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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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 |
format | Article |
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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 < 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 & 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&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 < 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 < 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 & 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 & 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 & 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 < 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 < 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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