Gymnastik- och idrottshögskolan, GIH

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Resistance Exercise Attenuates Mitochondrial Function: Effects Of NSAID Intake And Eccentric-Overload Training
Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Åstrand Laboratory of Work Physiology, Research group for Mitokondriell funktion och metabolisk kontroll.ORCID iD: 0000-0002-8607-550X
Karolinska Institutet, Stockholm, Sweden..
Karolinska Institutet, Stockholm, Sweden..
Karolinska Institutet, Stockholm, Sweden..
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2017 (English)In: Medicine & Science in Sports & Exercise. 49(5S):329, MAY 2017, 2017, Vol. 49, no 5, p. 329-329Conference paper, Oral presentation with published abstract (Refereed)
Abstract [en]

Although nonsteroidal antiinflammatorydrugs (NSAIDs) have been shown to modulate skeletal muscle adaptations and protein metabolism in response toresistance exercise, little is known about the effects of NSAIDs on mitochondrial function. Thus, the current study aimed to examine the effects of resistanceexercise with concomitant NSAID consumption on mitochondrial oxidative phosphorylation in skeletal muscle. Twenty participants were randomized in asingleblindedfashion to either an experimental group receiving ibuprofen (IBU: 27±5 yr; n=11; 1200 mg/d) or a control group receiving a lowdoseacetylsalicylic acid (CON: 26±4 yr; n=9; 75 mg/d) During this period, subjects performed 8 weeks of supervised resistance exercise involving the kneeextensors muscles. Each of the subject’s legs were randomized to complete the training program using either a flywheel (FW) device emphasizing eccentricoverload,or a traditional weight stack machine (WS). Maximal mitochondrial oxidative phosphorylation (OXPHOS) from permeabilized skeletal muscle bundleswas assessed using high resolution respirometry before and after the training intervention. Citrate synthase activity was assessed using spectrophotometrictechniques. After training, OXPHOS decreased (P<0.05) in both IBU (23%) and CON (29%) with no difference across medical treatments. Although OXPHOSdecreased in both legs, the decrease was greater (interaction P= 0.015) in WS (33%, P= 0.015) than in FW (19%, P= 0.078). Citrate synthase (CS) did notchange after the intervention. The increase in quadriceps muscle volume was not significantly correlated with the change in OXPHOS (R=0.15). These resultssuggest that 1) eight weeks of resistance training reduces mitochondrial function but not mitochondrial content, 2) The decreased mitochondrial function withresistance exercise was not affected by ibuprofen consumption, 3) flywheel resistance training, emphasizing eccentric overload, rescues some of thereduction in mitochondrial function seen with conventional resistance training.

Place, publisher, year, edition, pages
2017. Vol. 49, no 5, p. 329-329
Keywords [en]
Mitochondrial function, NSAID, resistance training
National Category
Sport and Fitness Sciences
Research subject
Medicine/Technology
Identifiers
URN: urn:nbn:se:gih:diva-5107DOI: 10.1249/01.mss.0000517772.05105.6aISI: 000415214600184OAI: oai:DiVA.org:gih-5107DiVA, id: diva2:1161894
Conference
Annual Meeting of the American-College-of-Sports-Medicine (ACSM), MAY 30-JUN 03, 2017, Denver, CO
Available from: 2017-12-01 Created: 2017-12-01 Last updated: 2022-12-06Bibliographically approved

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Cardinale, DanieleLarsen, Filip J.
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