Browsing by Subject "Psychology of Movement"
Now showing 1 - 6 of 6
- Results Per Page
- Sort Options
Item Baroreflex Mediated Autonomic Modulation by Acute Pain and Orthostatic Stress(2008-10-01) Raven, Joseph Simon; James Caffrey; Joan Carroll; Robert MalletRaven, Joseph Simon, Baroreflex Mediated Autonomic Modulation by Acute Pain and Orthostatic Stress. Doctor of Philosophy (Integrative Physiology), October 2008, 147 pp.; 23 figures; bibliography; 123 titles. Nociceptive and baroreceptor afferent neurons are implicated as the components responsible for carotid baroreceptor reflex (CBR) resetting. The purpose of this dissertation was to identify the effect of cold induced pain, and cardiopulmonary baroreceptor (CPBR) unloading accompanied by pain, on CBR resetting. First, the relationships between cold induced pain to cardiovascular responses, pain perception, and muscle sympathetic nerve activity (MSNA) were investigated. Questions were addressed through use of the cold pressor test (CPT), finger plethysmography, and microneurography. This study demonstrated perceived pain, MSNA, and blood pressure responses to a cold stimulus were reproducible. Furthermore, graded responses observed in mean arterial pressure (MAP) and MSNA directly correlated to the intensity of the pain stimulus. The next study examined cold induced pain on CBR gain and operational point resetting in healthy normotensive subjects. Using similar experimental methodologies to the previous study, the data demonstrated acute pain shifted the CBR operational point toward the lower limiting value of MSNA. These data also confirmed an upward-rightward shift and increased gain of the CBR function curve during pain. Finally, CBR gain and operational point resetting during simultaneous CPBR unloading and cold induced pain in healthy normotensive subjects was addressed. Using the previous experimental paradigm, this investigation revealed CPBR unloading during acute pain did not abolish the shift of the CBR operational point. Thus, the capacity for hypotensive buffering remained enhanced. This study also determined CPBR unloading during acute pain produced higher prevailing blood pressures compared to periods of CPBR unloading alone. In summary: 1)MSNA and cardiovascular responses were tightly coupled to pain. 2) The CPT was a reliable technique for producing repeated sympathoexcitation within a subject. 3) Acute pain increased CBR gain and induced a shift of the CBR operational point. 4) The CBR operational point shift remained in the presence of CPBR unloading, which precipitated increased MAP during hypotensive stimuli. These findings suggested pain improves blood pressure maintenance during central hypovolemic stress.Item Establishing the Effects of Exercise Schema and Self-Schema on Emotional Distress(2003-08-01) Rodriguez, Leslie R.; Claudia Coggin; Joseph Doster; Daisha CipherRodriguez, Leslie R., BSN, RN, Establishing the Effects of Exercise Schema and Self-Schema on Emotional Distress. Masters of Public Health (Health Behavior), August 2003, 78 pp., 4 tables, references, 81 titles. Chronic diseases’ resulting from anger and depression represents a significant problem. Vast amounts of resources and dollars are expended and utilized. Their link to the development of cardiovascular disease, hypertension, and diabetes is recognized. Physical activity produces improvements in self-esteem, increased alertness, and decreased anxiety. The purpose of this study was determining the effect exercise and exercise schema has on mood states. College age students (N=198) of a large North Texas University were recruited. Data collection included States of change, the Exerciser self-schema questionnaire, Clinical Analysis Questionnaire, and the State Trait Anger Expression Inventory. Significance in some mood states of those who were exercising and exercise schematic were found.Item Examining Coronary Heart Disease Risk Factors and Its Relationship with Physical Activity in a Self-Reported Survey(2004-05-01) Fernandes, Alroy H.; Frederick Fridinger; Daisha Cipher; Claudia CogginFernandes, Alroy H., Examining Coronary Heart Disease Risk Factors and its Relationship with Physical Activity in a Self-Reported Survey. Masters of Public Health (Community Health), May 2004, 49pp., 3 illustrations, references, 38 titles. This study uses ‘Healthstyles,’ a self reported survey of 3,719 respondents above the age of 18, to look at exercise behavior in people at risk for CHD. Married or higher earning