The DOI matches its Crossref record; 41 of the 41 references it cites were found in a registry or an index.
Resistance Exercise Training Alters Mitochondrial Function in Human Skeletal Muscle
Open accessAbstract
INTRODUCTION: Loss of mitochondrial competency is associated with several chronic illnesses. Therefore, strategies that maintain or increase mitochondrial function will likely be of benefit in numerous clinical settings. Endurance exercise has long been known to increase mitochondrial function in the skeletal muscle. Comparatively little is known regarding the effect of resistance exercise training (RET) on skeletal muscle mitochondrial respiratory function. PURPOSE: The purpose of the current study was to determine the effect of chronic resistance training on skeletal muscle mitochondrial respiratory capacity and function. METHODS: Here, we studied the effect of a 12-wk RET program on skeletal muscle mitochondrial function in 11 young healthy men. Muscle biopsies were collected before and after the 12-wk training program, and mitochondrial respiratory capacity was determined in permeabilized myofibers by high-resolution respirometry. RESULTS: RET increased lean body mass and quadriceps muscle strength by 4% and 15%, respectively (P < 0.001). Coupled mitochondrial respiration supported by complex I, and complex I and II substrates increased by 2- and 1.4-fold, respectively (P < 0.01). The ratio of coupled complex I-supported respiration to maximal respiration increased with RET (P < 0.05), as did complex I protein abundance (P < 0.05), whereas the substrate control ratio for succinate was reduced after RET (P < 0.001). Transcripts responsible for proteins critical to electron transfer and NAD production increased with training (P < 0.05), whereas transcripts involved in mitochondrial biogenesis were unaltered. CONCLUSIONS: Collectively, 12 wk of RET resulted in qualitative and quantitative changes in skeletal muscle mitochondrial respiration. This adaptation was accompanied by modest changes in mitochondrial proteins and transcript expression. RET seems to be a means to augment the respiratory capacity and intrinsic function of skeletal muscle mitochondria.
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In the citing paper
“Resistance training helps mitigate these effects by maintaining muscle mass and preserving metabolic capacity, including mitochondrial function and glucose utilization.”
From Weight maintenance after discontinuation of GLP-1 therapies (2026) · cites this paper as [77]
Experimental — accuracy not yet measuredIn the citing paper
“strong evidence shows that PRT increases mitochondrial protein fractional synthesis rates [119,371] and improves mitochondrial function [119,372].”
From Global consensus on optimal exercise recommendations for enhancing healthy longevity in older adults (ICFSR) (2025) · cites this paper as [372]
In the citing paper
“More recently, strong evidence shows that PRT increases mitochondrial protein fractional synthesis rates [119,371] and improves mitochondrial function [119,372].”
From Global consensus on optimal exercise recommendations for enhancing healthy longevity in older adults (ICFSR) (2025) · cites this paper as [372]
In the citing paper
“Both endurance and resistance exercise have been associated with elevated mitochondrial biogenesis (93, 109).”
From Mitochondria initiate and regulate sarcopenia (2017) · cites this paper as [109]
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Metadata
- Authors
- PORTER, C., REIDY, P. T., BHATTARAI, N., SIDOSSIS, L. S., & RASMUSSEN, B. B.
- Affiliations
- Shriners Hospitals for Children - Galveston (US)
- The University of Texas Medical Branch at Galveston (US)
- Venue
- Medicine & Science in Sports & Exercise
- Published
- 2015-09
- Volume
- 47
- Issue
- 9
- Pages
- 1922-1931
- ISSN
- 0195-9131 (ISSN-L)
- PMC
- PMC4478283
- OpenAlex
- W2018607292
- Cited by
- 288
- References
- 40
- Citations by year
- 2026: 26 · 2025: 41 · 2024: 36 · 2023: 37 · 2022: 28 · 2021: 28 · 2020: 25 · 2019: 22 · 2018: 23 · 2017: 9 · 2016: 6 · 2015: 7
- FWCI
- 3.00
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Medicine & Science in Sports & Exercise (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health (UL1TR000071)
- National Institute on Aging (P30AG024832)
- National Institute of Arthritis and Musculoskeletal and Skin Diseases (R01AR049877)
- NIH Clinical Center
- National Center for Advancing Translational Sciences
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Health Sciences › Medicine › Physiology (medical) › Cardiovascular and exercise physiology
- Health Sciences › Medicine › Physiology (medical) › Exercise and Physiological Responses
- Keywords
- resistance training, skeletal muscle mitochondria, mitochondrial respiration, complex I, succinic acid, mitochondrial biogenesis, electron transfer, muscle strength, lean body mass, exercise adaptation
- MeSH terms
- Adult, Humans, Male, Mitochondria, Muscle, Physical Education and Training, RNA, Messenger, Body Mass Index, Muscle, Skeletal, Cell Respiration, Electron Transport Chain Complex Proteins, Muscle Strength, Resistance Training, Young Adult
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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