Mobilisation of mesenchymal cells in cardiac patients: is intense exercise necessary?
A Lucia1, A De La Rosa, M Avila Silván
1Universidad Europea deMadrid, Spain. alejandro.lucia@uem.es
Insights
Intense exercise, particularly near myocardial ischemia, significantly increases circulating mesenchymal cells (cMCs). This finding suggests high-intensity physical activity may stimulate these cells for tissue repair.
Area of Science:
- Cardiovascular Medicine
- Regenerative Medicine
- Exercise Physiology
Background:
- Circulating mesenchymal cells (cMCs) show potential for damaged tissue regeneration, including ischemic myocardium.
- Understanding factors that mobilize cMCs is crucial for regenerative therapies.
Purpose of the Study:
- To investigate the effect of dynamic exercise intensity on circulating mesenchymal cell (cMC) levels in patients with stable coronary artery disease.
- To determine if exercise-induced myocardial ischemia influences cMC mobilization.
Main Methods:
- Assessed cMCs in patients (53-76 years) with stable coronary artery disease before and after exercise.
- Compared moderate-intensity exercise (< respiratory compensation threshold) versus high-intensity exercise (>RCT).
- Monitored for signs of myocardial ischemia and ventricular extrasystoles during exercise.
Main Results:
- High-intensity exercise significantly increased cMC levels (p = 0.009).
- This increase occurred in patients experiencing signs of myocardial ischemia or ventricular extrasystoles.
- Moderate-intensity exercise did not induce a significant change in cMCs.
Conclusions:
- Intense dynamic exercise, especially when approaching myocardial ischemia, is a potent stimulus for mobilizing circulating mesenchymal cells.
- These findings support the hypothesis that exercise-induced ischemia may enhance cMC availability for potential tissue repair mechanisms.
Abstract:
Circulating mesenchymal cells (cMCs) have a potential for regenerating damaged tissue, e.g., ischaemic myocardium. In patients (age range: 53-76 years) with stable coronary artery disease cMCs were determined before and after dynamic exercise of moderate (< respiratory compensation threshold (RCT)) (n = 9 patients) or high intensity (>RCT) (n = 11). Only high-intensity exercise (i.e., provoking signs of myocardial ischaemia in 3 patients and ventricular extrasystoles in another) induced a significant increase in cMCs (p = 0.009). These results support the hypothesis that intense exercise (near or at the point of myocardial ischaemia) is a potent stimulus for MC mobilisation.
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