The biomechanical principles underlying the organization of muscle activation patterns during standing balance are poorly understood. The goal of this study was to understand the influence of biomechanical inter-joint coupling on endpoint forces and accelerations induced by the activation of individual muscles during postural tasks. We calculated induced endpoint forces and accelerations of 31 muscles in a 7 degree-of-freedom, three-dimensional model of the cat hindlimb. To test the effects of inter-joint coupling, we systematically immobilized the joints (excluded kinematic degrees of freedom) and evaluated how the endpoint force and acceleration directions changed for each muscle in 7 different conditions. We hypothesized that altered inter-joint coupling due to joint immobilization of remote joints would substantially change the induced directions of endpoint force and acceleration of individual muscles. Our results show that for most muscles crossing the knee or the hip, joint immobilization altered the endpoint force or acceleration direction by more than 90° in the dorsal and sagittal planes. Induced endpoint forces were typically consistent with behaviorally observed forces only when the ankle was immobilized. We then activated a proximal muscle simultaneous with an ankle torque of varying magnitude, which demonstrated that the resulting endpoint force or acceleration direction is modulated by the magnitude of the ankle torque. We argue that this simple manipulation can lend insight into the functional effects of co-activating muscles. We conclude that inter-joint coupling may be an essential biomechanical principle underlying the coordination of proximal and distal muscles to produce functional endpoint actions during motor tasks.
Simulating realistic musculoskeletal dynamics is critical to understanding neural control of muscle activity evoked in sensorimotor feedback responses that have inherent neural transmission delays. Thus, the initial mechanical response of muscles to perturbations in the absence of any change in muscle activity determines which corrective neural responses are required to stabilize body posture. Muscle short-range stiffness, a history-dependent property of muscle that causes a rapid and transient rise in muscle force upon stretch, likely affects musculoskeletal dynamics in the initial mechanical response to perturbations. Here we identified the contributions of short-range stiffness to joint torques and angles in the initial mechanical response to support surface translations using dynamic simulation. We developed a dynamic model of muscle short-range stiffness to augment a Hill-type muscle model. Our simulations show that short-range stiffness can provide stability against external perturbations during the neuromechanical response delay. Assuming constant muscle activation during the initial mechanical response, including muscle short-range stiffness was necessary to account for the rapid rise in experimental sagittal plane knee and hip joint torques that occurs simultaneously with very small changes in joint angles and reduced root mean square errors between simulated and experimental torques by 56% and 47%, respectively. Moreover, forward simulations lacking short-range stiffness produced unreasonably large joint angle changes during the initial response. Using muscle models accounting for short-range stiffness along with other aspects of history-dependent muscle dynamics may be important to advance our ability to simulate inherently unstable human movements based on principles of neural control and biomechanics.
Total cavopulmonary connection is the result of a series of palliative surgical repairs performed on patients with single ventricle heart defects. The resulting anatomy has complex and unsteady hemodynamics characterized by flow mixing and flow separation. Although varying degrees of flow pulsatility have been observed in vivo, non-pulsatile (time-averaged) boundary conditions have traditionally been assumed in hemodynamic modeling, and only recently have pulsatile conditions been incorporated without completely characterizing their effect or importance. In this study, 3D numerical simulations with both pulsatile and non-pulsatile boundary conditions were performed for 24 patients with different anatomies and flow boundary conditions from Georgia Tech database. Flow structures, energy dissipation rates and pressure drops were compared under rest and simulated exercise conditions. It was found that flow pulsatility is the primary factor in determining the appropriate choice of boundary conditions, whereas the anatomic configuration and cardiac output had secondary effects. Results show that the hemodynamics can be strongly influenced by the presence of pulsatile flow. However, there was a minimum pulsatility threshold, identified by defining a weighted pulsatility index (wPI), above which the influence was significant. It was shown that when wPI < 30%, the relative error in hemodynamic predictions using time-averaged boundary conditions was less than 10% compared to pulsatile simulations. In addition, when wPI < 50, the relative error was less than 20%. A correlation was introduced to relate wPI to the relative error in predicting the flow metrics with non-pulsatile flow conditions.