Corticospinal excitability remains unchanged in the presence of residual force enhancement and does not contribute to increased torque production

Background Following stretch of an active muscle, muscle force is enhanced, which is known as residual force enhancement (rFE). As earlier studies found apparent corticospinal excitability modulations in the presence of rFE, this study aimed to test whether corticospinal excitability modulations contribute to rFE. Methods Fourteen participants performed submaximal plantar flexion stretch-hold and fixed-end contractions at 30% of their maximal voluntary soleus muscle activity in a dynamometer. During the steady state of the contractions, participants either received subthreshold or suprathreshold transcranial magnetic stimulation (TMS) of their motor cortex, while triceps surae muscle responses to stimulation were obtained via electromyography (EMG), and net ankle joint torque was recorded. B-mode ultrasound imaging was used to confirm muscle fascicle stretch during stretch-hold contractions in a subset of participants. Results Following stretch of the plantar flexors, an average rFE of 7% and 11% was observed for contractions with subthreshold and suprathreshold TMS, respectively. 41–46 ms following subthreshold TMS, triceps surae muscle activity was suppressed by 19–25%, but suppression was not significantly different between stretch-hold and fixed-end contractions. Similarly, the reduction in plantar flexion torque following subthreshold TMS was not significantly different between contraction conditions. Motor evoked potentials, silent periods and superimposed twitches following suprathreshold TMS were also not significantly different between contraction conditions. Discussion As TMS of the motor cortex did not result in any differences between stretch-hold and fixed-end contractions, we conclude that rFE is not linked to changes in corticospinal excitability.

Muscle Actuators, Not Springs, Drive Maximal Effort Human Locomotor Performance

The current investigation examined muscle-tendon unit kinematics and kinetics in human participants asked to perform a hopping task for maximal performance with variational preceding milieu. Twenty-four participants were allocated post-data collection into those participants with an average hop height of higher (HH) or lower (LH) than 0.1 m. Participants were placed on a customized sled at a 20º angle while standing on a force plate. Participants used their dominant ankle for all testing and their knee was immobilized and thus all movement involved only the ankle joint and corresponding propulsive unit (triceps surae muscle complex). Participants were asked to perform a maximal effort during a single dynamic countermovement hop (CMH) and drop hops from 10 cm (DH10) and 50 cm (DH50). Three-dimensional motion analysis was performed by utilizing an infrared camera VICON motion analysis system and a corresponding force plate. An ultrasound probe was placed on the triceps surae muscle complex for muscle fascicle imaging. HH hopped significantly higher in all hopping tasks in comparison to LH. In addition, the HH group concentric ankle work was significantly higher in comparison to LH during all of the hopping tasks. Active muscle work was significantly higher in HH in comparison to LH as well. Tendon work was not significantly different between HH and LH. Active muscle work was significantly correlated with hopping height (r = 0.97) across both groups and hopping tasks and contributed more than 50% of the total work. The data indicates that humans primarily use a motor-driven system and thus it is concluded that muscle actuators and not springs maximize performance in hopping locomotor tasks in humans.

The effects of triceps surae muscle stimulation on localized achilles subtendon tissue displacements

The triceps surae muscle tendon unit is comprised of the lateral and medial gastrocnemius (MG) and soleus (SOL) muscles and three in series elastic “subtendons” that form the Achilles tendon. Comparative literature and our own in vivo evidence suggests that sliding between adjacent subtendons may facilitate independent muscle actuation. We aim to more clearly define the relation between individual muscle activation and subtendon tissue displacements. Here, during fixed-end contractions, electrical muscle stimulation controlled the magnitude of force transmitted via individual triceps surae muscles while ultrasound imaging recorded resultant subtendon tissue displacements. We hypothesized that MG and SOL stimulation would elicit larger displacements in their associated subtendon. 10 young adults completed 4 experimental activations at 3 ankle angles (-20°, 0°, 20°) with knee flexed to approximately 20°: MG stimulation (STIMMG), SOL stimulation (STIMSOL), combined stimulation, and volitional contraction. At 20° plantarflexion, STIMSOL elicited 49% larger tendon non-uniformity (SOL – MG subtendon tissue displacement) than that of STIMMG (p=0.004). For STIMSOL, a one-way post-hoc ANOVA revealed a significant main effect of ankle angle (p=0.009) on Achilles tendon non-uniformity. However, peak tendon non-uniformity decreased by an average of 61% from plantarflexion to dorsiflexion, likely due to an increase in passive tension. Our results suggest that localized tissue displacements within the Achilles tendon respond in anatomically consistent ways to differential patterns of triceps surae muscle activation, but these relations are highly susceptible to ankle angle. This in vivo evidence points to at least some mechanical independence in actuation between the human triceps surae muscle-subtendon units.

Applying Stretch to Evoke Hyperreflexia in Spasticity Testing: Velocity vs. Acceleration

In neurological diseases, muscles often become hyper-resistant to stretch due to hyperreflexia, an exaggerated stretch reflex response that is considered to primarily depend on the muscle's stretch velocity. However, there is still limited understanding of how different biomechanical triggers applied during clinical tests evoke these reflex responses. We examined the effect of imposing a rotation with increasing velocity vs. increasing acceleration on triceps surae muscle repsonse in children with spastic paresis (SP) and compared the responses to those measured in typically developing (TD) children. A motor-operated ankle manipulator was used to apply different bell-shaped movement profiles, with three levels of maximum velocity (70, 110, and 150°/s) and three levels of maximum acceleration (500, 750, and 1,000°/s2). For each profile and both groups, we evaluated the amount of evoked triceps surae muscle activation. In SP, we evaluated two additional characteristics: the intensity of the response (peak EMG burst) and the time from movement initiation to onset of the EMG burst. As expected, the amount of evoked muscle activation was larger in SP compared to TD (all muscles: p < 0.001) and only sensitive to biomechanical triggers in SP. Further investigation of the responses in SP showed that peak EMG bursts increased in profiles with higher peak velocity (lateral gastrocnemius: p = 0.04), which was emphasized by fair correlations with increased velocity at EMG burst onset (all muscles: r > 0.33–0.36, p ≤ 0.008), but showed no significant effect for acceleration. However, the EMG burst was evoked faster with higher peak acceleration (all muscles p < 0.001) whereas it was delayed in profiles with higher peak velocity (medial gastrocnemius and soleus: p < 0.006). We conclude that while exaggerated response intensity (peak EMG burst) seems linked to stretch velocity, higher accelerations seem to evoke faster responses (time to EMG burst onset) in triceps surae muscles in SP. Understanding and controlling for the distinct effects of different biological triggers, including velocity, acceleration but also length and force of the applied movement, will contribute to the development of more precise clinical measurement tools. This is especially important when aiming to understand the role of hyperreflexia during functional movements where the biomechanical inputs are multiple and changing.