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  • 1.
    Tonkonogi, Michail
    et al.
    Högskolan Dalarna, Akademin Hälsa och samhälle, Medicinsk vetenskap.
    Fernström, Maria
    Walsh, Brandon
    Ji, Li Li
    Rooyackers, Olav
    Hammaqvist, Folke
    Wernerman, Jan
    Sahlin, Kent
    Reduced oxidative power but unchanged antioxidative capacity in skeletal muscle from aged humans.2003Ingår i: Pflügers Archiv: European Journal of Physiology, ISSN 0031-6768, E-ISSN 1432-2013, Vol. 446, nr 2, s. 261-269Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    The hypothesis that the aging process is associated with mitochondrial dysfunction and oxidative stress has been investigated in human skeletal muscle. Muscle biopsy samples were taken from seven old male subjects [OS; 75 (range 61-86) years] and eight young male subjects [YS; 25 (22-31) years]. Oxidative function was measured both in permeabilised muscle fibres and isolated mitochondria. Despite matching the degree of physical activity, OS had a lower training status than YS as judged from pulmonary maximal O2 consumption (V£O2max, m36%) and handgrip strength (m20%). Both maximal respiration and creatine-stimulated respiration were reduced in muscle fibres from OS (m32 and m34%, respectively). In contrast, respiration in isolated mitochondria was similar in OS and YS. The discrepancy might be explained by a biased harvest of "healthy" mitochondria and/or disruption of structural components during the process of isolation. Cytochrome C oxidase was reduced (m40%, P<0.01), whereas UCP3 protein tended to be elevated in OS (P=0.09). Generation of reactive oxygen species by isolated mitochondria and measures of antioxidative defence (muscle content of glutathione, glutathione redox status, antioxidative enzymes activity) were not significantly different between OS and YS. It is concluded that aging is associated with mitochondrial dysfunction, which appears to be unrelated to reduced physical activity. The hypothesis of increased oxidative stress in aged muscle could not be confirmed in this study.

  • 2.
    Tonkonogi, Michail
    et al.
    Högskolan Dalarna, Akademin Hälsa och samhälle, Medicinsk vetenskap.
    Walsh, Brandon
    Tiivel, Toomas
    Saks, Valdur
    Sahlin, Kent
    Mitochondrial function in human skeletal muscle is not impaired by high intensity exercise.1999Ingår i: Pflügers Archiv: European Journal of Physiology, ISSN 0031-6768, E-ISSN 1432-2013, Vol. 437, nr 4, s. 562-568Artikel i tidskrift (Refereegranskat)
    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.

  • 3. Walsh, Brandon
    et al.
    Tonkonogi, Michail
    Högskolan Dalarna, Akademin Hälsa och samhälle, Medicinsk vetenskap.
    Sahlin, Kent
    Effect of endurance training on oxidative and antioxidative function in human permeabilised muscle fibres.2001Ingår i: Pflügers Archiv: European Journal of Physiology, ISSN 0031-6768, E-ISSN 1432-2013, Vol. 442, s. 420-425Artikel i tidskrift (Refereegranskat)
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