Browsing by Subject "Other Kinesiology"
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Item Alterations in Beta-Adrenergic Receptor Density on Human Lymphocytes in Response to Chronic Exercise(2000-12-01) Brittain, Adam K.; Peter B. Raven; Stephen R. Grant; Michael W. MartinA number of cardiovascular adaptations have been shown to occur in healthy individuals as a result from regular, chronic exercise training. These changes include, but are not limited to, a lower resting heart rate, a lower heart rate at any given submaximal workload, an increase in stroke volume, an increase in maximal cardiac output due primarily to an increase in contractility, a decreased peripheral vascular resistance (increased peripheral vascular conductance), an overall increase in vascularity, an increase in left ventricular mass, and an increase in total body oxygen extraction (Raven, 1994). Some of these adaptations are also known to commonly occur in patients with coronary artery disease enabling them to increase their total work capacity. Therefore, exercise apparently adapts the heart to better cope with the adverse affects of coronary artery disease and helps to prevent the aforementioned disease from developing in healthy individuals. The beta-adrenergic receptor (β-AR) is essential for the activation of many aspects of the cardiovascular system during dynamic exercise (1). The catecholamines epinephrine and norepinephrine are released from the adrenal medulla and postganglionic fibers of the sympathetic nervous system respectively in response to dynamic exercise. Epinephrine and other beta-adrenergic receptor agonists bind and activate the β-AR on the cell membrane thus allowing it to couple with the stimulatory GTP-binding regulatory protein Gs. This step initiate the activation of adenylate cyclase and the synthesis of cyclic adenosine 3’,5’ monophosphate (cyclic AMP), a key intracellular second messenger. Cyclic AMP ultimately activates cyclic AMP-dependent protein kinase (PKA), an enzyme that phosphorylates a number of intracellular proteins that subsequently influence cell metabolism and function. Alterations in the activity of the adrenergic system seen in several clinical and physiological situations, including exercise, are directly associated with changes in lymphocytic β-AR density or function (2). Moreover, it has been suggested that the changes in receptor density on lymphocytes correlate closely with cardiovascular responsiveness to catecholamines in humans (3-6). Additionally, changes in catecholamine concentration within the physiological range have a regulatory effect on β-AR density and function (7). One particular study established an inverse relationship between plasma and urine catecholamine concentrations and lymphocytic β-AR density in man (8). It is the intent of this review to describe some of the cardiovascular adaptations that occur as a result of chronic exercise and how these changes could be caused by alterations in β-AR density and responsiveness. Additionally, the comparisons and contradictions between chronic heart failure and chronic exercise will be made. The role of the beta-adrenergic system in mediating the effects of exercise will be introduced. The structure of the β-AR will be described and how its molecular structure dictates its function. A brief synopsis will be presented on the mechanism in which β-AR operates subsequent to ligand binding. Alterations of the β-AR, particularly its expression in the heart, through transgenics will then be reviewed to show how this receptor could be responsive for some of the aforementioned adaptations to chronic exercise. In this, some of the differences between the β1- and β2-AR will be described as well as some of the therapeutic implications that could result from overexpression of the β-AR. Following this, alterations in the density of the β-AR after both short-term and long-term exposure to catecholamines will be examined. Included in this section with be the detailed description of the mechanism of receptor desensitization that precedes receptor down-regulation. A brief review will then be given on the effects of chronic exercise on β-AR density. The use of human lymphocytes as model cells will then be described. Binding theory will be explained as it will be the basis of methodology used in any subsequent studies. Along with this, [125 Iodo] cyanopindolol (125I-CYP) will be introduced and its advantages and disadvantages as a β-AR ligand probe will be discussed.Item Carotid Baroreflex of Leg Vasculature(2004-07-01) Keller, David Melvin; Peter A. Raven; H. Fred Downey; Patricia A. GwirtzKeller, David Melvin, Carotid Baroreflex Control of Leg Vasculature. Doctor of Philosophy (Biomedical Science), July 2004; 110 pp; 5 tables; 10 figures; bibliography. The carotid baroreflex (CBR) exerts control of arterial blood pressure primarily as a result of changes in total vascular conductance. In humans, understanding CBR control of the vasculature supplying a given vascular bed, such as the leg, remains unclear. Furthermore, it appears that metabolic attenuation of sympathetic vasoconstriction may modulate the CBR of the vasculature supplying contracting skeletal muscle during exercise. However, the balance between baroreflex-mediated vasoconstriction and the mechanisms responsible for the metabolic attenuation has not been fully elucidated. Therefore, the purpose of the investigations within this dissertation was to: i) explain CBR control of leg vascular conductance (LVC) and the relationship between changes in LVC and muscle sympathetic nerve activity at rest and during one-legged knee extension exercise, ii) examine the CBR control of the vasculature supplying an exercising leg and a non-exercising leg during exercise, and iii) demonstrate the role of the ATP-sensitive potassium channel in contributing to the metabolic attenuation of CBR-mediated vasoconstriction in the vasculature supplying contracting skeletal muscle. In the first investigation, we demonstrated: i) the stimulus response relationships for CBR control of LVC and MSNA at rest and during two intensities of one-legged knee extension exercise; ii) that CBR control of LVC was preserved during exercise; iii) that the attenuation of CBR-mediated vasoconstriction was no different between 7W and 25W exercise in the vasculature supplying an exercising leg; and iv) that the contribution of changes in LVC to CBR changes in mean arterial pressure was no different from rest to exercise in both the exercising leg and the non-exercising leg. In the second investigation, we examined the role of the ATP-sensitive potassium channel in modulating sympathetically-mediated vasoconstriction at rest and during exercise in the vasculature supplying an exercising leg and a non-exercising leg. The attenuated vasoconstrictor response to the carotid baroreceptor stimulated hypotension observed in the vasculature supplying an exercising leg was partially restored two to four hours after the oral ingestion of glyburide (5mg). This finding indicates that ATP-sensitive potassium channel activation plays a primary role in the effects of functional sympatholysis during leg exercise in humans. We further demonstrated that CBR control of MAP was not altered by oral glyburide administration in healthy subjects.Item Control of the Peripheral Vasculature During Exercise: Angiotensin II(2007-04-01) Brothers, Robert Matthew; Peter B. Raven; Michael Smith; Patricia GwirtzBrothers, Robert Matthew, Control of the Peripheral Vasculature During Exercise Angiotesin II. Doctor of Philosophy (Biomedical Science), April 2007, 126 pp; 3 tables; 12 figures; bibliography. Control of the vasculature during exercise is balance between sympathetic vasoconstriction and metabolic vasodilation. There is an exercise intensity dependent reduction in vasoconstriction resulting in a shift towards vasodilation within “metabolically active” muscle and tissues, a phenomena known as “functional sympatholysis”. Previous studies investigating the alpha-receptors during exercise have used intra-arterial infusions of alpha-agonists. These studies indicate that alpha-receptor vasoconstrictionis completely attenuated during mild intensity exercise. When the alpha receptors are pharmacologically blocked the magnitude and onset of “functional sympatholysis” is not as drastic when compared to the agonist infusion studies. Intense exercise also activates the renin-angiotesin-system leading to production of angiotensin II (AngII), which increases exponentially at approximately 55% maximal oxygen uptake (55% VO2max). While the mechanisms of “functional sympatholysis” has been extensively studied less is known about the role of AngII in the control of the vasculature during exercise. Therefore, the purpose of the investigations within this dissertation was to: i)determine if alpha-1- blockade in an exercising human model will identify a greater maintenance of alpha-1 mediated vasoconstriction when compared to agonist infusion studies; ii) to determine if the metabolites produced within the active skeletal muscle will attenuate angiotensin II vasoconstriction; and iii) to determine if AngII vasoconstriction provides a greater percentage contribution to vascular tone as exercise intensity increases. We demonstrated that i) pharmacologic alpha-1-blockade identified a greater maintenance of alpha-1 vasoconstriction during moderately heavy exercise; and ii) this effect decreased as intensity increased in the exercising leg and increased with intensity in the non-exercising leg. In the second investigation we demonstrated that AngII and phenylephrine (PE) mediated vasoconstriction were attenuated to a similar degree during low and mild intensity exercise. In the third investigation we observed that AT1-receptor blockade; 1) attenuated the increases in MAP that occur during high-intensity exercise; ii) did not affect the vasculature in the exercising leg but; iii) we identified that AngII does partially control the vasculature in a “non-metabolically active” muscle group.Item Elimination of Post-Exercise Hypotension Impairs Plasma Volume Recovery(1996-12-01) Hayes, Patrick M.; Peter B. RavenHayes, Patrick M., Elimination of Post-Exercise Hypotension Impairs Plasma Volume Recovery. Master of Science (Biomedical Sciences), December, 1996, 18 pp., 2 tables, 5 figures, bibliography, 20 titles. The aim of this study was to test the hypothesis that plasma volume (PV) recovery following exercise was facilitated by post-exercise hypotension. Seven volunteers performed 2 bouts of cycling exercise for 60 minutes followed by 90 minutes of seated recovery without intervention (trial 1) or with phenylephrine infusion (PE) started at 10 minutes of recovery (trial 2). Blood samples were taken throughout the protocol at specific times, and were analyzed to measure hematocrit (Hct), hemoglobin (Hb), protein content and electrolyte levels. Plasma volume was measured using the Evans Blue Dye dilution technique and estimates of changes from resting values were then calculated from Hct and Hb values. While PV approached baseline levels at 30 minutes into recovery in trial 1, the change in PV remained significantly below control values with PE. We concluded that the diminished gain in the change in total proteins (significant increase without PE, no difference from control with PE) contributed to the impaired recovery of PV observed in trial 2, and that this difference in protein shift is attributable to the elimination of post-exercise hypotension.Item Endurox R4® & Gatorade®: Effects of Recovery Drinks After Prolonged Glycogen-Depleting Exercise(1999-06-01) Williams, Michael Brandon; Raven, Peter B.; Smith, Michael; Shi, XiangrongWilliams, Michael B., Endurox R4® & Gatorade®: Effects of Recovery Drinks After Prolonged Glycogen-Depletion Exercise. Master of Science (Biomedical Sciences, Integrative Physiology), June, 1999, 73 pp., 2 tables, 18 figures, references. Purpose: Eight high-fit (bicycle Vo2max=62.4 ± 1.10 ml·kg-1·min-1) male cyclists, aged 28.4±1.65 yrs, performed a two-hour endurance bicycle exercise to achieve depletion of skeletal muscle and liver glycogen. During recovery, Endurox R4 Recovery Drink®, or Gatorade®, was ingested to investigate their relative restorative capacities to enable further exercise. Methods: Each subject performed two days of testing: one for each drink presented in random order. On each testing day, the twelve-hour fasted subject performed a two-hour cycling exercise bout at 75% VO2max followed by one to three five-minute sprints at 85% VO2max. At the end of the exercise blood glucose concentrations were 3.98±0.138 mmol/L. A four hour recovery period ensued in which the subject was given 24-ounces of the recovery drink. A performance test at 85% VO2max to exhaustion was then conducted. Ventilatory responses were collected breath-to-breath, while venous blood samples were measured for oxidation products, glucose and insulin concentrations. Results: The recovery phase showed significant increases in both plasma glucose and serum insulin following Endurox R4 Recovery Drink® ingestion as compared to Gatorade®. There was a significant increase in time to exhaustion (+55%) following Endurox R4 Recovery Drink® during the performance ride compared to Gatorade®. Final oxidation products following Endurox R4 Recovery Drink® ingestion were significantly decreased as compared to Gatorade® ingestion, in that Thiobarbituric Acid Reactive Substrates (T-BARS) were significantly decreased. Conclusions: These data indicate that the Endurox R4 Recovery Drink®, when compared to Gatorade®, significantly enhanced recovery from glycogen-depleting exercise. In addition, Endurox R4 Recovery® Drink decreased the formation of final oxidation products, when compared to Gatorade®.