Sportverletz Sportschaden 2018; 32(04): 243-250
DOI: 10.1055/a-0753-1884
Übersicht
© Georg Thieme Verlag KG Stuttgart · New York

Advances in Delayed-Onset Muscle Soreness (DOMS): Part I: Pathogenesis and Diagnostics

Delayed Onset Muscle Soreness – Teil I: Pathogenese und Diagnostik
Thilo Hotfiel
1   Department of Orthopedic Surgery, Friedrich-Alexander-University Erlangen-Nuremberg, Germany
2   Muscle Research Center Erlangen, Interdisciplinary Center for Muscle Research, Friedrich-Alexander-University Erlangen-Nuremberg, Germany
3   High Performance Sports Commission, German-Austrian-Swiss Society for Orthopaedic Traumatologic Sports Medicine (GOTS)
,
Jürgen Freiwald
3   High Performance Sports Commission, German-Austrian-Swiss Society for Orthopaedic Traumatologic Sports Medicine (GOTS)
4   Department of Movement and Training Science, University of Wuppertal, Germany
,
Matthias Wilhelm Hoppe
4   Department of Movement and Training Science, University of Wuppertal, Germany
5   Department of Orthopedic, Trauma and Hand Surgery, Klinikum Osnabrück, Germany
,
Christoph Lutter
6   Department of Orthopedic and Trauma Surgery, Sportsorthopedics and Sportsmedicine, Klinikum Bamberg, Germany
,
Raimund Forst
1   Department of Orthopedic Surgery, Friedrich-Alexander-University Erlangen-Nuremberg, Germany
,
Casper Grim
3   High Performance Sports Commission, German-Austrian-Swiss Society for Orthopaedic Traumatologic Sports Medicine (GOTS)
5   Department of Orthopedic, Trauma and Hand Surgery, Klinikum Osnabrück, Germany
,
Wilhelm Bloch
7   Department of Molecular and Cellular Sports Medicine, Institute of Cardiovascular Research and Sports Medicine, German Sport University Cologne, Cologne, Germany
,
Moritz Hüttel
1   Department of Orthopedic Surgery, Friedrich-Alexander-University Erlangen-Nuremberg, Germany
,
Rafael Heiss
2   Muscle Research Center Erlangen, Interdisciplinary Center for Muscle Research, Friedrich-Alexander-University Erlangen-Nuremberg, Germany
8   Department of Radiology, University Hospital Erlangen, Germany
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Publikationsverlauf

Publikationsdatum:
11. Dezember 2018 (online)

Abstract

Delayed-onset muscle soreness (DOMS) is a type of ultrastructural muscle injury. The manifestation of DOMS is caused by eccentric or unfamiliar forms of exercise. Clinical signs include reduced force capacities, increased painful restriction of movement, stiffness, swelling, and dysfunction of adjacent joints. Although DOMS is considered a mild type of injury, it is one of the most common reasons for compromised sportive performance. In the past few decades, many hypotheses have been developed to explain the aetiology of DOMS. Although the exact pathophysiological pathway remains unknown, the primary mechanism is currently considered to be the ultrastructural damage of muscle cells due to unfamiliar sporting activities or eccentric exercise, which leads to further protein degradation, apoptosis and local inflammatory response. The development of clinical symptoms is typically delayed (peak soreness at 48 – 72 h post-exercise) as a result of complex sequences of local and systemic physiological responses. The following narrative review was conducted to present an overview of the current findings regarding the damaging mechanisms as well as the pathophysiology of DOMS and its diagnostic evaluation.

Zusammenfassung

Die Delayed Onset Muscle Soreness (DOMS) oder auch „verzögert einsetzender Muskelkater" wird zu den ultrastrukturellen Muskelschädigungen gezählt. Ursächlich werden vorausgegangene exzentrische Kontraktionsformen oder ungewohnte Muskelbelastungen angesehen. Klinische Symptome imponieren in Form einer reduzierten Kraftentfaltung, schmerzhafter Bewegungseinschränkungen, einer Erhöhung des Muskeltonus, Schwellungen sowie Funktionseinschränkungen angrenzender Gelenke. Obwohl die DOMS den milden Schädigungsformen zugeordnet wird, hat sie aufgrund der leistungseinschränkenden Auswirkungen eine große Bedeutung – insbesondere für den Leistungssport. In den letzten Jahrzehnten sind viele Hypothesen zur Ursache und Pathophysiologie beschrieben worden. Auch, wenn der genaue pathophysiologische Signalweg bis heute nicht vollständig geklärt ist, gilt als primärer Schädigungsmechanismus eine mechanische, ultrastrukturelle Schädigung des Muskelparenchyms, die zu einer weiteren Proteindegradation, Autophagie und einer lokalen Entzündungsantwort führt. Klinische Symptome manifestieren sich typischerweise verzögert (Hauptmanifestation zwischen 24 und 72 h nach der Belastung), als Folge einer komplexen lokalen und systemischen Inflammationsphase. Die vorliegende Arbeit hat das Ziel, eine Übersicht über diese Schädigungsentität zu liefern und dabei Grundlagen der schädigenden Mechanismen, der Pathophysiologie und der Diagnostik aufzuzeigen.

 
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