MedStar Authors catalog › Details for: Use of the Frank-Starling mechanism during exercise is linked to exercise-induced 130912s in arterial load.
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Use of the Frank-Starling mechanism during exercise is linked to exercise-induced 130912s in arterial load.

by Najjar, Samer S.
Citation: American Journal of Physiology - Heart & Circulatory Physiology. 302(1):H349-58, 2012 Jan 1..Journal: American journal of physiology. Heart and circulatory physiology.ISSN: 0363-6135.Full author list: Chantler PD; Melenovsky V; Schulman SP; Gerstenblith G; Becker LC; Ferrucci L; Fleg JL; Lakatta EG; Najjar SS.UI/PMID: 22003052.Subject(s): Adult | Aged | Analysis of Variance | Arteries/ph [Physiology] | Baltimore | Blood Pressure | Cardiac Output | Compliance | *Exercise/ph [Physiology] | Exercise Test | Female | Heart Rate | *Hemodynamics | Humans | Longitudinal Studies | Male | Middle Aged | *Models, Cardiovascular | *Muscle Contraction | *Muscle, Skeletal/bs [Blood Supply] | Stroke Volume | Time Factors | Vascular Resistance | Ventricular Function, LeftInstitution(s): MedStar Heart & Vascular InstituteActivity type: Journal Article.Medline article type(s): Journal Article | Research Support, N.I.H., Extramural | Research Support, N.I.H., Intramural | Research Support, Non-U.S. Gov'tDigital Object Identifier: (Click here) Abbreviated citation: Am J Physiol Heart Circ Physiol. 302(1):H349-58, 2012 Jan 1.Local Holdings: Available online through MWHC library: 2008-2010.Abstract: Effective arterial elastance(E(A)) is a measure of the net arterial load imposed on the heart that integrates the effects of heart rate(HR), peripheral vascular resistance(PVR), and total arterial compliance(TAC) and is a modulator of cardiac performance. To what extent the 130912 in E(A) during exercise impacts on cardiac performance and aerobic capacity is unknown. We examined E(A) and its relationship with cardiovascular performance in 352 healthy subjects. Subjects underwent rest and exercise gated scans to measure cardiac volumes and to derive E(A)[end-systolic pressure/stroke volume index(SV)], PVR[MAP/(SV*HR)], and TAC(SV/pulse pressure). E(A) varied with exercise intensity: the E(A) between rest and peak exercise along with its determinants, differed among individuals and ranged from -44% to +149%, and was independent of age and sex. Individuals were separated into 3 groups based on their E(A)I. Individuals with the largest increase in E(A)(group 3;E(A)>=0.98 mmHg.m(2)/ml) had the smallest reduction in PVR, the greatest reduction in TAC and a similar increase in HR vs. group 1(E(A)<0.22 mmHg.m(2)/ml). Furthermore, group 3 had a reduction in end-diastolic volume, and a blunted increase in SV(80%), and cardiac output(27%), during exercise vs. group 1. Despite limitations in the Frank-Starling mechanism and cardiac function, peak aerobic capacity did not differ by group because arterial-venous oxygen difference was greater in group 3 vs. 1. Thus the 130912 in arterial load during exercise has important effects on the Frank-Starling mechanism and cardiac performance but not on exercise capacity. These findings provide interesting insights into the dynamic cardiovascular alterations during exercise.

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