Hypertrophy of skeletal muscle in diabetic rats in response to chronic resistance exercise

Noll Physiological Research Center and Department of Kinesiology, University Park 16802; and Department of Cellular and Molecular Physiology, Pennsylvania State University College of Medicine, Hershey, Pennsylvania 17033 This study had the following objectives: 1 ) to determine whether diabetic rats...

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Veröffentlicht in:Journal of applied physiology (1985) 1999-09, Vol.87 (3), p.1075-1082
Hauptverfasser: Farrell, Peter A, Fedele, Mark J, Hernandez, Jazmir, Fluckey, James D, Miller, John L., III, Lang, Charles H, Vary, Thomas C, Kimball, Scot R, Jefferson, Leonard S
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container_issue 3
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container_title Journal of applied physiology (1985)
container_volume 87
creator Farrell, Peter A
Fedele, Mark J
Hernandez, Jazmir
Fluckey, James D
Miller, John L., III
Lang, Charles H
Vary, Thomas C
Kimball, Scot R
Jefferson, Leonard S
description Noll Physiological Research Center and Department of Kinesiology, University Park 16802; and Department of Cellular and Molecular Physiology, Pennsylvania State University College of Medicine, Hershey, Pennsylvania 17033 This study had the following objectives: 1 ) to determine whether diabetic rats could increase muscle mass due to a physiological manipulation (chronic resistance exercise), 2 ) to determine whether exercise training status modifies the effect of the last bout of exercise on elevations in rates of protein synthesis, and 3 ) to determine whether chronic resistance exercise alters basal glycemia. Groups consisted of diabetic or nondiabetic rats that performed progressive resistance exercise for 8 wk, performed acute resistance exercise, or remained sedentary. Arterial plasma insulin in diabetic groups was reduced by about one-half ( P  <   0.05) compared with nondiabetic groups. Soleus and gastrocnemius-plantaris complex muscle wet weights were lower because of diabetes, but in response to chronic exercise these muscles hypertrophied in diabetic (0.028 ± 0.003 vs. 0.032 ± 0.0015 g/cm for sedentary vs. exercised soleus and 0.42 ± 0.068 vs. 0.53 ± 0.041 g/cm for sedentary vs. exercised gastrocnemius-plantaris, both P  
doi_str_mv 10.1152/jappl.1999.87.3.1075
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Groups consisted of diabetic or nondiabetic rats that performed progressive resistance exercise for 8 wk, performed acute resistance exercise, or remained sedentary. Arterial plasma insulin in diabetic groups was reduced by about one-half ( P  &lt;   0.05) compared with nondiabetic groups. Soleus and gastrocnemius-plantaris complex muscle wet weights were lower because of diabetes, but in response to chronic exercise these muscles hypertrophied in diabetic (0.028 ± 0.003 vs. 0.032 ± 0.0015 g/cm for sedentary vs. exercised soleus and 0.42 ± 0.068 vs. 0.53 ± 0.041 g/cm for sedentary vs. exercised gastrocnemius-plantaris, both P  &lt; 0.05) but not in nondiabetic (0.041 ± 0.0026 vs. 0.042 ± 0.003 g/cm for sedentary vs. exercised soleus and 0.72 ± 0.015 vs. 0.69 ±   0.013 g/cm for sedentary vs. exercised gastrocnemius-plantaris) rats when muscle weight was expressed relative to tibial length or body weight (data not shown). Another group of diabetic rats that lifted heavier weights showed muscle hypertrophy. Rates of protein synthesis were higher in red gastrocnemius in chronically exercised than in sedentary rats: 155 ± 11 and 170 ± 7 nmol phenylalanine incorporated · g muscle 1 · h 1 in exercised diabetic and nondiabetic rats vs. 110 ± 14 and 143   ± 7 nmol phenylalanine incorporated · g muscle 1 · h 1 in sedentary diabetic and nondiabetic