Effect of a myocardial volume overload on lactate transport in skeletal muscle sarcolemmal vesicles
1 Department of Health and Human Performance, Auburn University and 2 Department of Anatomy, Physiology, and Pharmacology, Auburn University College of Veterinary Medicine, Auburn, Alabama 36849; and 3 Department of Human Nutrition, Foods, and Exercise Science, Virginia Tech, Blacksburg, Virginia...
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| Veröffentlicht in: | American journal of physiology. Regulatory, integrative and comparative physiology integrative and comparative physiology, 2001-07, Vol.281 (1), p.176-R186 |
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| container_title | American journal of physiology. Regulatory, integrative and comparative physiology |
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| creator | Aschenbach, William G Brower, Gregory L Talmadge, Robert J Dobson, John L Gladden, L. Bruce |
| description | 1 Department of Health and Human Performance, Auburn
University and 2 Department of Anatomy, Physiology, and
Pharmacology, Auburn University College of Veterinary Medicine,
Auburn, Alabama 36849; and 3 Department of Human Nutrition,
Foods, and Exercise Science, Virginia Tech, Blacksburg, Virginia
24061
This study sought to determine
the effect of a myocardial volume overload (MVO) on sarcolemmal (SL)
lactate (La ) transport and the aerobic profile of
skeletal muscle. SL vesicles were obtained from female rats 10 wk after
either a MVO was induced by creation of an infrarenal fistula
( n = 10), or sham surgeries were performed
( n = 11). Influx of 14 C-labeled
L(+)-La was measured at various unlabeled
La concentrations under zero- trans conditions.
La transport kinetics were determined using a
Michaelis-Menten equation with an added linear component to
discriminate between carrier-mediated and diffusional transport.
Although heart and lung weights were significantly increased
( P |
| doi_str_mv | 10.1152/ajpregu.2001.281.1.r176 |
| format | Article |
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University and 2 Department of Anatomy, Physiology, and
Pharmacology, Auburn University College of Veterinary Medicine,
Auburn, Alabama 36849; and 3 Department of Human Nutrition,
Foods, and Exercise Science, Virginia Tech, Blacksburg, Virginia
24061
This study sought to determine
the effect of a myocardial volume overload (MVO) on sarcolemmal (SL)
lactate (La ) transport and the aerobic profile of
skeletal muscle. SL vesicles were obtained from female rats 10 wk after
either a MVO was induced by creation of an infrarenal fistula
( n = 10), or sham surgeries were performed
( n = 11). Influx of 14 C-labeled
L(+)-La was measured at various unlabeled
La concentrations under zero- trans conditions.
La transport kinetics were determined using a
Michaelis-Menten equation with an added linear component to
discriminate between carrier-mediated and diffusional transport.
Although heart and lung weights were significantly increased
( P < 0.0001) in the MVO group, left ventricular function was only modestly altered ( P < 0.05). A
significant reduction in type I myosin heavy chain (MHC) in the soleus
and a strong trend ( P = 0.06) for a reduced type IIx
MHC in the plantaris were observed in MVO rats, but no differences in
citrate synthase activity or monocarboxylate transporter proteins
(MCT)-1 expression were noted in any muscle. Carrier-mediated
La influx into SL vesicles was similar between sham and
MVO ( K m = 12 ± 1 and 18 ± 3 mM;
apparent V max = 772 ± 99 and 827 ± 80 nmol · mg 1 · min 1 ,
respectively). Total influx at 100 mM was lower in MVO, and this was due to a 30% reduction in membrane diffusion. In conclusion, a 10-wk MVO did not alter MCT-mediated La transport or
protein expression but was associated with modest changes in
myofibrillar proteins and impaired SL diffusive properties.
