Balance control after slip-like perturbations in human running when systematically altering forward trunk leaning

Human running is generally robust to external perturbations, yet the underlying whole-body mechanics governing perturbation recovery remain poorly understood. Existing research has primarily focused on perturbation recovery during walking, whereas running remains underrepresented despite its distinct mechanical characteristics. In the present study, 16 participants ran at 2.5 m s-1 while standardized late-stance slip-like anterior-posterior perturbations were induced. Perturbations were applied as sudden accelerations of the treadmill belt, expected but not predictable in timing. Sagittal whole-body angular momentum (WBAM) and external angular impulse were calculated to investigate the underlying mechanics of perturbation recovery. In addition, we investigated the effects of trunk forward leaning on perturbation recovery, as trunk kinematics strongly influence the whole-body center of mass position and thereby the generation of angular impulse during stance. Balance control was quantified using WBAM-based perturbation recovery time. Recovery was governed by reactive sagittal WBAM regulation through backward angular impulse generation, arising from sustained propulsive ground reaction forces (GRFs) and a pronounced initial vertical GRF peak across successive recovery steps. Forward leaning did not affect perturbation recovery time, indicating that forward leaning does not impair balance control. Instead, forward leaning reduced baseline steady-state WBAM range before perturbation onset and the peak forward WBAM excursion following perturbations. This suggests that leaning forward may lead to greater reliance on feedforward control mechanisms, as reflected in a tighter baseline sagittal WBAM control. These findings highlight that robust balance control following slip-like anterior-posterior perturbations in human running reflects regulation of sagittal WBAM through complementary reactive and feedforward mechanisms.