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 Exercise-Evoked Metabolic Adaptations in Canine Myocardium(1999-12-01) Stuewe, Steven Richard; Robert Mallet; Neeraj Agarwal; Patricia GwirtzStuewe, Steven Richard, Exercise-Evoked Metabolic Adaptations in Canine Myocardium. Doctor of Philosophy (Biomedical Sciences), November 1999; 128 pp; 4 tables; 17 figures; bibliography, 130 titles. Aerobic exercise training evokes adaptations in the myocardial contractile machinery that enhance cardiac functional capabilities, and the myocardium’s capacity to consume energy. Despite considerable investigative effort, the effects of exercise training on myocardial intermediary metabolism, the source of energy for cardiac function, have not been defined. The investigations described herein were undertaken to delineate the effects of aerobic exercise training on key rate-controlling enzymes of myocardial intermediary metabolism and energy transport, and to characterize the effects of acute exercise on cardiac messenger RNA transcripts encoding metabolic enzymes. To address these questions, dogs were conditioned by a 9 wk treadmill running program or cage rested for 4 wk. Exercise conditioning was documented by a significant decrease in heart rate at rest and during submaximal exercise. A panel of glycolytic and oxidative enzymes was measured in myocardial extracts. It was demonstrated that aerobic exercise training of dogs selectively increased capacities of key rate-controlling enzymes of each of the major pathways of intermediary metabolism in ventricular myocardium. In addition, it appeared that the training-evoked increases in enzyme activities were due to increased enzyme contents, not to changes in substrate affinity. The same training program was implemented to investigate the effects of aerobic exercise training on the myocardium’s energy shuttling system. Total creatine kinase (CK) activity and content of the CKMB isoenzyme were measured in canine myocardial extracts. It was demonstrated that aerobic exercise training increased total myocardial CK activity and CKMB content, although the CKMB isoenzyme remained minor component of the myocardial CK system. A third investigation was conducted to examine the effects of aerobic exercise on the abundance of messenger RNA (mRNA) encoding key enzymes involved in myocardial energy production and transport. Left ventricular myocardium was sampled 30 min after an exercise bout, and messenger RNA transcripts were analyzed by reverse transcriptase polymerase chain reaction. Exercise increased in the myocardial abundance of mRNA transcripts encoding glyceraldeheyde 3-phosphate dehydrogenase, citrate synthase, and the CK-M subunit. These mRNA enhancements could be responsible, at least in part, for exercise-evoked adaptations in myocardial metabolic enzymes demonstrated in the first two investigations.Item Firefighter Medical Surveillance/Duty Fitness Evaluation of Content and Reporting Format: Compliance with Federal and Other Recognized Standards(2003-05-01) Lin, Rick H.Lin, Rick H, Firefighter Medical Surveillance/Duty Fitness Evaluation of Content and Reporting Format: Compliance with Federal and Other Recognized Standards. Master of Public Health (DO/MPH Dual Degree Track), May, 2001, 41 pp., 7 tables, bibliography, 11 titles. The University of North Texas Health Science Center analyzed data collected by the Public Health Preventive Medicine (PHPM) Clinic at the University of North Texas Health Science Center (UNTHSC) in the course of medical surveillance and duty fitness exams for the City of Rowlett, Texas, HAZMAT Team. Data was analyzed for content and reporting format to determine compliance with federal and other recognized standards. An aggregate report of continuous and categorical data was also created. The subjects were all firefighters in the City of Rowlett Fire Department, Rowlett, Texas. The data was collected from the results of physical exams performed on the members of this population between the period of 1-1-1996 and 12-31-1996. There were a total of sixteen subjects. (n=16) These firefighters are all HAZMAT Team members. The overall content of the medical surveillance and duty fitness examinations was evaluated. The compliance in content of medical history and physical examination to the recognized standards established by OSHA, EPA, and NFPA was examined. The physical characteristics and health of this population of firefighters is described based on the data collected. The result of the comparison shows that the UNTHSC PHPM Clinic’s forms for the history and medical exams did not completely incorporate the recognized standards. The content of the medical surveillance and duty fitness exams was in compliance with and often exceeded recognized standards.Item Influence of Thermoregulatory and Nonthermoregulatory Control Mechanisms of Arterial Blood Pressure During Recivert from Exercise in Humans(2001-05-10) Carter, Robert; Michael L. Smith; Robert L. Kaman; Thomas YorioCarter, III Robert, Thermoregulatory and nonthermoregulatory control of arterial pressure during recovery from exercise in humans. Doctor of Philosophy (Biomedical Sciences). May 2001; 153p; 4 tables, 17 figures; 100 titles. The mechanisms of arterial blood pressure control during exercise is well established; however, much less is known about the regulation of arterial blood pressure immediately after intense or prolonged dynamic exercise. Inactive