School of Public Health
Permanent URI for this communityhttp://hdl.handle.net/1903/1633
The collections in this community comprise faculty research works, as well as graduate theses and dissertations.
Note: Prior to July 1, 2007, the School of Public Health was named the College of Health & Human Performance.
Browse
19 results
Search Results
Item THE RELATIONSHIP OF PERCEIVED WORKLOAD AND PSYCHOMOTOR PERFORMANCE TO BRAIN DYNAMICS DURING VARYING DEGREES OF TASK DEMAND AND CONTROLLABILITY IN A FLIGHT-RELATED COMPENSATORY TRACKING TASK(2024) Pietro, Kyle; Hatfield, Bradley D.; Kinesiology; Digital Repository at the University of Maryland; University of Maryland (College Park, Md.)The assessment and prediction of cognitive-motor performance holds great importance for any discipline connected to human operators in the context of safety-critical behavior. A study of mental workload is essential to understanding the intrinsic limitations of the human information processing system, and the resultant cognitive-motor behavior. Mental workload and the quality of cognitive-motor performance are generally known to be impacted by task demand. However, one feature of task demand far less understood is the controllability of a system (e.g. the responsiveness of a flight platform and its handling qualities). In the realm of Human-Machine Interface, the assessment of system controllability has typically been conducted through subjective measurements, such as the Cooper-Harper Rating Scale, a widely used metric in aircraft design to measure perceived operator workload and handling qualities, first proposed in 1969. A fundamental element of the decision making process for handling qualities associated with operator workload includes the reporting of the control compensation required to overcome deficiencies and errors that could impact and inhibit the successful completion of a task. Yet, the Cooper-Harper Rating Scale, and all other subjective rating scales are limited by a lack of objectivity, reliability, reduced sensitivity to dynamic changes in operator workload, and, are solely dependent on subjective estimates of effort to control compensation within a system, despite such wide usage in the field. To overcome such limitations, the contribution of this dissertation is the estimation of perceived operator workload, based on objective brain dynamics captured during varying levels of task demand and controllability. Therefore, the objective of this dissertation was to ascertain how objective brain dynamics and subjective ratings would respond to flight-related compensatory tracking tasks when handling qualities and task demand are manipulated. More specifically, this dissertation assessed the relationship between objective brain dynamics and subjective rating scales explicitly related to mental workload, as reported during compensatory tracking tasks of varying complexity, while also challenged with progressively increasing levels of controllability (i.e., levels of handling qualities). Thus, Aim 1 was to assess the effects of varying levels of handling qualities (i.e., HQR1, HQR2, HQR3) on mental workload and psychomotor performance. Aim 2 was to investigate the effects of increased task demand (i.e., Single-axis vs. Multi-axis) on mental workload and psychomotor performance. Finally, Aim 3 was to examine the empirical relationship between objective brain dynamics and subjective ratings of workload. Accordingly, this dissertation employed a 2 Condition (Single-axis vs. Multi-axis) x 3 Level of Handling Qualities (HQR1, HQR2, HQR3) design. Perceived workload, psychomotor performance, and brain dynamics, derived from EEG power spectra and spectro-temporal analyses, were assessed in twenty-two volunteer participants in the Naval Reserve Officers’ Training Corps. Overall, the findings of this dissertation support a characterization of the human information processing system as a finite resource with a limited capacity. When challenged with increasing levels of handling qualities, parietal alpha power decreased, behavioral performance was significantly attenuated, and subjective ratings of workload were higher, as was expected. Accordingly, there was a significant relationship between objective brain dynamics and subjective ratings of workload. Furthermore, an exploratory wavelet-based analysis revealed some generally high cross-correlations between brain dynamics and psychomotor performance, which may inform future research efforts of more dynamic measurement strategies to capture perceived workload with increased fidelity. Therefore, the results of this dissertation underscore the usage of objective brain dynamics to supplement subjective rating scales, which can provide additional insights to enhance our understanding of brain and motor coordination under varying levels of task demand and system handling qualities.Item HIPPOCAMPAL GLUCOSE TRANSPORT AND OXIDATION IN RESPONSE TO DISRUPTED BLOOD FLOW IN AN AGING RAT MODEL OF HEART FAILURE(2023) Pena, Gabriel Santiago; Smith, J. Carson; Kuzmiak-Glancy, Sarah; Kinesiology; Digital Repository at the University of Maryland; University of Maryland (College Park, Md.)The primary objective of this dissertation was to investigate, in a rodent model of