Impaired Skeletal Muscle Fatigue Resistance in Rats with Pressure Overload-induced Left Ventricular Hypertrophy
In rats with left ventricular (LV) hypertrophy, we investigated whether abnormalities of skeletal muscle could result in reduced exercise tolerance in the absence of reduced cardiac function. LV pressure overload was induced by partial constriction of the abdominal aorta (AC) with controls subjected...
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| Veröffentlicht in: | Journal of molecular and cellular cardiology 1996-01, Vol.28 (1), p.183-195 |
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| creator | Levy, Louis B. Avkiran, Metin Ferrari, Roberto Hearse, David J. |
| description | In rats with left ventricular (LV) hypertrophy, we investigated whether abnormalities of skeletal muscle could result in reduced exercise tolerance in the absence of reduced cardiac function. LV pressure overload was induced by partial constriction of the abdominal aorta (AC) with controls subjected to sham operation. Cardiac and skeletal muscle function and blood flow were assessed
in vivo3 and 6 weeks later. AC induced LV hypertrophy of 41 % and 37 % at 3 and 6 weeks post-operation. In AC rats, cardiac index was 31 ±8 and 35 ±4 ml /min /100 g at 3 and 6 weeks compared to 38 ±4 and 34 ±2 ml /min /100 g in controls (
n.s.). Fatigue index of the soleus (type-I rich) muscle in AC rats was reduced by 14 % (
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| doi_str_mv | 10.1006/jmcc.1996.0018 |
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in vivo3 and 6 weeks later. AC induced LV hypertrophy of 41 % and 37 % at 3 and 6 weeks post-operation. In AC rats, cardiac index was 31 ±8 and 35 ±4 ml /min /100 g at 3 and 6 weeks compared to 38 ±4 and 34 ±2 ml /min /100 g in controls (
n.s.). Fatigue index of the soleus (type-I rich) muscle in AC rats was reduced by 14 % (
P<0.05) at both time points, while that of the tibialis anterior (mixed fiber) muscle was unchanged at 3 weeks but reduced by 18 % (
P<0.05) at 6 weeks. Function of the extensor digitorum longus (type-II
Brich) muscle was unaltered at both time points. Blood flow at rest was paradoxically increased in muscles which exhibited increased fatigue susceptibility. At 3 weeks, blood flow during fatigue stimulation was reduced by 33 % in the soleus muscle; the only muscle to exhibit impaired fatigue resistance at this time point. Blood flow during stimulation remained unaltered in the EDL and TA muscles. Thus, impaired fatigue resistance was observed in skeletal muscle with high oxidative and oxidative glycolytic fiber content during the compensatory phase of LV hypertrophy, prior to overt cardiac dysfunction. A selective impairment of blood flow to these muscles during exercise may play a causal role in exercise intolerance.</description><identifier>ISSN: 0022-2828</identifier><identifier>EISSN: 1095-8584</identifier><identifier>DOI: 10.1006/jmcc.1996.0018</identifier><identifier>PMID: 8745226</identifier><language>eng</language><publisher>England: Elsevier Ltd</publisher><subject>Animals ; Blood flow ; Body Weight ; Cardiac Output ; Compensated hypertrophy ; Electric Stimulation ; Exercise intolerance ; Heart - physiology ; Heart - physiopathology ; Heart Rate ; Hypertrophy, Left Ventricular - physiopathology ; Male ; Muscle Contraction ; Muscle Fatigue ; Muscle function ; Muscle, Skeletal - blood supply ; Muscle, Skeletal - physiology ; Muscle, Skeletal - physiopathology ; Organ Size ; Rats ; Rats, Wistar ; Regional Blood Flow ; Sciatic Nerve - physiology ; Sciatic Nerve - physiopathology ; Soleus ; Stroke Volume ; Tibialis anterior ; Time Factors</subject><ispartof>Journal of molecular and cellular cardiology, 1996-01, Vol.28 (1), p.183-195</ispartof><rights>1996</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c339t-c2c4e7ca1441fcd6c6e5fe0d5ce6651d45accf7c644ce7638e0b7e7de48c6eb33</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1006/jmcc.1996.0018$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3548,27923,27924,45994</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/8745226$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Levy, Louis B.</creatorcontrib><creatorcontrib>Avkiran, Metin</creatorcontrib><creatorcontrib>Ferrari, Roberto</creatorcontrib><creatorcontrib>Hearse, David J.