recovery from dynamic exercise is associated with cessation of the primary exercise stimuli from the brain (central command), Skeletal muscle pumping, which contributes to increases in venous return during exercise is also stopped during inactive recovery from exercise. Thus, the skeletal muscle pump and central command each contribute importantly to elevation and maintenance of arterial blood pressure regulation and cerebral blood flow during exercise. When exercise is intense and/or prolonged, the resulting thermal load exacerbates the challenge to maintain arterial blood pressure and cerebral blood flow both during exercise and particularly during recovery from exercise and thereby increases the risk of syncope. Recently, we found that the skeletal muscle pump plays a major role in arterial blood pressure control during recovery from brief (3 min), mild (60% of maximal HR) exercise in which there was no thermal load. However, how the mechanisms of arterial pressure regulation operate during recovery from intense or prolonged exercise when a thermal load occurs is unknown. Therefore, the purpose of the investigations described herein, was to quantify the mechanisms of the carotid baroreflex function, central command, and the skeletal muscle pump when a thermal stress occurs on arterial blood pressure regulation during recovery from exercise in humans. In addition, differences in arterial blood pressure regulation in women and men during recovery from exercise were addressed in women and men. To investigate these mechanisms, we investigated the carotid-cardiac baroreflex function, cardiovascular, and thermoregulatory responses in volunteer subjects during inactive and active recovery from prolonged exercise improved the function of the baroreflex by increasing the functional reserve of the reflex to buffer against hypotensive stimuli. Our data also suggest that thermoregulatory factors contribute to decreases in MAP after inactive recovery from exercise. In addition, the metabolic state of skeletal muscle during longer duration exercise (15 min) may contribute to these responses during inactive recovery from exercise. These results support the hypothesis that thermal stress contributes to the rapid decreases in arterial blood pressure during inactive recovery following dynamic exercise. To investigate gender differences in arterial pressure regulation during recovery from exercise, we compared 11 women and 8 men during 3 min of exercise and 5 min of inactive and active recovery from exercise. Interestingly, at 1 minute after exercise, MAP decreased less during inactive recovery in men when compared to women. This difference was due to greater decreases in SV and less increase in TPR during inactive recovery from exercise in women compared to men. MAP decreased less during active recovery in men when compared to women. These findings suggest that women may have increased risk of post-exercise orthostatic hypotension and that active recovery from exercise may reduce this risk.Item Mechanisms of Right Ventricular Oxygen Supply/Demand Balance in the Concious Dog(2000-06-01) Hart, Bradley; H. Fred Downey; Patricia A. Gwirtz; James L. CaffreyHart, Bradley Joe. Mechanisms of Right Ventricular Oxygen Supply/Demand Balance in the Conscious Dog Doctor of Philosophy (Biomedical Sciences), August,2000, 119 pp, 4 tables, 13 figures, references, 79 titles. No data exist in the literature describing the myocardial oxygen supply/demand relationship of the right ventricle in a conscious, anaesthetized animal. A novel technique developed in our laboratory enables us to collect right ventricular (RV) venous blood samples from conscious dogs to determine RV myocardial oxygen consumption (MVO2). RV oxygen supply/demand balance was examined in conscious dogs, chronically instrumented to measure right coronary blood flow (RCBF), segmental shortening (%SS) and RV pressure (RVP) during increases and decreases in RV myocardial oxygen demand. Right ventricular MVO2 and O2 extraction (O2E2) were determined; RCBF, RVP, dP/dt, and %SS were recorded concomitantly. Acute increases in RV MVO2 were accomplished by atrial pacing (200 beats/min), increasing RV afterload by 65%, infusion of isoproterenol (0.1 μg/kg/min, i.v.), and by conducting a submaximal exercise routine (70-75% of maximum VO2). An acute decrease in RV MVO2 was created by propranolol administration (1 mg bolus, i.c.). During acute increases in RV MVO2, the extraction reserve is utilized primarily; flow is not affected in the absence of direct vasodilatory effects of the intervention. A decrease in RV oxygen demand is associated with a further increase in the RV extraction reserve. Since RV O2E increases linearly with increases in RV MVO2, these data show that changes in RV venous O2 tension can occur with little or no change in RCBF. LC resistance is very sensitive to alterations in LC venous pO2; therefore, there appear to be significant differences between the left and right ventricles concerning the matching of oxygen supply with myocardial oxygen demand.