cardiovascular disease promoted by transverse aortic constriction (TAC), whether cerebral hypoperfusion stemming from chronic high pulsatile blood flow, and cerebral hypoperfusion stemming from low cerebral blood flow differentially affected hippocampal glucose transport and hippocampal mitochondrial function. We first, characterized the changes in right and left carotid hemodynamics and diameter in response to TAC and in a SHAM control group at three different time points (20-, 30-, and 40 weeks) post-surgery. Then, right, and left hippocampal mitochondrial content and substrate oxidation were investigated, and protein expression of glucose transporters and mitochondrial quality control markers were quantified. In this study, both the SHAM and TAC conditions included male and female rats to address possible sex differences. We report that all time points within TAC, right carotid blood flow velocities and pulsatility were greater than the left, but did not worsen over time. No differences in mitochondrial content were found within TAC nor between TAC and SHAM, but within TAC animals there were impairments in right hippocampal coupled and uncoupled respiration when compared to the left. When compared to the SHAM controls, right and left hippocampi of TAC animals had higher protein expression of mitochondrial quality control markers, but no differences in glucose transporter expression were found. Thus, while both high blood flow and/or pulsatility as well as low cerebral blood flow may lead to brain hypoperfusion, the metabolic consequences of the two may not be the same. The results from this dissertation contribute to the expanding literature characterizing the intersection between cardiovascular disease and neurodegeneration.Item ALLOSTATIC LOAD INFLUENCES VASCULAR FUNCTION AND SYMPATHOLYSIS IN YOUNG BLACK ADULTS(2024) Eagan, Lauren Elizabeth; Ranadive, Sushant M; Kinesiology; Digital Repository at the University of Maryland; University of Maryland (College Park, Md.)In the U.S., Black individuals tend to face a disproportionately higher risk for hypertension. This is largely attributed to chronic sympathetic activation induced by heightened exposure to psychosocial stressors. Allostatic load (AL), an index of cumulative physiological dysfunction from chronic stress, is associated with hypertensive risk and is also heightened in Black adults compared to those of other racial groups. Indeed, increased sympathetic activity is a hallmark characteristic of both hypertension and AL. The inability to blunt sympathetic-induced vasoconstriction during exercise (impaired functional sympatholysis) is also associated with hypertension. This dissertation aimed to investigate whether AL was associated with measures of vascular health in young Black adults, both at rest and during a sympathetic stressor. In our first study, we examined associations between AL and indices of vascular function and structure among young Black adults at rest, finding that higher AL was associated with greater macrovascular dysfunction and amplified wave-reflections. Additionally, we identified significant correlations among greater self-perceived stress with smaller brachial artery diameters and greater wave-reflections. The second aim of this dissertation focused on the associations between AL and the magnitude of functional sympatholysis among this population. Results indicated a positive association between AL and functional sympatholysis, with amplified sympatholytic responses among young Black females, as compared to their male counterparts, when forearm volume was controlled for. Overall, our findings suggest that elevated AL might predict macrovascular dysfunction at rest, with larger arterial diameters potentially compensating for chronic stress. These adaptive mechanisms, commonly observed in aging and diseased states, may also explain the positive correlations between AL and the functional sympatholytic response in young Black adults. Our consistent observations of the redundant vascular mechanisms among young Black adults allowing for adaptation to chronic stress strengthen our findings and further highlight the complex interplay between stress and cardiovascular health in Black adults.Item SIMILAR VASCULAR RESPONSES TO A HIGH-FAT MEAL, REGARDLESS OF RACE AND SOCIAL DETERMINANTS OF HEALTH(2022) Weiner, Cynthia Marie; Ranadive, Sushant M; Kinesiology; Digital Repository at the University of Maryland; University of Maryland (College Park, Md.)Black individuals are at a higher risk for developing cardiovascular disease (CVD), including hypertension, compared to white individuals. Chronic low-grade inflammation contributes to hypertension by causing vascular dysfunction, including increased vascular resistance. Young, healthy, normotensive black individuals exhibit heightened inflammatory biomarkers at rest, a possible factor in the higher prevalence of hypertension seen within this population. Vascular function decreases transiently as a result of an acute inflammatory stimulus, such as with consumption of a high-fat meal (HFM). However, there is limited evidence regarding the racial differences in inflammatory and vascular responses to a HFM in young, healthy black and white individuals. Furthermore, there