Physical Activity, Blood Pressure, and Cardiac Structure and Function

Increased cardiac wall thickness, left ventricular (LV) chamber enlargement, and left ventricular hypertrophy (LVH) are characteristics of chronic, vigorous exercise endured by athletes and commonly referred to as “the athlete’s heart.” These cardiac structural and functional adaptations are specific to the workload demands imposed upon the myocardium, are considered normal physiologic responses, and are not associated with adverse prognosis. However, in young athletes, a thorough examination should be performed by a cardiologist to differentiation between physiological LVH (athlete’s heart) and hypertrophic cardiomyopathy, the commonest cause of non-traumatic exercise-related sudden cardiac death. Perhaps exercise-induced cardiac structural adaptations that improve cardiac efficiency and ultimately accommodate the imposed physiologic demand should be referred to as eutrophic. Conversely, hypertrophic cardiac adaptations should be considered exclusively those imposed by pathophysiologic and encroach upon cardiac efficiency, ultimately leading to compromised cardiac dysfunction and even death. Systolic blood pressure (BP) during daily activities may present the strongest impetus for cardiac adaptations. Exercise systolic BP ≥150 mmHg at the workload of approximately 4-5 METs (first stage of the Bruce protocol) closely represents the daily hemodynamic load threshold for cardiac adaptations. Moderate-intensity aerobic training lowers exercise systolic BP at absolute and maximal workloads, leading to a relatively lower hemodynamic load during daily activities and ultimately lowering the stimulus for increase in LV mass. This is in line with the LVH regression reported by aerobic exercise intervention studies.