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 Psychological Mechanisms and Physiological Consequences of Panic Attack in Recreational Scuba Diving(1996-12-01) May, Kyle P.; Michael Smith; David BarkerRecreational scuba diving has become increasingly popular in recent years. With the increasing number of participant, the risk associated with the sport needs to be addressed. Some authorities suggest it should be classified as a high-risk sport while others suggest that the dangers of the activity have been down-played due to the commercialization of the diving community. Panic is an important topic in assessing the risk to recreational divers. The National Underwater Accident Center, NUADC, for the period of 1976 to 1988 indicated that 19% of diving fatalities reported involved probable panic. Furthermore, in a sample of 245 male and female divers, 54% experienced panic or near-panic behavior while diving on one or more occasion. The physiological consequences of a panic attack while diving can be deadly. Instructors, physicians and dive students should be made aware of the risk to persons prone to panic attack. Instructors need to be trained in recognizing the manifestations of frank panic during instruction and discourage these students from continuing. More subtle cases of panic disorder must be screened out by a physician while performing a medical clearance physical for a recreational diving student. The physician can make subtle inquiries and through the answers screen out potentially panic prone divers. Such questions as “How many visits to the emergency room have you made?” as opposed to “Have you ever visited the emergency room?” will elicit a more complete history versus a blanket denial of previous illness or injury. The nature of the E.R. visits will often be revealing to the astute physician. Persons with histories of asthma attacks or hyperventilation syndrome may indicate an underlying panic disorder. The students themselves need to be warned of the hazards of diving if panic prone. The idea needs to be stressed in scuba diving books and manuals much more than it is currently. For example, one of the most popular scuba diving books, The Encyclopedia of Recreational Diving, does not cover panic or the problems that can result due to panic. If this concept is made clear to students while in class, those prone to panic episodes may then self-screen themselves and discontinue a scuba class thereby avoiding injury or death. Scuba diving should be considered a high-risk sport and participants screened for such activity. Not only does a panicked diver put himself in jeopardy, he risks the lives of others in a group with the loss of cognitive abilities seen during panic. Individuals with elevated anxiety levels are more likely to experience a panic episode while diving due to the number of stressors involved in the sport. These persons should be selectively screened out and encouraged to find other avenues for recreation.Item Regulation of Carotid Baroreflex Resetting During Arm Exercise(1999-06-01) Querry, Ross G.; Peter B. Raven; Patricia Gwirtz; Michael SmithQuerry, Ross G., Regulation of Carotid Baroreflex Resetting during Arm Exercise. Doctor of Philosophy (Biomedical Sciences), June 1999, 100 pp., 4 tables, 12 figures, bibliography, 56 titles. Cardiovascular responses to exercise are modulated by the integration of the central nervous system and afferent information from arterial baroreflexes and working skeletal muscle. Investigations have shown that during exercise, the carotid baroreflex (CBR) is reset in proportion to the exercise intensity. The role of the central nervous system contribution to the CBR resetting has not been elucidated. Investigations of CBR function in the animal model consistently report CBR variables such as maximal gain that are different than those reported in humans. These discrepancies may be due in part to methodological limitations in the neck pressure/neck suction (NP-NS) technique used to investigate the isolated CBR function in humans. To accurately examine the internal stimulus from the NP-NS maneuver, subjects were instrumented with a percutaneous catheter to record tissue pressure at the carotid sinus during five-second and rapid pulse NP-NS protocols. Carotid baroreflex function curves were analyzed with and without transmission correction of the carotid sinus pressure (CSP). Results indicated that positive pressure was more fully transmitted (~83%) than negative pressure (~65%) during the five-second-pulse, but not the rapid pulse protocol. Correction