Hyperactive muscle mTORC1 attenuates functional adaptations to endurance training despite alterations in mitochondrial and lipid profiles
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.
Authors
- Blake B. Rasmussen (ORCID: https://orcid.org/0000-0001-7854-5375)
- Jennifer J. Linares
- William K. Russell (ORCID: https://orcid.org/0000-0003-1931-4555)
- Sean P. Kilroe
- Vladislav Bugay
- Trevor B. Romsdahl (ORCID: https://orcid.org/0000-0001-9075-9771)
- Erik D. Marchant (ORCID: https://orcid.org/0000-0002-2222-7594)
- Rosario Maroto
- Jacquelyn May
- Hanna Kalenta (ORCID: https://orcid.org/0009-0000-7965-4733)
- Mandy R. Hinojosa
- Zhao Lai
Institutions
- The University of Texas at San Antonio Health Science Center (US)
- The University of Texas Medical Branch at Galveston (US)
Publication Details
- Journal
- Journal of Applied Physiology
- Published
- 2026-04-14
- DOI
- https://doi.org/10.1152/japplphysiol.00730.2025
- Primary Topic
- Muscle Physiology and Disorders
- Type
- article
- Field-Weighted Citation Impact
- 0.00
Funders
- Cancer Prevention and Research Institute of Texas
- National Institute on Aging
- NIH Office of the Director
- National Cancer Institute