Match tier
Listed
Presence
Current · Arkansas
Last published
2026
Sources
OpenAlex · ORCID
Refreshed
2026-08-08
C
Research Areas
Biomedical Subjects
Biography and Research Information
OverviewAI-generated summary
Calvin Peterson studies molecular mechanisms of skeletal muscle adaptation, particularly in response to exercise and disease states. His research investigates the role of MYC in promoting muscle growth following resistance exercise in humans and examines the impact of tumor induction on myocellular adaptations in mice. Peterson's work also explores the protective effects of promoting mitochondrial fusion against cancer-induced muscle detriments and the sufficiency of global mitophagy inhibition in mitigating skeletal muscle impairments in tumor-bearing mice. He has published six articles, accumulating 45 citations, and holds an h-index of 4. Peterson collaborates with researchers at the University of Arkansas at Fayetteville, including Pieter J Koopmans, Francielly Morena da Silva, Sabin Khadgi, and Nicholas P. Greene, with whom he shares multiple publications.
Metrics
- h-index: 4
- Publications: 6
- Citations: 50
Selected Publications
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Exercise training prior to and during cancer in mice preserves muscle mass, reduces tumour weight and suppresses molecular mediators of cachexia (2026)
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Promoting mitochondrial fusion is protective against cancer-induced muscle detriments in males and females (2025)
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Global mitophagy inhibition via BNIP3 ablation is not sufficient to alleviate skeletal muscle impairments in male and female tumor-bearing mice (2025)
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Myocellular adaptations to short‐term weighted wheel‐running exercise are largely conserved during C26‐tumour induction in male and female mice (2025)
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The 24-hour molecular landscape after exercise in humans reveals MYC is sufficient for muscle growth (2024)
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The 24-Hour Time Course of Integrated Molecular Responses to Resistance Exercise in Human Skeletal Muscle Implicates <i>MYC</i> as a Hypertrophic Regulator That is Sufficient for Growth (2024)
Collaboration Network
Top Collaborators
Sabin Khadgi
University of Arkansas at Fayetteville
5 shared publications
In database
- The 24-hour molecular landscape after exercise in humans reveals MYC is sufficient for muscle growth
- The 24-Hour Time Course of Integrated Molecular Responses to Resistance Exercise in Human Skeletal Muscle Implicates <i>MYC</i> as a Hypertrophic Regulator That is Sufficient for Growth
- Promoting mitochondrial fusion is protective against cancer-induced muscle detriments in males and females
- Myocellular adaptations to short‐term weighted wheel‐running exercise are largely conserved during C26‐tumour induction in male and female mice
- Global mitophagy inhibition via BNIP3 ablation is not sufficient to alleviate skeletal muscle impairments in male and female tumor-bearing mice
Francielly Morena da Silva
University of Arkansas at Fayetteville
5 shared publications
In database
- The 24-hour molecular landscape after exercise in humans reveals MYC is sufficient for muscle growth
- The 24-Hour Time Course of Integrated Molecular Responses to Resistance Exercise in Human Skeletal Muscle Implicates <i>MYC</i> as a Hypertrophic Regulator That is Sufficient for Growth
- Promoting mitochondrial fusion is protective against cancer-induced muscle detriments in males and females
- Myocellular adaptations to short‐term weighted wheel‐running exercise are largely conserved during C26‐tumour induction in male and female mice
- Global mitophagy inhibition via BNIP3 ablation is not sufficient to alleviate skeletal muscle impairments in male and female tumor-bearing mice
Nicholas P. Greene
University of Arkansas at Fayetteville
5 shared publications
In database
- The 24-hour molecular landscape after exercise in humans reveals MYC is sufficient for muscle growth
- The 24-Hour Time Course of Integrated Molecular Responses to Resistance Exercise in Human Skeletal Muscle Implicates <i>MYC</i> as a Hypertrophic Regulator That is Sufficient for Growth
- Promoting mitochondrial fusion is protective against cancer-induced muscle detriments in males and females
- Myocellular adaptations to short‐term weighted wheel‐running exercise are largely conserved during C26‐tumour induction in male and female mice
- Global mitophagy inhibition via BNIP3 ablation is not sufficient to alleviate skeletal muscle impairments in male and female tumor-bearing mice
Kevin A. Murach
University of Arkansas at Fayetteville
5 shared publications
In database
- The 24-hour molecular landscape after exercise in humans reveals MYC is sufficient for muscle growth
- The 24-Hour Time Course of Integrated Molecular Responses to Resistance Exercise in Human Skeletal Muscle Implicates <i>MYC</i> as a Hypertrophic Regulator That is Sufficient for Growth
- Promoting mitochondrial fusion is protective against cancer-induced muscle detriments in males and females
