Neural mechanisms underlying the adaptive plasticity of human locomotion

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The aim of the present work is to better understand the adaptive capacity/learning ability of the neural control of human locomotion. In the proposed experiments, locomotor control will be challenged by having subjects walk on a treadmill in altered force environments (“force fields”) generated by a custom-made robotized orthosis. In order to walk normally in the presence of the force field, participants need to temporarily modify their stereotypic muscle activation pattern, an experimental model of motor learning. Over the next five years, the following 3 objectives will be addressed:OBJ#1: Define the contribution of stretch and load inputs to locomotor adaptation.When walking in a force field, subjects obtain information about their movement errors through sensory feedback from muscle spindles (muscle length/velocity), Golgi tendon organs (GTOs; muscle loading), and foot cutaneous receptors (pressure distribution). We have recently shown that cutaneous receptors contribute to adaptation. In this proposal, we will focus on spindle and GTO contributions. We will use vibration (spindle) or electrical stimulation of the muscle (GTOs) during locomotor adaptation to selectively “scramble” the selected input (sensory barrage). Our hypothesis is that deficits in adaptation observed during sensory barrage will provide information on the role of this input for locomotor adaptation.OBJ#2: Test the extent of adaptive capacity of the muscle activation pattern to complex force fields. It has been hypothesized that adaptive plasticity during gait might be limited due to the important contribution of automatic locomotor networks to movement generation. Here we will use our rAFO to produce graded perturbations to ankle movement during gait. By going from resistance to increasing amounts of assistance, it will be possible to increase the level of difficulty of the learning, going from simple changes in muscle activation amplitude to a "phase-reversal" of activation, akin to antagonist tendon-transfer. Our hypothesis is that participants will be able to adapt to situations requiring changes in muscle activation amplitude, but incapable of phase reversal. OBJ#3: Better understand how central fatigue affects acquisition/retention of locomotor learning. Muscle fatigue is often present during motor learning. How it interferes with learning remains largely unknown. Here, we will test corticospinal excitability, ankle proprioception and locomotor adaptation/retention during gait after a short-duration fatiguing exercise. Our hypothesis is that fatigue will have a minimal effect on locomotor adaptation but a larger deleterious effect on retention. IMPACT. By methodically studying human walking under several complementary adaptive situations, this research program will make important discoveries about neural mechanisms underlying locomotor plasticity.