Prof. Kirsten Legerlotz

Profil

Zusammenfassung

Prof. Legerlotz erforscht die biomechanischen und molekularen Veränderungen in Sehnen und Muskeln unter mechanischer Belastung. Sie entwickelt experimentelle Systeme, um zu verstehen, wie wiederholte Belastung zu Sehnenschäden führt und wie Trainingsinterventionen diese verhindern oder behandeln können. Ihre Expertise verbindet Laboranalytik auf Zellebene mit funktionalen Bewegungsstudien und ist für die Optimierung von Trainingstherapien und Prävention von Überlastungsverletzungen relevant.

Skills

Name

Prof. Kirsten Legerlotz

Titel

Prof.

Fakultät

Kultur-, Sozial- und Bildungswissenschaftliche Fakultät

Institut

Institut für Sportwissenschaft

Arbeitsgruppe

Movement Biomechanics (J)

E-Mail

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Telefon

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HU-FIS-Profil

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Zuletzt gescrapt

28.6.2026, 01:08:55

• EXIST Gründerstipendium SURF ERA

  Quelle ↗

  Förderer: BMWE: EXIST Zeitraum: 09/2019 - 11/2020 Projektleitung: Prof. Kirsten Legerlotz

• GSC BSRT: JP- Movement Biomechanics

  Quelle ↗

  Zeitraum: 10/2014 - 10/2017 Projektleitung: Prof. Kirsten Legerlotz

• Optimierung der Trainingstherapie zur Behandlung von Sportlern mit Achilles-Tendinopathie

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  Förderer: Bundesministerien Zeitraum: 01/2016 - 09/2018 Projektleitung: Prof. Kirsten Legerlotz

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• Increased expression of IL-6 family members in tendon pathology

  2012

  Lara D. Veeken · 146 Zitationen · DOI

  OBJECTIVES: Histological examination of pathological tendon generally does not reveal signs of inflammation. However, the inflammatory cytokine IL-6 has been shown to be expressed in ruptured rotator cuff tendon. The aim of this study was to investigate the expression of IL-6 family members in painful posterior tibialis tendon (PTT) and in painful and ruptured Achilles tendon (AT) compared with normal tendon. METHODS: AT samples were obtained from cadavers (normal) or from patients undergoing surgical procedures to treat chronic painful tendinopathy or ruptured tendon. PTT samples were obtained from patients undergoing surgery for other reasons (normal) and from patients with PTT dysfunction (painful). Total RNA was extracted and mRNA expression was analysed by quantitative real-time PCR. RESULTS: Collagen type I α-chain I (COL1A1) expression was increased in both painful PTT and AT compared with normal. Ciliary neurotrophic factor levels were increased in painful PTT only. In the painful AT, cyclooxygenase-2 (COX2) and IL-6 expression increased compared with normal. In the ruptured AT, levels of VEGF A, COX2, oncostatin-M, leukaemia inhibitory factor and IL-6 expression were higher compared with both normal and painful AT. IL-6R expression decreased in both painful and ruptured AT compared with normal. CONCLUSION: Painful AT and PTT show different expression patterns, indicating a substantial difference between those two tendinopathies. Inflammatory markers are up-regulated in painful and particularly in ruptured AT, pointing towards a role of inflammation not only in rupture healing, but also in Achilles tendinopathy.

• Cyclic loading of tendon fascicles using a novel fatigue loading system increases interleukin‐6 expression by tenocytes

  2011

  Scandinavian Journal of Medicine and Science in Sports · 89 Zitationen · DOI

  Repetitive strain or 'overuse' is thought to be a major factor contributing to the development of tendinopathy. The aims of our study were to develop a novel cyclic loading system, and use it to investigate the effect of defined loading conditions on the mechanical properties and gene expression of isolated tendon fascicles. Tendon fascicles were dissected from bovine-foot extensors and subjected to cyclic tensile strain (1 Hz) at 30% or 60% of the strain at failure, for 0 h (control), 15 min, 30 min, 1 h, or 5 h. Post loading, a quasi-static test to failure assessed damage. Gene expression at a selected loading regime (1 h at 30% failure strain) was analyzed 6 h post loading by quantitative real-time polymerase chain reaction. Compared with unloaded controls, loading at 30% failure strain took 5 h to lead to a significant decrease in failure stress, whereas loading to 60% led to a significant reduction after 15 min. Loading for 1 h at 30% failure strain did not create significant structural damage, but increased Collagen-1-alpha-chain-1 and interleukin-6 (IL6) expression, suggesting a role of IL6 in tendon adaptation to exercise. Correlating failure properties with fatigue damage provides a method by which changes in gene expression can be associated with different degrees of fatigue damage.

• Specimen dimensions influence the measurement of material properties in tendon fascicles

  2010

  Journal of Biomechanics · 82 Zitationen · DOI

  Stress, strain and modulus are regularly used to characterize material properties of tissue samples. However, when comparing results from different studies it is evident the reported material properties, particularly failure strains, vary hugely. The aim of our study was to characterize how and why specimen length and cross-sectional area (CSA) appear to influence failure stress, strain and modulus in fascicles from two functionally different tendons. Fascicles were dissected from five rat tails and five bovine foot extensors, their diameters determined by a laser micrometer, and loaded to failure at a range of grip-to-grip lengths. Strain to failure significantly decreased with increasing in specimen length in both rat and bovine fascicles, while modulus increased. Specimen length did not influence failure stress in rat tail fascicles, although in bovine fascicles it was significantly lower in the longer 40 mm specimens compared to 5 and 10mm specimens. The variations in failure strain and modulus with sample length could be predominantly explained by end-effects. However, it was also evident that strain fields along the sample length were highly variable and notably larger towards the ends of the sample than the mid-section even at distances in excess of 5mm from the gripping points. Failure strain, stress and modulus correlated significantly with CSA at certain specimen lengths. Our findings have implications for the mechanical testing of tendon tissue: while it is not always possible to control for fascicle length and/or CSA, these parameters have to be taken into account when comparing samples of different dimensions.

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