Hyperactive muscle mTORC1 attenuates functional adaptations to endurance training despite alterations in mitochondrial and lipid profiles

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Authors: Hanna Kalenta, Erik D. Marchant, Sean Paul Kilroe, Rosario Maroto, Jacquelyn T. May, Vladislav Bugay, Trevor B. Romsdahl, Jennifer J. Linares, Mandy R. Hinojosa, Zhao Lai, William K. Russell, Blake B. Rasmussen
Cited by: 1
References: 55

Abstract

Endurance exercise training in mice with hyperactive muscle mechanistic target of rapamycin complex I (mTORC1) was associated with increase in mitochondrial activity and TA muscle mass despite lack of changes in physical function. These findings could be attributed to altered autophagy-related signaling and a reduction in the phosphorylation of ribosomal protein S6, downstream target of mTORC1, after exercise training in DEPDC5 mKO mice. Reduction in phosphatidylcholines (PCs) and triglycerides (TGs) may suggest an increase in lipid fuel use and alterations in lipid membrane composition due to an increase in mitochondrial activity.

Fields of Study & Subjects

Muscle Physiology and Disorders Adipose Tissue and Metabolism Mitochondrial Function and Pathology

Publication details

Journal / source
Journal of Applied Physiology
Publisher
American Physiological Society
Volume
140
Issue
5
Pages
1338–1354
Publication date
14 April 2026
Language
EN