Neural contributions to maximal muscle performance
2014-06-06T08:32:53Z (GMT) by
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.