<abstract xmlns="http://www.w3.org/1999/xhtml"><sec id="j_1905-7415.0904.415_s_001_w2aab3b7b2b1b6b1aab1c16b1Aa"><h3>Background</h3><p>Performing regular exercise may be beneficial to delay aging. During aging, numerous biochemical and molecular changes occur in cells, including increased DNA instability, epigenetic alterations, cell-signaling disruptions, decreased protein synthesis, reduced adenosine triphosphate (ATP) production capacity, and diminished oxidative phosphorylation.</p></sec><sec id="j_1905-7415.0904.415_s_002_w2aab3b7b2b1b6b1aab1c16b2Aa"><h3>Objectives</h3><p>To identify the types of exercise and the molecular mechanisms associated with antiaging phenotypes by comparing the profiles of gene expression in skeletal muscle after various types of exercise and aging.</p></sec><sec id="j_1905-7415.0904.415_s_003_w2aab3b7b2b1b6b1aab1c16b3Aa"><h3>Methods</h3><p>We used bioinformatics data from skeletal muscles reported in the Gene Expression Omnibus repository and used Connection Up- and Down-Regulation Expression Analysis of Microarrays to identify genes significant in antiaging. The significant genes were mapped to molecular pathways and reviewed for their molecular functions, and their associations with molecular and cellular phenotypes using the Database for Annotation, Visualization and Integrated Discovery and Kyoto Encyclopedia of Genes and Genomes informatics resources, and GeneCards databases, respectively.</p></sec><sec id="j_1905-7415.0904.415_s_004_w2aab3b7b2b1b6b1aab1c16b4Aa"><h3>Results</h3><p>The results showed that endurance exercise has an antiaging potential (Pearson χ<sup>2</sup>, P &lt; 0.01) by upregulating genes coding for components of the oxidative phosphorylation pathway (Benjamini false discovery rate Q &lt; 0.05). We found that numerous genes coding for components of other pathways were also upregulated (Pearson χ<sup>2</sup> P &lt; 0.01) as a chronic adaptation to endurance exercise, including <italic>ATP5C1</italic>, involved in ATP synthesis, <italic>CYCS</italic>, involved in electron transfer in the mitochondrial respiratory chain, and <italic>GSTK1</italic>, involved in cellular detoxification.</p></sec><sec id="j_1905-7415.0904.415_s_005_w2aab3b7b2b1b6b1aab1c16b5Aa"><h3>Conclusions</h3><p>Endurance exercise may be the best type to promote antiaging phenotypes by increasing mitochondrial biogenesis and ATP production capacity.</p></sec></abstract>

BackgroundPerforming regular exercise may be beneficial to delay aging. During aging, numerous biochemical and molecular changes occur in cells, including increased DNA instability, epigenetic alterations, cell-signaling disruptions, decreased protein synthesis, reduced adenosine triphosphate (ATP) production capacity, and diminished oxidative phosphorylation.ObjectivesTo identify the types of exercise and the molecular mechanisms associated with antiaging phenotypes by comparing the profiles of gene expression in skeletal muscle after various types of exercise and aging.MethodsWe used bioinformatics data from skeletal muscles reported in the Gene Expression Omnibus repository and used Connection Up- and Down-Regulation Expression Analysis of Microarrays to identify genes significant in antiaging. The significant genes were mapped to molecular pathways and reviewed for their molecular functions, and their associations with molecular and cellular phenotypes using the Database for Annotation, Visualization and Integrated Discovery and Kyoto Encyclopedia of Genes and Genomes informatics resources, and GeneCards databases, respectively.ResultsThe results showed that endurance exercise has an antiaging potential (Pearson χ2, P < 0.01) by upregulating genes coding for components of the oxidative phosphorylation pathway (Benjamini false discovery rate Q < 0.05). We found that numerous genes coding for components of other pathways were also upregulated (Pearson χ2 P < 0.01) as a chronic adaptation to endurance exercise, including ATP5C1, involved in ATP synthesis, CYCS, involved in electron transfer in the mitochondrial respiratory chain, and GSTK1, involved in cellular detoxification.ConclusionsEndurance exercise may be the best type to promote antiaging phenotypes by increasing mitochondrial biogenesis and ATP production capacity.

Antiaging phenotype in skeletal muscle after endurance exercise is associated with the oxidative phosphorylation pathway

Department of Anatomy, Faculty of Medicine

Center of Excellence in Molecular Genetics of Cancer and Human Diseases

Asian Biomedicine

This work is licensed under the Creative Commons Attribution-NonCommercial-NoDerivatives 3.0 License.

BackgroundPerforming regular exercise may be beneficial to delay aging. During aging, numerous biochemical and molecular changes occur in cells, including...

Antiaging phenotype in skeletal muscle after endurance exercise is associated with the oxidative phosphorylation pathway

Article Category: Original article

Online veröffentlicht: 31. Jan. 2017

Seitenbereich: 455 - 471

DOI: https://doi.org/10.5372/1905-7415.0904.415

Schlüsselwörter
Aging, endurance exercise, mitochondrial biogenesis, mitochondrial dysfunction, oxidative phosphorylation, skeletal muscle

© 2015 Wasin Laohavinij, Apiwat Mutirangura

This work is licensed under the Creative Commons Attribution-NonCommercial-NoDerivatives 3.0 License.

Antiaging phenotype in skeletal muscle after endurance exercise is associated with the oxidative phosphorylation pathway

Article Category: Original article

Online veröffentlicht: 31. Jan. 2017

Seitenbereich: 455 - 471

DOI: https://doi.org/10.5372/1905-7415.0904.415

SchlüsselwörterAging, endurance exercise, mitochondrial biogenesis, mitochondrial dysfunction, oxidative phosphorylation, skeletal muscle

© 2015 Wasin Laohavinij, Apiwat Mutirangura

This work is licensed under the Creative Commons Attribution-NonCommercial-NoDerivatives 3.0 License.

Schlüsselwörter
Aging, endurance exercise, mitochondrial biogenesis, mitochondrial dysfunction, oxidative phosphorylation, skeletal muscle