rats. These elevations, however, were lower than in acutely exercised (but untrained) rats: 176 ± 15 and 193 ± 8 nmol phenylalanine incorporated · g muscle 1 · h 1 in diabetic and nondiabetic rats. Finally, chronic exercise training in diabetic rats was associated with reductions in basal glycemia, and such reductions did not occur in sedentary diabetic groups. These data demonstrate that, despite lower circulating insulin concentrations, diabetic rats can increase muscle mass in response to a physiological stimulus. protein synthesis; insulin; insulin-like growth factor I; muscle mass</description><identifier>ISSN: 8750-7587</identifier><identifier>EISSN: 1522-1601</identifier><identifier>DOI: 10.1152/jappl.1999.87.3.1075</identifier><identifier>PMID: 10484579</identifier><identifier>CODEN: JAPHEV</identifier><language>eng</language><publisher>Bethesda, MD: Am Physiological Soc</publisher><subject>Animals ; Biological and medical sciences ; Blood Glucose - metabolism ; Body Weight - physiology ; Diabetes ; Diabetes Mellitus, Experimental - blood ; Diabetes Mellitus, Experimental - physiopathology ; Diabetes. Impaired glucose tolerance ; Endocrine pancreas. Apud cells (diseases) ; Endocrinopathies ; Etiopathogenesis. Screening. Investigations. Target tissue resistance ; Exercise ; Insulin ; Insulin - blood ; Insulin-Like Growth Factor I - metabolism ; Kinetics ; Male ; Medical sciences ; Muscle Development ; Muscle Proteins - biosynthesis ; Muscle, Skeletal - growth &amp; development ; Muscle, Skeletal - pathology ; Muscular system ; Organ Size - physiology ; Pancreatectomy ; Physical Conditioning, Animal - physiology ; Physical Exertion - physiology ; Proteins ; Rats ; Rats, Sprague-Dawley ; Rodents ; Space life sciences</subject><ispartof>Journal of applied physiology (1985), 1999-09, Vol.87 (3), p.1075-1082</ispartof><rights>1999 INIST-CNRS</rights><rights>Copyright American Physiological Society Sep 1999</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c503t-2ab9cd6a24b76dc08c0b456ef0d7b00d9f736174affdb247673e91b42798f95a3</citedby><cites>FETCH-LOGICAL-c503t-2ab9cd6a24b76dc08c0b456ef0d7b00d9f736174affdb247673e91b42798f95a3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,3026,27901,27902</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&amp;idt=1960097$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/10484579$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Farrell, Peter A</creatorcontrib><creatorcontrib>Fedele, Mark J</creatorcontrib><creatorcontrib>Hernandez, Jazmir</creatorcontrib><creatorcontrib>Fluckey, James D</creatorcontrib><creatorcontrib>Miller, John L., III</creatorcontrib><creatorcontrib>Lang, Charles H</creatorcontrib><creatorcontrib>Vary, Thomas C</creatorcontrib><creatorcontrib>Kimball, Scot R</creatorcontrib><creatorcontrib>Jefferson, Leonard S</creatorcontrib><title>Hypertrophy of skeletal muscle in diabetic rats in response to chronic resistance exercise</title><title>Journal of applied physiology (1985)</title><addtitle>J Appl Physiol (1985)</addtitle><description>Noll Physiological Research Center and Department of Kinesiology, University Park 16802; and Department of Cellular and Molecular Physiology, Pennsylvania State University College of Medicine, Hershey, Pennsylvania 17033 This study had the following objectives: 1 ) to determine whether diabetic rats could increase muscle mass due to a physiological manipulation (chronic resistance exercise), 2 ) to determine whether exercise training status modifies the effect of the last bout of exercise on elevations in rates of protein synthesis, and 3 ) to determine whether chronic resistance exercise alters basal glycemia. Groups consisted of diabetic or nondiabetic rats that performed progressive resistance exercise for 8 wk, performed