- Myocellular adaptations to short‐term weighted wheel‐running exercise are largely conserved during C26‐tumour induction in male and female mice
- Global mitophagy inhibition via BNIP3 ablation is not sufficient to alleviate skeletal muscle impairments in male and female tumor-bearing mice
Pieter J. Koopmans
University of Arkansas at Fayetteville
3 shared publications
In database
- The 24-Hour Time Course of Integrated Molecular Responses to Resistance Exercise in Human Skeletal Muscle Implicates <i>MYC</i> as a Hypertrophic Regulator That is Sufficient for Growth
- Myocellular adaptations to short‐term weighted wheel‐running exercise are largely conserved during C26‐tumour induction in male and female mice
- Global mitophagy inhibition via BNIP3 ablation is not sufficient to alleviate skeletal muscle impairments in male and female tumor-bearing mice
Toby L. Chambers
University of Arkansas at Fayetteville
3 shared publications
In database
- The 24-hour molecular landscape after exercise in humans reveals MYC is sufficient for muscle growth
- Promoting mitochondrial fusion is protective against cancer-induced muscle detriments in males and females
- Global mitophagy inhibition via BNIP3 ablation is not sufficient to alleviate skeletal muscle impairments in male and female tumor-bearing mice
Stavroula Tsitkanou
University of Arkansas at Fayetteville
3 shared publications
In database
- Promoting mitochondrial fusion is protective against cancer-induced muscle detriments in males and females
- Myocellular adaptations to short‐term weighted wheel‐running exercise are largely conserved during C26‐tumour induction in male and female mice
- Global mitophagy inhibition via BNIP3 ablation is not sufficient to alleviate skeletal muscle impairments in male and female tumor-bearing mice
Ana Regina Cabrera
University of Arkansas at Fayetteville
3 shared publications
In database
- Promoting mitochondrial fusion is protective against cancer-induced muscle detriments in males and females
- Myocellular adaptations to short‐term weighted wheel‐running exercise are largely conserved during C26‐tumour induction in male and female mice
- Global mitophagy inhibition via BNIP3 ablation is not sufficient to alleviate skeletal muscle impairments in male and female tumor-bearing mice
Ruqaiza Muhyudin
University of Arkansas at Fayetteville
3 shared publications
In database
- Promoting mitochondrial fusion is protective against cancer-induced muscle detriments in males and females
- Myocellular adaptations to short‐term weighted wheel‐running exercise are largely conserved during C26‐tumour induction in male and female mice
- Global mitophagy inhibition via BNIP3 ablation is not sufficient to alleviate skeletal muscle impairments in male and female tumor-bearing mice
Tyrone A. Washington
University of Arkansas at Fayetteville
3 shared publications
In database
- Promoting mitochondrial fusion is protective against cancer-induced muscle detriments in males and females
- Myocellular adaptations to short‐term weighted wheel‐running exercise are largely conserved during C26‐tumour induction in male and female mice
- Global mitophagy inhibition via BNIP3 ablation is not sufficient to alleviate skeletal muscle impairments in male and female tumor-bearing mice
Sebastian Edman
Karolinska Institutet (SE)
2 shared publications
- The 24-hour molecular landscape after exercise in humans reveals MYC is sufficient for muscle growth
- The 24-Hour Time Course of Integrated Molecular Responses to Resistance Exercise in Human Skeletal Muscle Implicates <i>MYC</i> as a Hypertrophic Regulator That is Sufficient for Growth
Ronald G. Jones
University of Arkansas at Fayetteville
2 shared publications
In database
- The 24-hour molecular landscape after exercise in humans reveals MYC is sufficient for muscle growth
- The 24-Hour Time Course of Integrated Molecular Responses to Resistance Exercise in Human Skeletal Muscle Implicates <i>MYC</i> as a Hypertrophic Regulator That is Sufficient for Growth
Paulo R. Jannig
Karolinska Institutet (SE)
2 shared publications
- The 24-hour molecular landscape after exercise in humans reveals MYC is sufficient for muscle growth
- The 24-Hour Time Course of Integrated Molecular Responses to Resistance Exercise in Human Skeletal Muscle Implicates <i>MYC</i> as a Hypertrophic Regulator That is Sufficient for Growth
Rodrigo Fernandez‐Gonzalo
Karolinska University Hospital (SE)
2 shared publications
- The 24-hour molecular landscape after exercise in humans reveals MYC is sufficient for muscle growth
- The 24-Hour Time Course of Integrated Molecular Responses to Resistance Exercise in Human Skeletal Muscle Implicates <i>MYC</i> as a Hypertrophic Regulator That is Sufficient for Growth
Jessica Norrbom
Karolinska Institutet (SE)
2 shared publications
- The 24-hour molecular landscape after exercise in humans reveals MYC is sufficient for muscle growth
- The 24-Hour Time Course of Integrated Molecular Responses to Resistance Exercise in Human Skeletal Muscle Implicates <i>MYC</i> as a Hypertrophic Regulator That is Sufficient for Growth
Similar Researchers
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