Limb movement-induced hyperemia has a central hemodynamic component: evidence from a neural blockade study

Abstract

Limb movement-induced hyperemia has a central hemodynamic component: evidence from a neural blockade study. Am J Physiol Heart Circ Physiol 299: H1693-H1700, 2010. First published August 27, 2010; doi:10.1152/ajpheart.00482.2010.-The purpose of this investigation was to partially remove feedback from type III/IV skeletal muscle afferents and determine how this feedback influences the central and peripheral hemodynamic responses to passive leg movement. Heart rate (HR), stroke volume (SV), cardiac output (CO), mean arterial pressure, leg vascular conductance (LVC), and leg blood flow (LBF) were measured during 2 min of passive knee extension in eight young men before and after intrathecal fentanyl injection. Passive movement increased HR by 14 beats/min from baseline to maximal response during control (CON) (65 Ϯ 4 to 79 Ϯ 5 beats/min, P Ͻ 0.05), whereas HR did not significantly increase with the fentanyl block (BLK). LBF and LVC increased in both conditions; however, these increases were attenuated and delayed during BLK [%change from baseline to maximum, LBF: CON 295 Ϯ 109 vs. BLK 210 Ϯ 86%, (P Ͻ 0.05); LVC: CON 322 Ϯ 40% vs. BLK 231 Ϯ 32%, (P Ͻ 0.04)]. In CON, HR, SV, CO, and LVC increased contributing to the hyperemic response. However, under BLK conditions, statistically insignificant increases in HR and SV combined to yield a small, but significant, increase in CO and an attenuated hyperemic response. Therefore, partially blocking skeletal muscle afferent feedback blunts the central hemodynamic response due to passive limb movement, which then results in an attenuated and delayed movement-induced hyperemia. In combination, these findings provide evidence that limb movement-induced hyperemia has a significant central hemodynamic component induced by peripheral nerve activation. afferent nerve fiber; blood flow; hemodynamics CENTRAL AND PERIPHERAL HEMODYNAMIC factors contribute to the hyperemic response at the onset of exercise. These factors include the muscle pump (24, 38) mechanically induced vasodilation (6,19,41), mechanical deformation of arterioles (37), flow-mediated vasodilation (22, 34), and cardioacceleration (26, 30 -33, 43) due to stimulation of afferent mechanosensitive and metabosensitive fibers in the working muscles (25,36). Isolating the relative importance of these numerous mechanisms is difficult and requires a systematic approach to understand the nature of any single mechanism.One approach to study the movement-induced central and peripheral hemodynamic responses to the onset of exercise is to perform passive movement, thereby minimizing the metabolic contribution of voluntary exercise. Recently, our group (26, 43) and others (30,31,33) have highlighted the role of cardioacceleration in the hyperemic responses to passive movement. Wray et al. (43) reported that passive knee extension resulted in significant tachycardia and increased leg blood flow (LBF) during the first 5 s of movement. However, in this study, stroke volume (SV) was not measured, and cardiac output (CO) was assumed to r...

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

“…3). Although even more clear here, this annulling of the central hemodynamic response to limb movement was similar to our previously published findings of an attenuated response (33% reduced) with the partial pharmacological blockade (fentanyl) of type III and IV afferents in able-bodied volunteers (22). Therefore, in combination with our previous work (22), these data not only highlight the importance of afferent signals from the passively moved limb in the instigation of a central hemodynamic response but also provide the opportunity to document that arousal (which was evident in the ventilatory response of these subjects) does not appear to play a significant role in terms of central cardiovascular responses to passive limb movement.…”

“…It has been well documented that in the intact human, passive limb movement induces a significant, albeit transient, increase in central hemodynamic variables (HR, SV, CO, and MAP) (17,22). In contrast, in the present subjects with a SCI, central hemodynamics did not significantly differ from baseline Data are means Ϯ SE.…”

“…Recently, our group (17,22,26) and others (19) have underlined the role of afferent signals that invoke cardioacceleration, which supports the hyperemic response to passive limb movement. Similarly, efferent signals from the brain have been documented to invoke cardiovascular responses (11,21).…”

“…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.…”

“…Indeed, our group (22) recently used an intrathecal fentanyl injection to partially block this afferent nerve traffic and identified a critical role for this feedback in both central and peripheral hemodynamic responses as well as ventilatory responses to passive limb movement. Although it would have been interesting to take advantage of this reduced afferent feedback to examine the role of efferent signals in isolation, the fentanyl block allows enough sensory perception for this to be impossible.…”