Physical Activity and Cardiac Morphologic Adaptations

Chronic and intense exercise programs lead to cardiac adaptations, followed by increased left ventricular wall thickness cavity diameter, at times meeting the criteria for hypertrophy (LVH), commonly referred as “athlete’s heart”. Recent studies have also reported that extremely vigorous practices been associated with heightened trabeculation extent, fulfilling noncompaction cardiomyopathy criteria, part of exercise-induced structural adaptation. These changes are specific type, intensity, duration, volume workload demands imposed on myocardium. They considered physiologic adaptations not a negative prognosis. Conversely, hypertrophic resulting from chronic elevations in blood pressure (BP) or overload due valvular regurgitation, compromised function, cardiovascular events, even death. In younger athletes, (HCM) is usual cause non-traumatic, exercise-triggered sudden Thus, an extended examination should be performed, differentiate between HCM non-pathological exercise-related LVH athlete’s heart. The functional normal responses designed accommodate exercise. we propose such defined “eutrophic” reserved pathologic adaptations. Systolic BP during daily activities may strongest predictor metabolic demand most approximately 3–5 equivalents (METs) (1 MET = 3.5 mL O2 kg body weight per minute). This similar treadmill first stage Bruce protocol. Some evidence supports systolic response ≥150 mmHg end strong hypertrophy, this reflects hemodynamic burden physical tasks. Aerobic training moderate intensity lowers resting absolute workloads, leading lower activities, ultimately reducing stimulus LVH. mechanism explains significant regression addressed aerobic intervention clinical studies.