of the CSP in either protocol resulted in significant increases in CBR maximal gain and threshold and a reduced saturation pressure. These methodological refinements were then utilized to investigate the role of central command on CBR function during exercise. Subjects performed static and rhythmic handgrip exercise before and after regional anesthesia. Carotid baroreflex curves were analyzed at rest and during exercise before and after blockade at the same absolute workload. Muscle weakness from the blockade required an increased effort to maintain control tension. Heart rate, arterial pressure and perceived exertion during exercise were increased following blockade. During control exercise the CBR function curves were reset upward and rightward compared to rest with a further parallel shift during exercise with blockade. The operating point of the CBR was reset along with the centering point, but did not show the divergence toward the threshold pressure that had been previously described during dynamic exercise. The results support the proposal that central command was a primary mechanism for the resetting of the carotid baroreflex during exercise, but may not be the primary mechanism in the resetting of the operating point of the reflex.Item Regulation of Myocardial Blood Flow and Function During Exercise in Dogs(1995-06-01) Kim, Song-Jung; Patricia A. Gwirtz; Peter B. Raven; James L. CaffreyIntroduction. Background. Coronary circulation during exercise. Coronary blood flow is regulated primarily by local metabolic mechanisms according to the oxygen and nutrient needs of the heart (2, 4, 19). The local “metabolic signal” involves vasoactive metabolites, such as adenosine, released from myocytes in direct proportion to myocardial work (Figure 1). However, other external factors are superimposed on local regulatory mechanisms and can substantially modulate coronary blood flow. One of these modulatory factors is the sympathetic nervous system. Sympathetic vasoconstriction mediated by α-adrenergic receptors in the coronary circulation has been shown to oppose metabolic vasodilation and limit oxygen supply to the myocardium during physiologic and pathophysiological cardiac stresses, such as exercise and myocardial hypoperfusion (1, 6, 7, 8, 10-14, 17, 18, 21). This limitation on myocardial oxygenation appears to impose a restriction on the increase in regional left ventricular subendocardial contractile function during submaximal exercise (7). In this regard, studies have shown that removing this α1-constrictor tone leads to an increase in coronary blood flow and, as a result, regional contractile function (8). This adrenergic coronary constriction during exercise is mediated by neutrally released norepinephrine, not by circulating catecholamines (8). Endothelial-mediated control of coronary vascular tone. Recent investigations indicate that another factor involved in modulating coronary blood flow is the vascular endothelium. The endothelium exerts an influence on vascular smooth muscle vasomotor tone by releasing an endothelium-derived relaxing factor (EDRF) or nitric oxide (NO), which is derived from the amino acid L-arginine by nitric oxide synthase (5, 22). Synthesized NO diffuses into the underlying vascular smooth muscle to activate cytosolic guanylate cyclase (GC), thereby stimulating the intracellular accumulation of cyclic GMP (cGMP). This is illustrated in Figure 2. NO is released by the stimulation of muscarinic receptors on endothelial cells by acetylcholine, as well as by other agonists or physical stimuli (e.g., shear stress) at the interface between blood and endothelial cell surface (15). During exercise, for example, the work output of the normal heart may increase several-fold by the stimulation of sympathetic nerves to heart. The increased work output of the heart increases myocardial oxygen demand. Consequently, the coronary circulation undergoes vasodilation due to local metabolic mechanisms. The elevation in shear stress caused by increases in coronary blood flow triggers release of NO from the endothelium because of the extremely pulsatile nature of the flow. Therefore, it is likely that during exercise, release of NO by shear stress and by neurohormonal stimuli, concomitant with local release of metabolites, contributes to coronary dilation. These vasodilatory influences counteract a sympathetic α-adrenergic coronary constriction, which limits the increase in coronary blood flow and cardiac performance. Accordingly, coronary vascular smooth muscle tone during exercise is modulated by the endothelium, which responds to the increased shear stress and adrenergic stimulation, which provides the major extrinsic input.Item Role of Adenosine in Acute Hibernation of Guinea-Pig Myocardium(1995-08-01) Gao, Zhi-Ping; H. Fred Downey; James