(Georgia Institute of Technology, 2010-11-03)
Auyang, Arick Gin-Yu
The kinematic motor redundancy of the human legs provides more local degrees of freedom than are necessary to achieve low degree of freedom performance variables like leg length and orientation. The purpose of this dissertation is to investigate how the neuromuscular skeletal system simplifies control of a kinematically redundant system to achieve stable locomotion under different conditions. I propose that the neuromuscular skeletal system minimizes step to step variance of leg length and orientation while allowing segment angles to vary within the set of acceptable combinations of angles that achieves the desired leg length and orientation. I find that during human hopping, control of the locomotor system is organized hierarchically such that leg length and orientation are achieved by structuring segment angle variance. I also found that leg length and leg orientation was minimized for a variety of conditions and perturbations, including frequency, constrained foot placement, and different speeds. The results of this study will give valuable information on interjoint compensation strategies used when the locomotor system is perturbed. This work also provides evidence for neuromuscular system strategies in adapting to novel, difficult tasks. This information can be extended to give insight into new and different areas to focus on during gait rehabilitation of humans suffering from motor control deficits in movement and gait.
(Georgia Institute of Technology, 2009-11-17)
Brown, Mary Beth
Our aim was to understand mechanisms responsible for excessive electrolyte loss in the sweat gland and the potential impact on fluid balance during exercise in heat stress conditions. Human physiological testing under exercise/heat stress and immunofluorescence staining of sweat glands from skin biopsies were compared between healthy individuals (with normal and high sweat sodium chloride concentration, [NaCl]) and with cystic fibrosis patients (CF), who exhibit excessively salty sweat due to a defect of Cl- channel cystic fibrosis transmembrane conductance regulator (CFTR). Three novel findings are presented. First, excessively salty sweat may be associated with reduced expression of CFTR in the sweat gland reabsorptive duct of healthy individuals in addition to in those with CF; however, although a link to a CF gene mutation in healthy individuals with high sweat [NaCl] was not demonstrated, the possibility of an undetected CFTR mutation or polymorphism remains to be investigated as an underlying mechanism. Two, CF and healthy individuals with excessively salty sweat respond to moderate dehydration (3% body weight loss during exercise) with an attenuated rise in serum osmolality, greater relative loss in plasma volume, but similar perceived thirst compared to healthy individuals with "normal" sweat [NaCl]. However, individuals with CF respond to rehydration with hypotonic beverage by drinking less ad libitum in response to reduced serum [NaCl], suggesting that thirst-guided fluid replacement may be more appropriate for this population rather than restoring 100% of sweat loss following dehydration as is often recommended in healthy individuals.