</creatorcontrib><title>Impaired Skeletal Muscle Fatigue Resistance in Rats with Pressure Overload-induced Left Ventricular Hypertrophy</title><title>Journal of molecular and cellular cardiology</title><addtitle>J Mol Cell Cardiol</addtitle><description>In rats with left ventricular (LV) hypertrophy, we investigated whether abnormalities of skeletal muscle could result in reduced exercise tolerance in the absence of reduced cardiac function. LV pressure overload was induced by partial constriction of the abdominal aorta (AC) with controls subjected to sham operation. Cardiac and skeletal muscle function and blood flow were assessed
in vivo3 and 6 weeks later. AC induced LV hypertrophy of 41 % and 37 % at 3 and 6 weeks post-operation. In AC rats, cardiac index was 31 ±8 and 35 ±4 ml /min /100 g at 3 and 6 weeks compared to 38 ±4 and 34 ±2 ml /min /100 g in controls (
n.s.). Fatigue index of the soleus (type-I rich) muscle in AC rats was reduced by 14 % (
P<0.05) at both time points, while that of the tibialis anterior (mixed fiber) muscle was unchanged at 3 weeks but reduced by 18 % (
P<0.05) at 6 weeks. Function of the extensor digitorum longus (type-II
Brich) muscle was unaltered at both time points. Blood flow at rest was paradoxically increased in muscles which exhibited increased fatigue susceptibility. At 3 weeks, blood flow during fatigue stimulation was reduced by 33 % in the soleus muscle; the only muscle to exhibit impaired fatigue resistance at this time point. Blood flow during stimulation remained unaltered in the EDL and TA muscles. Thus, impaired fatigue resistance was observed in skeletal muscle with high oxidative and oxidative glycolytic fiber content during the compensatory phase of LV hypertrophy, prior to overt cardiac dysfunction. A selective impairment of blood flow to these muscles during exercise may play a causal role in exercise intolerance.</description><subject>Animals</subject><subject>Blood flow</subject><subject>Body Weight</subject><subject>Cardiac Output</subject><subject>Compensated hypertrophy</subject><subject>Electric Stimulation</subject><subject>Exercise intolerance</subject><subject>Heart - physiology</subject><subject>Heart - physiopathology</subject><subject>Heart Rate</subject><subject>Hypertrophy, Left Ventricular - physiopathology</subject><subject>Male</subject><subject>Muscle Contraction</subject><subject>Muscle Fatigue</subject><subject>Muscle function</subject><subject>Muscle, Skeletal - blood supply</subject><subject>Muscle, Skeletal - physiology</subject><subject>Muscle, Skeletal - physiopathology</subject><subject>Organ Size</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Regional Blood Flow</subject><subject>Sciatic Nerve - physiology</subject><subject>Sciatic Nerve - physiopathology</subject><subject>Soleus</subject><subject>Stroke Volume</subject><subject>Tibialis anterior</subject><subject>Time Factors</subject><issn>0022-2828</issn><issn>1095-8584</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1996</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kD1v2zAQQIkiQeqmWbsV4JRNDilRFDUGRh0HcJHAbbMS9PHU0NVXSMqF_31p2OiW6YZ794B7hHzhbM4Zk3e7DmDO61rOGePqA5lxVpeZKpW4IDPG8jzLVa4-kk8h7BhjtSiKK3KlKlHmuZyR4bEbjfNo6Y8_2GI0Lf0-BWiRLk10vyekGwwuRNMDUtfTjYmB_nXxlT57DGHySJ_26NvB2Mz1doJkWmMT6Qv20TuYWuPp6jCij34YXw-fyWVj2oA353lNfi2__VyssvXTw-Pifp1BUdQxgxwEVmC4ELwBK0Fi2SCzJaCUJbeiNABNBVIIwEoWCtm2wsqiUAndFsU1uT15Rz-8TRii7lwAbFvT4zAFXalcpAAygfMTCH4IwWOjR-864w-aM30srI-F9bGwPhZOB1_P5mnbof2Pn5OmvTrtMb23d-h1AIcpn02ZIWo7uPfU_wA-vo1o</recordid><startdate>19960101</startdate><enddate>19960101</enddate><creator>Levy, Louis B.</creator><creator>Avkiran, Metin</creator><creator>Ferrari, Roberto</creator><creator>Hearse, David J.</creator><general>Elsevier Ltd</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>7X8</scope></search><sort><creationdate>19960101</creationdate><title>Impaired Skeletal Muscle Fatigue Resistance in Rats with Pressure Overload-induced Left Ventricular Hypertrophy</title><author>Levy, Louis B. ; Avkiran, Metin ; Ferrari, Roberto ; Hearse, David J.