Editorial: Cardiovascular responses to exercise: clinical and pathological perspectives in athletes

It is well known and accepted that regular physical activity is a cornerstone of cardiovascular health and longevity, yet the spectrum of cardiovascular responses to exercise extends beyond merely beneficial adaptation. Increasing recognition of exercise-induced arrhythmias, maladaptive remodeling, and sudden cardiac death, particularly among the athletic population, has sharpened the need for nuanced, mechanistically informed investigation. This research topic, Cardiovascular Responses to Exercise: Clinical and Pathological Perspectives in Athletes, was designed to address this complexity by bringing together clinical, translational, and mechanistic studies that examine how exercise influences cardiovascular structure, function, and risk.The eight articles published within this special topic collectively highlight the dual nature of exercise as both a potent therapeutic intervention and a contributor to pathological cardiovascular remodeling, under specific conditions. Importantly, the articles published within this topic highlight the value of advanced imaging, rigorous physiological assessment, and individualized exercise prescription in separating adaptive from maladaptive responses.Several contributions focus on structural and functional cardiac remodeling in response to sustained exercise. The study of amateur marathon runners from Wang et al. [1] provides critical insight into left ventricular hypertrophy (LVH) as a potential marker of excessive cardiac remodeling. Using pressure-strain loop-derived myocardial work indices, the authors demonstrate that while moderate exercise adaptations are associated with higher global myocardial work, excessive weekly running distance correlates with reduced myocardial work efficiency and increased wasted work, particularly in male athletes. These findings refine the concept of the "athlete's heart" by suggesting that myocardial efficiency may serve as a more sensitive indicator of maladaptive remodeling compared with myocardial size and mass alone. At the mechanistic level, a preclinical study from Jun Zhang and colleagues [5]