The purpose of this study was to display increase in eccentric hamstring strength after 10-weeks training program. Secondly, if such an increase occurred, would this strength change result in altered landing kinetics and improved jumping performance? 27 recreational female athletes assigned into experimental (n = 14) and control (n = 13) groups. Baseline measures of landing kinetics were collected using a force plate, strength data and proprioceptive measurements were evaluated using an isokinetic dynamometer and vertical jump performance were determined by a jumping mat. Results indicated that NHST group increased their eccentric hamstring strength after eccentric strength training program (week-1 = 233.6&plusmn / 27.5, week-10 = 253.8&plusmn / 28.4 Nm/kgbw / p&lt / .05). The results demonstrated that there were significant differences in landing mechanics for NHST group. PVGRF (week-1 = 6.2&plusmn / 0.9, week-5 = 5.3&plusmn / 0.9 / p&lt / .05), PAPGRF (week-1 = 1.1&plusmn / 0.2 &amp / week-10 = 0.8&plusmn / 0.3 / p&lt / .05) and APImp results demonstrated significant differences in trained group (week-1 = 78.1&plusmn / 13.6 &amp / week-10 = 67.8&plusmn / 9.2 / p&lt / .05). NHST group exhibited significant increase in vertical jumping ability (week-1 = 0.25&plusmn / 0.0 &amp / week-10 = 0.27&plusmn / 0.0 cm / p&lt / .01). This study supported the following points: 1) increases in the eccentric hamstring strength were evident after NHST program, 2) the increases in isokinetic strength were sufficient to cause alterations in landing kinetics to decrease the applied joint forces, so the NHST program would be an influential factor in decreasing the lower extremity injuries, and 3) the increase in the efficiency of force transfer at the final take off phase of jumping contributed to a higher performance in vertical jump.

Kinematic analysis of basketball shooting is evolving, however the effects of fatigue on free throw shooting have not been studied. Therefore the effects of fatigue on the kinematics of free throw shooting among elite male basketball players was assessed. Ten healthy male collegiate basketball players participated in the study. Resting and fatigue heart rates of the participants were measured. After a 15 minute warm-up period, markers were placed on seven locations on the shooting arm&rsquo / s side upper and lower extremities. The free throw shots were recorded with two digital cameras at a speed of 60 frames/s at a stereoscopic position. Data were analyzed with the photogrammetry technique. Each participant performed free throw shots (pre-fatigue condition) until the two successful and two unsuccessful shots were collected. Then participants completed a fatigue protocol, which included sprints and squat jumping, until reaching their volitional exhaustion and free throw shots were repeated (post-fatigue condition). The elbow, trunk, knee and ankle joint angles were measured. Successful and unsuccessful shots were compared for pre- and post-fatigue conditions. The results demonstrated that fatigue did not affect free throw shooting and there was no significant joint angle difference (p&gt / .05) between successful and unsuccessful shots (p&gt / .05). It was concluded that fatigue does not affect the kinematics of free throw shooting of healthy male collegiate basketball players and there were no differences in the kinematics of selected joint angles for successful and unsuccessful free throw shots.

Skeletal muscle is defined to be atrophic in osteoporosis models and therefore is a potential target tissue for osteoporosis research. The aim of this longitudinal randomized controlled interdisciplinary study was to analyze the functional, histological, ultra-structral and molecular changes and the role of cachectic muscle atrophy inducer TNF-alpha in the skeletal muscles of the ovariectomized (OVX) rat model which mimics postmenopausal osteoporosis. Female Sprague-Dawley rats were randomly assigned to the control, the OVX and the OVX+10&amp / #956 / g/g/week TNF-alpha antagonist (Remicade) treated OVX-TNF groups. Maximum isometric and tetanic-twitch amplitudes were lower than the control group in the OVX group. Maximum isometric twitch amplitudes recovered in the fast-twitch extensor digitorum longus (EDL) muscles but not in the slow-twitch soleus muscles in the OVX-TNF group. The decrease in tetanic-twitch amplitudes recovered in the OVX-TNF group in both muscle types. Splitting and size variations of fibers, central nuclei and well-preserved overall ultrastructure were noted in the OVX and the OVX-TNF groups. Slow-twitch Type I fiber percentage, areas and diameters increased in EDL muscles of the OVX and the OVX-TNF group comparing to the control group. p65 and MyoD immune-labeling increased in OVX group whereas MyoD and C-Rel increased and p50 decreased in OVX-TNF group. Expressions of 61 genes and 42 unidentified transcripts were significantly different between the control, the OVX and the OVX-TNF groups. To sum up TNF-alpha has a role in skeletal muscle dysfunction in OVX rats and TNF-alpha antagonist administration recovered it. But this modulation was not sufficient for total structural recovery.

