Changes in calpain activity, muscle structure, and function after eccentric exercise
Purpose: The aim of this study was to investigate changes in muscle function, muscle structure, and calpain activity after high-force eccentric exercise. Methods: Eleven healthy males performed 300 maximal voluntary eccentric actions with knee extensors in one leg. Maximal force-generating capacity...
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creator | Raastad, Truls Owe, Simen Gylterud Paulsen, Gøran Enns, Deborah Overgaard, Kristian Crameri, Regina Kiil, Steinar Belcastro, Angelo Bergersen, Linda Hildegard Hallén, Jostein |
description | Purpose: The aim of this study was to investigate changes in muscle function, muscle structure, and calpain activity after high-force eccentric exercise. Methods: Eleven healthy males performed 300 maximal voluntary eccentric actions with knee extensors in one leg. Maximal force-generating capacity was measured before exercise and regularly during the next 7 d. Biopsies from musculus vastus lateralis were taken in both control and exercised legs 0.5, 4, 8, 24, 96, and 168 h after exercise for evaluation of myofibrillar structure, extracellular matrix proteins, and calpain activity. Results: In the exercised leg, peak torque was reduced by 47 ± 5% during exercise and was still 22 ± 5% lower than baseline 4 d after the exercise. Calpain activity was three times higher in the exercised leg compared with the control leg 30 min after exercise. Myofibrillar disruptions were observed in 36 ± 6% of all fibers in exercised muscle and in 2 ± 1% of fibers in control muscle. The individual reductions in peak torque correlated with the proportion of fibers with myofibrillar disruptions (r = 0.89). The increase in calpain activity was not correlated to the proportion of fibers with myofibrillar disruptions. Nevertheless, the characteristics of the myofibrillar disruptions mimicked calpain-mediated degradation of myofibrils. Tenascin-C and the N-terminal propeptide of procollagen type III showed increased staining intensity on cross-sections 4-7 d after the exercise. Conclusions: Myofibrillar disruptions seem to be a main cause for the long-lasting reduction in force-generating capacity after high-force eccentric exercise. The increase in calpain activity, but the lack of a relationship between calpain activity and the amount of muscle damage, suggests multiple roles of calpain in the damage and repair process. |
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fullrecord | <record><control><sourceid>cristin_3HK</sourceid><recordid>TN_cdi_cristin_nora_11250_170663</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>11250_170663</sourcerecordid><originalsourceid>FETCH-cristin_nora_11250_1706633</originalsourceid><addsrcrecordid>eNqNyrENwkAMAMA0FAjYwQMEKU9EGCACMUD6l2X8YClxkN-PYHtSMADVNbeuhv6BeucMokA4PnERyeUl_qlhKplGhuxWyItxDag3SEWXMS8xORswEaubEPCbjSTztlolHDPvfm4quJyH_ronk-yiUWfDGMLh2MRwarqubf8oXxeVOA0</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype></control><display><type>article</type><title>Changes in calpain activity, muscle structure, and function after eccentric exercise</title><source>NORA - Norwegian Open Research Archives</source><creator>Raastad, Truls ; Owe, Simen Gylterud ; Paulsen, Gøran ; Enns, Deborah ; Overgaard, Kristian ; Crameri, Regina ; Kiil, Steinar ; Belcastro, Angelo ; Bergersen, Linda Hildegard ; Hallén, Jostein</creator><creatorcontrib>Raastad, Truls ; Owe, Simen Gylterud ; Paulsen, Gøran ; Enns, Deborah ; Overgaard, Kristian ; Crameri, Regina ; Kiil, Steinar ; Belcastro, Angelo ; Bergersen, Linda Hildegard ; Hallén, Jostein</creatorcontrib><description>Purpose: The aim of this study was to investigate changes in muscle function, muscle structure, and calpain activity after high-force eccentric exercise. Methods: Eleven healthy males performed 300 maximal voluntary eccentric actions with knee extensors in one leg. Maximal force-generating capacity was measured before exercise and regularly during the next 7 d. Biopsies from musculus vastus lateralis were taken in both control and exercised legs 0.5, 4, 8, 24, 96, and 168 h after exercise for evaluation of myofibrillar structure, extracellular matrix proteins, and calpain activity. Results: In the exercised leg, peak torque was reduced by 47 ± 5% during exercise and was still 22 ± 5% lower than baseline 4 d after the exercise. Calpain activity was three times higher in the exercised leg compared with the control leg 30 min after exercise. Myofibrillar disruptions were observed in 36 ± 6% of all fibers in