Cardiac Output Enhancement: New Insights into the Mechanisms That Engage Diastolic Function Optimization during Aerobic Exercise

Aerobic exercise elicits profound cardiovascular adaptations focused on maximizing diastolic function, which enables the heart to meet the increased circulatory demands imposed by physical exertion. This chapter explores how the low-pressure compartments contribute to improving cardiac output through optimized diastolic filling. Central to these adaptations are structural and functional changes in venous conduit vessels, such as the inferior vena cava (IVC) and the pulmonary vasculature. Aerobic exercise-induced IVC remodeling, blood volume mobilization, and pulmonary transit time reduction all facilitate preload augmentation without significant increases in venous resistance. At the myocardial level, cardiac auxotonic relaxation supports early diastolic filling during shortened diastolic phases, aided by physiological left ventricular eccentric hypertrophy and coronary vascular expansion, which leads to metabolic balance between substrate supply and energy production. Another critical mediator of the processes enhancing diastolic function is adenosine, which not only promotes vasodilation in conduit and coronary vessels but also supports auxotonic relaxation and capillary angiogenesis. Together, these integrated adaptations in the venous, pulmonary, myocardial, and coronary systems underscore the critical role of diastolic enhancement in sustaining high cardiac output during aerobic performance. This chapter offers a comprehensive review of the structural and functional mechanisms underlying these processes and highlights the underappreciated but essential contributions of the low-pressure compartment in enhancing diastolic function and achieving maximal aerobic exercise capacity.