The influence of training-detraining upon the heart, muscle and adipose tissue of female rats

The purpose of this study was to measure the effects of a 10 week training, 3 week detraining cycle upon heart, muscle and adipose tissue of the rat. Specific pathogen-free female Wistar rats, 175 g at the onset of the experiments, were separated into three treatment groups; Sedentary Control (SC),...

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Veröffentlicht in:Mechanisms of ageing and development 1991, Vol.57 (1), p.49-61
Hauptverfasser: Craig, B.W., Martin, G., Betts, J., Lungren, M., Lambret, V., Kaiserauer, S.
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container_end_page 61
container_issue 1
container_start_page 49
container_title Mechanisms of ageing and development
container_volume 57
creator Craig, B.W.
Martin, G.
Betts, J.
Lungren, M.
Lambret, V.
Kaiserauer, S.
description The purpose of this study was to measure the effects of a 10 week training, 3 week detraining cycle upon heart, muscle and adipose tissue of the rat. Specific pathogen-free female Wistar rats, 175 g at the onset of the experiments, were separated into three treatment groups; Sedentary Control (SC), Trained (T) and Detrained (DT). Animals from the T group were killed at 2, 4, 6, 8, 10 weeks and animals from the DT group were killed at 7, 14 and 21 days after the last day of training. Unweighted swimming — 6 h/day, 5 day/week, was the form of training employed. The animals, after being sacrified, were anesthetized with nembutal (45 mg/kg body wt.) and muscle samples and heart removed. These tissues were frozen and analyzed at a later date for succinate dehydrogenase (SDH) activity (muscles), total protein (TP), total hydroxylprotein (TH) and wet and dryg weight (heart). Adipose tissue was removed last, digested in collagenase (5 mg/ ml) and the isolated cells used to measured 2-[ 3H]deoxyglucose uptake (DOG) and the conversion of D-[1- 14C]glucose (C-1) and D-[6- 14C]glucose (C-6) to CO 2. The results of this study show that 10 weeks of endurance training induced myocardial hypertrophy ( P < 0.05) which involved increases in both TP and TH, the heart of the trained animals having 20.8% more protein and a 28.5% more hydroxlprotein than the sedentary controls. With detraining hypertrophy was lost within 21 days. Training maintained fat cell size at its pre-trained diameter, while inactivity allowed growth in the adipocytes of the control animals. The uptake of DOG and the conversion of glucose C-1 and glucose C-6 to CO 2, were significantly ( P < 0.05) higher in the adipocytes of trained animals indicating that they were more responsive to insulin than the sedentary controls, which corresponded to increases in the respiratory enzyme levels of the muscles. During the first 7 days of detraining DOG uptake and both C-1 and C-6 glucose oxidation remained elevated. In conclusion the results of this study clearly demonstrate that there is a direct relationship between adiposity and training that can be related to the insulin responsiveness of the adipose tissue.
doi_str_mv 10.1016/0047-6374(91)90023-S
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The results of this study show that 10 weeks of endurance training induced myocardial hypertrophy ( P &lt; 0.05) which involved increases in both TP and TH, the heart of the trained animals having 20.8% more protein and a 28.5% more hydroxlprotein than the sedentary controls. With detraining hypertrophy was lost within 21 days. Training maintained fat cell size at its pre-trained diameter, while inactivity allowed growth in the adipocytes of the control animals. The uptake of DOG and the conversion of glucose C-1 and glucose C-6 to CO 2, were significantly ( P &lt; 0.05) higher in the adipocytes of trained animals indicating that they were more responsive to insulin than the sedentary controls, which corresponded to increases in the respiratory enzyme levels of the muscles. During the first 7 days of detraining DOG uptake and both C-1 and C-6 glucose oxidation remained elevated. 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Specific pathogen-free female Wistar rats, 175 g at the onset of the experiments, were separated into three treatment groups; Sedentary Control (SC), Trained (T) and Detrained (DT). Animals from the T group were killed at 2, 4, 6, 8, 10 weeks and animals from the DT group were killed at 7, 14 and 21 days after the last day of training. Unweighted swimming — 6 h/day, 5 day/week, was the form of training employed. The animals, after being sacrified, were anesthetized with nembutal (45 mg/kg body wt.) and muscle samples and heart removed. These tissues were frozen and analyzed at a later date for succinate dehydrogenase (SDH) activity (muscles), total protein (TP), total hydroxylprotein (TH) and wet and dryg weight (heart). Adipose tissue was removed last, digested in collagenase (5 mg/ ml) and the isolated cells used to measured 2-[ 3H]deoxyglucose uptake (DOG) and the conversion of D-[1- 14C]glucose (C-1) and D-[6- 14C]glucose (C-6) to CO 2. The results of this study show that 10 weeks of endurance training induced myocardial hypertrophy ( P &lt; 0.05) which involved increases in both TP and TH, the heart of the trained animals having 20.8% more protein and a 28.5% more hydroxlprotein than the sedentary controls. With detraining hypertrophy was lost within 21 days. Training maintained fat cell size at its pre-trained diameter, while inactivity allowed growth in the adipocytes of the control animals. The uptake of DOG and the conversion of glucose C-1 and glucose C-6 to CO 2, were significantly ( P &lt; 0.05) higher in the adipocytes of trained animals indicating that they were more responsive to insulin than the sedentary controls, which corresponded to increases in the respiratory enzyme levels of the muscles. During the first 7 days of detraining DOG uptake and both C-1 and C-6 glucose oxidation remained elevated. 