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Lifelong endurance training keeps the mitochondria young.
Gymnastik- och idrottshögskolan, GIH, Institutionen för idrotts- och hälsovetenskap, Åstrandlaboratoriet.
2014 (Engelska)Ingår i: Proceedings of the Physiological Society 2014, 2014, s. 276P-277PKonferensbidrag, Publicerat paper (Refereegranskat)
Abstract [en]

It is an ongoing debate whether mitochondrial function deteriorates with aging. Some studies demonstrate metabolic dysfunction and increased ROS production (Squier, 2001) while others find no bioenergetics alterations (Rasmussen, et al., 2003). The extent to which exercise maintains or restores mitochondrial function is unknown. Methods: A unique group of elderly lifelong trained males (64±2 yr, BMI=24.5±0.4 kg/m2, VO2max=3.5±0.07 L/min), who maintained road cycling training ~250 km/week 50 years were recruited for the experiment (group ET) along with a group of healthy age matched untrained males (age 65±2 yr, BMI=27±1, VO2max=2.4±0.1), who lived a sedentary lifestyle (group UT). A biopsy was obtained from Vastus lateralis under local anaesthesia. 15-25 mg muscle was immediately prepared and permeabilized for High Resolution Respirometry as previously described (Boushel, et al., 2011). LEAK respiration was assessed by addition of malate (2 mM) and octanoyl-carnitine (0.2 mM). Coupled ADP-stimulated respiration (OXPHOS) of complex I was assessed with pyruvate (5mM) and glutamate (10 mM), and ADP (5 mM). Maximal OXPHOS was determined by addition of succinate (10 mM) for convergent electron input to both complexes I and II. The isolated activity of cytochrome c oxidase (COX), was determined in a redox reaction with TMPD (N,N,N,N-tetramethyl-p-phenylenediamine dihydrochloride) (0.5 mM) and ascorbate (2mM) after blockade of electron flow through complex III with antimycin A (2.5μM) followed by sodium azide (100 mM). Findings: All values are mean±S.E.M. Preliminary findings show that mitochondrial OXPHOS capacity for CI (PI) is substantially higher (50±3 vs. 30±1 pmol.sec-1.mg-1, p<0.0001) in the ET compared to the UT, and maximal OXPHOS with CI+CII (PI+PII) was 2-fold higher (103±3 vs. 51±2 pmol.sec-1.mg-1, p<5*10-5). The higher substrate control ratio (CI+II/CI) in ET (2.05±0.09) compared to UT (1.7±0.06) suggests less substrate competition at the mitochondrial level. These findings indicate that exercise training throughout life induces both regulatory and mitochondrial density changes that optimize mitochondrial function. The observed OXPHOS capacities in the ET subjects are fully comparable to values reported in young elite trained subjects (Jacobs & Lundby, 2013), illustrating no mitochondrial age-related deteriorating in these subjects.

Ort, förlag, år, upplaga, sidor
2014. s. 276P-277P
Nationell ämneskategori
Idrottsvetenskap
Forskningsämne
Medicin/Teknik
Identifikatorer
URN: urn:nbn:se:gih:diva-3504OAI: oai:DiVA.org:gih-3504DiVA, id: diva2:756397
Konferens
Physiology 2014 (London, UK)
Tillgänglig från: 2014-10-17 Skapad: 2014-10-17 Senast uppdaterad: 2014-10-17Bibliografiskt granskad

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