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  • 1. Fernström, Maria
    et al.
    Tonkonogi, Michail
    Dalarna University, School of Health and Social Studies, Medical Science.
    Sahlin, Kent
    Effects of acute and chronic exercise on mitochondrial uncoupling in human skeletal muscle2004In: Journal of Physiology, ISSN 0022-3751, E-ISSN 1469-7793, Vol. 554, no 3, p. 755-763Article in journal (Refereed)
    Abstract [en]

    Mitochondrial proteins such as uncoupling protein 3 (UCP3) and adenine nucleotide translocase (ANT) may mediate back-leakage of protons and serve as uncouplers of oxidative phosphorylation. We hypothesized that UCP3 and ANT increase after prolonged exercise and/or endurance training, resulting in increased uncoupled respiration (UCR). Subjects were investigated with muscle biopsies before and after acute exercise (75 min of cycling at 70% of ) or 6 weeks endurance training. Mitochondria were isolated and respiration measured in the absence (UCR or state 4) and presence of ADP (coupled respiration or state 3). Protein expression of UCP3 and ANT was measured with Western blotting. After endurance training , citrate synthase activity (CS), state 3 respiration and ANT increased by 24, 47, 40 and 95%, respectively (all P< 0.05), whereas UCP3 remained unchanged. When expressed per unit of CS (a marker of mitochondrial volume) UCP3 and UCR decreased by 54% and 18%(P < 0.05). CS increased by 43% after acute exercise and remained elevated after 3 h of recovery (P < 0.05), whereas the other muscle parameters remained unchanged. An intriguing finding was that acute exercise reversibly enhanced the capacity of mitochondria to accumulate Ca2+(P < 0.05) before opening of permeability transition pores. In conclusion, UCP3 protein and UCR decrease after endurance training when related to mitochondrial volume. These changes may prevent excessive basal thermogenesis. Acute exercise enhances mitochondrial resistance to Ca2+ overload but does not influence UCR or protein expression of UCP3 and ANT. The increased Ca2+ resistance may prevent mitochondrial degradation and the mechanism needs to be further explored.

  • 2. Sahlin, Kent
    et al.
    Fernström, Maria
    Tonkonogi, Michail
    Dalarna University, School of Health and Social Studies, Medical Science.
    No evidence of an intracellular lactate shuttle in rat skeletal muscle2002In: Journal of Physiology, ISSN 0022-3751, E-ISSN 1469-7793, Vol. 541, no 2, p. 569-574Article in journal (Refereed)
    Abstract [en]

    The concerted view is that cytosolic pyruvate is transferred into mitochondria and after oxidative decarboxylation further metabolized in the tricarboxylic acid cycle. Recently this view has been challenged. Based on experimental evidence from rat skeletal muscle it has been concluded that mitochondria predominantly oxidize lactate in vivo and that this constitutes part of an 'intracellular lactate shuttle'. This view appears to be gaining acceptance in the scientific community and due to its conceptual importance, confirmation by independent experiments is required. We have repeated the experiments in mitochondria isolated from rat soleus muscle. Contrary to the previously published findings we cannot find any mitochondrial respiration with lactate. Analysis of lactate dehydrogenase (LDH) by spectrophotometry demonstrated that the activity in the mitochondrial fraction was only 0.7 % of total activity. However, even when external LDH was added to mitochondria, there were no signs of respiration with lactate. In the presence of conditions where lactate is converted to pyruvate (external additions of both LDH and NAD+), mitochondrial oxygen consumption increased. Furthermore, we provide theoretical evidence that direct mitochondrial lactate oxidation is energetically unlikely. Based on the present data we conclude that direct mitochondrial lactate oxidation does not occur in skeletal muscle. The presence of an 'intracellular lactate shuttle' can therefore be questioned.

  • 3.
    Tonkonogi, Michail
    et al.
    Dalarna University, School of Health and Social Studies, Medical Science.
    Harris, Bearn
    Sahlin, Kent
    Mitochondrial oxidative function in human saponin-skinned muscle fibres: effects of prolonged exercise.1998In: Journal of Physiology, ISSN 0022-3751, E-ISSN 1469-7793, Vol. 510, p. 279-286Article in journal (Refereed)
    Abstract [en]

    1. The influence of prolonged exhaustive exercise on mitochondrial oxidative function was investigated in ten men. 2. Muscle biopsies were taken before and after exercise and mitochondrial respiration investigated in fibre bundles made permeable by pretreatment with saponin. 3. After exercise, respiration in the absence of ADP increased by 18 % (P< 0.01), but respiration at suboptimal ADP concentration (0.1 mM) and maximal ADP-stimulated respiration (1 mM ADP) remained unchanged. 4. In the presence of creatine (20 mM), mitochondrial affinity for ADP increased markedly and respiration at suboptimal ADP concentration (0.1 mM) was similar (pre-exercise) or higher (post-exercise; P< 0.05) than with 1 mM ADP alone. The increase in respiratory rate with creatine was correlated to the relative type I fibre area (r = 0.84). Creatine-stimulated respiration increased after prolonged exercise (P< 0.01). 5. The respiratory control index (6.8 ± 0.4, mean ± s.e.m.) and the ratio between respiration at 0.1 and 1 mM ADP (ADP sensitivity index, 0.63 ± 0.03) were not changed after exercise. The sensitivity index was negatively correlated to the relative type I fibre area (r = -0.86). 6. The influence of exercise on muscle oxidative function has for the first time been investigated with the skinned-fibre technique. It is concluded that maximal mitochondrial oxidative power is intact or improved after prolonged exercise, while uncoupled respiration is increased. The latter finding may contribute to the elevated post-exercise oxygen consumption. The finding that the sensitivity of mitochondrial respiration for ADP and creatine are related to fibre-type composition indicates intrinsic differences in the control of mitochondrial respiration between fibres.

