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Myofibrillar proteolysis in response to voluntary or electrically stimulated muscle contractions in humans
Author(s) -
Hansen M.,
Trappe T.,
Crameri R. M.,
Qvortrup K.,
Kjaer M.,
Langberg H.
Publication year - 2009
Publication title -
scandinavian journal of medicine and science in sports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.575
H-Index - 115
eISSN - 1600-0838
pISSN - 0905-7188
DOI - 10.1111/j.1600-0838.2007.00766.x
Subject(s) - myofibril , skeletal muscle , medicine , myocyte , endocrinology , protein turnover , chemistry , biochemistry , protein biosynthesis
Knowledge about the effects of exercise on myofibrillar protein breakdown in human subjects is limited. Our purpose was to measure the changes in the degradation of myofibrillar proteins in response to different ways of eliciting muscle contractions using the local interstitial 3‐methyl‐histidine (3‐MH) concentration as a marker for myofibrillar protein breakdown. Untrained males ( n =8, 22–27 years, range) performed 210 maximal isokinetic eccentric contractions with each leg on an isokinetic dynamometer. One leg performed voluntary (VOL) and the other leg performed electrically induced contractions (ES). Microdialysis probes were placed in m. vastus lateralis in both the legs immediately after, and 1 and 3 days post‐exercise. Interstitial 3‐MH was higher in ES vs VOL immediately after exercise ( P <0.05). One and 3 days post‐exercise no difference between the two exercise types was observed. Only after ES did the histochemical stainings show significant disruption of cytoskeletal proteins. Furthermore, intracellular disruption and destroyed Z‐lines were markedly more pronounced in ES vs VOL. In conclusion, the local level of interstitial 3‐MH in the skeletal muscle was significantly enhanced after ES compared with VOL immediately after exercise, while the level of 3‐MH did not change in the post‐exercise period after VOL. These results indicate that the local myofibrillar breakdown is accelerated after ES associated with severe myofiber damage.