Abstract
The purpose of this study was to evaluate the role of sirtuin 1 (SirT1) in exercise- and resveratrol (RSV)-induced skeletal muscle mitochondrial biogenesis. Using muscle-specific SirT1-deficient (KO) mice and a cell culture model of differentiated myotubes, we compared the treatment of resveratrol, an activator of SirT1, with that of exercise in inducing mitochondrial biogenesis. These experiments demonstrated that SirT1 plays a modest role in maintaining basal mitochondrial content and a larger role in preserving mitochondrial function. Furthermore, voluntary exercise and RSV treatment induced mitochondrial biogenesis in a SirT1-independent manner. However, when RSV and exercise were combined, a SirT1-dependent synergistic effect was evident, leading to enhanced translocation of PGC-1α and SirT1 to the nucleus and stimulation of mitochondrial biogenesis. Thus, the magnitude of the effect of RSV on muscle mitochondrial biogenesis is reliant on SirT1, as well as the cellular environment, such as that produced by repeated bouts of exercise.
Highlights
sirtuin 1 (SirT1) regulates mitochondrial biogenesis in various tissues
Because the effects of RSV and Contractile Activity (CA) on early signaling pathways linked to mitochondrial biogenesis were distinct, we combined these treatments in subsequent long term experiments (4-day protocol) to see if they exhibited an additive effect on mitochondrial content and function
The goal of this study was to delineate the role of SirT1 on mitochondrial function and biogenesis in both resting and exercising muscle and the consequent effects of the lack of SirT1 on muscle performance
Summary
Results: Exercise combined with resveratrol has a SirT1-dependent synergistic effect on mitochondrial biogenesis, despite individual treatments being SirT1-independent. Using muscle-specific SirT1-deficient (KO) mice and a cell culture model of differentiated myotubes, we compared the treatment of resveratrol, an activator of SirT1, with that of exercise in inducing mitochondrial biogenesis. These experiments demonstrated that SirT1 plays a modest role in maintaining basal mitochondrial content and a larger role in preserving mitochondrial function. When RSV and exercise were combined, a SirT1-dependent synergistic effect was evident, leading to enhanced translocation of PGC-1␣ and SirT1 to the nucleus and stimulation of mitochondrial biogenesis. The magnitude of the effect of RSV on muscle mitochondrial biogenesis is reliant on SirT1, as well as the cellular environment, such as that produced by repeated bouts of exercise
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