Walking-Induced Inertial Effects on the Cardiovascular System

Aurora Rosato^1,2Emanuele Perra^1,2Eric Rullman³Seraina A Dual^1,2*

• ¹Royal Institute of Technology, Stockholm, Sweden
• ²Intelligent Heart Technology Lab, Department of Biomedical Engineering and Health Systems, KTH Royal Institute of Technology, Stockholm, Sweden
• ³Division of Clinical Physiology, Department of Laboratory Medicine, Karolinska Institute, Stockholm, Sweden

During exercise, the cardiovascular, respiratory, and locomotor systems interplay dynamically, yet the specific mechanisms of cardiovascular and locomotor interaction during simple rhythmic exercise like walking remain unclear. Computational models constitute a powerful tool to investigate the interplay of networked physiological systems, but while gravitational and postural effects on circulation have been explored, the influence of inertial forces from body motion on hemodynamics has not been addressed. Here, we present a closed-loop cardiovascular model that incorporates inertial effects during walking to study dynamic hemodynamic changes caused by bodily acceleration. The model is a lumped parameter system with 25 vascular compartments and a four-chamber heart with valves, including pericardial and intrathoracic pressures and interventricular septal interactions. Inertial effects are modeled as additional hydrostatic pressure in each vascular segment, caused by acceleration of blood mass influenced by gravity and motion. A baroreflex mechanism regulates time-averaged aortic pressure by adjusting heart rate, vascular resistance, and ventricular elastance to maintain target pressures. We tested the model using three protocols: a head-up tilt test to validate baroreflex and gravity effects; a synthetic walking simulation with controlled heart rate (HR) and step rate (SR) using a cyclic acceleration waveform; a human walking experiment comparing simulated aortic pressure with measured brachial blood pressure using acquired HR and chest acceleration data. The model accurately reproduces physiological responses to head-up tilt, consistent with previous literature. When HR and SR are equal, pressure augmentations linked to walking-induced inertial effects are observed, with phase shifts causing increased systolic or diastolic peaks. The model follows the pressure changes at different phase shifts between heart contraction and stepping and shows good agreement with experimental results. When SR exceeds HR, phase variability produces a low-frequency “beating” in the pressure waveform and mean arterial pressure, corresponding to the difference between SR and HR. Introducing contributions of body acceleration as an additional dynamic component of the pressure source in the vascular compartments seems a valid way to capture walking-induced inertial effects. This work contributes to the broader effort to characterize physiological network adaptations to exercise and offers a foundation for future research studying and optimizing cardiac-locomotor interaction.