acute resistance exercise, or remained sedentary. Arterial plasma insulin in diabetic groups was reduced by about one-half ( P  &lt;   0.05) compared with nondiabetic groups. Soleus and gastrocnemius-plantaris complex muscle wet weights were lower because of diabetes, but in response to chronic exercise these muscles hypertrophied in diabetic (0.028 ± 0.003 vs. 0.032 ± 0.0015 g/cm for sedentary vs. exercised soleus and 0.42 ± 0.068 vs. 0.53 ± 0.041 g/cm for sedentary vs. exercised gastrocnemius-plantaris, both P  &lt; 0.05) but not in nondiabetic (0.041 ± 0.0026 vs. 0.042 ± 0.003 g/cm for sedentary vs. exercised soleus and 0.72 ± 0.015 vs. 0.69 ±   0.013 g/cm for sedentary vs. exercised gastrocnemius-plantaris) rats when muscle weight was expressed relative to tibial length or body weight (data not shown). Another group of diabetic rats that lifted heavier weights showed muscle hypertrophy. Rates of protein synthesis were higher in red gastrocnemius in chronically exercised than in sedentary rats: 155 ± 11 and 170 ± 7 nmol phenylalanine incorporated · g muscle 1 · h 1 in exercised diabetic and nondiabetic rats vs. 110 ± 14 and 143   ± 7 nmol phenylalanine incorporated · g muscle 1 · h 1 in sedentary diabetic and nondiabetic rats. These elevations, however, were lower than in acutely exercised (but untrained) rats: 176 ± 15 and 193 ± 8 nmol phenylalanine incorporated · g muscle 1 · h 1 in diabetic and nondiabetic rats. Finally, chronic exercise training in diabetic rats was associated with reductions in basal glycemia, and such reductions did not occur in sedentary diabetic groups. These data demonstrate that, despite lower circulating insulin concentrations, diabetic rats can increase muscle mass in response to a physiological stimulus. protein synthesis; insulin; insulin-like growth factor I; muscle mass</description><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Blood Glucose - metabolism</subject><subject>Body Weight - physiology</subject><subject>Diabetes</subject><subject>Diabetes Mellitus, Experimental - blood</subject><subject>Diabetes Mellitus, Experimental - physiopathology</subject><subject>Diabetes. Impaired glucose tolerance</subject><subject>Endocrine pancreas. Apud cells (diseases)</subject><subject>Endocrinopathies</subject><subject>Etiopathogenesis. Screening. Investigations. Target tissue resistance</subject><subject>Exercise</subject><subject>Insulin</subject><subject>Insulin - blood</subject><subject>Insulin-Like Growth Factor I - metabolism</subject><subject>Kinetics</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Muscle Development</subject><subject>Muscle Proteins - biosynthesis</subject><subject>Muscle, Skeletal - growth &amp; development</subject><subject>Muscle, Skeletal - pathology</subject><subject>Muscular system</subject><subject>Organ Size - physiology</subject><subject>Pancreatectomy</subject><subject>Physical Conditioning, Animal - physiology</subject><subject>Physical Exertion - physiology</subject><subject>Proteins</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Rodents</subject><subject>Space life sciences</subject><issn>8750-7587</issn><issn>1522-1601</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1999</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kU1v1DAQhi0EokvhHyAUIYS4JIwTO46PqKItUiUu5cLFcpxx14s3DnYiuv8eh12VDwlfLHmed2b0mJCXFCpKef1-p6fJV1RKWXWiaioKgj8im1yqS9oCfUw2neBQCt6JM_IspR0AZYzTp-SMAusYF3JDvl4fJoxzDNP2UARbpG_ocda-2C_JeCzcWAxO9zg7U0Q9p_UhYprCmLCYQ2G2MYxrDZNLsx4NFniP0biEz8kTq33CF6f7nHy5_Hh7cV3efL76dPHhpjQcmrmsdS_N0Oqa9aIdDHQGesZbtDCIHmCQVjQtFUxbO_Q1E61oUNKe1UJ2VnLdnJO3x75TDN8XTLPau2TQez1iWJISADVvO8jg63_AXVjimHdTdT7Q8YZniB0hE0NKEa2aotvreFAU1Cpe_RKvVvGqE6pRq_gce3XqvfR7HP4IHU1n4M0J0Mlob2N25dJvTrYAUmTs3RHburvtDxdR5Y9JLvhwd1gn_zWS_R-9XLy_xft5zTxE1DTY5ic8EK7A</recordid><startdate>19990901</startdate><enddate>19990901</enddate><creator>Farrell, Peter