Although people can typically maintain balance on moving trains, or press the appropriate button on an elevator with little conscious effort, the apparent ease of these sensorimotor tasks is courtesy of neural mechanisms that continuously interpret many sensory input signals to activate muscles throughout the body. The overall hypothesis of this work is that motor behaviors emerge from the interacting constraints and features of the nervous and musculoskeletal systems. The nervous system may simplify the control problem by recruiting muscles in groups called muscle synergies rather than individually. Because muscles cannot be recruited individually, muscle synergies may represent a neural constraint on behavior. However, the constraints of the musculoskeletal system and environment may also contribute to determining motor behaviors, and so must be considered in order to identify and interpret muscle synergies. Here, I integrated techniques from musculoskeletal modeling, control systems engineering, and data analysis to identify neural and biomechanical constraints that determine the muscle activity and ground reaction forces during the automatic postural response (APR) in cats. First, I quantified the musculoskeletal constraints on force production during postural tasks in a detailed, 3D musculoskeletal model of the cat hindlimb. I demonstrated that biomechanical constraints on force production in the isolated hindlimb do not uniquely determine the characteristic patterns of force activity observed during the APR. However, when I constrained the muscles in the model to activate in a few muscle synergies based on experimental data, the force production capability drastically changed, exhibiting a characteristic rotation with the limb axis as the limb posture was varied that closely matched experimental data. Finally, after extending the musculoskeletal model to be quadrupedal, I simulated the optimal feedforward control of individual muscles or muscle synergies to regulate the center of mass (CoM) during the postural task. I demonstrated that both muscle synergy control and optimal muscle control reproduced the characteristic force patterns observed during postural tasks. These results are consistent with the hypothesis that the nervous system may use a low-dimension control scheme based on muscle synergies to approximate the optimal motor solution for the postural task given the constraints of the musculoskeletal system. One primary contribution of this work was to demonstrate that the influences of biomechanical mechanisms in determining motor behaviors may be unclear in reduced models, a factor that may need to be considered in other studies of motor control. The biomechanical constraints on force production in the isolated hindlimb did not predict the stereotypical forces observed during the APR unless a muscle synergy organization was imposed, suggesting that neural constraints were critical in resolving musculoskeletal redundancy during the postural task. However, when the model was extended to represent the quadrupedal system in the context of the task, the optimal control of the musculoskeletal system predicted experimental force patterns in the absence of neural constraints. A second primary contribution of this work was to test predictions concerning muscle synergies developed in theoretical neuromechanical models in the context of a natural behavior, suggesting that these concepts may be generally useful for understanding motor control. It has previously been shown in abstract neuromechanical models that low-dimension motor solutions such as muscle synergies can emerge from the optimal control of individual muscles. This work demonstrates for the first time that low-dimension motor solutions can emerge from optimal muscle control in the context of a natural behavior and a realistic musculoskeletal model. This work also represents the first explicit comparison of muscle synergy control and optimal muscle control during a natural behavior. It demonstrates that an explicit low-dimension control scheme based on muscle synergies is competent for performance of the postural task across biomechanical conditions, and in fact, may approximate the motor solution predicted by optimal muscle control. This work advances our understanding how the constraints and features of the nervous and musculoskeletal systems interact to produce motor behaviors. In the future, this understanding may inform improved clinical interventions, prosthetic applications, and the general design of distributed, hierarchal systems.

Thesis (Ph.D.)--Indiana University, 2009. / Title from screen (viewed on December 9, 2009). Department of Biochemistry and Molecular Biology, Indiana University-Purdue University Indianapolis (IUPUI). Advisor(s): Jeffrey S. Elmendorf, Peter J. Roach, Joseph T. Brozinick, Michael S. Sturek, Robert V. Considine. Includes vitae. Includes bibliographical references (leaves 97-124).

