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- W2593229620 abstract "Exercise is the most effective treatment for sarcopenia, the age-related loss of muscle mass and function. Despite its positive effects, many studies indicate that adaptive signaling with exercise is altered or attenuated with age. We and others have found that aging muscle presents with increased mitochondrial reactive oxygen species (ROS) generation, decreased mitochondrial function, and an oxidized redox status. The extent to which mitochondrial ROS contribute to exercise adaptation and excitation/contraction (EC) coupling remains controversial, but evidence suggests that oxidative modifications to protein thiols may alter the activity of transcription factors, kinases, and the function of contractile proteins. In this study, we hypothesized that an acute decrease in mitochondrial ROS will rescue the age-related changes in skeletal muscle EC coupling and contractile signaling. To test this hypothesis, we performed acute fatiguing contractions using an in vivo stimulation protocol on young (7-10 months) and old (28-32 month) CB6F1 (BALB/cBy x C57BL/6) mice pretreated for one hour with elamipretide (SS-31), a mitochondrially-targeted peptide that reduces mitochondrial ROS and improves bioenergetics in dysfunctional mitochondria. Contraction kinetics were monitored by a force transducer throughout the fatiguing stimulations, and the phosphorylation status of AKT, P38/MAPK, AMPK, and P70S6K were measured in the stimulated and non-stimulated gastrocnemius to address the extent of contractile signaling. Force production was significantly lower in the aged mice compared to young, consistent with sarcopenia. One hour of SS-31 restored the age-related loss of contraction and relaxation rates, but no changes in fatigability or max contraction were observed. In vivo stimulation resulted in significant changes in kinase phosphorylation, however, exercise induced changes in AKT were blunted in aged muscle, but restored with SS-31. Together, these data suggest a direct role of mitochondrial ROS and bioenergetics on EC coupling and kinase activity, and implicate the use of mitochondrially-targeted therapies to improve exercise adaptation in aged muscle." @default.
- W2593229620 created "2017-03-16" @default.
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- W2593229620 date "2016-11-01" @default.
- W2593229620 modified "2023-09-27" @default.
- W2593229620 title "Mitochondrially-Targeted Intervention to Improve Contractile Signaling and Kinetics in Aged Muscle" @default.
- W2593229620 doi "https://doi.org/10.1016/j.freeradbiomed.2016.10.213" @default.
- W2593229620 hasPublicationYear "2016" @default.
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