  • 4.
    Tonkonogi, Michail
    et al.
    Dalarna University, School of Health and Social Studies, Medical Science.
    Walsh, Brandon
    Svensson, Michael
    Sahlin, Kent
    Mitochondrial function and antioxidative defence in human muscle: Effects of endurance training and oxidative stress.2000In: Journal of Physiology, ISSN 0022-3751, E-ISSN 1469-7793, Vol. 528, no 2, p. 379-388Article in journal (Refereed)
    Abstract [en]

    1. The influence of endurance training on oxidative phosphorylation and the susceptibility of mitochondrial oxidative function to reactive oxygen species (ROS) was investigated in skeletal muscle of four men and four women. Mitochondria were isolated from muscle biopsies taken before and after 6 weeks of endurance training. Mitochondrial respiration was measured before and after exposure of mitochondria to exogenous ROS (H2O2+ FeCl2). 2. Endurance training increased peak pulmonary O2 uptake (VO2,peak) by 24 % and maximal ADP-stimulated mitochondrial oxygen consumption (state 3) by 40 % (P< 0.05). Respiration in the absence of ADP (state 4), the respiratory control ratio (RCR = state 3/state 4) and the ratio between added ADP and consumed oxygen (P/O) remained unchanged by the training programme. 3. Exposure to ROS reduced state 3 respiration but the effect was not significantly different between pre- and post-training samples. State 4 oxygen consumption increased after exposure to ROS both before (+189 %, P< 0.05) and after training (+243 %, P< 0.05) and the effect was significantly higher after training (P< 0.05, pre- vs. post-training). The augmented state 4 respiration could in part be attenuated by atractyloside, which indicates that ADP/ATP translocase was affected by ROS. The P/O ratio in ROS-treated mitochondria was significantly lower (P< 0.05) compared to control conditions, both before (-18.6 ± 2.2 %) and after training (-18.5 ± 1.1 %). 4. Muscle activities of superoxide dismutase (mitochondrial and cytosolic), glutathione peroxidase and muscle glutathione status were unaffected by training. There was a positive correlation between muscle superoxide dismutase activity and age (r= 0.75; P< 0.05; range of age 20–37 years), which may reflect an adaptation to increased generation of ROS in senescent muscle. The muscle glutathione pool was more reduced in subjects with high activity of glutathione peroxidase (r= 0.81; P< 0.05). 5. The influence of short-term training on mitochondrial oxygen consumption has for the first time been investigated in human skeletal muscle. The results showed that maximal mitochondrial oxidative power is increased after endurance training but that the efficiency of energy transfer (P/O ratio) remained unchanged. Antioxidative defence was unchanged after training when expressed relative to muscle weight. Although this corresponds to a reduced antioxidant protection per individual mitochondrion, the sensitivity of aerobic energy transfer to ROS was unchanged. However, the augmented ROS-induced non-coupled respiration after training indicates an increased susceptibility of mitochondrial membrane proton conductance to oxidative stress.

  • 5.
    Tonkonogi, Michail
    et al.
    Dalarna University, School of Health and Social Studies, Medical Science.
    Walsh, Brandon
    Söderlund, Karin
    Hultman, Erik
    Saks, Valdur
    Sahlin, Kent
    The role of phosphorylcreatine in the regulation of mitochondrial respiration in human skeletal muscle.2001In: Journal of Physiology, ISSN 0022-3751, E-ISSN 1469-7793, Vol. 537, no 3, p. 971-978Article in journal (Refereed)
    Abstract [en]

    1. The role of phosphorylcreatine (PCr) and creatine (Cr) in the regulation of mitochondrial respiration was investigated in permeabilised fibre bundles prepared from human vastus lateralis muscle. 2. Fibre respiration was measured in the absence of ADP (V0) and after sequential additions of submaximal ADP (0.1 mm ADP, Vsubmax), PCr (or Cr) and saturating [ADP] (Vmax). 3. Vsubmax increased by 55% after addition of saturating creatine (P< 0.01; n = 8) and half the maximal effect was obtained at 5 mm [Cr]. In contrast, Vsubmax decreased by 54% after addition of saturating phosphorylcreatine (P< 0.01; n = 8) and half the maximal effect was obtained at 1 mm [PCr]. Vmax was not affected by Cr or PCr. 4. Vsubmax was similar when PCr and Cr were added simultaneously at concentrations similar to those in muscle at rest (PCr/Cr = 2) and at low-intensity exercise (PCr/Cr = 0.5). At conditions mimicking high-intensity exercise (PCr/Cr = 0.1), Vsubmax increased to 60% of Vmax (P< 0.01) vs. rest and low-intensity exercise). 5. Eight of the subjects participated in a 16 day Cr supplementation programme. Following Cr supplementation, V0 decreased by 17% (P< 0.01) vs. prior to Cr supplementation), whereas ADP-stimulated respiration (with and without Cr or PCr) was unchanged. 6. For the first time evidence is given that PCr is an important regulator of mitochondrial ADP-stimulated respiration. Phosphorylcreatine decreases the sensitivity of mitochondrial respiration to ADP whereas Cr has the opposite effect. During transition from rest to high-intensity exercise, decreases in the PCr/Cr ratio will effectively increase the sensitivity of mitochondrial respiration to ADP. The decrease in V0 after Cr supplementation indicates that intrinsic changes in membrane proton conductance occur.

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