U
Ulrik Wisløff
Researcher at Norwegian University of Science and Technology
Publications - 376
Citations - 32133
Ulrik Wisløff is an academic researcher from Norwegian University of Science and Technology. The author has contributed to research in topics: Interval training & Aerobic exercise. The author has an hindex of 82, co-authored 347 publications receiving 27648 citations. Previous affiliations of Ulrik Wisløff include University of Queensland & Baylor College of Medicine.
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Journal ArticleDOI
Long-term Changes in Depressive Symptoms and Estimated Cardiorespiratory Fitness and Risk of All-Cause Mortality: The Nord-Trøndelag Health Study
Trude Carlsen,Øyvind Salvesen,Xuemei Sui,Carl J. Lavie,Steven N. Blair,Ulrik Wisløff,Ulrik Wisløff,Linda Ernstsen +7 more
TL;DR: Maintaining low DSs and high e CRF was independently associated with a lower risk of all‐cause mortality, and the lowest mortality risk was observed for persistently high eCRF combined with decreased or persistently lowDSs.
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Trimetazidine does not alter metabolic substrate oxidation in cardiac mitochondria of target patient population
Marija Cavar,Marko Ljubkovic,C Bulat,Darija Bakovic,Damir Fabijanić,Jasenka Kraljević,N Karanovic,Zeljko Dujic,Carl J. Lavie,Ulrik Wisløff,Jasna Marinovic +10 more
TL;DR: The goal of the current study was to assess the effect of trimetazidine on mitochondrial substrate oxidation directly in left ventricular myocardium from CAD patients.
Journal ArticleDOI
Exercise training reverses myocardial dysfunction induced by CaMKIIδC overexpression by restoring Ca2+ homeostasis
Morten A. Høydal,Tomas Stølen,Sarah Kettlewell,Lars S. Maier,Joan Heller Brown,Tomas Sowa,Daniele Catalucci,Gianluigi Condorelli,Ole J. Kemi,Godfrey L. Smith,Ulrik Wisløff +10 more
TL;DR: Exercise training improves global cardiac function as well as cardiomyocyte function in the presence of a maintained high CaMKII activity and the main mechanisms of exercise-induced improvements in TG Ca MKIIδC mice are mediated via increased L-type Ca(2+) channel currents and improved SR Ca( 2+) handling by restoration of SERCA2a function.
Journal ArticleDOI
Skeletal muscle heme oxygenase-1 activity regulates aerobic capacity.
Rodrigo W. Alves de Souza,Rodrigo W. Alves de Souza,David Gallo,Ghee Rye Lee,Eri Katsuyama,Alexa Schaufler,Janick Weber,Eva Csizmadia,George C. Tsokos,Lauren G. Koch,Steven L. Britton,Ulrik Wisløff,Patricia Chakur Brum,Leo E. Otterbein +13 more
TL;DR: In this article, the authors found that the benefits of exercise on muscle function are linked partly to microtraumatic events that result in accumulation of circulating heme, which is controlled by Heme Oxygenase-1 (HO-1, Hmox1) and showed that mouse skeletal muscle-specific HO-1 deletion (Tam-Cre-HSA-Hmox 1fl/fl) shifts the proportion of muscle fibers from type IIA to type IIB concomitant with a disruption in mitochondrial content and function.