exercised muscle and in 2 ± 1% of fibers in control muscle. The individual reductions in peak torque correlated with the proportion of fibers with myofibrillar disruptions (r = 0.89). The increase in calpain activity was not correlated to the proportion of fibers with myofibrillar disruptions. Nevertheless, the characteristics of the myofibrillar disruptions mimicked calpain-mediated degradation of myofibrils. Tenascin-C and the N-terminal propeptide of procollagen type III showed increased staining intensity on cross-sections 4-7 d after the exercise. Conclusions: Myofibrillar disruptions seem to be a main cause for the long-lasting reduction in force-generating capacity after high-force eccentric exercise. The increase in calpain activity, but the lack of a relationship between calpain activity and the amount of muscle damage, suggests multiple roles of calpain in the damage and repair process.</description><language>eng</language><publisher>LWW</publisher><subject>analysis of variance ; biopsy ; calpain ; exercise ; immunohistochemistry ; leg ; muscle contraction ; muscle fatigue ; muscle, skeletal ; myofibrils ; torque</subject><creationdate>2010</creationdate><rights>info:eu-repo/semantics/openAccess</rights><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,782,887,26574</link.rule.ids><linktorsrc>$$Uhttp://hdl.handle.net/11250/170663$$EView_record_in_NORA$$FView_record_in_$$GNORA$$Hfree_for_read</linktorsrc></links><search><creatorcontrib>Raastad, Truls</creatorcontrib><creatorcontrib>Owe, Simen Gylterud</creatorcontrib><creatorcontrib>Paulsen, Gøran</creatorcontrib><creatorcontrib>Enns, Deborah</creatorcontrib><creatorcontrib>Overgaard, Kristian</creatorcontrib><creatorcontrib>Crameri, Regina</creatorcontrib><creatorcontrib>Kiil, Steinar</creatorcontrib><creatorcontrib>Belcastro, Angelo</creatorcontrib><creatorcontrib>Bergersen, Linda Hildegard</creatorcontrib><creatorcontrib>Hallén, Jostein</creatorcontrib><title>Changes in calpain activity, muscle structure, and function after eccentric exercise</title><description>Purpose: The aim of this study was to investigate changes in muscle function, muscle structure, and calpain activity after high-force eccentric exercise. Methods: Eleven healthy males performed 300 maximal voluntary eccentric actions with knee extensors in one leg. Maximal force-generating capacity was measured before exercise and regularly during the next 7 d. Biopsies from musculus vastus lateralis were taken in both control and exercised legs 0.5, 4, 8, 24, 96, and 168 h after exercise for evaluation of myofibrillar structure, extracellular matrix proteins, and calpain activity. Results: In the exercised leg, peak torque was reduced by 47 ± 5% during exercise and was still 22 ± 5% lower than baseline 4 d after the exercise. Calpain activity was three times higher in the exercised leg compared with the control leg 30 min after exercise. Myofibrillar disruptions were observed in 36 ± 6% of all fibers in exercised muscle and in 2 ± 1% of fibers in control muscle. The individual reductions in peak torque correlated with the proportion of fibers with myofibrillar disruptions (r = 0.89). The increase in calpain activity was not correlated to the proportion of fibers with myofibrillar disruptions. Nevertheless, the characteristics of the myofibrillar disruptions mimicked calpain-mediated degradation of myofibrils. Tenascin-C and the N-terminal propeptide of procollagen type III showed increased staining intensity on cross-sections 4-7 d after the exercise. Conclusions: Myofibrillar disruptions seem to be a main cause for the long-lasting reduction in force-generating capacity after high-force eccentric exercise. The increase in calpain activity, but the lack of a relationship between calpain activity and the amount of muscle damage, suggests multiple roles of calpain in the damage and repair process.</description><subject>analysis of variance</subject><subject>biopsy</subject><subject>calpain</subject><subject>exercise</subject><subject>immunohistochemistry</subject><subject>leg</subject><subject>muscle contraction</subject><subject>muscle fatigue</subject><subject>muscle, skeletal</subject><subject>myofibrils</subject><subject>torque</subject><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2010</creationdate><recordtype>article</recordtype><sourceid>3HK</sourceid><recordid>eNqNyrENwkAMAMA0FAjYwQMEKU9EGCACMUD6l2X8YClxkN-PYHtSMADVNbeuhv6BeucMokA4PnERyeUl_qlhKplGhuxWyItxDag3SEWXMS8xORswEaubEPCbjSTztlolHDPvfm4quJyH_ronk-yiUWfDGMLh2MRwarqubf8oXxeVOA0</recordid><startdate>2010</startdate><enddate>2010</enddate><creator>Raastad, Truls</creator><creator>Owe, Simen