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

The exact role of arousal in the central and peripheral hemodynamic responses to passive limb movement in humans is unclear, but has been proposed as a potential contributor. Thus, we utilized a human model with no lower limb afferent feedback to determine the role of arousal on the hemodynamic response to passive-leg movement. In 9 people with a spinal cord injury (SCI), we compared central, and peripheral hemodynamic and ventilatory responses to one-leg passive knee-extension with and without visual feedback (M+VF, M-VF, respectively) and a third trial with no movement or visual feedback, but the perception of movement (F). Ventilation (VE), heart rate (HR), stroke volume (SV), cardiac output (CO), mean arterial pressure (MAP), and leg blood flow (LBF) were evaluated during the 3 protocols. VE increased rapidly from baseline in M+VF (55 ± 11\%), M-VF (63 ± 13\%), and F (48 ± 12\%). Central hemodynamics (HR, SV, CO, and MAP) were unchanged in all trials. LBF increased from baseline by 126 ± 18 ml/min, and 109 ± 23 ml/min in M+VF and M-VF, respectively, but was unchanged in F. Therefore, by using a paradigm that is devoid of afferent feedback from the legs, this study has revealed that, although arousal is invoked by passive movement or the thought of passive movement, as evidenced by an increase in VE, there is no central or peripheral hemodynamic impact of this increased neural activity. Additionally, this study reveals that a central hemodynamic response is not an obligatory component of movement-induced LBF.