CAI patients displayed altered movement strategies, perhaps in an attempt to avoid perceived positions of risk. Although sagittal joint positions seemed to increase the external torque on the knee and hip extensors, frontal joint positions appeared to reduce the muscular demands on evertor and hip abductor muscles.

Context The literature on gait kinematics and muscle activation in chronic ankle instability (CAI) is limited. A comprehensive evaluation of all relevant gait measures is needed to examine alterations in gait neuromechanics that may contribute to recurrent sprain. Objective To compare walking neuromechanics, including kinematics, muscle activity, and kinetics (ie, ground reaction force [GRF], moment, and power), between participants with and those without CAI by applying a novel statistical analysis to data from a large sample. Design Controlled laboratory study. Setting Biomechanics laboratory. Patients or Other Participants A total of 100 participants with CAI (49 men, 51 women; age = 22.2 ± 2.3 years, height = 174.0 ± 9.7 cm, mass = 70.8 ± 14.4 kg) and 100 individuals without CAI serving as controls (55 men, 45 women; age = 22.5 ± 3.3 years, height = 173.1 ± 13.3 cm, mass = 72.6 ± 18.7 kg). Intervention(s) Participants performed 5 trials of walking (shod) at a self-selected speed over 2 in-ground force plates. Main Outcome Measure(s) Three-dimensional GRFs, lower extremity joint angles, internal joint moments, joint powers, and activation amplitudes of 6 muscles were recorded during stance. Results Compared with the control group, the CAI group demonstrated (1) increased plantar flexion or decreased dorsiflexion, increased inversion or decreased eversion, decreased knee flexion, decreased knee abduction, and increased hip-flexion angles; (2) increased or decreased inversion, increased plantar flexion, decreased knee extension, decreased knee abduction, and increased hip-extension moments; (3) increased vertical, braking, and propulsive GRFs; (4) increased hip eccentric and concentric power; and (5) altered muscle activation in all 6 lower extremity muscles. Conclusions The CAI group demonstrated a hip-dominant strategy by limiting propulsive forces at the ankle while increasing force generation at the hip. The different walking neuromechanics exhibited by the CAI group could represent maladaptive strategies that developed after the initial sprain or an injurious gait pattern that may have predisposed the participants to their initial injuries. Increased joint loading and altered kinematics at the foot and ankle complex during initial stance could affect the long-term health of the ankle articular cartilage.

CAI patients seemed to use a hip-dominant strategy by increasing the hip extension moment, stiffness, and eccentric and concentric power during landing and jumping. This apparent compensation may be due to decreased capabilities to produce sufficient joint moment, stiffness, and power at the ankle and knee. These differences might have injury risk and performance implications.

Centrally mediated changes in sensorimotor function have been reported in patients with chronic ankle instability (CAI). However, little is known regarding supraspinal/spinal adaptations during lower‐extremity dynamic movement during a multiplanar, single‐leg landing/cutting task. The purpose of this study was to investigate the effect of CAI on landing/cutting neuromechanics, including lower‐extremity kinematic, electromyography (EMG) activation, and ground reaction force (GRF) characteristics. One hundred CAI patients and 100 matched healthy controls performed five trials of a jump landing/cutting task. Sagittal‐ and frontal‐plane ankle, knee and hip kinematics, EMG activation in eight lower‐extremity muscles, and 3D GRF were collected during jump landing/cutting. Functional analyses of variance (FANOVA) were used to evaluate between‐group differences for dependent variables throughout the entire ground contact of the task. Relative to the control group, the CAI group revealed (a) reduced dorsiflexion, increased knee and hip flexion angles, (b) increased inversion and hip adduction angles, (c) increased EMG activation of medial gastrocnemius, peroneus longus, adductor longus, vastus lateralis, gluteus medius, and gluteus maximus, and (d) increased posterior and vertical GRF during initial landing, and reduced medial, posterior, and vertical GRF during mid‐landing and mid‐cutting. CAI patients demonstrated alterations in landing/cutting movement strategies as demonstrated by a higher susceptibility of foot placement for lateral ankle sprains, and more flexed positions of the knee and hip with higher EMG activation of knee and hip extensors to modulate GRF to compensate for the unstable ankle. This apparent compensation may be due to mechanical (limited dorsiflexion angle) and/or sensorimotor deficits in the ankle.

Knee joint pain (KJP) is a cardinal symptom in knee pathologies, and quadriceps inhibition is commonly observed among KJP patients. Previously, KJP independently reduced quadriceps strength and activation. However, it remains unknown how disinhibitory transcutaneous electrical nerve stimulation (TENS) will affect inhibited quadriceps motor function. This study aimed at examining changes in quadriceps maximum voluntary contraction (MVC) and central activation ratio (CAR) before and after sensory TENS following experimental knee pain. Thirty healthy participants were assigned to either the TENS or placebo groups. All participants underwent three separate data collection sessions consisting of two saline infusions and one no infusion control in a crossover design. TENS or placebo treatment was administered to each group for 20 min. Quadriceps MVC and CAR were measured at baseline, infusion, treatment, and post-treatment. Perceived knee pain intensity was measured on a 100-mm visual analogue scale. Post-hoc analysis revealed that hypertonic saline infusion significantly reduced the quadriceps MVC and CAR compared with control sessions (P < 0.05). Sensory TENS, however, significantly restored inhibited quadriceps motor function compared with placebo treatment (P < 0.05). There was a negative correlation between changes in MVC and knee pain (r = 0.33, P < 0.001), and CAR and knee pain (r = 0.62, P < 0.001), respectively.