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.

Central and peripheral hemodynamic responses to passive limb movement: the role of arousal

“…4). However, it should be noted that, in agreement with our other recent work (12), where there was a greatly attenuated central hemodynamic response in heart transplant recipients, the magnitude of the hyperemic response in people with a SCI was limited (ϳ90% increase) compared with our previously published data from healthy subjects in a supine position of ϳ285% (22). Moreover, even when normalized for the somewhat reduced thigh muscle mass, the magnitude of hyperemia was ϳ38 ml·min Ϫ1 ·kg Ϫ1 in the present subjects with a SCI compared with ϳ190 ml·min Ϫ1 ·kg Ϫ1 in able-bodied subjects (23), implying that this attenuated hyperemic response was not just a consequence of reduced limb volume.…”

“…At the onset of exercise, a complex combination of both peripheral and central hemodynamic factors contribute to the increase in blood flow to active skeletal muscle. Recently, our group (12,18,22,23) has used passive movement as a reductionist model in which exercise-induced hyperemia can be studied without the increased complexity of altered muscle metabolism. To better understand the integration of mechanical and neurological factors that contribute to the immediate increase in blood flow to a moving limb, we (12,22) studied heart transplant recipients with denervated hearts and young subjects with a partial block of afferent nerve fibers.…”

“…Recently, our group (12,18,22,23) has used passive movement as a reductionist model in which exercise-induced hyperemia can be studied without the increased complexity of altered muscle metabolism. To better understand the integration of mechanical and neurological factors that contribute to the immediate increase in blood flow to a moving limb, we (12,22) studied heart transplant recipients with denervated hearts and young subjects with a partial block of afferent nerve fibers. These studies revealed that passive movement-induced hyperemia in the intact human is associated with a significant central hemodynamic response (ϳ5-24%), which, in turn, supports and sustains the elevated limb blood flow (12,22).…”

“…A 3-s rolling average was applied to the data for HR, SV, CO, MAP, blood flow, and vascular conductance. For this study and in other our investigations (12,18,22,23), we compared data that were averaged across 3, 5, 10, and 15 s. The 3-s averages provided the best balance between the quality and real variance of the signal. V E was measured breath by breath and averaged second by second; V O2 and V CO2 were assessed with 20-s averaging throughout the protocols.…”

Impact of body position on central and peripheral hemodynamic contributions to movement-induced hyperemia: implications for rehabilitative medicine

“…By the removal of the increase in metabolism associated with exercise, the independent effect of movement on central and peripheral hemodynamic mechanisms governing exercise hyperemia can be identified and studied. This approach has been used by our laboratory to identify that movement-induced hyperemia is transient in nature (22,40), that central hemodynamics and afferent feedback are integral parts of the hyperemic response (14,36), and that aging results in a reduction in movement-induced hyperemia that is independent of metabolism (23). At the onset of passive movement, the mechanical deformation of the vascular bed coupled with stimulation of group III afferent fibers initiates a cascade of events resulting in both peripheral vasodilation and a heart rate (HR)-driven increase in cardiac output (CO) and a subsequent increase in leg blood flow (LBF) (36).…”