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Cardiac function after exhaustive open-sea swimming
S Alexiou1, E Kouidi, A Fahadidou-Tsiligiroglou
1Laboratory of Sports Medicine, TEFAA, Aristotle University of Thessaloniki, Thessaloniki, Greece.
The Journal of Sports Medicine and Physical Fitness
|October 7, 2005
Summary
Exhaustive 25-km swimming significantly impairs left ventricular (LV) function in elite athletes, primarily due to increased afterload. This results in reduced ejection fraction and stroke volume, impacting cardiac performance.
Area of Science:
- Cardiology
- Sports Medicine
- Exercise Physiology
Background:
- Elite athletes push physiological limits during prolonged endurance events.
- Understanding cardiac adaptations and potential impairments post-exercise is crucial for athlete health.
- Open-sea swimming presents unique physiological demands compared to pool-based training.
Purpose of the Study:
- To investigate the acute effects of a 25-km open-sea swim on left ventricular (LV) function and morphology.
- To assess cardiac sympathetic outflow and key hematological markers post-exhaustive swimming.
Main Methods:
- Echocardiography and cardiovascular tracings were used to evaluate LV function and morphology pre- and post-swim.
- Blood samples were analyzed for hematocrit and plasma concentrations of various biomarkers (e.g., a-ANP, renin, lactate).
- Twenty elite male swimmers participated in this exhaustive 25-km open-sea swimming study.
Main Results:
- Significant reductions in LV fractional shortening (-13%), ejection fraction (-11%), and stroke volume (-25%) were observed.
- Increased cardiac index (+31%) and significantly elevated LV wall stress (+101-102%) indicated higher afterload.
- Post-exercise blood analysis revealed elevated hematocrit, a-ANP, renin, lactate, myoglobin, and CPK-MB.
Conclusions:
- Prolonged exhaustive swimming leads to depressed LV function in elite athletes.
- Reduced stroke volume and ejection fraction are key indicators of this functional impairment.
- Increased afterload is identified as the primary factor contributing to the observed cardiac alterations.