Gylterud</creator><creator>Paulsen, Gøran</creator><creator>Enns, Deborah</creator><creator>Overgaard, Kristian</creator><creator>Crameri, Regina</creator><creator>Kiil, Steinar</creator><creator>Belcastro, Angelo</creator><creator>Bergersen, Linda Hildegard</creator><creator>Hallén, Jostein</creator><general>LWW</general><scope>3HK</scope></search><sort><creationdate>2010</creationdate><title>Changes in calpain activity, muscle structure, and function after eccentric exercise</title><author>Raastad, Truls ; Owe, Simen Gylterud ; Paulsen, Gøran ; Enns, Deborah ; Overgaard, Kristian ; Crameri, Regina ; Kiil, Steinar ; Belcastro, Angelo ; Bergersen, Linda Hildegard ; Hallén, Jostein</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-cristin_nora_11250_1706633</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2010</creationdate><topic>analysis of variance</topic><topic>biopsy</topic><topic>calpain</topic><topic>exercise</topic><topic>immunohistochemistry</topic><topic>leg</topic><topic>muscle contraction</topic><topic>muscle fatigue</topic><topic>muscle, skeletal</topic><topic>myofibrils</topic><topic>torque</topic><toplevel>online_resources</toplevel><creatorcontrib>Raastad, Truls</creatorcontrib><creatorcontrib>Owe, Simen Gylterud</creatorcontrib><creatorcontrib>Paulsen, Gøran</creatorcontrib><creatorcontrib>Enns, Deborah</creatorcontrib><creatorcontrib>Overgaard, Kristian</creatorcontrib><creatorcontrib>Crameri, Regina</creatorcontrib><creatorcontrib>Kiil, Steinar</creatorcontrib><creatorcontrib>Belcastro, Angelo</creatorcontrib><creatorcontrib>Bergersen, Linda Hildegard</creatorcontrib><creatorcontrib>Hallén, Jostein</creatorcontrib><collection>NORA - Norwegian Open Research Archives</collection></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext_linktorsrc</fulltext></delivery><addata><au>Raastad, Truls</au><au>Owe, Simen Gylterud</au><au>Paulsen, Gøran</au><au>Enns, Deborah</au><au>Overgaard, Kristian</au><au>Crameri, Regina</au><au>Kiil, Steinar</au><au>Belcastro, Angelo</au><au>Bergersen, Linda Hildegard</au><au>Hallén, Jostein</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Changes in calpain activity, muscle structure, and function after eccentric exercise</atitle><date>2010</date><risdate>2010</risdate><abstract>Purpose: The aim of this study was to investigate changes in muscle function, muscle structure, and calpain activity after high-force eccentric exercise. Methods: Eleven healthy males performed 300 maximal voluntary eccentric actions with knee extensors in one leg. Maximal force-generating capacity was measured before exercise and regularly during the next 7 d. Biopsies from musculus vastus lateralis were taken in both control and exercised legs 0.5, 4, 8, 24, 96, and 168 h after exercise for evaluation of myofibrillar structure, extracellular matrix proteins, and calpain activity. Results: In the exercised leg, peak torque was reduced by 47 ± 5% during exercise and was still 22 ± 5% lower than baseline 4 d after the exercise. Calpain activity was three times higher in the exercised leg compared with the control leg 30 min after exercise. Myofibrillar disruptions were observed in 36 ± 6% of all fibers in exercised muscle and in 2 ± 1% of fibers in control muscle. The individual reductions in peak torque correlated with the proportion of fibers with myofibrillar disruptions (r = 0.89). The increase in calpain activity was not correlated to the proportion of fibers with myofibrillar disruptions. Nevertheless, the characteristics of the myofibrillar disruptions mimicked calpain-mediated degradation of myofibrils. Tenascin-C and the N-terminal propeptide of procollagen type III showed increased staining intensity on cross-sections 4-7 d after the exercise. Conclusions: Myofibrillar disruptions seem to be a main cause for the long-lasting reduction in force-generating capacity after high-force eccentric exercise. The increase in calpain activity, but the lack of a relationship between calpain activity and the amount of muscle damage, suggests multiple roles of calpain in the damage and repair process.</abstract><pub>LWW</pub><oa>free_for_read</oa></addata></record> |
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subjects | analysis of variance biopsy calpain exercise immunohistochemistry leg muscle contraction muscle fatigue muscle, skeletal myofibrils torque |
title | Changes in calpain activity, muscle structure, and function after eccentric exercise |
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