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Erschienen in: Der Unfallchirurg 4/2009

01.04.2009 | Leitthema

Körperliches Training und zelluläre Anpassung des Muskels

verfasst von: Prof. Dr. U. Tegtbur, M.W. Busse, H.P. Kubis

Erschienen in: Die Unfallchirurgie | Ausgabe 4/2009

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Zusammenfassung

Ausdauer bzw. Krafttraining induzieren in der Muskelzelle verschiedene Signalwege zur Proteinsynthese. Muskelfasern können die Struktur ihrer schweren Myosinketten in Abhängigkeit von Reiz und Immobilisation in beide Richtungen (I↔IIA↔IIX) anpassen. Exzentrisches Krafttraining ist effektiv und führt zur Neubildung von Sarkomeren in Längsrichtung des Muskels. Die Wirkung erfolgt über die Regeneration der zerstörten Sarkomerstruktur. Konzentrisches Krafttraining führt zur Muskelzellhypertrophie und induziert auch im hohen Alter noch die Proteinsynthese. Der durch Krafttraining aktivierte mTOR-Signalweg wird auch durch freie Aminosäuren stimuliert. Die Anpassung an Ausdauertraining läuft über den Kalzium-Calcineurin-NFATc1-Signalweg. Die Anzahl der Kalziumtransienten, erhöht durch Kontraktionsfrequenz und Trainingsdauer, ist ein wichtiger Stimulus zur Entwicklung der Fasertyp-I-Muskeln. Daher sollte Ausdauertraining durch lange Belastungen von >30 min mit hoher Bewegungsfrequenz dominiert werden. Muskuläre Aktivität, Zellstretch oder Sarkomerrisse können zur Teilung der Satellitenzellen führen. Die Satellitenzelle fusioniert mit der Muskelfaser, der neue Myonukleus wird Teil des Muskelkfasersynzitiums und fördert so die trainingsinduzierte Proteinsynthese. Neue Erkenntnisse der intrazellulären Vorgänge geben Einblick in die direkten Effekte von körperlichem Training, Immobilisation bzw. Alterung auf die Muskelplastizität und körperliche Leistungsfähigkeit.
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Metadaten
Titel
Körperliches Training und zelluläre Anpassung des Muskels
verfasst von
Prof. Dr. U. Tegtbur
M.W. Busse
H.P. Kubis
Publikationsdatum
01.04.2009
Verlag
Springer-Verlag
Erschienen in
Die Unfallchirurgie / Ausgabe 4/2009
Print ISSN: 2731-7021
Elektronische ISSN: 2731-703X
DOI
https://doi.org/10.1007/s00113-009-1627-9

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