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Resistance Exercise Attenuates Mitochondrial Function: Effects Of NSAID Intake And Eccentric-Overload Training
Gymnastik- och idrottshögskolan, GIH, Institutionen för idrotts- och hälsovetenskap, Åstrandlaboratoriet, Forskningsgruppen 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 (Engelska)Ingår i: Medicine & Science in Sports & Exercise. 49(5S):329, MAY 2017, 2017, Vol. 49, nr 5, s. 329-329Konferensbidrag, Muntlig presentation med publicerat abstract (Refereegranskat)
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.

Ort, förlag, år, upplaga, sidor
2017. Vol. 49, nr 5, s. 329-329
Nyckelord [en]
Mitochondrial function, NSAID, resistance training
Nationell ämneskategori
Idrottsvetenskap
Forskningsämne
Medicin/Teknik
Identifikatorer
URN: urn:nbn:se:gih:diva-5107DOI: 10.1249/01.mss.0000517772.05105.6aISI: 000415214600184OAI: oai:DiVA.org:gih-5107DiVA, id: diva2:1161894
Konferens
Annual Meeting of the American-College-of-Sports-Medicine (ACSM), MAY 30-JUN 03, 2017, Denver, CO
Tillgänglig från: 2017-12-01 Skapad: 2017-12-01 Senast uppdaterad: 2018-01-18Bibliografiskt granskad

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Cardinale, DanieleLarsen, Filip J.
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