Abstract
The hemodynamic consequences of aging have been extensively investigated during maximal incremental exercise. However, less is known about the effects of aging on hemodynamics during submaximal steady-state exercise. The aim of the present investigation was to compare the hemodynamics of healthy elderly and young subjects during an exercise bout conducted at the gas threshold (GET) intensity. Two groups of healthy, physically active subjects were studied: the elderly group—EG (n = 11; > 60 years old) and the young group—YG (n = 13; < 35 years old). Both groups performed a 5-min rectangular exercise test at the GET intensity. Hemodynamics were measured using echocardiography. The main finding was that stroke volume responses were higher in the YG than the EG (72.5 ± 16.7 vs. 52.4 ± 8.4 ml, respectively). The increased stroke volume capacity in the YG was the consequence of a greater capacity to increase cardiac preload and contractility and, to a lesser extent, to reduce systemic vascular resistance. Importantly, the atrial contribution to ventricular diastolic filling was substantially higher in the YG when compared to the EG.
Highlights
The hemodynamic consequences of aging have been extensively investigated during maximal incremental exercise
Maximum heart rate (HR) ( HRmax), Wmax, V O2max, maximum carbon dioxide production ( V CO2max), and maximum pulmonary ventilation ( VEmax) were all higher in the young group (YG) compared to the EG, whereas the maximum respiratory exchange ratio (RER) was not significantly different
Information about expected values may aid in establishing targets and providing parameters to evaluate the impact of training interventions
Summary
The hemodynamic consequences of aging have been extensively investigated during maximal incremental exercise. The cardiovascular response during exercise encompasses complex changes in heart rate (HR), myocardial contractility, preload, and afterload[2–7] This response is influenced by many factors, including aging, which substantially reduces the capacity to augment cardiac output (CO), and to exercise[1,8–11]. Older individuals showed a blunted capacity to reduce left ventricular end-systolic volume (ESV), and to increase ejection fraction (EF) in response to effort, this deficit was offset by increasing end-diastolic volume (EDV) via the Frank-Starling mechanism. This increase in preload was made possible due to the slower HR, and subsequent longer diastolic interval, as compared to young subjects[14]. The underlying mechanisms for the age-associated reduction in maximal EF are multifactorial and likely include impaired myocardial performance, increased vascular resistance, impaired autonomic nervous system modulation of myocardial contractility, and an intrinsic impairment in cardiomyocyte contractile function[1,9,14] available data suggest that diastolic function deteriorates with age, likely due to the age-associated increases in cardiac stiffness and impairment in ventricular relaxation[16–20]
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