2009
DOI: 10.1016/j.addr.2009.06.006
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Mitochondrial biogenesis in exercise and in ageing☆

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Cited by 205 publications
(146 citation statements)
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References 30 publications
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“…Vina et al (2009) concluded that exercise, and particularly aerobic exercise, activated mitochondriogenesis in young animals, although its influence on older animals required further investigation. Eight weeks of treadmill training in a murine model augmented mitochondrial function, as reflected by increased mitochondrial enzyme activities, maximal rate of ATP synthesis in isolated mitochondria, and whole-body maximal O2 uptake (Chow et al, 2007).…”
Section: Exercise and Its Effect On Mitochondriamentioning
confidence: 99%
“…Vina et al (2009) concluded that exercise, and particularly aerobic exercise, activated mitochondriogenesis in young animals, although its influence on older animals required further investigation. Eight weeks of treadmill training in a murine model augmented mitochondrial function, as reflected by increased mitochondrial enzyme activities, maximal rate of ATP synthesis in isolated mitochondria, and whole-body maximal O2 uptake (Chow et al, 2007).…”
Section: Exercise and Its Effect On Mitochondriamentioning
confidence: 99%
“…In addition, PGC‐1α extends health span and life span of a mouse model of premature aging arising from mitochondria defects (Sahin et al., 2011). Importantly, in line with the mitochondrial decline, PGC‐1α expression decreases during muscle aging in different species, including humans (Ghosh et al., 2011; Kang, Chung, Diffee, & Ji, 2013; Short et al., 2005; Vina et al., 2009). Moreover, PGC‐1α improves various muscle disorders, for example, denervation‐induced fiber atrophy (Sandri et al., 2006) or Duchenne muscular dystrophy (Handschin, Kobayashi et al., 2007).…”
Section: Introductionmentioning
confidence: 99%
“…Thus, to identify genotypes related to mitochondriogenesis (involving the PPARD-PPARGC1A-NRF-TFAM pathway) is of interest from a broader health perspective in aged people because these genotypes theoretically could be associated with muscle capacity and frailty in the elderly. Indeed, mitochondriogenesis is critical for the normal function of cells and the PPARD-PPARGC1A-NRF-TFAM pathway is impaired by chronic physical inactivity (Vina, Gomez-Cabrera, Borras, Froio, Sanchis-Gomar, Martinez-Bello & Pallardo, 2009a) and ageing (Hood, 2009). Reduced mitochondriogenesis can result in reduced muscle aerobic capacity (which is in itself an important health indicator), increased tendency for mitochondrially-mediated apoptosis, and, ultimately, accelerated sarcopenia (Hood, 2009).…”
Section: Discussionmentioning
confidence: 99%
“…As more individuals live longer, we should try to elucidate the mechanisms involved in healthy ageing and preserving functional independence in later life. With regards to this, mitochondria are one of the most important organelles for understanding the ageing process (Vina, Gomez-Cabrera, Borras, Froio, Sanchis-Gomar, Martinez-Bello, & Pallardo, 2009b). A constant renewal of these organelles is crucial for maintaining their normal function.…”
Section: Introductionmentioning
confidence: 99%