The aim of this thesis is to investigate the responses of the neuromuscular system to changes and constraints during explosive multi-segment movements of the lower limbs. The trunk segment was constrained into different positions during pendulum rebound exercises to observe how the neuromuscular system reorganises the movement. It was also aimed to examine how the neuromuscular system coordinates maximal countermovement jumps when the muscle forcegenerating properties of part and all muscles involved in these movements are reduced by the acute effects of fatigue or increased after training. The kinematic characteristics of pendulum rebound exercises were affected by constraining the trunk segment. Greater knee joint angular velocity was achieved when the movements were performed in the upright sitting posture (90) in comparison to the other sitting conditions (135° and 180°). The constraint applied on the trunk segment did not result in the emergence of a particular segmental movement between the hip, knee and ankle joints and variability was observed in the initiation of the joint extension of all rebound conditions. The absence of a fixed order for joint extension initiation showed that sequential and temporal variances can emerge during rebound jumps, where the hip joint, in most cases,e xtendedb efore the other joints. The biarticular musclesw ere suggestedto regulatet he distribution of forces between joints by transporting the large amounts of energy produced by monoarticular muscles, irrespective of the constraints imposed on the trunk segment. It was proposed the existence of a pre-programmed pattern that guides the execution of the movement irrespective of the constraints applied on the trunk segment. Fatiguing part and/or all muscle groups involved in maximal countermovemenjtu mps suggestedt he existence of a common drive that mediates and controls the activation timing between agonistantagonist muscle pairs. A similar muscle activation pattern found after fatigue indicated that the neuromuscular system does not reorganise the co-ordination strategy of explosive movements to compensate for the acute effects of muscular fatigue and acts without the knowledge of the muscle force-generating properties. The decline in the ability of the muscles to produce force was the major factor responsible for the decreases observed in jump height and changes in several kinematic and kinetic variables of the movement. The early occurrence of the peak joint angular velocity may have contributed to jump height decrease and indicated that an "optimal" solution (high countermovement jump performance) was not found under fatigue. It was suggested that training under fatigue should be avoided because the subjects may learn a muscle activation pattern that does not represent an optimal solution. Countermovement jump training (specific stimulus) was more effective than a weight lifting programme (non-specific stimulus) to improve jump height performance. This occurred despite the greater gains in isokinetic peak torque of the knee flexor and extensor muscles achieved after the nonspecific training programme in comparison to the specific training programme. It was observed that the training using non-specific stimulus did not cause the neuromuscular system to reorganise the controls. The neuromuscular system was able to reorganise the movement after the training programme that used a specific stimulus. It was concluded that the increased jump height performance observed after the countermovement jump programme can be attributed to a compounded effect, in which the increased ability of the extensor muscles to generate large amounts of energy around the hip joint was linked to the ability of the biarticular muscles to transfer part of this energy to the distal joints. It was noticed that movement co-ordination changes are sensitive to the order in which the training stimuli are introduced. Jump height performance was improved to a greater extent when the countermovement jumps programme followed the knee extensor and flexor muscles strengthening programme than when the training programmes were introduced in the opposite order.

Salamanders have a remarkable ability to regenerate complex body parts including the limb, tail, and central nervous system. Although salamander regeneration has been studied for several hundred years, molecular-level studies have been limited to a relatively few important transcription factors and signaling molecules that are highly conserved among animals. Physiological genomic approaches were used here to investigate spinal cord and limb regeneration. Chapter 2 reports that hundreds of gene expression changes were identified during spinal cord regeneration, showing that a diverse injury response is activated in concert with extracellular matrix remodeling mechanisms during the early acute phase of natural spinal cord regeneration. Chapter 3 presents results that identify the salamander ortholog of mammalian Nogo-A, a gene known to inhibit mammalian nerve axon regeneration. Nogo-A gene expression was characterized during salamander development and adulthood in order to address the roles of Nogo-A in the nervous system. Chapters 4 and 5 use physiological genomic approaches to examine limb regeneration and why this process is dependent upon an intact nerve supply. Results presented in Chapter 4 showed that many processes regulated during early limb regeneration do not depend upon nerve-derived factors, but striking differences arise between innervated and denervated limbs by 14 days after amputation. Chapter 5 identified genes associated with peripheral nerve axon regeneration and identified gene candidates that may be secreted by nerves to support limb regeneration. Lastly, chapter 6 characterizes the expression of a developmentally important family of genes, matrix metalloproteinases, during tail regeneration. These results suggest that matrix metalloproteinases play multiple roles throughout the regeneration process. Primarily, this dissertation presents data from the first genomic studies of salamander regeneration. The results suggest genes such as matrix metalloproteinases, and molecular pathways such as the Wnt and FGF signaling pathways that can be exploited to enhance regenerative ability in humans.

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