Blood flow restricted training leads to myocellular macrophage infiltration and upregulation of heat shock proteins, but no apparent muscle damage
| Autor: | Ulrik Frandsen, Tobias Nygaard, Jakob Lindberg Nielsen, Tatyana A. Prokhorova, Charlotte Suetta, Per Aagaard, Rune Dueholm Bech |
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| Rok vydání: | 2017 |
| Předmět: |
0301 basic medicine
medicine.medical_specialty Pathology Physiology Inflammation medicine.disease_cause 03 medical and health sciences 0302 clinical medicine Downregulation and upregulation Hsp27 Heat shock protein Internal medicine Medicine Kaatsu biology business.industry Skeletal muscle 030229 sport sciences 030104 developmental biology Endocrinology medicine.anatomical_structure biology.protein Tumor necrosis factor alpha medicine.symptom business Oxidative stress |
| Zdroj: | The Journal of Physiology. 595:4857-4873 |
| ISSN: | 0022-3751 |
| DOI: | 10.1113/jp273907 |
| Popis: | Previous studies indicate that low-load muscle contractions performed under local blood-flow restriction (BFR) may initially induce muscle damage and stress. However, whether these factors are evoked with longitudinal BFR training remains unexplored at the myocellular level. Two distinct study protocols were conducted (3 wk/1 wk). Subjects performed BFR exercise (100 mmHg, 20%-1RM) to concentric failure (BFRE) (3 wk/1 wk), while controls performed work-matched (LLE)(3 wk) or high-load (HLE; 70%-1RM)(1 wk), free-flow exercise. Muscle biopsies (3 wk) were obtained at baseline (Pre), 8 days into the intervention (Mid8) and 3 and 10 days after training cessation (Post3,Post10) to examine macrophage (M1/M2) content as well as heat-shock protein (HSP27/70) and tenascin-C expression. Blood samples (1 wk) were collected before and after (0.1–24 h) the first and last training session to examine markers of muscle damage (CK), oxidative stress (TAC,GSH) and inflammation (MCP1,IL-6,TNFa). M1-macrophage content increased 108–165% with BFRE and LLE at Post3 (P |
| Databáze: | OpenAIRE |
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