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c339t-c2c4e7ca1441fcd6c6e5fe0d5ce6651d45accf7c644ce7638e0b7e7de48c6eb33</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1996</creationdate><topic>Animals</topic><topic>Blood flow</topic><topic>Body Weight</topic><topic>Cardiac Output</topic><topic>Compensated hypertrophy</topic><topic>Electric Stimulation</topic><topic>Exercise intolerance</topic><topic>Heart - physiology</topic><topic>Heart - physiopathology</topic><topic>Heart Rate</topic><topic>Hypertrophy, Left Ventricular - physiopathology</topic><topic>Male</topic><topic>Muscle Contraction</topic><topic>Muscle Fatigue</topic><topic>Muscle function</topic><topic>Muscle, Skeletal - blood supply</topic><topic>Muscle, Skeletal - physiology</topic><topic>Muscle, Skeletal - physiopathology</topic><topic>Organ Size</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>Regional Blood Flow</topic><topic>Sciatic Nerve - physiology</topic><topic>Sciatic Nerve - physiopathology</topic><topic>Soleus</topic><topic>Stroke Volume</topic><topic>Tibialis anterior</topic><topic>Time Factors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Levy, Louis B.</creatorcontrib><creatorcontrib>Avkiran, Metin</creatorcontrib><creatorcontrib>Ferrari, Roberto</creatorcontrib><creatorcontrib>Hearse, David J.</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>Journal of molecular and cellular cardiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Levy, Louis B.</au><au>Avkiran, Metin</au><au>Ferrari, Roberto</au><au>Hearse, David J.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Impaired Skeletal Muscle Fatigue Resistance in Rats with Pressure Overload-induced Left Ventricular Hypertrophy</atitle><jtitle>Journal of molecular and cellular cardiology</jtitle><addtitle>J Mol Cell Cardiol</addtitle><date>1996-01-01</date><risdate>1996</risdate><volume>28</volume><issue>1</issue><spage>183</spage><epage>195</epage><pages>183-195</pages><issn>0022-2828</issn><eissn>1095-8584</eissn><abstract>In rats with left ventricular (LV) hypertrophy, we investigated whether abnormalities of skeletal muscle could result in reduced exercise tolerance in the absence of reduced cardiac function. LV pressure overload was induced by partial constriction of the abdominal aorta (AC) with controls subjected to sham operation. Cardiac and skeletal muscle function and blood flow were assessed
in vivo3 and 6 weeks later. AC induced LV hypertrophy of 41 % and 37 % at 3 and 6 weeks post-operation. In AC rats, cardiac index was 31 ±8 and 35 ±4 ml /min /100 g at 3 and 6 weeks compared to 38 ±4 and 34 ±2 ml /min /100 g in controls (
n.s.). Fatigue index of the soleus (type-I rich) muscle in AC rats was reduced by 14 % (
P<0.05) at both time points, while that of the tibialis anterior (mixed fiber) muscle was unchanged at 3 weeks but reduced by 18 % (
P<0.05) at 6 weeks. Function of the extensor digitorum longus (type-II
Brich) muscle was unaltered at both time points. Blood flow at rest was paradoxically increased in muscles which exhibited increased fatigue susceptibility. At 3 weeks, blood flow during fatigue stimulation was reduced by 33 % in the soleus muscle; the only muscle to exhibit impaired fatigue resistance at this time point. Blood flow during stimulation remained unaltered in the EDL and TA muscles. Thus, impaired fatigue resistance was observed in skeletal muscle with high oxidative and oxidative glycolytic fiber content during the compensatory phase of LV hypertrophy, prior to overt cardiac dysfunction. A selective impairment of blood flow to these muscles during exercise may play a causal role in exercise intolerance.</abstract><cop>England</cop><pub>Elsevier Ltd</pub><pmid>8745226</pmid><doi>10.1006/jmcc.1996.0018</doi><tpages>13</tpages></addata></record> |
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| subjects | Animals Blood flow Body Weight Cardiac Output Compensated hypertrophy Electric Stimulation Exercise intolerance Heart - physiology Heart - physiopathology Heart Rate Hypertrophy, Left Ventricular - physiopathology Male Muscle Contraction Muscle Fatigue Muscle function Muscle, Skeletal - blood supply Muscle, Skeletal - physiology Muscle, Skeletal - physiopathology Organ Size Rats Rats, Wistar Regional Blood Flow Sciatic Nerve - physiology Sciatic Nerve - physiopathology Soleus Stroke Volume Tibialis anterior Time Factors |
| title | Impaired Skeletal Muscle Fatigue Resistance in Rats with Pressure Overload-induced Left Ventricular Hypertrophy |
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