L. Caffrey; Patricia A. GwirtzGao, Zhi-Ping, Role of Adenosine in Acute Hibernation of Guinea-Pig Myocardium Doctor of Philosophy (Biomedical Sciences), August, 1995; 111 pp; 3 tables; 15 figures, bibliography, 158 titles. Myocardial hibernation is a state of depressed contractile function and energy demand during chronic ischemia. When coronary flow is restored, depressed contractile function can partially or completely recover to the pre-ischemic level, and ischemic injury of the myocardium in not evident. This project tested the hypothesis that endogenous adenosine mediates hibernation in guinea-pig myocardium. Isolated working guinea-pig hearts, perfused with glucose fortified Krebs-Henseleit buffer, were subjected to global low-flow ischemia. Left ventricular performance and cytosolic energy level were assessed. Lactate and purine nucleotides were measured in venous effluent. Heart were perfused with [U-14C]glucose to investigate the role of adenosine on glucose metabolism in myocardium. Left ventricular function in untreated hearts decreased by 80% and remained stable during ischemia, and completely recovered upon reperfusion. Neither adenosine receptor blockade with 8-p-sulfophenyl theophylline (8-SPT; 20 μM) nor ecto 5’-nucleotidase inhibitor αβ-methylene adenosine 5’-diphosphonate (AOPCP; 50μM) affected left ventricular function either ischemia or during reperfusion. Cytosolic energy level fell by 67% at 10 min ischemia in untreated hearts, but subsequently recovered to the pre-ischemic level despite continued ischemia. Adenosine receptor blockade increased cytosolic energy level at 10 min ischemia relative to untreated hearts, but blunted the subsequent rebound of phosphorylation potential. Moreover, 8-SPT doubled ischemic lactate release. Adenosine receptor blockade also increased glucose uptake during pre-ischemia and hypoperfusion, but did not stimulate glucose oxidation. Crossover plots of glycolytic intermediates revealed that phosphofructokinase, a key rate-controlling step in glycolysis, was activated by adenosine receptor blockade in both pre-ischemic and hibernating myocardium. We conclude that 1) activation of adenosine receptors results in recovery of cytosolic energy level of moderately ischemic working myocardium, but this energetic recover is not solely responsible for post-ischemic contractile recovery; 2) endogenous adenosine attenuates anaerobic glycolysis during myocardial hibernation by blunting phosphofructokinase activity.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.Item The Acute and Chronic Effects of Beta Blockade on Dynamic Exercise Performance and Cardiac Adaptation to Dynamic Exercise Training(1998-06-01) Robbins, H. Bart; Peter B. Raven; Patricia A. Gwirtz; Robert MalletWidespread use of beta-adrenergic blocking agents as treatments for hypertension, ischemic heart disease and postmyocardial infarction has raised many questions concerning the effect of these drugs during exercise. Since exercise is often prescribed as an adjunct treatment in combination with beta blockade, the effect of these drugs on cardiac function during exercise is important to know. It is also important to ascertain if patients taking beta blockers will benefit from chronic dynamic exercise training the same way as normal subjects or if they should be viewed differently. This review of the current biomedical literature is meant to elucidate the cardiac effects, both acute and chronic, of beta-adrenoceptor blockade during dynamic exercise. The acute effects during dynamic exercise and the compensatory mechanisms in the cardiovascular system will be outlined. I will further explore if and how beta blockade significantly affects cardiac adaptation to chronic exercise training. Be reviewing the current literature I will show what is already known and will demonstrate where current knowledge is lacking and where further research is needed. There are two questions which will be addressed by this research. The first question is: “What happens to the cardiovascular system during dynamic exercise when a beta blocker is present in the system?” This question deals with the acute effects of such agents on exercise performance and cardiac function. The second question is: “What effect does beta blockade have on the cardiac adaptations to chronic dynamic exercise training?” This question examines areas of cardiac adaptation that have been postulated to be mediated by beta-adrenergic receptor stimulation (e.g. myocardial hypertrophy). I hypothesize that the acute effects of beta blockade on exercise performance are minimal, while the chronic effects on cardiac adaptation to dynamic exercise training may be significant.Item The Effect of Exercise Training on Behavior and Oxidative Stress in Aging Mice(2005-08-01) Taylor, Sara A.; Michael Forster; