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During an acute bout of upright progressive exercise in a healthy, untrained person, stroke volume typically rises by 20-30% at low work intensities, then changes little (or 'plateaus') to the point of subject exhaustion.[1-3] The initial increase presumably reflects mobilization of blood sequestered by gravity in the lower extremities upon assuming the upright position,[4] as evidenced by failure to observe such a rise when exercise conditions are independent of gravity (supine cycling,[5,6] arm exercise,[7] weightlessness in space,[8] swimming[9] and aquatic exercise[10]). Other than during this initial phase of ventricular refilling, then, it can be assumed that stroke volume does not contribute to the rise in cardiac output during progressive upright exercise. (Some have contended that stroke volume may actually decrease in the last seconds of an exhaustive test.[11,12])
As work intensity increases, left ventricular end-diastolic dimension (LVED) in healthy subjects remains stable or slightly declines.[13,14] This more or less constant ventricular filling volume (preload) during progressive exercise is achieved as heart rate rises to match increases in systemic venous return (Bainbridge reflex).[15] Systolic and diastolic function improve in parallel as exercise intensity increases.[16] These changes in inotropic and lusitropic function serve to maintain a constant stroke volume and ventricular filling volume, respectively, as time periods of systolic ejection and diastolic filling shorten with increasing heart rate.
This model of cardiovascular response, derived from studies initially performed in the 1950s,[17] has been supported by more contemporary techniques.[2] It indicates a primary role of peripheral, non-cardiac factors (particularly fall in peripheral vascular resistance from arteriolar dilatation triggered by local metabolic regulators) in facilitating and controlling blood circulation with exercise. In this schema, the heart is relegated to a secondary role as a force-feed pump, its dynamics dictated by the magnitude of systemic venous return.
Highly trained endurance athletes are characterized by their superior cardiac functional capacity - higher maximal stroke volume and cardiac output - compared with non-athletes. Athletes have been found in some studies to exhibit the same pattern of stroke volume response to progressive exercise as non-athletes (a plateau after an early rise), their greater maximal values being accounted for by a shift upwards of the work intensity-stroke volume curve.[18,19] By this interpretation, functional characteristics of the heart are no different in endurance athletes than...