A</creator><creator>Fedele, Mark J</creator><creator>Hernandez, Jazmir</creator><creator>Fluckey, James D</creator><creator>Miller, John L., III</creator><creator>Lang, Charles H</creator><creator>Vary, Thomas C</creator><creator>Kimball, Scot R</creator><creator>Jefferson, Leonard S</creator><general>Am Physiological Soc</general><general>American Physiological Society</general><scope>IQODW</scope><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>7U7</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>P64</scope><scope>7X8</scope></search><sort><creationdate>19990901</creationdate><title>Hypertrophy of skeletal muscle in diabetic rats in response to chronic resistance exercise</title><author>Farrell, Peter A ; Fedele, Mark J ; Hernandez, Jazmir ; Fluckey, James D ; Miller, John L., III ; Lang, Charles H ; Vary, Thomas C ; Kimball, Scot R ; Jefferson, Leonard S</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c503t-2ab9cd6a24b76dc08c0b456ef0d7b00d9f736174affdb247673e91b42798f95a3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1999</creationdate><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Blood Glucose - metabolism</topic><topic>Body Weight - physiology</topic><topic>Diabetes</topic><topic>Diabetes Mellitus, Experimental - blood</topic><topic>Diabetes Mellitus, Experimental - physiopathology</topic><topic>Diabetes. Impaired glucose tolerance</topic><topic>Endocrine pancreas. Apud cells (diseases)</topic><topic>Endocrinopathies</topic><topic>Etiopathogenesis. Screening. Investigations. Target tissue resistance</topic><topic>Exercise</topic><topic>Insulin</topic><topic>Insulin - blood</topic><topic>Insulin-Like Growth Factor I - metabolism</topic><topic>Kinetics</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Muscle Development</topic><topic>Muscle Proteins - biosynthesis</topic><topic>Muscle, Skeletal - growth &amp; development</topic><topic>Muscle, Skeletal - pathology</topic><topic>Muscular system</topic><topic>Organ Size - physiology</topic><topic>Pancreatectomy</topic><topic>Physical Conditioning, Animal - physiology</topic><topic>Physical Exertion - physiology</topic><topic>Proteins</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Rodents</topic><topic>Space life sciences</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Farrell, Peter A</creatorcontrib><creatorcontrib>Fedele, Mark J</creatorcontrib><creatorcontrib>Hernandez, Jazmir</creatorcontrib><creatorcontrib>Fluckey, James D</creatorcontrib><creatorcontrib>Miller, John L., III</creatorcontrib><creatorcontrib>Lang, Charles H</creatorcontrib><creatorcontrib>Vary, Thomas C</creatorcontrib><creatorcontrib>Kimball, Scot R</creatorcontrib><creatorcontrib>Jefferson, Leonard S</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Calcium &amp; 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><collection>MEDLINE - Academic</collection><jtitle>Journal of applied physiology (1985)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Farrell, Peter A</au><au>Fedele, Mark J</au><au>Hernandez, Jazmir</au><au>Fluckey, James D</au><au>Miller, John L., III</au><au>Lang, Charles H</au><au>Vary, Thomas C</au><au>Kimball, Scot R</au><au>Jefferson, Leonard S</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Hypertrophy of skeletal muscle in diabetic rats in response to chronic resistance exercise</atitle><jtitle>Journal of applied physiology (1985)</jtitle><addtitle>J Appl Physiol (1985)</addtitle><date>1999-09-01</date><risdate>1999</risdate><volume>87</volume><issue>3</issue><spage>1075</spage><epage>1082</epage><pages>1075-1082</pages><issn>8750-7587</issn><eissn>1522-1601</eissn><coden>JAPHEV</coden><abstract>Noll Physiological Research Center and Department