Please use this identifier to cite or link to this item: http://hdl.handle.net/10553/53399
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dc.contributor.authorBoushel, R.
dc.contributor.authorAra, I.
dc.contributor.authorGnaiger, E.
dc.contributor.authorHelge, J. W.
dc.contributor.authorGonzalez-Alonso, J.
dc.contributor.authorMunck-Andersen, T.
dc.contributor.authorSondergaard, H.
dc.contributor.authorDamsgaard, R.
dc.contributor.authorvan Hall, G.
dc.contributor.authorSaltin, B.
dc.contributor.authorCalbet, J. A. L.
dc.contributor.otherCalbet, Jose A
dc.contributor.otherHelge, Jorn
dc.contributor.othervan Hall, Gerrit
dc.contributor.otherGnaiger, Erich
dc.contributor.otherAra Royo, Ignacio
dc.date.accessioned2019-02-04T16:28:13Z-
dc.date.available2019-02-04T16:28:13Z-
dc.date.issued2014
dc.identifier.issn1748-1708
dc.identifier.urihttp://hdl.handle.net/10553/53399-
dc.description.abstractAimIt is an ongoing discussion the extent to which oxygen delivery and oxygen extraction contribute to an increased muscle oxygen uptake during dynamic exercise. It has been proposed that local muscle factors including the capillary bed and mitochondrial oxidative capacity play a large role in prolonged low-intensity training of a small muscle group when the cardiac output capacity is not directly limiting. The purpose of this study was to investigate the relative roles of circulatory and muscle metabolic mechanisms by which prolonged low-intensity exercise training alters regional muscle VO2.MethodsIn nine healthy volunteers (seven males, two females), haemodynamic and metabolic responses to incremental arm cycling were measured by the Fick method and biopsy of the deltoid and triceps muscles before and after 42days of skiing for 6hday(-1) at 60% max heart rate.ResultsPeak pulmonary VO2 during arm crank was unchanged after training (2.380.19 vs. 2.18 +/- 0.2Lmin(-1) pre-training) yet arm VO2 (1.04 +/- 0.08 vs. 0.83 +/- 0.1Lmin(1), P<0.05) and power output (137 +/- 9 vs. 114 +/- 10 Watts) were increased along with a higher arm blood flow (7.9 +/- 0.5 vs. 6.8 +/- 0.6Lmin(-1), P<0.05) and expanded muscle capillary volume (76 +/- 7 vs. 62 +/- 4mL, P<0.05). Muscle O-2 diffusion capacity (16.2 +/- 1 vs. 12.5 +/- 0.9mLmin(-1)mHg(-1), P<0.05) and O-2 extraction (68 +/- 1 vs. 62 +/- 1%, P<0.05) were enhanced at a similar mean capillary transit time (569 +/- 43 vs. 564 +/- 31ms) and P-50 (35.8 +/- 0.7 vs. 35 +/- 0.8), whereas mitochondrial O-2 flux capacity was unchanged (147 +/- 6mLkgmin(-1) vs. 146 +/- 8mLkgmin(-1)).ConclusionThe mechanisms underlying the increase in peak arm VO2 with prolonged low-intensity training in previously untrained subjects are an increased convective O-2 delivery specifically to the muscles of the arm combined with a larger capillary-muscle surface area that enhance diffusional O-2 conductance, with no apparent role of mitochondrial respiratory capacity.
dc.publisher1748-1708
dc.relation.ispartofActa Physiologica
dc.sourceActa Physiologica[ISSN 1748-1708],v. 211 (1), p. 122-134
dc.subject.otherSkeletal-Muscle
dc.subject.otherOxygen
dc.subject.otherExercise
dc.subject.otherAdaptations
dc.subject.otherTransport
dc.subject.otherCapacity
dc.subject.otherCapillaries
dc.subject.otherPerfusion
dc.subject.otherTissues
dc.subject.otherSystem
dc.titleLow-intensity training increases peak arm VO2 by enhancing both convective and diffusive O-2 delivery
dc.typeinfo:eu-repo/semantics/Article
dc.typeArticle
dc.identifier.doi10.1111/apha.12258
dc.identifier.scopus84899103782
dc.identifier.isi000334488200015
dcterms.isPartOfActa Physiologica
dcterms.sourceActa Physiologica[ISSN 1748-1708],v. 211 (1), p. 122-134
dc.contributor.authorscopusid7003471688
dc.contributor.authorscopusid6603689982
dc.contributor.authorscopusid55365839300
dc.contributor.authorscopusid20334409300
dc.contributor.authorscopusid7004397216
dc.contributor.authorscopusid56063746100
dc.contributor.authorscopusid36958968500
dc.contributor.authorscopusid6506963877
dc.contributor.authorscopusid57191983922
dc.contributor.authorscopusid7103099936
dc.contributor.authorscopusid7004323423
dc.description.lastpage134
dc.identifier.issue1
dc.description.firstpage122
dc.relation.volume211
dc.type2Artículo
dc.identifier.wosWOS:000334488200015
dc.contributor.daisngid220476
dc.contributor.daisngid238859
dc.contributor.daisngid156181
dc.contributor.daisngid147585
dc.contributor.daisngid326233
dc.contributor.daisngid9620399
dc.contributor.daisngid21581881
dc.contributor.daisngid33551240
dc.contributor.daisngid1592176
dc.contributor.daisngid1055810
dc.contributor.daisngid209461
dc.contributor.daisngid13919
dc.contributor.daisngid90295
dc.identifier.investigatorRIDH-6693-2015
dc.identifier.investigatorRIDI-7096-2012
dc.identifier.investigatorRIDNo ID
dc.identifier.investigatorRIDNo ID
dc.identifier.investigatorRIDNo ID
dc.contributor.wosstandardWOS:Boushel, R
dc.contributor.wosstandardWOS:Ara, I
dc.contributor.wosstandardWOS:Gnaiger, E
dc.contributor.wosstandardWOS:Helge, JW
dc.contributor.wosstandardWOS:Gonzalez-Alonso, J
dc.contributor.wosstandardWOS:Munck-Andersen, T
dc.contributor.wosstandardWOS:Sondergaard, H
dc.contributor.wosstandardWOS:Damsgaard, R
dc.contributor.wosstandardWOS:van Hall, G
dc.contributor.wosstandardWOS:Saltin, B
dc.contributor.wosstandardWOS:Calbet, JAL
dc.date.coverdateEnero 2014
dc.identifier.ulpgces
dc.description.sjr1,793
dc.description.jcr4,382
dc.description.sjrqQ1
dc.description.jcrqQ1
dc.description.scieSCIE
item.fulltextSin texto completo-
item.grantfulltextnone-
crisitem.author.deptGIR IUIBS: Rendimiento humano, ejercicio físico y salud-
crisitem.author.deptIU de Investigaciones Biomédicas y Sanitarias-
crisitem.author.deptDepartamento de Educación Física-
crisitem.author.orcid0000-0002-9215-6234-
crisitem.author.parentorgIU de Investigaciones Biomédicas y Sanitarias-
crisitem.author.fullNameLópez Calbet, José Antonio-
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