are limited data regarding the association between social determinants of health (SDH) factors and the physiological components of inflammation and vascular responses. Therefore, the goal of the present study was twofold: to evaluate the racial differences in inflammatory and vascular responses to a HFM and to evaluate the potential impact of SDH factors on these relationships. Five black individuals (5 males, 21.2 ± 1.5 yrs) and 14 white individuals (7 males/7 females, 25 ± 4.1 yrs) completed the study. White individuals were significantly older than black individuals, but were similar in fitness status (VO2peak; 43.4 ± 10.8 ml/kg/min vs. 40.5 ± 5.9 ml/kg/min) and BMI (22.6 ± 2.9 kg/m2 vs. 23.5 ± 3.3 kg/m2). Black and white individuals exhibited similar vascular function, arterial stiffness, wave reflection, and hemodynamic variables (BP, HR) at baseline and following the HFM. Black individuals had a significantly lower total SDH score compared to white individuals, indicating lower SDH across seven domains assessed in the SDH questionnaire. However, SDH was not associated with any of the vascular measurements at baseline or following the HFM. Inflammation was not detected at baseline and following the HFM, as measured by a multiplex immunoassay. Therefore young, healthy black and white individuals maintain vascular function following a HFM, regardless of SDH status.Item Cardiac Mitochondrial Function and Exertional Tolerance in a Rat Model of Pressure-Overload Induced Heart Failure(2022) Li, Harry Zichen; Kuzmiak-Glancy, Sarah; Kinesiology; Digital Repository at the University of Maryland; University of Maryland (College Park, Md.)Heart failure (HF) is characterized by the inability of the heart to provide adequate cardiac output to meet their body’s demand for fuel and oxygen, particularly during periods of exertion. In fact, a hallmark characteristic of HF is exertional intolerance where performing activities brings about, or exacerbates, symptoms of dyspnea and/or fatigue. This exercise intolerance has been attributed to altered cardiac and skeletal muscle function. The myocardium of the heart is reliant upon cardiac mitochondria to generate sufficient ATP to fuel this highly metabolically active tissue. Therefore, reduced mitochondrial ATP production may play a role in myocardial dysfunction and contribute to reduced cardiac output in HF. Mitochondria react to intracellular signals to respond to energetic demands, and therefore, mitochondrial function is a product of both the mitochondria itself and the environment in which it resides. Intracellular Ca2+ and Na+ are of particular interest as they play a role in regulating mitochondrial function and the intracellular concentrations are elevated in ventricular myocytes in HF. Therefore, a goal of these investigations was to evaluate how altered Na+ and Ca2+ can impact the ability of cardiac mitochondria to respond to an increase in demand in mitochondria isolated from young healthy rat hearts, as well as rats with pressure-overload induced HF. A second goal of these investigations was to determine if pressure-overload induced heart failure altered exercise capacity, as well as in vivo and ex vivo skeletal muscle strength. In the first study, mitochondria were isolated from the ventricular tissue of young, healthy male rats, and oxygen consumption and mitochondrial activation by Ca2+ was assessed in the presence of elevated Na+ to mimic the cellular environment of HF. Ca2+ effectively activated mitochondrial ATP production, despite elevated Na+, suggesting that the ionic conditions of HF ventricular myocytes alone are not sufficient to disrupt mitochondrial function. In the second study, mitochondrial function was assessed under the same ionic conditions as the previous study, however, mitochondria were isolated from male rats with pressure-overload induced hypertrophy or sham-operated controls. Ca2+ was able to activate mitochondrial function regardless of Na+ concentration in both HF and sham mitochondria; however, failing mitochondria exhibited depolarized mitochondrial membrane values across these respiration rates, implicating an impaired potential for ATP production in failing ventricular mitochondria. In the third study, HF and sham male and female rats were evaluated for their exertional tolerance, and the results indicated that HF rats tolerated treadmill running and showed no deficits in grip exercise; however, solei muscle from female heart failure rats exhibited diminished contractile capacity, suggesting female skeletal muscle may respond differently than male skeletal muscle to heart failure. These findings indicate that failing mitochondria may be intrinsically dysfunctional regardless of an altered ionic environment and that there may be sexual dimorphism in the skeletal muscle function and its role in exercise intolerance in HF.Item CONCENTRATION- AND TIME-DEPENDENT EFFECTS OF PROGESTERONE ON ENDOTHELIAL CELLS(2022) Kim, Katherine In-Wha; Prior, Steven J; Kinesiology; Digital Repository at the University of Maryland; University of Maryland (College Park, Md.)The termination of endogenous sex hormone release is thought to account for increases in cardiovascular disease (CVD) incidence in postmenopausal