferent reflex could sympathetically restrain exercising muscle blood flow. Furthermore, while deficits in endothelial function are common in Type 2 diabetes and are often cited as impairing exercising muscle oxygen delivery, no direct evidence in exercise exists, and there are several other vasoregulatory mechanisms whose dysfunction could contribute. Finally, while there are findings of impaired oxygen delivery, conflicting evidence also exists. A definitive conclusion that Type 2 diabetes compromises exercising muscle oxygen delivery remains premature. We review these potentially dysfunctional mechanisms in terms of how they could impair oxygen delivery in exercise, evaluate the current literature on whether an oxygen delivery deficit is actually manifest, and correspondingly identify key directions for future research.</abstract><cop>Bethesda</cop><pub>American Physiological Society</pub></addata></record> |
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subjects | Blood Blood flow Cardiac output Cardiovascular system Diabetes Diabetes mellitus Diabetes mellitus (non-insulin dependent) Exercise Intolerance Muscles Muscular system Oxygen Oxygenation Physical activity Physical training Sensory neurons |
title | Exercise intolerance in Type 2 diabetes: is there a cardiovascular contribution?Synthesis |
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