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Neural activation is thought to be essential for the expression of maximal muscle performance, but the exact contribution of neural mechanisms such as the level of agonist, antagonist and stabiliser muscle activation to muscle strength is not fully understood. Explosive neuromuscular performance, including the ability to initiate (the electromechanical delay, EMD) and develop force rapidly (termed, rate of force development, RFD) are considered essential for the performance of explosive sporting tasks and joint stabilisation and thus injury avoidance. The thesis aimed to improve our understanding of the contribution of neural factors to muscle performance, with a specific focus on explosive neuromuscular performance. The work in this thesis utilised a range of approaches to achieve this aim. Initially, the association between muscle activation and rate of force development and EMD was established. Comparison of unilateral and bilateral actions was then undertaken. Finally interventions with the aim to both negatively affect and improve muscle strength, which included fatigue and resistance training (RT), respectively was undertaken and the neural contributions to changes in performance established. Agonist activation during the early phase of voluntary force production was shown to be an important determinant of voluntary EMD, explaining 41% of its inter-individual variability. Agonist activation was an important determinant of early, but not late phase RFD. Use of bilateral actions resulted in a reduction in explosive strength, which was thought to be due to differences in postural stability between unilateral and bilateral strength tasks. The level of stabiliser activation was strongly related to the level of agonist activation during the early phase of explosive force development and had a high association with explosive force production. Task-specific adaptations following isoinertial RT, specifically, the greater increase in isoinertial lifting strength than maximal isometric strength were due to training-specific changes in the level of agonist activation. High-intensity fatigue achieved a more substantial decline in explosive than maximal isometric strength, and this was postulated to be due to neural mechanisms, specifically decreased agonist activation. This work provides an in depth analysis of the neural contributions to maximal muscle performance.

Turning is an important activity of daily living and often compromised post-stroke. The fall rate for post-stroke individuals while turning is nearly four times as high compared to healthy adults, with most falls resulting in injury. Thus, there is a need for evidence-based rehabilitation targets to improve turning performance for post-stroke individuals. To produce well-coordinated movements, muscles can be organized into muscle modules (i.e., groups of co-excited muscles). Post-stroke these modules can be merged, leading to impaired muscle coordination and walking performance. However, the relationship between impaired coordination and turning performance is not well understood. Thus, the purpose of this study was to analyze the influence of impaired muscle coordination (i.e., merged modules) on turning performance (i.e., time to complete a turn, number of steps required to complete a turn, smoothness of performing the turn and balance control during a turn). Post-stroke individuals and healthy controls performed three tasks including overground straight line walking, a 90-degree turn and a 180-degree turn. The number of muscle modules during straight line walking were determined using non-negative matrix factorization. As few as two modules were found in post-stroke individuals. Differences in turning performance were only seen in the 180-degree turning performance measures. Those with two modules took longer to turn, used more steps and had less smooth movement. These results suggest obtaining independent modules should be an important aim in locomotor therapies aimed at improving turning performance. In addition, the time it takes to complete a 180-degree turn may be a useful clinical assessment measure of the degree of muscle coordination impairment post-stroke.

Abnormal motor coordination affects motor function following stroke, yet we lack a complete characterization of how such abnormal coordination affects movements such as gait. Previous research found that post-stroke gait exhibited fewer movement primitives, or muscle modules, than healthy individuals, suggesting abnormal coordination may affect gait function. However, aside from abnormal coordination, the reduced number of modules could also be due to compensations in response to other impairments such as increased muscle tone and spasticity. Our previous research compared gait in those with post-stroke Stiff-Knee Gait (SKG) to healthy individuals with kinematically constrained knee flexion. While healthy individuals compensated with pelvic obliquity, those with post-stroke SKG also exhibited greater hip abduction, suggesting the motion may be related to neural impairments such as abnormal coordination. We hypothesize that abnormal coordination, not the compensations due to restricted ranges of motion induced by other impairments, is associated with reduced gait function. In this experiment, we compared muscle coordination patterns emerging from healthy individuals with and without restricted knee kinematics to a cohort of individuals post-stroke, both with and without SKG. We predicted the number of muscle modules would be fewer than healthy individuals with similar gait kinematics and found that mechanical knee restriction reduced the number of modules similar to those with post-stroke SKG in walking. Constraining healthy motions resulted in similar muscular coordination patterns to unrestricted gait suggesting the robustness of muscle recruitment despite a kinematic perturbation. The composition of modules in the pre-swing phase between those with SKG and the mechanically restricted group differed (Spearman’s ρ = -0.024), whereas comparisons between post-stroke individuals without SKG (NSKG) and the healthy group were similar (Spearman’s ρ = 0.833). We found those with SKG relied less on hamstrings than healthy counterparts, suggesting an altered motor command beyond adaptation. Muscle coordination patterns in constrained motions during gait were not similar to SKG while the NSKG group showed greater similarity to normal walking. Thus, our data suggests that abnormal coordination may play a greater role in SKG than those without SKG. The results of this comparison will help develop more accurate interventions for clinical treatment.

When the human skeleton is moved by muscles, the resulting movement is inherently unsteady. This work introduces two new approaches for using motor unsteadiness as a window into central nervous system function. The first approach, termed "Force Covariance Mapping" (FCM), demonstrates experimentally that there can be systematic differences in how forces exerted by limbs fluctuate depending on the direction of intended movement. Forces exerted in different directions by the human index finger were measured using a sensitive load cell. In certain directions of intended movement, forces were found to fluctuate in magnitude only, while in other directions of intended movement, forces were found to fluctuate in both direction and magnitude. Along with electromyographic (EMG) recordings and biomechanical estimates, force fluctuation data indicates that the central nervous system uses different muscular control strategies for different directions of intended movement: some movement directions are generated primarily by single muscles while others involve cooperation among multiple muscles. The second approach, termed "EMG-weighted averaging" (EWA), couples measures of electrical activity with concurrent motor unsteadiness to estimate the direction of mechanical contribution (action) for a muscle of interest. EWA tracks how exerted forces fluctuate after EMG in a particular muscle increases. This approach allows the exploration of complex neuromechanical phenomena "in vivo". EWA was applied to forces exerted isometrically by the human index finger and EMG data from two muscles: the first dorsal interosseous (FDI) and extensor indicis proprius (EIP) muscles. EWA estimates for the action direction of these muscles were found to change depending on the intended movement direction. These changes could relate to several hypotheses of muscle action, including differential control of motor units within a muscle as well as nonlinear summation of force among muscles. In addition, this work presents novel predictive equations describing spike-triggered averaging, a commonly-used neuroscience tool for understanding motor unit function that works by coupling motor unit electrical discharges with motor unsteadiness. Studying human motor unsteadiness, in the detail presented in this work, holds great promise for increasing our understanding human motor function and pathology.