of Kinesiology, University Park 16802; and Department of Cellular and Molecular Physiology, Pennsylvania State University College of Medicine, Hershey, Pennsylvania 17033 This study had the following objectives: 1 ) to determine whether diabetic rats could increase muscle mass due to a physiological manipulation (chronic resistance exercise), 2 ) to determine whether exercise training status modifies the effect of the last bout of exercise on elevations in rates of protein synthesis, and 3 ) to determine whether chronic resistance exercise alters basal glycemia. Groups consisted of diabetic or nondiabetic rats that performed progressive resistance exercise for 8 wk, performed acute resistance exercise, or remained sedentary. Arterial plasma insulin in diabetic groups was reduced by about one-half ( P  &lt;   0.05) compared with nondiabetic groups. Soleus and gastrocnemius-plantaris complex muscle wet weights were lower because of diabetes, but in response to chronic exercise these muscles hypertrophied in diabetic (0.028 ± 0.003 vs. 0.032 ± 0.0015 g/cm for sedentary vs. exercised soleus and 0.42 ± 0.068 vs. 0.53 ± 0.041 g/cm for sedentary vs. exercised gastrocnemius-plantaris, both P  &lt; 0.05) but not in nondiabetic (0.041 ± 0.0026 vs. 0.042 ± 0.003 g/cm for sedentary vs. exercised soleus and 0.72 ± 0.015 vs. 0.69 ±   0.013 g/cm for sedentary vs. exercised gastrocnemius-plantaris) rats when muscle weight was expressed relative to tibial length or body weight (data not shown). Another group of diabetic rats that lifted heavier weights showed muscle hypertrophy. Rates of protein synthesis were higher in red gastrocnemius in chronically exercised than in sedentary rats: 155 ± 11 and 170 ± 7 nmol phenylalanine incorporated · g muscle 1 · h 1 in exercised diabetic and nondiabetic rats vs. 110 ± 14 and 143   ± 7 nmol phenylalanine incorporated · g muscle 1 · h 1 in sedentary diabetic and nondiabetic rats. These elevations, however, were lower than in acutely exercised (but untrained) rats: 176 ± 15 and 193 ± 8 nmol phenylalanine incorporated · g muscle 1 · h 1 in diabetic and nondiabetic rats. Finally, chronic exercise training in diabetic rats was associated with reductions in basal glycemia, and such reductions did not occur in sedentary diabetic groups. These data demonstrate that, despite lower circulating insulin concentrations, diabetic rats can increase muscle mass in response to a physiological stimulus. protein synthesis; insulin; insulin-like growth factor I; muscle mass</abstract><cop>Bethesda, MD</cop><pub>Am Physiological Soc</pub><pmid>10484579</pmid><doi>10.1152/jappl.1999.87.3.1075</doi><tpages>8</tpages></addata></record>
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source MEDLINE; American Physiological Society; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Alma/SFX Local Collection
subjects Animals
Biological and medical sciences
Blood Glucose - metabolism
Body Weight - physiology
Diabetes
Diabetes Mellitus, Experimental - blood
Diabetes Mellitus, Experimental - physiopathology
Diabetes. Impaired glucose tolerance
Endocrine pancreas. Apud cells (diseases)
Endocrinopathies
Etiopathogenesis. Screening. Investigations. Target tissue resistance
Exercise
Insulin
Insulin - blood
Insulin-Like Growth Factor I - metabolism
Kinetics
Male
Medical sciences
Muscle Development
Muscle Proteins - biosynthesis
Muscle, Skeletal - growth & development
Muscle, Skeletal - pathology
Muscular system
Organ Size - physiology
Pancreatectomy
Physical Conditioning, Animal - physiology
Physical Exertion - physiology
Proteins
Rats
Rats, Sprague-Dawley
Rodents
Space life sciences
title Hypertrophy of skeletal muscle in diabetic rats in response to chronic resistance exercise
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