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Plasticity of skeletal muscle mitochondria in response to contractile activity.
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Role of gp130 in basal and exercise-trained skeletal muscle mitochondrial quality control.
J Appl Physiol (1985). 2018 Jun 1;124(6):1456-1470. doi: 10.1152/japplphysiol.01063.2017. Epub 2018 Feb 1.
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Exercise and the Regulation of Mitochondrial Turnover.
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Short-term intensified training temporarily impairs mitochondrial respiratory capacity in elite endurance athletes.
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Skeletal muscle metabolic adaptations to endurance exercise training are attainable in mice with simvastatin treatment.
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Maintenance of Skeletal Muscle Mitochondria in Health, Exercise, and Aging.
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Endurance Exercise and the Regulation of Skeletal Muscle Metabolism.
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Resistance exercise enhances the molecular signaling of mitochondrial biogenesis induced by endurance exercise in human skeletal muscle.
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The Role of Mitochondria in Mediation of Skeletal Muscle Repair.
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Diaphragm Muscle: A Pump That Can Not Fail.
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The musculotendinous interface: insights into development, injury, and recovery for military medical applications.
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The mitochondrial multi-omic response to exercise training across rat tissues.
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Correlates of physical activity levels, muscle strength, working memory, and cognitive function in older adults.
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The mitochondrial multi-omic response to exercise training across tissues.
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本文引用的文献

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Exercise-induced BCL2-regulated autophagy is required for muscle glucose homeostasis.
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Single bout of running exercise changes LC3-II expression in rat cardiac muscle.
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Exercise protects against doxorubicin-induced markers of autophagy signaling in skeletal muscle.
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Nuclear SIRT1 activity, but not protein content, regulates mitochondrial biogenesis in rat and human skeletal muscle.
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The autophagy initiating kinase ULK1 is regulated via opposing phosphorylation by AMPK and mTOR.
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Mitofusin-2 maintains mitochondrial structure and contributes to stress-induced permeability transition in cardiac myocytes.
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Mitochondrial fusion and fission in cell life and death.
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The importance of PGC-1α in contractile activity-induced mitochondrial adaptations.
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