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  • 1. Sahlin, Kent
    et al.
    Shabalina, Irina G
    Stockholm University, Faculty of Science, The Wenner-Gren Institute , Physiology.
    Mattsson, C Mikael
    Bakkman, Linda
    Fernström, Maria
    Rozhdestvenskaya, Zinaida
    Enqvist, Jonas K
    Nedergaard, Jan
    Stockholm University, Faculty of Science, The Wenner-Gren Institute , Physiology.
    Ekblom, Björn
    Tonkonogi, Michail
    Ultraendurance exercise increases the production of reactive oxygen species in isolated mitochondria from human skeletal muscle2010In: Journal of applied physiology, ISSN 8750-7587, E-ISSN 1522-1601, Vol. 108, no 4, p. 780-7Article in journal (Refereed)
    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 yr) performed ultraendurance exercise (kayaking/running/cycling) with an average work intensity of 55% V(O(2peak)) for 24 h. Muscle biopsies were taken from vastus lateralis before exercise, immediately after exercise, and after 28 h of recovery. The production of H(2)O(2) was measured fluorometrically in isolated mitochondria with the Amplex red and peroxidase system. Succinate-supported mitochondrial H(2)O(2) 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 fourfold and exceeded 1.2 mmol/l 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, ultraendurance 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.

  • 2.
    Timmons, James A.
    et al.
    Stockholm University, Faculty of Science, The Wenner-Gren Institute .
    Knudsen, Steen
    Rankinen, Tuomo
    Koch, Lauren G.
    Sarzynski, Mark
    Jensen, Thomas
    Keller, Pernille
    Scheele, Camilla
    Stockholm University, Faculty of Science, The Wenner-Gren Institute .
    Vollaard, Niels B. J.
    Nielsen, Soren
    Akerstrom, Thorbjoern
    MacDougald, Ormond A.
    Jansson, Eva
    Greenhaff, Paul L.
    Tarnopolsky, Mark A.
    van Loon, Luc J. C.
    Pedersen, Bente K.
    Sundberg, Carl Johan
    Wahlestedt, Claes
    Britton, Steven L.
    Bouchard, Claude
    Using molecular classification to predict gains in maximal aerobic capacity following endurance exercise training in humans2010In: Journal of applied physiology, ISSN 8750-7587, E-ISSN 1522-1601, Vol. 108, no 6, p. 1487-1496Article in journal (Refereed)
    Abstract [en]

    Timmons JA, Knudsen S, Rankinen T, Koch LG, Sarzynski M, Jensen T, Keller P, Scheele C, Vollaard NB, Nielsen S, Akerstrom T, MacDougald OA, Jansson E, Greenhaff PL, Tarnopolsky MA, van Loon LJ, Pedersen BK, Sundberg CJ, Wahlestedt C, Britton SL, Bouchard C. Using molecular classification to predict gains in maximal aerobic capacity following endurance exercise training in humans. J Appl Physiol 108: 1487-1496, 2010. First published February 4, 2010; doi:10.1152/japplphysiol.01295.2009.-A low maximal oxygen consumption ((V) over dotO(2max)) is a strong risk factor for premature mortality. Supervised endurance exercise training increases (V) over dotO(2max) with a very wide range of effectiveness in humans. Discovering the DNA variants that contribute to this heterogeneity typically requires substantial sample sizes. In the present study, we first use RNA expression profiling to produce a molecular classifier that predicts (V) over dotO(2max) training response. We then hypothesized that the classifier genes would harbor DNA variants that contributed to the heterogeneous (V) over dotO(2max) response. Two independent preintervention RNA expression data sets were generated (n = 41 gene chips) from subjects that underwent supervised endurance training: one identified and the second blindly validated an RNA expression signature that predicted change in (V) over dotO(2max) (""predictor"" genes). The HERITAGE Family Study (n = 473) was used for genotyping. We discovered a 29-RNA signature that predicted (V) over dotO(2max) training response on a continuous scale; these genes contained similar to 6 new single-nucleotide polymorphisms associated with gains in (V) over dotO(2max) in the HERITAGE Family Study. Three of four novel candidate genes from the HERITAGE Family Study were confirmed as RNA predictor genes (i.e., ""reciprocal"" RNA validation of a quantitative trait locus genotype), enhancing the performance of the 29-RNA-based predictor. Notably, RNA abundance for the predictor genes was unchanged by exercise training, supporting the idea that expression was preset by genetic variation. Regression analysis yielded a model where 11 single-nucleotide polymorphisms explained 23% of the variance in gains in (V) over dotO(2max), corresponding to similar to 50% of the estimated genetic variance for (V) over dotO(2max). In conclusion, combining RNA profiling with single-gene DNA marker association analysis yields a strongly validated molecular predictor with meaningful explanatory power. (V) over dotO(2max) responses to endurance training can be predicted by measuring a similar to 30-gene RNA expression signature in muscle prior to training. The general approach taken could accelerate the discovery of genetic biomarkers, sufficiently discrete for diagnostic purposes, for a range of physiological and pharmacological phenotypes in humans.