individuals were more likely to show sufficient exercise levels. Individuals with high blood pressure, high blood cholesterol, diabetes, obesity or family history of heart disease reported lesser levels of sufficient exercise than those without these conditions. People with CHD risk factor reported lower scores on questions that dealt with attitude and opinions about exercise behavior, and this was significantly correlated with lower levels of sufficient exercise. This supports the ‘positive attributes of the behavior’ aspect of the social cognitive theory of exercise. The attitude questions used, although not specific, could be included in a self-reported survey for the purpose of qualitatively and quantitatively assessing exercise intervention; albeit more studies are required to validate this claim.Item Interactive Effects of Mental and Physical Stress on Cardiovascular Control(1998-08-01) Westerholm, Erin Carpenter; Smith, Michael; Raven, Peter B.; Shi, XiangrongWesterholm, Erin C., Interactive Effects of Mental and Physical Stress on Cardiovascular Control. Master of Science (Biomedical Sciences, Integrative Physiology), August, 1998, 42 pp., 1 table, 13 figures, 35 references. Mental task and exercise often occur together. Physiological responses to each of these stressors have been studied independently, yet the interactive effects of these stressors are unknown. Hypothesis: Combined mental and physical stress will produce a synergistic interaction. Methods: Twelve healthy subjects were studied by measuring cardiovascular responses to five minutes of static left handgrip alone (25-35% of maximal handgrip strength), mental arithmetic alone, and combined stimuli in random order. Sympathetic nerve activity (SNA, microneurography), mean arterial blood pressure (MAP, Finapres), heart rate (HR, ECG), and vascular resistance (Doppler) were measured. Results: Physical and combined stressors significantly changed SNA, MAP, HR, and FVR. SNA responses to handgrip and the combined stimuli exceeded responses to mental arithmetic alone (p [less than] 0.05), yet no significant difference existed between responses to handgrip alone and the combined stimuli (p=0.33). The three stimuli increased heart rate similarity (p [less than] 0.0006). Conclusion: The data refuted the hypothesis: mental task did not synergistically interact or even add to the stress response elicited by handgrip exercise. Thus these data suggest that mental task and static exercise interact in a redundant manner.Item Neural Control of the Carotid Baroreflex During Exercise(2000-05-01) Gallagher, Kevin Matthew; Peter B. Raven; Stephen R. Grant; H. Fred DowneyGallagher, Kevin Matthew, Neural Control of the Carotid Baroreflex During Exercise. Doctor of Osteopathic Medicine/Doctor of Philosophy (Biomedical Sciences), May 2000; 151 pages; 13 tables; 19 figures; bibliography; 161 titles. Carotid baroreflex (CBR) function is reset upward and rightward to the prevailing blood pressure during dynamic and static exercise. Feedforward central neural inputs (central command) and negative feedback from skeletal muscle (exercise pressor reflex) both contribute to the resetting. The purpose of this investigation was to identify the individual roles of central command and the exercise pressor reflex in the resetting of the CBR during dynamic and static exercise. First, it was necessary to determine which receptor group that comprises the exercise pressor reflex, chemically-sensitive (chemoreceptors) or mechanically-sensitive (mechanoreceptors) receptors, was primarily involved in the regulation of the cardiovascular system. We observed the cardiovascular responses during exercise to individual action of the chemoreceptors and the mechanoreceptors. We demonstrated an increased mean arterial pressure (MAP) response to mechanoreceptor activation that was not identified during chemoreceptor stimulation. This finding suggested that the mechanoreflex was the primary exercise pressor mediated of arterial blood pressure during exercise. To identify the role of central command on CBR resetting, a second investigation increased central command by partial neuromuscular blockade during dynamic and static exercise. Resetting of CBR control of heart rate (carotid-cardiac; CSP-HR) and MAP (carodtid-vasomotor; CSP-MAP) during control exercise was further reset upward and rightward by increased central command without alterations in sensitivity. In conclusion, central command, a feedforward mechanism, was