ArticleJournal of the International Society of Sports Nutrition2023
The dose-response effects of arachidonic acid on primary human skeletal myoblasts and myotubes.
Article in Journal of the International Society of Sports Nutrition, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
6 citing papers in PubMed, 17 citations in OpenAlex.
- A single, maximal dose of celecoxib, ibuprofen, or flurbiprofen does not reduce the muscle signalling response to plyometric exercise in young healthy adults.European journal of applied physiology · 2024Trial
- Dietary omega-6 arachidonic acid and omega-3 docosahexaenoic acid supplementation differentially impact skeletal muscle inflammaging in mice.bioRxiv : the preprint server for biology · 2026Article
- Ibuprofen, Flurbiprofen or Naproxen Sodium Minimally Influences Musculoskeletal Adaptations to Treadmill Exercise in Rats.Journal of cachexia, sarcopenia and muscle · 2025Article
- The dose-response effects of flurbiprofen, indomethacin, ibuprofen, and naproxen on primary skeletal muscle cells.Journal of the International Society of Sports Nutrition · 2024Article
- Article
- Differential activation of AKT isoforms by growth factors in human myotubes.Physiological reports · 2023Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Cellular inflammatory response, mediated by arachidonic acid (AA) and cyclooxygenase, is a highly regulated process that leads to the repair of damaged tissue. Recent studies on murine C2C12 cells have demonstrated that AA supplementation leads to myotube hypertrophy. However, AA has not been tested on primary human muscle cells. Therefore, the purpose of this study was to determine whether AA supplementation has similar effects on human muscle cells. Methods: Proliferating and differentiating human myoblasts were exposed to AA in a dose-dependent manner (50-0.80 µM) for 48 (myoblasts) or 72 (myotubes) hours. Cell viability was tested using a 3-(4,5-Dimethylthiazol-2-Yl)-2,5-Diphenyltetrazolium Bromide (MTT) assay and cell counting; myotube area was determined by immunocytochemistry and confocal microscopy; and anabolic signaling pathways were evaluated by western blot and RT-PCR. Results: Our data show that the treatment of primary human myoblasts treated with 50 µM and 25 µM of AA led to the release of PGE Conclusion: Together, our data demonstrate that high concentrations of AA inhibit myoblast proliferation, myotube fusion, and myotube hypertrophy, thus revealing potential deleterious effects of AA on human skeletal muscle cell health and viability.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.