ArticleEuropean journal of applied physiology2021
Long-term physical training in adolescent sprint and middle distance swimmers alters the composition of circulating T and NK cells which correlates with soluble ICAM-1 serum concentrations.
Article in European journal of applied physiology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed, 4 citations in OpenAlex.
- Regulatory mechanisms of high-polyphenol dietary intervention on exercise-induced immunosuppression during high-intensity training periods in adolescent athletes: a systems biology analysis based on immune-metabolic pathways.Nutrition & metabolism · 2026Article
- One Sprinter, Two Olympic Preparations: A Single-Athlete Longitudinal Observational Study of Training-Intensity Distribution and Implications for Future 50 m Events.Sports (Basel, Switzerland) · 2026Article
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Authors and funding
6 authors at 2 institutions in 1 country.
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Abstract
purposeIt remains unknown how different training intensities and volumes chronically impact circulating lymphocytes and cellular adhesion molecules. First, we aimed to monitor changes in NK and T cells over a training season and relate these to training load. Second, we analyzed effects of training differences between swimmers on these cells. Finally, we examined if changes in lymphocytes were associated with sICAM-1 concentrations.
methodsWe analyzed weekly training volume, training intensity, proportions of T and NK cells and serum sICAM-1 in eight sprint (SS) and seven middle-distance swimmers (MID) at three points over a 16-week training period: at the start (t
resultsTraining volume of all swimmers was statistically higher and training intensity lower from t
conclusionThese results indicate that intensified training in swimmers resulted in transient changes in T and NK cells. Further, NK cells are sensitive to high training volumes. Lastly, sICAM-1 concentrations may be associated with the migration and maturation of CD4
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