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Ultra-endurance exercise increases the production of reactive oxygen species in isolated mitochondria from human skeletal muscle.
Gymnastik- och idrottshögskolan, GIH, Institutionen för idrotts- och hälsovetenskap, Åstrandlaboratoriet, Forskningsgruppen Mitokondriell funktion och metabolisk kontroll.
Gymnastik- och idrottshögskolan, GIH, Institutionen för idrotts- och hälsovetenskap, Åstrandlaboratoriet. Stockholm University.
Gymnastik- och idrottshögskolan, GIH, Institutionen för idrotts- och hälsovetenskap, Åstrandlaboratoriet, Björn Ekbloms forskningsgrupp.ORCID-id: 0000-0002-0642-4838
Gymnastik- och idrottshögskolan, GIH, Institutionen för idrotts- och hälsovetenskap, Åstrandlaboratoriet. Karolinska Institutet.
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2010 (Engelska)Ingår i: Journal of applied physiology, ISSN 8750-7587, E-ISSN 1522-1601, Vol. 108, nr 4, s. 780-787Artikel i tidskrift (Refereegranskat) Published
Abstract [en]

Exercise-induced oxidative stress is important for the muscular adaptation to training but may also cause muscle damage. We hypothesized that prolonged exercise would increase mitochondrial production of reactive oxygen species (ROS) measured in vitro and that this correlates with oxidative damage. Eight male athletes (24-32 years) performed ultra-endurance exercise (kayaking/running/cycling) with an average work intensity of 55% VO2peak for 24 h. Muscle biopsies were taken from vastus lateralis before exercise, immediately after exercise and after 28 h of recovery. The production of H2O2 was measured fluorometrically in isolated mitochondria with the Amplex red and peroxidase system. Succinate-supported mitochondrial H2O2 production was significantly increased after exercise (73% higher, P=0.025) but restored to the initial level at recovery. Plasma level of free fatty acids (FFA) increased 4-fold and exceeded 1.2 mmol l(-1) during the last 6 h of exercise. Plasma FFA at the end of exercise was significantly correlated to mitochondrial ROS production (r=0.74, P<0.05). Mitochondrial content of 4-hydroxy-nonenal-adducts (a marker of oxidative damage) was increased only after recovery and was not correlated with mitochondrial ROS production. Total thiol-group level and glutathione peroxidase activity were elevated after recovery. In conclusion: ultra-endurance exercise increases ROS production in isolated mitochondria but this is reversed after 28 h recovery. Mitochondrial ROS production was not correlated with oxidative damage of mitochondrial proteins, which was increased at recovery but not immediately after exercise. Key words: antioxidative defence, fatty acids, oxidative stress.

Ort, förlag, år, upplaga, sidor
2010. Vol. 108, nr 4, s. 780-787
Nyckelord [en]
antioxidative defence, fatty acids, oxidative stress
Nationell ämneskategori
Fysiologi
Forskningsämne
Medicin/Teknik
Identifikatorer
URN: urn:nbn:se:gih:diva-1104DOI: 10.1152/japplphysiol.00966.2009PubMedID: 20110545OAI: oai:DiVA.org:gih-1104DiVA, id: diva2:291626
Projekt
Physiology of Adventure RacingTillgänglig från: 2010-02-02 Skapad: 2010-02-02 Senast uppdaterad: 2018-01-12Bibliografiskt granskad

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Sahlin, KentMattsson, C MikaelEnqvist, Jonas KEkblom, Björn T

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Sahlin, KentMattsson, C MikaelFernström, MariaEnqvist, Jonas KEkblom, Björn T
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Forskningsgruppen Mitokondriell funktion och metabolisk kontrollÅstrandlaboratorietBjörn Ekbloms forskningsgrupp
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