congestive heart failure; monocarboxylate transporter proteins; monocarboxylate; membrane diffusion</description><identifier>ISSN: 0363-6119</identifier><identifier>EISSN: 1522-1490</identifier><identifier>DOI: 10.1152/ajpregu.2001.281.1.r176</identifier><identifier>PMID: 11404292</identifier><language>eng</language><publisher>United States</publisher><subject>Animals ; Cardiac Volume - physiology ; Carrier Proteins - metabolism ; Citrate (si)-Synthase - metabolism ; Female ; Heart Failure - metabolism ; Heart Failure - pathology ; Heart Failure - physiopathology ; Lactic Acid - metabolism ; Lanthanum - pharmacokinetics ; Microscopy, Electron ; Monocarboxylic Acid Transporters ; Motor Activity ; Muscle, Skeletal - metabolism ; Myofibrils - metabolism ; Myosin Heavy Chains - metabolism ; Organ Size ; Rats ; Rats, Sprague-Dawley ; Sarcoplasmic Reticulum - metabolism ; Sarcoplasmic Reticulum - ultrastructure ; Ventricular Function, Left - physiology</subject><ispartof>American journal of physiology. Regulatory, integrative and comparative physiology, 2001-07, Vol.281 (1), p.176-R186</ispartof><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c397t-56e4ba379fd96bbc5207450b079d57dcccf557ce9135e87f44fec709f7d89b1a3</citedby><cites>FETCH-LOGICAL-c397t-56e4ba379fd96bbc5207450b079d57dcccf557ce9135e87f44fec709f7d89b1a3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,3025,27903,27904</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/11404292$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Aschenbach, William G</creatorcontrib><creatorcontrib>Brower, Gregory L</creatorcontrib><creatorcontrib>Talmadge, Robert J</creatorcontrib><creatorcontrib>Dobson, John L</creatorcontrib><creatorcontrib>Gladden, L. Bruce</creatorcontrib><title>Effect of a myocardial volume overload on lactate transport in skeletal muscle sarcolemmal vesicles</title><title>American journal of physiology. Regulatory, integrative and comparative physiology</title><addtitle>Am J Physiol Regul Integr Comp Physiol</addtitle><description>1 Department of Health and Human Performance, Auburn
University and 2 Department of Anatomy, Physiology, and
Pharmacology, Auburn University College of Veterinary Medicine,
Auburn, Alabama 36849; and 3 Department of Human Nutrition,
Foods, and Exercise Science, Virginia Tech, Blacksburg, Virginia
24061
This study sought to determine
the effect of a myocardial volume overload (MVO) on sarcolemmal (SL)
lactate (La ) transport and the aerobic profile of
skeletal muscle. SL vesicles were obtained from female rats 10 wk after
either a MVO was induced by creation of an infrarenal fistula
( n = 10), or sham surgeries were performed
( n = 11). Influx of 14 C-labeled
L(+)-La was measured at various unlabeled
La concentrations under zero- trans conditions.
La transport kinetics were determined using a
Michaelis-Menten equation with an added linear component to
discriminate between carrier-mediated and diffusional transport.
Although heart and lung weights were significantly increased
( P < 0.0001) in the MVO group, left ventricular function was only modestly altered ( P < 0.05). A
significant reduction in type I myosin heavy chain (MHC) in the soleus
and a strong trend ( P = 0.06) for a reduced type IIx
MHC in the plantaris were observed in MVO rats, but no differences in
citrate synthase activity or monocarboxylate transporter proteins
(MCT)-1 expression were noted in any muscle. Carrier-mediated
La influx into SL vesicles was similar between sham and
MVO ( K m = 12 ± 1 and 18 ± 3 mM;
apparent V max = 772 ± 99 and 827 ± 80 nmol · mg 1 · min 1 ,
respectively). Total influx at 100 mM was lower in MVO, and this was due to a 30% reduction in membrane diffusion. In conclusion, a 10-wk MVO did not alter MCT-mediated La transport or
protein expression but was associated with modest changes in
myofibrillar proteins and impaired SL diffusive properties.
