High-volume endurance exercise training stimulates hematopoiesis by increasing ACE NH2-terminal activity
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Tipo de produção
article
Data de publicação
2021
Título da Revista
ISSN da Revista
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Editora
PORTLAND PRESS LTD
Autores
MAGALHAES, Flavio de Castro
FERNANDES, Tiago
BASSANEZE, Vinicius
MATTOS, Katt Coelho
SCHETTERT, Isolmar
NAVA, Roberto
BARAUNA, Valerio Garrone
OLIVEIRA, Edilamar Menezes de
Citação
CLINICAL SCIENCE, v.135, n.20, p.2377-2391, 2021
Resumo
One of the health benefits of endurance exercise training (ET) is the stimulation of hematopoiesis. However, the mechanisms underlying ET-induced hematopoietic adaptations are understudied. N-Acetyl-Seryl-Aspartyl-Lysyl-Proline (Ac-SDKP) inhibits proliferation of early hematopoietic progenitor cells. The angiotensin I-converting enzyme (ACE) NH2-terminal promotes hematopoiesis by inhibiting the anti-hematopoietic effect of Ac-SDKP. Here we demonstrate for the first time the role of ACE NH2-terminal in ET-induced hematopoietic adaptations. Wistar rats were subjected to 10 weeks of moderate-(T1) and high-(T2) volume swimming-training. Although both protocols induced classical ET-associated adaptations, only T2 increased plasma ACE NH2-domain activity (by 40%, P=0.0003) and reduced Ac-SDKP levels (by 50%, P<0.0001). T2 increased the number of hematopoietic stem cells (HSCs; similar to 200%, P=0.0008), early erythroid progenitor colonies (similar to 300%, P<0.0001) and reticulocytes (similar to 500%, P=0.0007), and reduced erythrocyte lifespan (similar to 50%, P=0.022). Following, Wistar rats were subjected to T2 or T2 combined with ACE NH2-terminal inhibition (captopril (Cap) treatment: 10 mg.kg(-1).day(-1)). T2 combined with ACE NH2-terminal inhibition prevented Ac-SDKP decrease and attenuated ET-induced hematopoietic adaptations. Altogether, our findings show that ET-induced hematopoiesis was at least partially associated with increased ACE NH2-terminal activity and reduction in the hematopoietic inhibitor Ac-SDKP.
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Referências
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