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Resistance Exercise Attenuates Mitochondrial Function : Effects Of NSAID Intake And Eccentric-Overload Training

Cardinale, Daniele (författare)
Gymnastik- och idrottshögskolan,Forskningsgruppen Mitokondriell funktion och metabol kontroll
Lilja, Mats (författare)
Karolinska Institutet, Stockholm, Sweden.
Mandic, Mirko (författare)
Karolinska Institutet, Stockholm, Sweden.
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Gustafsson, Thomas (författare)
Karolinska Institutet, Stockholm, Sweden.
Larsen, Filip J. (författare)
Gymnastik- och idrottshögskolan,Forskningsgruppen Mitokondriell funktion och metabol kontroll
Lundberg, Tommy R. (författare)
Karolinska Institutet Stockholm, Sweden.
visa färre...
 (creator_code:org_t)
Ovid Technologies (Wolters Kluwer Health), 2017
2017
Engelska.
Ingår i: Medicine & Science in Sports & Exercise. 49(5S):329, MAY 2017. - : Ovid Technologies (Wolters Kluwer Health). ; , s. 329-329
  • Konferensbidrag (refereegranskat)
Abstract Ämnesord
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  • 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.

Ämnesord

MEDICIN OCH HÄLSOVETENSKAP  -- Hälsovetenskap -- Idrottsvetenskap (hsv//swe)
MEDICAL AND HEALTH SCIENCES  -- Health Sciences -- Sport and Fitness Sciences (hsv//eng)

Nyckelord

Mitochondrial function
NSAID
resistance training
Medicin/Teknik
Medicine/Technology

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