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Impact of acute exercise on peripheral blood mononuclear cells nutrient sensing and mitochondrial oxidative capacity in healthy young adults
Regular exercise is associated with changes in peripheral blood mononuclear cell (PBMC) proportions that have enhanced effector functions in young and old adults; however, the effects of acute exercise on PBMC nutrient sensors and metabolic function in active young adults is unknown. To fill this ga...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
John Wiley and Sons Inc.
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8661513/ https://www.ncbi.nlm.nih.gov/pubmed/34889067 http://dx.doi.org/10.14814/phy2.15147 |
Sumario: | Regular exercise is associated with changes in peripheral blood mononuclear cell (PBMC) proportions that have enhanced effector functions in young and old adults; however, the effects of acute exercise on PBMC nutrient sensors and metabolic function in active young adults is unknown. To fill this gap, activation status and nutrient‐sensing mechanisms of PBMCs isolated from 21 healthy active adults (20–35 yr; 36.5 ± 6.3 V̇O(2peak)) were characterized before and after 30 min of moderate‐to‐vigorous cycling (65%–75% V̇O(2peak)). In addition, changes in PBMC mitochondrial respiratory function in response to exercise were assessed using high‐resolution respirometry. There was an increase in the number of activated CD69+/CD4 (79% increase) and CD69+/CD8 (166% increase) T‐cells in response to the acute bout of exercise, while the nutrient‐sensing mechanisms remained unchanged. PBMC mitochondrial respiration did not increase on a cell‐per‐cell basis, however, mitochondrial oxidative capacity (OXPHOS) increased at the tissue level (18.6 pmol/(s*ml blood) versus 29.3 pmol/(s*ml blood); p < 0.05) in response to acute exercise. Thus, this study shows that acute exercise preferentially mobilizes activated T‐cells while concomitantly increasing PBMC mitochondrial oxidative capacity at the tissue level, rather than acutely changing mitochondrial oxidative capacity at the cellular level in young adults. |
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