Use of the Frank-Starling mechanism during exercise is linked to exercise-induced changes in arterial load

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 change 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 ΔE(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 ΔE(A)I. Individuals with the largest increase in ΔE(A)(group 3;ΔE(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(ΔE(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 change 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.

Fig. 1.

The distribution of the change in E_AI during exercise A: The frequency distribution of the change in effective arterial elastance index (ΔE_AI) from rest to peak exercise. B: The relationship of ΔE_AI to age in men (closed symbols) and women (open symbols).

Fig. 2.

The change in E_AI and its components across relative exercise workloads. Comparisons of E_AI(A), heart rate (HR: B), peripheral vascular resistance (PVRI: C), total arterial compliance (TACI: D), and systolic blood pressure (SBP: E) among the 3 E_AI groups at rest, at 25% and 50% of peak, and at peak exercise (data shown as means ± SEM).*P < 0.05 E_AI group 1 vs. 2, ‡P < 0.05 E_AI group 1 vs. 3, ^†P < 0.05 E_AI group 2 vs. 3, adjusted for age, sex and maximal workload.

Fig. 3.

The change in cardiac volumes across relative exercise workloads Comparisons of ESVI(A), EDVI(B), and SVI(C), among the 3 E_AI groups at rest, at 25% and 50% of peak, and at peak exercise (data shown as means ± SEM). *P < 0.05 vs. E_AI group 1 vs. 2, ‡P < 0.05 E_AI group 1 vs. 3, ^†P < 0.05 E_AI group 2 vs. 3, adjusted for age, sex and maximal workload.

Fig. 4.

The change in cardiac performance across relative exercise workloads. Comparisons of cardiac index (CI: A), ejection fraction (EF: B), EDVI adjusted values of stroke work (SWI: C), and end-systolic elastance (E_LVI: D) among the 3 E_AI groups at rest, at 25% and 50% of peak, and at peak exercise (data shown as means ± SEM). *P < 0.05 vs. E_AI group 1 vs. 2, ‡P < 0.05 E_AI group 1 vs. 3, ^†P < 0.05 E_AI group 2 vs. 3, adjusted for age, sex and MWL.