Parkinson's disease (PD) is an age-related neurodegenerative disease characterized by the selective loss of dopaminergic neurons in the substantia nigra of the brain. The pathogenesis and etiology of PD are unclear. Mitochondrial dysfunction occurs in PD, causing a decrease in complex I activity in postmortem brain, and exacerbating reactive oxygen species production and ATP deficiency contributing to neuronal cell death. Mutation of leucine-rich-repeat kinase 2 (LRRK2) gene is the most common genetic factor identified in both familial and sporadic PD cases. Several mutations in LRRK2 have been linked to PD, in which R1441G is the second commonest mutation after G2019S. LRRK2 protein is ubiquitously expressed in human body, in which a portion is localized to the mitochondria. Mutations of LRRK2 directly or indirectly cause mitochondria dysfunction. Dysfunction of mitochondrial respiratory complexes has been described in skin fibroblasts and skeletal muscle of PD patients. Therefore, these clinically accessible tissues are good for monitoring disease progression. The objectives of this study were to investigate how LRRK2 R1441G mutation affects normal mitochondrial function, and whether this specific LRRK2 mutation potentiates age-dependent deterioration of mitochondrial function. To achieve these aims, colonies of skin fibroblast carrying LRRK2 R1441G mutation or wild-type LRRK2 were derived from a novel LRRK2 R1441G knock-in (KI) mouse model and its wild-type (WT) littermates. Skeletal muscles were dissected from the hind legs of WT and KI mice. The effects of aging and LRRK2 R1441G mutation on mitochondrial function were investigated in vitro using these derived skin fibroblast cultures, and ex vivo using skeletal muscle obtained from young (3-month-old) and aged (18-month-old) WT and KI mice. Reduction-oxidation activities of mitochondrial complex I and complex II in skin fibroblasts and skeletal muscle were measured spectrophotometrically. Intracellular ATP levels in skin fibroblasts were determined by bioluminescent assay. Phase-contrast microscopy showed that aging and LRRK2 R1441G mutation did not affect cell morphology of the derived skin fibroblast cultures. Complex I activity determined in skin fibroblasts and skeletal muscle derived from KI and their WT littermates revealed that, aging caused a significant increase in complex I activity in WT but not KI skin fibroblasts. Conversely, a significant decrease in complex I activity was observed in both WT and KI skeletal muscle, demonstrating an aging effect ex vivo. LRRK2 R1441G mutation did not affect complex I activity in WT and KI skin fibroblasts and skeletal muscle. Moreover, complex II activity in these two tissues was neither affected by aging nor R1441G LRRK2 mutation. Intracellular ATP levels in the skin fibroblast cultures were also unaltered by aging and LRRK2 R1441G mutation. In conclusion, my current findings indicated a significant aging effect on mitochondrial complex I activity ex vivo, supporting the role of age-dependent deterioration of complex I activity in mitochondrial dysfunction of PD. LRRK2 R1441G mutation did not affect complex I and II activities in both skin fibroblasts and skeletal muscle. Also, this mutation did not potentiate the age-dependent deterioration of complex I activities as observed in skin fibroblasts and skeletal muscle of the LRRK2 R1441G knock-in mice. / published_or_final_version / Medicine / Master / Master of Philosophy

Not available / text

Ectotherms regulate body temperature (Tb) primarily through behavioral interactions with their environment. These animals also have limited aerobic scopes and must rely on anaerobic metabolism to support intense activity; lactate byproduct and glycogen depletion are two consequences of anaerobic metabolism that must be dealt with during exercise recovery. It has been suggested that, in many ectothermic species, Tb may affect the rate of lactate clearance and glycogen repletion during recovery from intense exercise. This study investigated thermoregulatory behavior in Western Fence Lizards (Sceloporus occidentalis) to determine preferred Tb during exercise recovery. I hypothesized that animals would select higher Tb’sduring the recovery period on the basis that biochemical processes occur at faster rates at high temperatures, which may facilitate a more rapid reduction of lactate and replenishment of glycogen stores. However, it was found that control animals maintained a constant Tb of 33°C, while exercised animals cooled Tb to 30°C 20 minutes after exercising, and eventually warmed to 32°C by the 2 hour mark. Animals were found to be able to cool Tb by a maximum of 0.175°C/min given the available temperatures, which negated possible effects of temperature variation on Tb during exercise trials and transport. My results suggest a benefit of lowered Tb to facilitate exercise recovery in these animals. Behavioral hypothermia in S. occidentalis may be caused by physiological triggers associated with intense activity such as hypoxia, hypercapnia, or elevated blood lactate concentration. However, these speculations must be confirmed by further research.

No description available.

Locomotion persists despite changes in external and internal circumstances. Motor responses to gait impairment exhibit commonalities across various taxa and types of injury, yet we lack a systematic understanding of compensation strategies. The objective of this dissertation is to uncover principles governing implicit goals within the control of locomotion. I propose that coordination of injured locomotion will demonstrate that these goals follow a hierarchical organization of the neuromuscular system. Accurate quantification of gait deficits in rodents demands sophisticated measurement techniques. I utilize X-ray technology to examine intralimb and interlimb coordination after unilateral injury in rats. My findings indicate that compensation to injury involves the coordination of lower-order motor elements to preserve the pre-injury behaviors of higher-order elements. Specifically I present evidence that preservation of limb angle and limb length are critical task goals that transcend injury states and afferent sensory feedback conditions. Broadening my investigation to include interlimb coordination revealed that task goals may change to satisfy the goals of a higher hierarchical level. This work is a necessary precursor to study locomotor coordination and injury compensation in more complex rodent injury models such as self-reinnervation, sciatic nerve, and spinal cord injury. These results could also translate to clinical gait rehabilitation through future protocols that address motor patterns of the entire limb over the behavior of individual joints.