Cardiovascular Responses to Endurance Exercise

Endurance exercise imposes a sustained haemodynamic load on the heart and vasculature, eliciting both acute and chronic adaptations in structure, function and biomarker profiles. Acutely, prolonged exertion increases cardiac output through elevated heart rate and stroke volume, while diastolic filling and contractile mechanics may transiently decline, a phenomenon often termed exercise-induced cardiac fatigue. Circulating biomarkers such as cardiac troponins and natriuretic peptides rise in proportion to exercise intensity and duration, reflecting reversible myocardial stress rather than irreversible injury in most healthy individuals. Chronically, regular endurance training promotes eccentric ventricular remodelling, characterised by enlarged chamber volumes with preserved or enhanced systolic function, as well as improved endothelial function and reduced arterial stiffness. These adaptations underpin the cardiovascular protection conferred by habitual moderate-to-vigorous exercise, while also raising important questions about the limits of safe high-intensity or ultra-endurance participation.

Research from Nature Portfolio

Recent studies have probed how different endurance modalities influence myocardial biomarker release and cardiac dimensions without causing overt dysfunction. One foundational investigation compared short-duration repeated sprint sessions with moderate-intensity continuous running in healthy adults. Although repeated sprints generated significantly higher post-exercise rises in cardiac troponin T, serum lactate and perceived exertion, echocardiographic and electrocardiographic indices of ventricular function remained within normal ranges. These findings support a physiological interpretation of biomarker elevations during intermittent high-intensity endurance work and underscore the heart’s resilience to transient biochemical stress.

Cardiovascular Responses to Endurance Exercise publication trend

The graph below shows the total number of articles in cardiovascular responses to endurance exercise across all publications each year (not limited to Nature Index journals).

Technical terms

Cardiac troponin I (cTnI): A myocardial protein released into the circulation during cardiomyocyte stress or injury, used as a biomarker of exercise-induced myocardial strain.

Cardiac troponin T (cTnT): A regulatory protein in the cardiac contractile apparatus, whose elevation is more specific for pathological myocardial damage than cTnI in athletic settings.

Left ventricular ejection fraction (LVEF): The proportion of blood ejected from the left ventricle with each heartbeat, expressed as a percentage of end-diastolic volume.

Right ventricular fractional area change (RVFAC): A measure of right ventricular systolic function calculated from differences in end-diastolic and end-systolic areas on echocardiography.

Speckle-tracking echocardiography: An imaging technique that tracks natural acoustic markers (‘speckles’) within the myocardium to quantify strain and detect subtle changes in cardiac mechanics.

References

1. Cardiac troponin T and echocardiographic dimensions after repeated sprint vs. moderate intensity continuous exercise in healthy young males. Scientific Reports (2016).
2. Impact of an Ultra-Endurance Marathon on Cardiac Function in Association with Cardiovascular Biomarkers. Sports Medicine - Open (2024).
3. Differences in Troponin I and Troponin T Release in High-Performance Athletes Outside of Competition. International Journal of Molecular Sciences (2024).
4. Effects of Long-Term Endurance Exercise on Cardiac Morphology, Function, and Injury Indicators among Amateur Marathon Runners. International Journal of Environmental Research and Public Health (2023).