congestive heart failure; monocarboxylate transporter proteins; monocarboxylate; membrane diffusion</description><subject>Animals</subject><subject>Cardiac Volume - physiology</subject><subject>Carrier Proteins - metabolism</subject><subject>Citrate (si)-Synthase - metabolism</subject><subject>Female</subject><subject>Heart Failure - metabolism</subject><subject>Heart Failure - pathology</subject><subject>Heart Failure - physiopathology</subject><subject>Lactic Acid - metabolism</subject><subject>Lanthanum - pharmacokinetics</subject><subject>Microscopy, Electron</subject><subject>Monocarboxylic Acid Transporters</subject><subject>Motor Activity</subject><subject>Muscle, Skeletal - metabolism</subject><subject>Myofibrils - metabolism</subject><subject>Myosin Heavy Chains - metabolism</subject><subject>Organ Size</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Sarcoplasmic Reticulum - metabolism</subject><subject>Sarcoplasmic Reticulum - ultrastructure</subject><subject>Ventricular Function, Left - physiology</subject><issn>0363-6119</issn><issn>1522-1490</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2001</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kNFOHCEUhonR6Nb6Cpar3s0UBhiWS2PUNjFpYuw1YZjD7lhmGYGx3beXzW6zvfGK5PD9_zn5EPpCSU2paL6ZlynCaq4bQmjdLGlN60hle4IW5bepKFfkFC0Ia1nVUqou0KeUXgghnHF2ji4o5YQ3qlkge-cc2IyDwwaP22BN7Afj8Vvw8wg4vEH0wfQ4bLA3NpsMOEezSVOIGQ8bnH6Dh1wC45ysB5xMtMHDOO46IA1llj6jM2d8gqvDe4l-3d89336vHn8-_Li9eawsUzJXogXeGSaV61XbdVY0RHJBOiJVL2RvrXVCSAuKMgFL6Tgvl0uinOyXqqOGXaKv-94phtcZUtbjkCx4bzYQ5qQL21AhlwWUe9DGkFIEp6c4jCZuNSV651cf_OqdX138aqqfit-SvD6smLsR-mPuILQA1R5YD6v1nyGCntbbNAQfVttj6_-F6mP-fvb-Gf7mf8FjTk-9Y-8iUaCS</recordid><startdate>20010701</startdate><enddate>20010701</enddate><creator>Aschenbach, William G</creator><creator>Brower, Gregory L</creator><creator>Talmadge, Robert J</creator><creator>Dobson, John L</creator><creator>Gladden, L. Bruce</creator><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>7X8</scope></search><sort><creationdate>20010701</creationdate><title>Effect of a myocardial volume overload on lactate transport in skeletal muscle sarcolemmal vesicles</title><author>Aschenbach, William G ; Brower, Gregory L ; Talmadge, Robert J ; Dobson, John L ; Gladden, L. Bruce</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c397t-56e4ba379fd96bbc5207450b079d57dcccf557ce9135e87f44fec709f7d89b1a3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2001</creationdate><topic>Animals</topic><topic>Cardiac Volume - physiology</topic><topic>Carrier Proteins - metabolism</topic><topic>Citrate (si)-Synthase - metabolism</topic><topic>Female</topic><topic>Heart Failure - metabolism</topic><topic>Heart Failure - pathology</topic><topic>Heart Failure - physiopathology</topic><topic>Lactic Acid - metabolism</topic><topic>Lanthanum - pharmacokinetics</topic><topic>Microscopy, Electron</topic><topic>Monocarboxylic Acid Transporters</topic><topic>Motor Activity</topic><topic>Muscle, Skeletal - metabolism</topic><topic>Myofibrils - metabolism</topic><topic>Myosin Heavy Chains - metabolism</topic><topic>Organ Size</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Sarcoplasmic Reticulum - metabolism</topic><topic>Sarcoplasmic Reticulum - ultrastructure</topic><topic>Ventricular Function, Left - physiology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Aschenbach, William G</creatorcontrib><creatorcontrib>Brower, Gregory L</creatorcontrib><creatorcontrib>Talmadge, Robert J</creatorcontrib><creatorcontrib>Dobson, John L</creatorcontrib><creatorcontrib>Gladden, L. Bruce</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>American journal of physiology. Regulatory, integrative and comparative physiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Aschenbach, William G</au><au>Brower, Gregory