  • 3. Vollaard, Niels B. J.
    et al.
    Constantin-Teodosiu, Dimitru
    Fredriksson, Katarina
    Rooyackers, Olav
    Jansson, Eva
    Greenhaff, Paul L.
    Timmons, James A.
    Stockholm University, Faculty of Science, The Wenner-Gren Institute .
    Sundberg, Carl Johan
    Systematic analysis of adaptations in aerobic capacity and submaximal energy metabolism provides a unique insight into determinants of human aerobic performance2009In: Journal of applied physiology, ISSN 8750-7587, E-ISSN 1522-1601, Vol. 106, no 5, p. 1479-1486Article in journal (Refereed)
    Abstract [en]

    Vollaard NB, Constantin-Teodosiu D, Fredriksson K, Rooyackers O, Jansson E, Greenhaff PL, Timmons JA, Sundberg CJ. Systematic analysis of adaptations in aerobic capacity and submaximal energy metabolism provides a unique insight into determinants of human aerobic performance. J Appl Physiol 106: 1479-1486, 2009. First published February 5, 2009; doi:10.1152/japplphysiol.91453.2008.-It has not been established which physiological processes contribute to endurance training-related changes (Delta) in aerobic performance. For example, the relationship between intramuscular metabolic responses at the intensity used during training and improved human functional capacity has not been examined in a longitudinal study. In the present study we hypothesized that improvements in aerobic capacity ((V) over dotO(2max)) and metabolic control would combine equally to explain enhanced aerobic performance. Twenty-four sedentary males (24 +/- 2 yr; 1.81 +/- 0.08 m; 76.6 +/- 11.3 kg) undertook supervised cycling training (45 min at 70% of pretraining (V) over dotO(2max)) 4 times/wk for 6 wk. Performance was determined using a 15-min cycling time trial, and muscle biopsies were taken before and after a 10-min cycle at 70% of pretraining (V) over dotO(2max) to quantify substrate metabolism. Substantial interindividual variability in training-induced adaptations was observed for most parameters, yet ""low responders"" for Delta(V) over dotO(2max) were not consistently low responders for other variables. While (V) over dotO(2max) and time trial performance were related at baseline (r(2) = 0.80, P < 0.001), the change in (V) over dotO(2max) was completely unrelated to the change in aerobic performance. The maximal parameters Delta(V) over dotE(max) and Delta Veq(max) (Delta(V) over dotE/(V) over dotO(2max)) accounted for 64% of the variance in Delta(V) over dotO(2max) (P < 0.001), whereas Delta performance was related to changes in the submaximal parameters Veq(submax) (r(2) = 0.33; P < 0.01), muscle Delta lactate (r(2) = 0.32; P < 0.01), and Delta acetyl-carnitine (r(2) = 0.29; P < 0.05). This study demonstrates that improvements in high-intensity aerobic performance in humans are not related to altered maximal oxygen transport capacity. Altered muscle metabolism may provide the link between training stimulus and improved performance, but metabolic parameters do not change in a manner that relates to aerobic capacity changes.

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