women. Thus, hormone replacement therapy may be a preventive measure against cardiovascular disease. To date, most research has been focused on estrogen treatment, but the effects of progesterone, a vasoactive hormone with effects on the endothelium, have received less attention. Two progesterone receptor subtypes, nuclear and membrane, are known to enact the effects of progesterone in endothelial cells which mediate the release of nitric oxide (NO). There is also some evidence that the two subtypes function in a coordinated manner. The aims of this thesis study are to assess the effects of different concentrations of progesterone on endothelial cells and isolate the actions of the progesterone receptor subtypes. Outcomes of this study include migration and proliferation assays to assess endothelial cell function and Western blotting to quantify endothelial nitric oxide synthase expression and phosphorylation. Progesterone and the membrane progesterone receptor agonist were found to inhibit migration and proliferation of human umbilical vein endothelial cells (HUVECs), while progesterone alone or in combination with the membrane progesterone receptor agonist increased endothelial nitric oxide synthase (eNOS) phosphorylation in HUVECs after 24 hours of incubation. While increased eNOS phosphorylation is thought to be beneficial to HUVEC function, other factors released in the presence of progesterone or progesterone receptor agonists may be scavenging bioavailable NO, thus reducing the angiogenic potential of HUVECs.Item RACIAL DIFFERENCES IN VASCULAR FUNCTION FOLLOWING INDUCED ACUTE INFLAMMATION(2020) Chesney, Catalina Anne; Ranadive, Sushant M; Kinesiology; Digital Repository at the University of Maryland; University of Maryland (College Park, Md.)African-Americans (AAs) have higher rates of cardiovascular disease (CVD), including hypertension and stroke, as compared to their Caucasian-American (CA) counterparts. High resting concentrations of systemic inflammatory biomarkers contribute to vascular dysfunction and are predictive of future cardiovascular events; differential resting levels of inflammatory markers between groups may reveal increased potential for CVD in at-risk groups. Additionally, impaired endothelial function and increased arterial stiffness, subclinical measures of CVD progression, have been reported in AA groups. The purpose of this study was to examine race differences between young, healthy AA and CA adults after a systemic inflammatory stimulus and subsequent endothelial responses to inflammation. Endothelial function, arterial stiffness, and hemodynamic variables were measured. The results suggest there were no race differences in vascular function or hemodynamic responses following an acute inflammatory stimulus.Item The Impact of Acute Aerobic Exercise on Semantic Memory Activation in Healthy Older Adults(2018) Won, Junyeon; Smith, Jerome C; Kinesiology; Digital Repository at the University of Maryland; University of Maryland (College Park, Md.)Background: A growing body of exercise literature use functional magnetic resonance imaging (fMRI) technique to measure the effects of exercise on the brain. Findings suggest that regular participation of long-term exercise is associated with enhanced cognitive function. However, fundamental questions regarding the beneficial effects of acute exercise on semantic memory have been ignored. Purpose: This study investigated the effects of a single session of exercise on brain activation during recognition of Famous names and Non-Famous names compared to seated-rest in healthy older adults (age 65-85) using fMRI. We also aimed to measure whether there are differences in brain activation during retrieval of Famous names from three distinct time epochs (Remote, Enduring, and Recent) following acute exercise. Methods: Using a within-subjects counterbalanced design, 30 participants (ages 55-85) will undergo two experimental visits on separate days. During each visit, participants will engage in 30-minutes of rest or stationary cycling exercise immediately followed by the famous name discrimination task (FNT). Neuroimaging and behavioral data will be processed using AFNI (version 17.1.06) and SPSS (version 23), respectively. Results: HR and RPE were significantly higher during exercise. Acute exercise was associated with significantly greater semantic memory activation (Famous > Non-Famous) in five out of nine regions (p-value ranged 0.027 to 0.046). In an exploratory epoch analysis, five out of 14 brain regions activated ruing the semantic memory task showed significantly greater activation intensity following the exercise intervention (Enduringly Famous > Non-Famous). Conclusions: Enhanced semantic memory processing is observed following acute exercise, characterized by greater fMRI response to Famous than Non-Famous names. Enduringly Famous names exhibited significantly greater activation after exercise compared to Non-Famous names. These findings suggest that exercise may improve semantic memory retrieval in healthy older adults, and may lead to enhancement of cognitive function.Item BIOLOGICAL AND FUNCTIONAL CHANGES IN SUPRASPINATUS MUSCLE AFTER ROTATOR CUFF TEAR(2017) Valencia, Ana Patricia; Spangenburg, Espen E; Hagberg, James