High-volume endurance exercise training stimulates hematopoiesis by increasing ACE NH2-terminal activity

Area of Science:

• Physiology
• Hematology
• Exercise Science

Background:

• Endurance exercise training (ET) benefits health by stimulating hematopoiesis.
• Mechanisms of ET-induced hematopoietic adaptations are not fully understood.
• N-Acetyl-Seryl-Aspartyl-Lysyl-Proline (Ac-SDKP) inhibits hematopoietic progenitor cell proliferation.
• Angiotensin I-converting enzyme (ACE) NH2-terminal activity promotes hematopoiesis by counteracting Ac-SDKP.

Purpose of the Study:

• To investigate the role of ACE NH2-terminal activity in ET-induced hematopoietic adaptations.
• To elucidate the relationship between ACE, Ac-SDKP, and hematopoiesis following endurance exercise.

Main Methods:

• Wistar rats underwent 10 weeks of moderate- (T1) and high- (T2) volume swimming training.
• Plasma ACE NH2-domain activity and Ac-SDKP levels were measured.
• Hematopoietic stem cells (HSCs), erythroid progenitor colonies, and reticulocytes were quantified.
• Erythrocyte lifespan was assessed.
• The effect of ACE NH2-terminal inhibition (captopril) on ET-induced changes was evaluated.

Main Results:

• High-volume training (T2) significantly increased plasma ACE NH2-domain activity (40%) and decreased Ac-SDKP levels (50%).
• T2 elevated HSCs (∼200%), early erythroid progenitor colonies (∼300%), and reticulocytes (∼500%), while reducing erythrocyte lifespan (∼50%).
• ACE NH2-terminal inhibition with captopril prevented Ac-SDKP reduction and attenuated ET-induced hematopoietic adaptations.

Conclusions:

• ET-induced hematopoiesis is, at least partially, mediated by increased ACE NH2-terminal activity.
• This process involves a reduction in the hematopoietic inhibitor Ac-SDKP.
• ACE NH2-terminal activity plays a crucial role in exercise-related blood cell production.