High Intensity Acute Aerobic Exercise Elicits Alterations in Circulating and Skeletal Muscle Tissue Expression of Neuroprotective Exerkines.
Autor: | Mazo CE; School of Kinesiology, University of Michigan, Ann Arbor, MI, USA., Miranda ER; School of Kinesiology, University of Michigan, Ann Arbor, MI, USA., Shadiow J; School of Kinesiology, University of Michigan, Ann Arbor, MI, USA., Vesia M; School of Kinesiology, University of Michigan, Ann Arbor, MI, USA., Haus JM; School of Kinesiology, University of Michigan, Ann Arbor, MI, USA. |
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Jazyk: | angličtina |
Zdroj: | Brain plasticity (Amsterdam, Netherlands) [Brain Plast] 2022 Oct 21; Vol. 8 (1), pp. 5-18. Date of Electronic Publication: 2022 Oct 21 (Print Publication: 2022). |
DOI: | 10.3233/BPL-220137 |
Abstrakt: | Background: Cathepsin B (CTSB) and brain derived neurotrophic factor (BDNF) are increased with aerobic exercise (AE) and skeletal muscle has been identified as a potential source of secretion. However, the intensity of AE and the potential for skeletal muscle contributions to circulating CTSB and BDNF have not been fully studied in humans. Objective: Determine the effects of AE intensity on circulating and skeletal muscle CTSB and BDNF expression profiles. Methods: Young healthy subjects ( n = 16) completed treadmill-based AE consisting of VO Results: Serum CTSB increased by 20±7% ( p = 0.02) and 30±18% ( p = 0.04) after 80% and VO Conclusions: High intensity AE elicits greater increases in circulating CTSB compared with lower intensities. Skeletal muscle protein and gene expression corroborate the potential role of skeletal muscle in generating and releasing neuroprotective exerkines into the circulation.NEW AND NOTEWORTHY: 1) CTSB is enriched in the circulation in an aerobic exercise intensity dependent manner. 2) Skeletal muscle tissue expresses both message and protein of CTSB and BDNF. 3) BDNF is highly expressed in glycolytic skeletal muscle fibers. Competing Interests: The authors have no conflict of interest to report. (© 2022 – The authors. Published by IOS Press.) |
Databáze: | MEDLINE |
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