Endurance training restores ageing-impaired lysosomal biogenesis factors in rest and response to acute exercise in rat skeletal muscle
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Lysosomes, crucial for autophagy, play a pivotal role in cellular processes influenced by exercise. This study investigates the impact of ageing on lysosomal function, focusing on Transcription Factor E3 and its regulators, mTORC1 and Calcineurin, emphasizing their response and adaptation to endurance training. Twenty-five male Sprague-Dawley rats were categorised into Young (2 months), Aged sedentary and Aged sedentary single session (18 months), Aged long-term trained, and Aged trained-single session (17 months). Changes in variables were explored concerning sarcopenia by Soleus muscle fibre diameter and number measured via Eosin & Hematoxylin, phosphorylated and total TFEB protein levels via western blot, mTORC1 and Calcineurin mRNA levels via real-time PCR. Ageing happened with increased pTFE3/TFE3 total protein (BF=579) and declined mTORC1 mRNA (BF=3.99) and muscle diameter (BF=87), signifying sarcopenia and potential contributors. Conversely, Calcineurin mRNA (BF=0.67) and muscle fibre number (BF=0.31) remained unaltered during ageing. Endurance exercise induced acute responses, reducing pTFE3/TFE3 total protein (BF=306) and elevating mTORC1 (BF=1.57) and Calcineurin mRNA levels (BF=3.19). Three weeks of endurance training further decreased resting pTFE3/TFE3 total protein (BF=174) while increasing Calcineurin mRNA (BF=12), and muscle fibre diameter (BF=126), with no changes in mTORC1 mRNA levels (BF=0.46) and muscle fibre number. Post-exercise, trained rats sustained decreased pTFE3/TFE3 total protein (BF=56) and elevated mTORC1 mRNA (BF=1.16). In conclusion, this study underscores the involvement of TFE3, MTORC1, and Calcineurin in sarcopenia, proposing endurance training as an effective strategy to mitigate age-related changes and enhance muscle function in aged rats. Additionally, it suggests impairments in TFE3 possibly contribute to sarcopenia in ageing.
key point
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Given the pivotal role lysosomes play in multiple homeostatic processes, investigating mTORC1, Calcineurin, and TFE3, an overlooked lysosome biogenesis factor directly involved in the metabolic effects of exercise, could help understand the metabolic state of sarcopenia and the role exercise plays in it.
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Through eosin & hematoxylin, western blotting and real-time PCR, we found Aging results in Sarcopenia, reduced TFE3 activity and mTORC1 gene expression.
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We saw a single bout of exercise elicit a response by increasing TFE3 protein activation, mTORC1, and Calcineurin gene expression, which is directed to improved sarcopenia.
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Three weeks of exercise improved sarcopenia and was accompanied by elevated only with resting levels of TFE3 protein activation, and Calcineurin gene expression.
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Endurance training was still able to licit post exercise response in TFE3 protein activation, and Calcineurin gene expression
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Endurance training is a beneficial remedy for sarcopenia, and TFE3 protein is a major crucial player in inducing its effects.
