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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Hauptverfasser: Raastad, Truls, Owe, Simen Gylterud, Paulsen, Gøran, Enns, Deborah, Overgaard, Kristian, Crameri, Regina, Kiil, Steinar, Belcastro, Angelo, Bergersen, Linda Hildegard, Hallén, Jostein
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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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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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source NORA - Norwegian Open Research Archives
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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