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Psychology</subject><subject>General aspects</subject><subject>Heart - physiology</subject><subject>Muscles - enzymology</subject><subject>Muscles - physiology</subject><subject>Myocardium - enzymology</subject><subject>Physical Exertion - physiology</subject><subject>Rats</subject><subject>Rats, Inbred Strains</subject><subject>Space life sciences</subject><subject>Specific Pathogen-Free Organisms</subject><subject>Succinate Dehydrogenase - metabolism</subject><subject>Swimming</subject><subject>Training</subject><subject>Vertebrates: anatomy and physiology, studies on body, several organs or systems</subject><issn>0047-6374</issn><issn>1872-6216</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1991</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kElLAzEYhoMotS7_QCEHEQVHs0yTzEWQ4gYFD61HCWnyjUZmqcmM4L83XdSblyTwPt-b5EHoiJJLSqi4IiSXmeAyPyvoeUEI49l0Cw2pkiwTjIptNPxFdtFejO-EEJozMUADqthICTpEL7M3wL4pqx4aC7gtcReMb3zzmjn4OeJ-0Ta4S-QbmNBd4LqPtgJsGoeN84s2Au58jP2qoITapDCYLh6gndJUEQ43-z56vrudjR-yydP94_hmklmuRJcxIt3cKWcFZ6XlxHJmrbFUOVlIpUjJeDEyKXIu_VIImdaCKymMHCnGCd9Hp-veRWg_eoidrn20UFWmgbaPWiUPnKs8gfkatKGNMUCpF8HXJnxpSvTSql4q00tluqB6ZVVP09jxpr-f1-D-htYaU36yyU20piqDaayPv9iIFTxdn7DrNQbJxaeHoKP1S-_OB7Cddq3__x3f89CSrg</recordid><startdate>1991</startdate><enddate>1991</enddate><creator>Craig, B.W.</creator><creator>Martin, G.</creator><creator>Betts, J.</creator><creator>Lungren, M.</creator><creator>Lambret, V.</creator><creator>Kaiserauer, S.</creator><general>Elsevier Ireland Ltd</general><general>Elsevier Science</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>7X8</scope></search><sort><creationdate>1991</creationdate><title>The influence of training-detraining upon the heart, muscle and adipose tissue of female rats</title><author>Craig, B.W. ; Martin, G. ; Betts, J. ; Lungren, M. ; Lambret, V. ; Kaiserauer, S.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c386t-207dbd8dc632fc30c32ccac18d797880f2395a2fcdd02366702393876a7582303</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1991</creationdate><topic>Adipose Tissue - cytology</topic><topic>Adipose Tissue - enzymology</topic><topic>Adipose Tissue - physiology</topic><topic>Adiposity</topic><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Cardiac hypertrophy</topic><topic>Deoxyglucose - metabolism</topic><topic>Detraining</topic><topic>Female</topic><topic>Fundamental and applied biological sciences. 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Specific pathogen-free female Wistar rats, 175 g at the onset of the experiments, were separated into three treatment groups; Sedentary Control (SC), Trained (T) and Detrained (DT). Animals from the T group were killed at 2, 4, 6, 8, 10 weeks and animals from the DT group were killed at 7, 14 and 21 days after the last day of training. Unweighted swimming — 6 h/day, 5 day/week, was the form of training employed. The animals, after being sacrified, were anesthetized with nembutal (45 mg/kg body wt.) and muscle samples and heart removed. These tissues were frozen and analyzed at a later date for succinate dehydrogenase (SDH) activity (muscles), total protein (TP), total hydroxylprotein (TH) and wet and dryg weight (heart). Adipose tissue was removed last, digested in collagenase (5 mg/ ml) and the isolated cells used to measured 2-[ 3H]deoxyglucose uptake (DOG) and the conversion of D-[1- 14C]glucose (C-1) and D-[6- 14C]glucose (C-6) to CO 2. The results of this study show that 10 weeks of endurance training induced myocardial hypertrophy ( P &lt; 0.05) which involved increases in both TP and TH, the heart of the trained animals having 20.8% more protein and a 28.5% more hydroxlprotein than the sedentary controls. With detraining hypertrophy was lost within 21 days. Training maintained fat cell size at its pre-trained diameter, while inactivity allowed growth in the adipocytes of the control animals. The uptake of DOG and the conversion of glucose C-1 and glucose C-6 to CO 2, were significantly ( P &lt; 0.05) higher in the adipocytes of trained animals indicating that they were more responsive to insulin than the sedentary controls, which corresponded to increases in the respiratory enzyme levels of the muscles. During the first 7 days of detraining DOG uptake and both C-1 and C-6 glucose oxidation remained elevated. In conclusion the results of this study clearly demonstrate that there is a direct relationship between adiposity and training that can be related to the insulin responsiveness of the adipose tissue.</abstract><cop>Shannon</cop><pub>Elsevier Ireland Ltd</pub><pmid>1825861</pmid><doi>10.1016/0047-6374(91)90023-S</doi><tpages>13</tpages></addata></record>
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subjects Adipose Tissue - cytology
Adipose Tissue - enzymology
Adipose Tissue - physiology
Adiposity
Animals
Biological and medical sciences
Cardiac hypertrophy
Deoxyglucose - metabolism
Detraining
Female
Fundamental and applied biological sciences. Psychology
General aspects
Heart - physiology
Muscles - enzymology
Muscles - physiology
Myocardium - enzymology
Physical Exertion - physiology
Rats
Rats, Inbred Strains
Space life sciences
Specific Pathogen-Free Organisms
Succinate Dehydrogenase - metabolism
Swimming
Training
Vertebrates: anatomy and physiology, studies on body, several organs or systems
title The influence of training-detraining upon the heart, muscle and adipose tissue of female rats
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