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  • 101.
    Tonkonogi, Michail
    et al.
    Dalarna University, School of Health and Social Studies, Medical Science.
    Sahlin, Kent
    Fernström, Maria
    The leaky mitochondrion2004In: Physiology News, ISSN 1476-7996, Vol. 56, p. 27-28Article in journal (Refereed)
  • 102.
    Tonkonogi, Michail
    et al.
    Dalarna University, School of Education, Health and Social Studies, Medical Science.
    Tonkonogi, Aleksandra
    Grundläggande muskel- och neurofysiologi2019In: Motorisk kontroll och inlärning: Med inriktning på muskoloskeletal rehabilitering / [ed] Ulrik Röijezon, Studentlitteratur AB, 2019, 1, p. 25-36Chapter in book (Other academic)
  • 103.
    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.

  • 104.
    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.

  • 105.
    Tonkonogi, Michail
    et al.
    Dalarna University, School of Health and Social Studies, Medical Science.
    Walsh, Brandon
    Tiivel, Toomas
    Saks, Valdur
    Sahlin, Kent
    Mitochondrial function in human skeletal muscle is not impaired by high intensity exercise.1999In: Pflügers Archiv: European Journal of Physiology, ISSN 0031-6768, E-ISSN 1432-2013, Vol. 437, no 4, p. 562-568Article in journal (Refereed)
    Abstract [en]

    The hypothesis that high-intensity (HI) intermittent exercise impairs mitochondrial function was investigated with different microtechniques in human muscle samples. Ten male students performed three bouts of cycling at 130% of peak O2 consumption (V·O2,peak). Muscle biopsies were taken from the vastus lateralis muscle at rest, at fatigue and after 110 min recovery. Mitochondrial function was measured both in isolated mitochondria and in muscle fibre bundles made permeable with saponin (skinned fibres). In isolated mitochondria there was no change in maximal respiration, rate of adenosine 5'-triphosphate (ATP) production (measured with bioluminescence) and respiratory control index after exercise or after recovery. The ATP production per consumed oxygen (P/O ratio) also remained unchanged at fatigue but decreased by 4% (P<0.05) after recovery. In skinned fibres, maximal adenosine 5'-diphosphate (ADP)-stimulated respiration increased by 23% from rest to exhaustion (P<0.05) and remained elevated after recovery, whereas the respiratory rates in the absence of ADP and at 0.1 mM ADP (submaximal respiration) were unchanged. The ratio between respiration at 0.1 and 1 mM ADP (ADP sensitivity index) decreased at fatigue (P<0.05) but after the recovery period was not significantly different from that at rest. It is concluded that mitochondrial oxidative potential is maintained or improved during exhaustive HI exercise. The finding that the sensitivity of mitochondrial respiration to ADP is reversibly decreased after strenuous exercise may indicate that the control of mitochondrial respiration is altered.

  • 106. Walsh, Brandon
    et al.
    Tiivel, Toomas
    Tonkonogi, Michail
    Dalarna University, School of Health and Social Studies, Medical Science.
    Sahlin, Kent
    Increased concentrations of Pi and lactic acid reduce creatine stimulated respiration in muscle fibres.2002In: Journal of applied physiology, ISSN 8750-7587, E-ISSN 1522-1601, Vol. 92, p. 2273-2276Article in journal (Refereed)
    Abstract [en]

    We tested the hypothesis that the respiratory function of skeletal muscle mitochondria is impaired by lactic acidosis and elevated concentrations of Pi. The rate of respiration of chemically skinned fiber bundles from rat soleus muscle was measured at [Pi] (brackets denote concentration) and pH values similar to those at rest (3 mM Pi, pH 7.0) and high-intensity exercise (20 mM Pi, pH 6.6). Respiration was measured in the absence of ADP and after sequential additions of 0.1 mM ADP, 20 mM creatine (Cr; VCr), and 4 mM ADP. Respiration at 0.1 mM ADP increased after addition of Cr. However, VCr was 23% lower (P < 0.05) during high-intensity conditions than during resting conditions. VCr was also reduced when Pi or H+ was increased separately (P < 0.05). Respiration in the absence of ADP and after additions of 0.1 mM ADP and 4 mM ADP was not affected by changes in [Pi] or [H+]. The response was similar, irrespective of when acidosis was induced (i.e., quiescent or actively respiring mitochondria). In conclusion, Cr-stimulated respiration is impaired by increases in [H+] and [Pi] corresponding to those in exercising muscle. Although the reduced Cr-stimulated respiration could be compensated for by increased [ADP], this might have implications for intracellular homeostasis.

