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Cycling efficiency in humans is related to low UCP3 content and to type I fibres but not to mitochondrial efficiency
Gymnastik- och idrottshögskolan, GIH, Institutionen för idrotts- och hälsovetenskap.ORCID-id: 0000-0001-9526-2967
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2006 (Engelska)Ingår i: Journal of Physiology, ISSN 0022-3751, E-ISSN 1469-7793, Vol. 571, nr 3, s. 669-681Artikel i tidskrift (Refereegranskat) Published
Abstract [en]

The purpose of this study was to investigate the hypothesis that cycling efficiency in vivo is related to mitochondrial efficiency measured in vitro and to investigate the effect of training status on these parameters. Nine endurance trained and nine untrained male subjects ( , respectively) completed an incremental submaximal efficiency test for determination of cycling efficiency (gross efficiency, work efficiency (WE) and delta efficiency). Muscle biopsies were taken from m. vastus lateralis and analysed for mitochondrial respiration, mitochondrial efficiency (MEff; i.e. P/O ratio), UCP3 protein content and fibre type composition (% MHC I). MEff was determined in isolated mitochondria during maximal (state 3) and submaximal (constant rate of ADP infusion) rates of respiration with pyruvate. The rates of mitochondrial respiration and oxidative phosphorylation per muscle mass were about 40% higher in trained subjects but were not different when expressed per unit citrate synthase (CS) activity (a marker of mitochondrial density). Training status had no influence on WE (trained 28.0 +/- 0.5, untrained 27.7 +/- 0.8%, N.S.). Muscle UCP3 was 52% higher in untrained subjects, when expressed per muscle mass (P < 0.05 versus trained). WE was inversely correlated to UCP3 (r=-0.57, P < 0.05) and positively correlated to percentage MHC I (r= 0.58, P < 0.05). MEff was lower (P < 0.05) at submaximal respiration rates (2.39 +/- 0.01 at 50% ) than at state 3 (2.48 +/- 0.01) but was neither influenced by training status nor correlated to cycling efficiency. In conclusion cycling efficiency was not influenced by training status and not correlated to MEff, but was related to type I fibres and inversely related to UCP3. The inverse correlation between WE and UCP3 indicates that extrinsic factors may influence UCP3 activity and thus MEff in vivo.

Ort, förlag, år, upplaga, sidor
2006. Vol. 571, nr 3, s. 669-681
Nationell ämneskategori
Odontologi
Identifikatorer
URN: urn:nbn:se:gih:diva-197OAI: oai:DiVA.org:gih-197DiVA, id: diva2:552
Anmärkning

The definitive version is available at www.blackwell-synergy.com

Tillgänglig från: 2007-05-08 Skapad: 2007-05-08 Senast uppdaterad: 2017-09-19
Ingår i avhandling
1. Effects of endurance exercise on mitochondrial efficiency, uncoupling and lipid oxidation in human skeletal muscle
Öppna denna publikation i ny flik eller fönster >>Effects of endurance exercise on mitochondrial efficiency, uncoupling and lipid oxidation in human skeletal muscle
2006 (Engelska)Doktorsavhandling, sammanläggning (Övrigt vetenskapligt)
Abstract [en]

During the last years the importance of muscle mitochondria, and mitochondrial function, not only for performance but also for health has been highlighted. The main function of the mitochondria is to produce ATP by oxidative phosphorylation (coupled respiration). In skeletal muscle a substantial part of the energy is lost in non-coupled reactions, it has been estimated that non-coupled respiration accounts for as much as 20-25% of the total energy expenditure. It is now almost 10 years since the discovery of uncoupling protein 3 (UCP3), but the functional role of UCP3 in non-coupled respiration is not completely understood. The aim of this thesis was to investigate mitochondrial efficiency (P/O ratio), mitochondrial fat oxidation, non-coupled respiration (state 4) and protein expression of UCP3 in response to exercise and training in human skeletal muscle.

In study I eight healthy subjects endurance trained for 6 weeks and 9 subjects performed one exercise session (75 min). In the cycling efficiency study II, and in the study on mitochondrial lipid oxidation III, 9 healthy trained and 9 healthy untrained men participated. In study IV mitochondrial function and reactive oxygen species (ROS) production was studied in 9 elite athletes after extreme exercise, 24 hours of cycling, running and paddling.

Endurance training increased whole body oxygen uptake (VO2 peak) by 24% and muscle citrate synthase (CS) activity (marker of mitochondrial volume) by 47% (P< 0.05), but non-coupled respiration and UCP3 adjusted for mitochondrial volume were reduced (P< 0.05). One session of exercise did not affect non-coupled respiration or UCP3.

Cycling efficiency (expressed as work efficiency) was inversely related to protein expression of UCP3 (r= 0.57) and correlated to type 1 fibers (r= 0.58). Work efficiency was not influenced by training status or correlated to mitochondrial efficiency. UCP3 was 52% higher in the untrained men (P< 0.05). Mitochondrial capacity for fat oxidation was not influenced by training status, but related to fiber type composition. The hypothesis that mitochondrial fat oxidation is related to whole body lipid oxidation during low-intensity exercise was confirmed (r= 0.62).

Mitochondrial capacity for fat oxidation increased after 24 hours of exercise, whereas mitochondrial efficiency (P/O ratio) decreased. P/O ratio remained reduced also after 28 hours of recovery. Formation of ROS by isolated mitochondria increased after exercise. Non-coupled respiration (state 4), however, decreased and UCP3 tended to be reduced after recovery from ultra-endurance exercise (P= 0.07).

In conclusion: UCP3 does not follow exercise induced mitochondrial biogenesis. UCP3 is reduced by endurance training and lower in trained men compared with untrained men. Non-coupled respiration, measured in isolated mitochondria was reduced by endurance training and reduced after recovery from ultra-endurance exercise, but similar in trained and untrained men. In these studies UCP3 and non-coupled respiration follow the same pattern but are not correlated. Further studies are needed to understand the complex role of UCP3 in skeletal muscle metabolism.

Ort, förlag, år, upplaga, sidor
Department of Physiology and Pharmacology, Karolinska Institutet, 2006
Identifikatorer
urn:nbn:se:gih:diva-13 (URN)91-7357-059-1 (ISBN)
Disputation
2007-01-19, Aulan, GIH, 09:00 (Engelska)
Opponent
Handledare
Tillgänglig från: 2007-01-25 Skapad: 2007-01-25 Senast uppdaterad: 2017-09-26

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