actively involved in the resetting of the CBR during exercise. To investigate the role of the exercise pressor reflex on CBR function, a third investigation activated by the exercise pressor reflex with the application of medical anti-shock trousers (MAS) during dynamic and static exercise. From control exercise, carotid-vasomotor function was further reset upward and rightward by the application of MAS trousers while CSP-HR function was only reset rightward. Sensitivity of the CSP-MAP and CSP-HR function curves were unaltered. The negative feedback mechanism of exercise pressor reflex, primarily mediated by mechanoreceptors, appeared to act as a modulator of CBR resetting during exercise.Item Sympathetic Responses to Dynamic Arm Ergometry in Humans(2001-05-11) Wasmund, Stephen Lee; Patricia A. Gwirtz; Peter B. Raven; H. Fred DowneyWasmund, Stephen L, Sympathetic Responses to Dynamic Arm Ergometry. Doctor of Philosophy (Biomedical Sciences), May 2001; 96 pp; 1 table; 15 figures; bibliography. Cardiovascular control during exercise is of obvious importance due to the need for an increase in cardiac output and maintenance of blood pressure when metabolic demands increase. While investigations during exercise have been conducted for some time, and much is known about the responses to dynamic exercise, the understanding of the signals that elicit the cardiovascular changes, particularly as mediated by sympathetic nerve activity (SNA) is incomplete. Sympathetic nerve activity plays an important role during exercise by causing vasoconstriction in non-working vascular beds, probably causing vasoconstriction in the vascular beds of working muscles to partially counteract the profound vasodilation caused by locally produced metabolites and by stimulating the heart to increase contractility and heart rate. It is possible to directly measure electrical activity in sympathetic nerves supplying the vasculature of skeletal muscles, however few investigations have reported on this activity during strenuous dynamic exercise. The investigations described in this dissertation extend the understanding of muscle sympathetic nerve responses to dynamic exercise. The first investigation evaluated SNA during a graded arm ergometry test to near volitional fatigue and demonstrated that increases in SNA began to occur at approximately 40% of peak exercise and then increase in a linear fashion until exercise is stopped. This relation is more closely linked to relative workload rather than heart rate as previously suggested. We also sought to determine the relationship between the increase in SNA and the ventilator threshold, hypothesizing that the two would occur at similar times, and concluded that the exercise protocol utilized did not elicit a distinct breakpoint in ventilation. However, a ventilator threshold did occur in two subjects and there appeared to be an accelerated increase in SNA. The second investigation assessed the dynamics of SNA, blood pressure and heart rate responses during the onset and termination of dynamic arm ergometry at mild, moderate and intense workloads to determine the relationship between changes in sympathetic nerve activity and blood pressure. When analyzing data every 10 seconds we determined that modest increases in SNA tend to occur at the onset of exercise in most subjects, but this response did not reach significance. This finding suggests that a neural mechanism, likely central command, plays a minor role in the initial activation of SNA, although this is probably attenuated or overridden by cardiopulmonary reflex mediated sympathoinhibition as has been previously proposed. The delay (30 s) in frank sympathetic nerve activation during strenuous exercise strongly suggests that a delayed signal, probably muscle metaboreceptor stimulation, is the primary stimulus for activation of SNA. At the termination of 5 minutes of exercise SNA, blood pressure and heart rate all decreased significantly below peak values within 10 seconds. We propose that metabolites rapidly drop below a threshold level that allows SNA to decrease significantly towards baseline values. A rapid control mechanism, such as central command or mechanoreceptor stimulation, might also play an important role in returning SNA towards resting values following exercise. We conclude that SNA remains active throughout relatively strenuous dynamic exercise, and that multiple control mechanisms are likely responsible for its control during the onset and termination of exercise.