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Wang, Li
Publications (3 of 3) Show all publications
Hey-Mogensen, M., Højlund, K., Vind, B. F., Wang, L., Dela, F., Beck-Nielsen, H., . . . Sahlin, K. (2010). Effect of physical training on mitochondrial respiration and reactive oxygen species release in skeletal muscle in patients with obesity and type 2 diabetes.. Diabetologia, 53(9), 1976-85
Open this publication in new window or tab >>Effect of physical training on mitochondrial respiration and reactive oxygen species release in skeletal muscle in patients with obesity and type 2 diabetes.
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2010 (English)In: Diabetologia, ISSN 0012-186X, E-ISSN 1432-0428, Vol. 53, no 9, p. 1976-85Article in journal (Refereed) Published
Abstract [en]

AIM/HYPOTHESIS: Studies have suggested a link between insulin resistance and mitochondrial dysfunction in skeletal muscles. Our primary aim was to investigate the effect of aerobic training on mitochondrial respiration and mitochondrial reactive oxygen species (ROS) release in skeletal muscle of obese participants with and without type 2 diabetes. METHODS: Type 2 diabetic men (n = 13) and control (n = 14) participants matched for age, BMI and physical activity completed 10 weeks of aerobic training. Pre- and post-training muscle biopsies were obtained before a euglycaemic-hyperinsulinaemic clamp and used for measurement of respiratory function and ROS release in isolated mitochondria. RESULTS: Training significantly increased insulin sensitivity, maximal oxygen consumption and muscle mitochondrial respiration with no difference between groups. When expressed in relation to a marker of mitochondrial density (intrinsic mitochondrial respiration), training resulted in increased mitochondrial ADP-stimulated respiration (with NADH-generating substrates) and decreased respiration without ADP. Intrinsic mitochondrial respiration was not different between groups despite lower insulin sensitivity in type 2 diabetic participants. Mitochondrial ROS release tended to be higher in participants with type 2 diabetes. CONCLUSIONS/INTERPRETATION: Aerobic training improves muscle respiration and intrinsic mitochondrial respiration in untrained obese participants with and without type 2 diabetes. These adaptations demonstrate an increased metabolic fitness, but do not seem to be directly related to training-induced changes in insulin sensitivity.

National Category
Endocrinology and Diabetes Physiology
Research subject
Medicine/Technology
Identifiers
urn:nbn:se:gih:diva-1579 (URN)10.1007/s00125-010-1813-x (DOI)20526759 (PubMedID)
Available from: 2010-12-06 Created: 2010-12-06 Last updated: 2019-09-17Bibliographically approved
Psilander, N., Wang, L., Westergren, J., Tonkonogi, M. & Sahlin, K. (2010). Mitochondrial gene expression in elite cyclists: effects of high-intensity interval exercise.. European Journal of Applied Physiology, 110(3), 597-606
Open this publication in new window or tab >>Mitochondrial gene expression in elite cyclists: effects of high-intensity interval exercise.
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2010 (English)In: European Journal of Applied Physiology, ISSN 1439-6319, E-ISSN 1439-6327, Vol. 110, no 3, p. 597-606Article in journal (Refereed) Published
Abstract [en]

Little is known about the effect of training on genetic markers for mitochondrial biogenesis in elite athletes. We tested the hypothesis that low-volume sprint interval exercise (SIE) would be as effective as high-volume interval exercise (IE). Ten male cyclists competing on national elite level (W (max) 403 ± 13 W, VO(2peak) 68 ± 1 mL kg(-1) min(-1)) performed two interval exercise protocols: 7 × 30-s "all-out" bouts (SIE) and 3 × 20-min bouts at ~87% of VO(2peak) (IE). During IE, the work was eightfold larger (1,095 ± 43 vs. 135 ± 5 kJ) and the exercise duration 17 times longer (60 vs. 3.5 min) than during SIE. Muscle samples were taken before and 3 h after exercise. The mRNA of upstream markers of mitochondrial biogenesis [peroxisome proliferator-activated receptor-γ coactivator-1 (PGC-1α), PGC-1α-related coactivator (PRC) and peroxisome proliferator-activated receptor δ (PPARδ)] increased to the same extent after SIE and IE (6-, 1.5- and 1.5-fold increase, respectively). Of the downstream targets of PGC-1α, mitochondrial transcription factor A (Tfam) increased only after SIE and was significantly different from that after IE (P < 0.05), whereas others increased to the same extent (pyruvate dehydrogenase kinase, PDK4) or was unchanged (nuclear respiratory factor 2, NRF2). We conclude that upstream genetic markers of mitochondrial biogenesis increase in a similar way in elite athletes after one exercise session of SIE and IE. However, since the volume and duration of work was considerably lower during SIE and since Tfam, the downstream target of PGC-1α, increased only after SIE, we conclude that SIE might be a time-efficient training strategy for highly trained individuals.

National Category
Physiology
Research subject
Medicine/Technology
Identifiers
urn:nbn:se:gih:diva-1590 (URN)10.1007/s00421-010-1544-1 (DOI)20571821 (PubMedID)
Available from: 2010-12-06 Created: 2010-12-06 Last updated: 2018-01-12Bibliographically approved
Wang, L., Psilander, N., Tonkonogi, M., Ding, S. & Sahlin, K. (2009). Similar expression of oxidative genes after interval and continuous exercise.. Medicine & Science in Sports & Exercise, 41(12), 2136-44
Open this publication in new window or tab >>Similar expression of oxidative genes after interval and continuous exercise.
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2009 (English)In: Medicine & Science in Sports & Exercise, ISSN 0195-9131, E-ISSN 1530-0315, Vol. 41, no 12, p. 2136-44Article in journal (Refereed) Published
Abstract [en]

PURPOSE: There is a debate whether interval or traditional endurance training is the most effective stimulus of mitochondrial biogenesis. Here, we compared the effects of acute interval exercise (IE) or continuous exercise (CE) on the muscle messenger RNA (mRNA) content for several genes involved in mitochondrial biogenesis and lipid metabolism. METHODS: Nine sedentary subjects cycled for 90 min with two protocols: CE (at 67% VO2max) and IE (12 s at 120% and 18 s at 20% of VO2max). The duration of exercise and work performed with CE and IE was identical. Muscle biopsies were taken before and 3 h after exercise. RESULTS: There were no significant differences between the two exercise protocols in the increases in VO2 and HR, the reduction in muscle glycogen (35%-40% with both protocols) or the changes in blood metabolites (lactate, glucose, and fatty acids). The mRNA content for major regulators of mitochondrial biogenesis [peroxisome proliferator-activated receptor (PPAR) gamma coactivator 1alpha (PGC-1alpha), PGC-1-related coactivator, PPARbeta/delta] and of lipid metabolism [pyruvate dehydrogenase kinase isozyme 4 (PDK4)] increased after exercise, but there was no significant difference between IE and CE. However, the mRNA content for several downstream targets of PGC-1alpha increased significantly only after CE, and mRNA content for nuclear respiratory factor 2 was significantly higher after CE (P < 0.025 vs IE). CONCLUSIONS: The present findings demonstrate that, when the duration of exercise and work performed is the same, IE and CE influence the transcription of genes involved in oxidative metabolism in a similar manner.

National Category
Physiology
Identifiers
urn:nbn:se:gih:diva-1583 (URN)10.1249/MSS.0b013e3181abc1ec (DOI)19915506 (PubMedID)
Available from: 2010-12-06 Created: 2010-12-06 Last updated: 2018-01-12Bibliographically approved
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