Oliver's mTOR Atlas Evidence Platform
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James A. Carson

Muscle physiologist studying cancer-associated cachexia and how chemotherapy and exercise remodel skeletal-muscle metabolism

Professor, Department of Kinesiology & Sport Management, and Executive Director, Huffines Institute for Sports Medicine & Human Performance, Texas A&M University (since 2024) · formerly Senior Associate Dean for Research and Graduate Studies, College of Health Professions, University of Tennessee Health Science Center (2018–2024) · 19 years on faculty at the University of South Carolina, where he built its muscle-biology research program and directed its Exercise Science PhD program

Integrative Muscle Biology Laboratory, Texas A&M University (College Station, Texas, USA) ↗ ORCID0000-0003-3733-8796 ↗

Carson leads the Integrative Muscle Biology Laboratory and is among the field's established voices on cancer-associated cachexia — the muscle wasting that accompanies tumours and their treatment. He moved the laboratory to Texas A&M University in 2024, after six years at the University of Tennessee Health Science Center (2018–2024) and, before that, 19 years at the University of South Carolina building a muscle-biology research program and its Exercise Science doctoral program.

His laboratory combines in vivo and in vitro models to examine how mechanical, inflammatory and hormonal signals converge on skeletal-muscle anabolic and metabolic plasticity. The 2026 study he senior-authored asked a narrower version of that question: whether the muscle damage caused by FOLFOX chemotherapy runs through mTORC1 and AMPK's control of autophagy, and whether rapamycin — by restoring autophagy flux — could partly undo it.

Milestones in the Atlas

YearEvidenceStudy
2026 M 5-Fluorouracil-based chemotherapy disrupts autophagy flux and protein synthesis in cultured myotubes: a role for mTORC1 signaling HAL2026 Senior and corresponding author; his laboratory's long-standing work on cancer-associated cachexia framed the study's focus on chemotherapy-induced disruption of muscle mTORC1/AMPK signalling.

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