Understanding exercise-induced hyperemia: central and peripheral hemodynamic responses to passive limb movement in heart transplant recipients

Abstract

To better characterize the contribution of both central and peripheral mechanisms to passive limb movement-induced hyperemia, we studied nine recent (<2 yr) heart transplant (HTx) recipients (56 ± 4 yr) and nine healthy controls (58 ± 5 yr). Measurements of heart rate (HR), stroke volume (SV), cardiac output (CO), and femoral artery blood flow were recorded during passive knee extension. Peripheral vascular function was assessed using brachial artery flow-mediated dilation (FMD). During passive limb movement, the HTx recipients lacked an HR response (0 ± 0 beats/min, Δ0%) but displayed a significant increase in CO (0.4 ± 0.1 l/min, Δ5%) although attenuated compared with controls (1.0 ± 0.2 l/min, Δ18%). Therefore, the rise in CO in the HTx recipients was solely dependent on increased SV (5 ± 1 ml, Δ5%) in contrast with the controls who displayed significant increases in both HR (6 ± 2 beats/min, Δ11%) and SV (5 ± 2 ml, Δ7%). The transient increase in femoral blood volume entering the leg during the first 40 s of passive movement was attenuated in the HTx recipients (24 ± 8 ml) compared with controls (93 ± 7 ml), whereas peripheral vascular function (FMD) appeared similar between HTx recipients (8 ± 2%) and controls (6 ± 1%). These data reveal that the absence of an HR increase in HTx recipients significantly impacts the peripheral vascular response to passive movement in this population and supports the concept that an increase in CO is a major contributor to exercise-induced hyperemia.

Fig. 1.

Central and peripheral hemodynamic responses to passive exercise in heart transplant (HTx) recipients and controls. Values are means ± SE of passive leg blood flow (A), control leg blood flow (B), cardiac output (CO; C), heart rate (HR; D), stroke volume (SV; E), and mean arterial pressure (MAP; F) for the first 40 s of the exercise protocol. bpm, Beats/min. The transition from rest to movement occurs at 0 on the axis. Note: these figures are presented to illustrate the general trends. As the analyses were performed on data from individuals who exhibited varying response kinetics, averaging removes some of the information in the original individual recordings. Therefore, maximum change tends to be underestimated here but is represented in Fig. 2.

Fig. 2.

Maximum relative changes in passive leg blood flow, control leg blood flow, vascular conductance, CO, HR, SV, and MAP in HTx recipients and controls. Values are means ± SE.*Significantly different from control. Note: y-axis scale for the blood flow data is different from y-axis scale for the central variables (dashed vertical line separates the variables associated with the y-axis scales on left and right).

Fig. 3.

Brachial artery flow-mediated dilation (FMD) following 5-min cuff occlusion expressed as a percent change from precuff baseline (A) and after normalizing FMD for shear rate (B) in HTx recipients and controls. Values are means ± SE. There were no significant differences.

Fig. 4.

Resting brachial artery blood flow and reactive hyperemia following cuff occlusion in healthy controls and HTx recipients.