L</au><au>Talmadge, Robert J</au><au>Dobson, John L</au><au>Gladden, L. Bruce</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Effect of a myocardial volume overload on lactate transport in skeletal muscle sarcolemmal vesicles</atitle><jtitle>American journal of physiology. Regulatory, integrative and comparative physiology</jtitle><addtitle>Am J Physiol Regul Integr Comp Physiol</addtitle><date>2001-07-01</date><risdate>2001</risdate><volume>281</volume><issue>1</issue><spage>176</spage><epage>R186</epage><pages>176-R186</pages><issn>0363-6119</issn><eissn>1522-1490</eissn><abstract>1 Department of Health and Human Performance, Auburn
University and 2 Department of Anatomy, Physiology, and
Pharmacology, Auburn University College of Veterinary Medicine,
Auburn, Alabama 36849; and 3 Department of Human Nutrition,
Foods, and Exercise Science, Virginia Tech, Blacksburg, Virginia
24061
This study sought to determine
the effect of a myocardial volume overload (MVO) on sarcolemmal (SL)
lactate (La ) transport and the aerobic profile of
skeletal muscle. SL vesicles were obtained from female rats 10 wk after
either a MVO was induced by creation of an infrarenal fistula
( n = 10), or sham surgeries were performed
( n = 11). Influx of 14 C-labeled
L(+)-La was measured at various unlabeled
La concentrations under zero- trans conditions.
La transport kinetics were determined using a
Michaelis-Menten equation with an added linear component to
discriminate between carrier-mediated and diffusional transport.
Although heart and lung weights were significantly increased
( P < 0.0001) in the MVO group, left ventricular function was only modestly altered ( P < 0.05). A
significant reduction in type I myosin heavy chain (MHC) in the soleus
and a strong trend ( P = 0.06) for a reduced type IIx
MHC in the plantaris were observed in MVO rats, but no differences in
citrate synthase activity or monocarboxylate transporter proteins
(MCT)-1 expression were noted in any muscle. Carrier-mediated
La influx into SL vesicles was similar between sham and
MVO ( K m = 12 ± 1 and 18 ± 3 mM;
apparent V max = 772 ± 99 and 827 ± 80 nmol · mg 1 · min 1 ,
respectively). Total influx at 100 mM was lower in MVO, and this was due to a 30% reduction in membrane diffusion. In conclusion, a 10-wk MVO did not alter MCT-mediated La transport or
protein expression but was associated with modest changes in
myofibrillar proteins and impaired SL diffusive properties.
congestive heart failure; monocarboxylate transporter proteins; monocarboxylate; membrane diffusion</abstract><cop>United States</cop><pmid>11404292</pmid><doi>10.1152/ajpregu.2001.281.1.r176</doi></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0363-6119 |
| ispartof | American journal of physiology. Regulatory, integrative and comparative physiology, 2001-07, Vol.281 (1), p.176-R186 |
| issn | 0363-6119 1522-1490 |
| language | eng |
| recordid | cdi_pubmed_primary_11404292 |
| source | MEDLINE; American Physiological Society; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals |
| subjects | Animals Cardiac Volume - physiology Carrier Proteins - metabolism Citrate (si)-Synthase - metabolism Female Heart Failure - metabolism Heart Failure - pathology Heart Failure - physiopathology Lactic Acid - metabolism Lanthanum - pharmacokinetics Microscopy, Electron Monocarboxylic Acid Transporters Motor Activity Muscle, Skeletal - metabolism Myofibrils - metabolism Myosin Heavy Chains - metabolism Organ Size Rats Rats, Sprague-Dawley Sarcoplasmic Reticulum - metabolism Sarcoplasmic Reticulum - ultrastructure Ventricular Function, Left - physiology |
| title | Effect of a myocardial volume overload on lactate transport in skeletal muscle sarcolemmal vesicles |
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