M; Kinesiology; Digital Repository at the University of Maryland; University of Maryland (College Park, Md.)Rotator cuff (RTC) tears impair upper limb mobility and affect 20% of the adult population. Unfortunately, surgical repair of major RTC tears often fails to restore shoulder function and has a high risk of re-tear. RTC tears induce irreversible, degenerative changes to the muscle that may hinder the recovery of shoulder function. Currently, very few studies have comprehensively assessed RTC muscle function, thus, little is known about which markers may be able predict changes in function after RTC tear. In this dissertation, I present three studies designed to systemically determine the impact of a RTC tear on contractile function of the supraspinatus (SS), the muscle most commonly affected in the RTC. In study #1 I developed a novel method to test in vivo SS contractile function using animal species common to RTC research. In study #2, I found that the SS exhibited a 30% loss in force prior to onset of muscle atrophy after acute RTC tear using the rat model. The initial loss of force was associated with a decrease in the size and continuity of the neuromuscular junction (NMJ). The SS muscle was also more susceptible to injury, which was associated with a reduction in collagen packing density. Therefore, SS size is not the strongest predictor of force output with acute RTC tears. In addition, the increased susceptibility to injury could compound the dysfunction already apparent in the SS muscle after RTC tear. In study #3, I found that the rabbit model experienced a 40% loss of force after 6 weeks of RTC tear that persisted at 12 weeks. Using a number of different in vivo and ex vivo imaging approaches I found the degree of fatty infiltration (FI) to be the strongest predictor of muscle force production after RTC tear. Surprisingly, the data suggested that muscle atrophy only explained the loss in force in torn muscles when little to no FI was present. Therefore, FI is a prognostic marker for muscle weakness after RTC tear, and can help clinicians predict the force generating capacity of the SS for surgery and rehabilitation decision-making. Results from both studies found that SS contractile function was significantly impaired after RTC tear, and identified measureable markers beyond muscle atrophy that were associated with the loss in muscle force that may act as potential therapeutic targets to improve functional outcomes after RTC tear.Item The role of intracellular calcium perturbations in muscle damage and dysfunction in mouse models of muscular dystrophy(2016) Mázala, Davi Augusto Garcia; Chin, Eva R; Kinesiology; Digital Repository at the University of Maryland; University of Maryland (College Park, Md.)Duchenne muscular dystrophy (DMD) is a neuromuscular disease caused by mutations in the dystrophin gene. DMD is clinically characterized by severe, progressive and irreversible loss of muscle function, in which most patients lose the ability to walk by their early teens and die by their early 20’s. Impaired intracellular calcium (Ca2+) regulation and activation of cell degradation pathways have been proposed as key contributors to DMD disease progression. This dissertation research consists of three studies investigating the role of intracellular Ca2+ in skeletal muscle dysfunction in different mouse models of DMD. Study one evaluated the role of Ca2+-activated enzymes (proteases) that activate protein degradation in excitation-contraction (E-C) coupling failure following repeated contractions in mdx and dystrophin-utrophin null (mdx/utr-/-) mice. Single muscle fibers from mdx/utr-/- mice had greater E-C coupling failure following repeated contractions compared to fibers from mdx mice. Moreover, protease inhibition during these contractions was sufficient to attenuate E-C coupling failure in muscle fibers from both mdx and mdx/utr-/- mice. Study two evaluated the effects of overexpressing the Ca2+ buffering protein sarcoplasmic/endoplasmic reticulum Ca2+-ATPase 1 (SERCA1) in skeletal muscles from mdx and mdx/utr-/- mice. Overall, SERCA1 overexpression decreased muscle damage and protected the muscle from contraction-induced injury in mdx and mdx/utr-/- mice. In study three, the cellular mechanisms underlying the beneficial effects of SERCA1 overexpression in mdx and mdx/utr-/- mice were investigated. SERCA1 overexpression attenuated calpain activation in mdx muscle only, while partially attenuating the degradation of the calpain target desmin in mdx/utr-/- mice. Additionally, SERCA1 overexpression decreased the SERCA-inhibitory protein sarcolipin in mdx muscle but did not alter levels of Ca2+ regulatory proteins (parvalbumin and calsequestrin) in either dystrophic model. Lastly, SERCA1 overexpression blunted the increase in endoplasmic reticulum stress markers Grp78/BiP in mdx mice and C/EBP homologous protein (CHOP) in mdx and mdx/utr-/- mice. Overall, findings from the studies presented in this dissertation provide new insight into the role of Ca2+ in muscle dysfunction and damage in different dystrophic mouse models. Further, these findings support the overall strategy for improving intracellular Ca2+ control for the development of novel therapies for DMD.