  • 107. Walsh, Brandon
    et al.
    Tonkonogi, Michail
    Dalarna University, School of Health and Social Studies, Medical Science.
    Malm, Christer
    Ekblom, Björn
    Sahlin, Kent
    Effect of eccentric exercise on muscle oxidative function in man.2001In: Medicine & Science in Sports & Exercise, ISSN 0195-9131, E-ISSN 1530-0315, Vol. 33, no 3, p. 436-441Article in journal (Refereed)
    Abstract [en]

    Purpose: The purpose of this study was to evaluate the effects of eccentric exercise on muscle oxidative function. Methods: Thirteen subjects performed high-intensity eccentric cycling for 30 min. Muscle oxidative function in vastus lateralis was evaluated by measurements of respiration in permeabilized muscle fibers (skinned fibers) and from the kinetics of oxyhemoglobin (oxyHb) saturation measured with near infrared spectroscopy (NIRS). Results: After eccentric cycling, all subjects reported extensive delayed onset muscle soreness (DOMS), but plasma markers of muscle damage (creatine kinase and [beta]-glucuronidase activity) were not significantly altered. The half time of oxyHb desaturation after circulatory occlusion (128 +/- 11 s, mean +/- SE) and oxyHb resaturation after restoration of blood flow (13.8 +/- 0.7 s) were not significantly changed after eccentric cycling (N = 7). Respiration in skinned muscle fibers measured in the absence of ADP and in the presence of a submaximal (0.1 mM) or maximal ADP concentration (1 mM) was not significantly changed after eccentric cycling (N = 6). The sensitivity of respiration to ADP was not significantly changed after eccentric cycling. Conclusions: Muscle oxidative function (maximal respiration and respiratory control by ADP) was not compromised after high-intensity eccentric cycle exercise. Furthermore, NIRS indicates that after eccentric cycling muscle oxygen utilization and local oxygen transport at rest are unchanged. It is concluded that eccentric cycling, although causing DOMS, does not negatively affect skeletal muscle oxidative function.

  • 108. Walsh, Brandon
    et al.
    Tonkonogi, Michail
    Dalarna University, School of Health and Social Studies, Medical Science.
    Sahlin, Kent
    Effect of endurance training on oxidative and antioxidative function in human permeabilised muscle fibres.2001In: Pflügers Archiv: European Journal of Physiology, ISSN 0031-6768, E-ISSN 1432-2013, Vol. 442, p. 420-425Article in journal (Refereed)
  • 109. Wang, Li
    et al.
    Psilander, Niklas
    Tonkonogi, Michail
    Dalarna University, School of Education, Health and Social Studies, Sport and Health Science.
    Ding, Shuzhe
    Sahlin, Kent
    Similar expression of oxidative genes after interval and continuous exercise2009In: Medicine & Science in Sports & Exercise, ISSN 0195-9131, E-ISSN 1530-0315, Vol. 41, no 12, p. 2136-2144Article in journal (Refereed)
    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% V?O2max) and IE (12 s at 120% and 18 s at 20% of V?O2max). 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 V?O2 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) ? coactivator 1a (PGC-1a), PGC-1-related coactivator, PPAR/d] 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-1a 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.

  • 110.
    Westergren, Jens
    et al.
    Dalarna University, School of Education, Health and Social Studies, Sport and Health Science.
    Tonkonogi, Michail
    Dalarna University, School of Education, Health and Social Studies, Sport and Health Science.
    No difference in sprint cycling performance tests on a stationary and mobile ergometer2011In: Medicine & Science in Sports & Exercise, ISSN 0195-9131, E-ISSN 1530-0315, Vol. 43, no 5, p. 161-161Article in journal (Other academic)
123 101 - 110 of 110
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