Mitochondrial Biogenesis in Skeletal Muscle in Response to Endurance Exercises

Freyssenet, Damien; Berthon, Pierre; Denis, Christian

doi:10.1076/apab.104.2.129.12878

Cited by 57 publications

(29 citation statements)

References 72 publications

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“…It is believed to involve *1,000 genes and to affect 20% of the cellular proteins (4,79,136,137,168,260). As nonfunctional mitochondria are eliminated by autophagy, mitochondrial biogenesis is needed to sustain energy production and physiological homeostasis in the cell.…”

Section: Mitochondrial Biogenesismentioning

confidence: 99%

Mitochondrial Turnover and Aging of Long-Lived Postmitotic Cells: The Mitochondrial–Lysosomal Axis Theory of Aging

Terman

Kurz

Navrátil

et al. 2010

Antioxidants & Redox Signaling

427

375

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It is now generally accepted that aging and eventual death of multicellular organisms is to a large extent related to macromolecular damage by mitochondrially produced reactive oxygen species, mostly affecting long-lived postmitotic cells, such as neurons and cardiac myocytes. These cells are rarely or not at all replaced during life and can be as old as the whole organism. The inherent inability of autophagy and other cellular-degradation mechanisms to remove damaged structures completely results in the progressive accumulation of garbage, including cytosolic protein aggregates, defective mitochondria, and lipofuscin, an intralysosomal indigestible material. In this review, we stress the importance of crosstalk between mitochondria and lysosomes in aging. The slow accumulation of lipofuscin within lysosomes seems to depress autophagy, resulting in reduced turnover of effective mitochondria. The latter not only are functionally deficient but also produce increased amounts of reactive oxygen species, prompting lipofuscinogenesis. Moreover, defective and enlarged mitochondria are poorly autophagocytosed and constitute a growing population of badly functioning organelles that do not fuse and exchange their contents with normal mitochondria. The progress of these changes seems to result in enhanced oxidative stress, decreased ATP production, and collapse of the cellular catabolic machinery, which eventually is incompatible with survival. Antioxid. Redox Signal. 12, 503-535.

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Section: Mitochondrial Biogenesismentioning

confidence: 99%

Mitochondrial Turnover and Aging of Long-Lived Postmitotic Cells: The Mitochondrial–Lysosomal Axis Theory of Aging

Terman

Kurz

Navrátil

et al. 2010

Antioxidants & Redox Signaling

427

375

View full text Add to dashboard Cite

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“…In mice and humans, endurance exercise is known to improve glucose sensitivity (Henriksson, 1995;Hayashi et al, 1997), while in mice and flies, endurance exercise is known to increase autophagy (He et al, 2012;Sujkowski et al, 2012). In all species tested, endurance exercise increases mitochondrial biogenesis (Freyssenet et al, 1996;Irrcher et al, 2003;Tinkerhess et al, 2012b). Because of these conserved changes, endurance exercise is thought to be a potential low-cost intervention that may provide increased healthspan to the human population by alleviating pathological states related to obesity and glucose insenstivity (Hopps and Caimi, 2011;Chudyk and Petrella, 2011).…”

Section: Introductionmentioning

confidence: 99%

Dietary composition regulatesDrosophilamobility and cardiac physiology

Bazzell

Ginzberg

Healy

et al. 2012

Journal of Experimental Biology

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SUMMARYThe impact of dietary composition on exercise capacity is a subject of intense study in both humans and model organisms. Interactions between diet and genetics are a crucial component of optimized dietary design. However, the genetic factors governing exercise response are still not well understood. The recent development of invertebrate models for endurance exercise is likely to facilitate study designs examining the conserved interactions between diet, exercise and genetics. As a first step, we used the Drosophila model to describe the effects of varying dietary composition on several physiological indices, including fatigue tolerance and climbing speed, cardiac performance, lipid storage and autophagy. We found that flies of two divergent genetic backgrounds optimize endurance and cardiac performance on relatively balanced low calorie diets. When flies are provided with unbalanced diets, diets higher in sugar than in yeast facilitate greater endurance at the expense of cardiac performance. Importantly, we found that dietary composition has a profound effect on various physiological indices, whereas total caloric intake per se has very little predictive value for performance. We also found that the effects of diet on endurance are completely reversible within 48h if flies are switched to a different diet. Supplementary material available online at

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“…The function and number of mitochondria in skeletal muscle cells can change in response to stimulation. For example, endurance exercise increases the number of mitochondria and improves energy metabolism in skeletal muscle (12,32). Mechanisms of mitochondrial biogenesis have been the subject of much research, and some transcription factors, such as peroxisome proliferator-activated receptor-␥ coactivator-1␣ (PGC1-␣) and nuclear respiratory factor 1, are thought to play a primary role in mitochondrial biogenesis within skeletal muscle (11,16,31,36); however, the mechanisms involved have not been identified.…”

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confidence: 99%