Effects of Intense Physical Training on Left Ventricular Hemodynamic Forces in Endurance Athletes: A Feature-Tracking Cardiac Magnetic Resonance Study.

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Tác giả: Makhabbat Bekbossynova, Tairkhan Dautov, Dinara Jumadilova, Zaukiya Kamitova, Nail Khissamutdinov, Yeltay Rakhmanov, Alessandro Salustri, Bauyrzhan Toktarbay, Aizhan Zankorazhova, Nurmakhan Zholshybek

Ngôn ngữ: eng

Ký hiệu phân loại:

Thông tin xuất bản: United States : Medicine and science in sports and exercise , 2025

Mô tả vật lý:

Bộ sưu tập: NCBI

ID: 707800

 PURPOSE: We sought to evaluate the effect of intensive physical training on left ventricular (LV) hemodynamic forces (HDF) in athletes. METHODS: Forty professional endurance athletes were evaluated at the beginning of their training cycle (off-season) and after a period of aerobic isotonic dynamic exercise (peak training period) using cardiac magnetic resonance (CMR). Images were analyzed off-line using dedicated software. LV HDF for the whole cardiac cycle and the different cardiac phases were measured. Standard statistics were used to compare off-season and peak training period values. RESULTS: The average sport experience was 11 ± 7 years. There were no differences in LV volumes, stroke volume, LVEF and LV mass between off-season and peak training CMR. Similarly, there were no changes induced by physical training in the strain parameters. Physical training induced a significant increase of the longitudinal HDF (18.7 vs 21.2, p = 0.023) and an increase of the transverse HDF (3.4 vs 4.0, p = 0.048) throughout the entire heartbeat. After physical training, the peak values and the hemodynamic work (expressed as AUC) of the first part of the systole were significantly higher compared to off-season values (63.9 vs 53.9, p = 0.034
  4.67 vs 3.79, p = 0.015, respectively). The difference in the elastic rebound between off-season and peak training (-0.22 vs -0.37) did not reach statistical significance (p = 0.056). CONCLUSIONS: Intense physical training induces an increase in LV HDF of the first part of the systole and of the elastic rebound phase, independent from geometric cardiac remodeling.
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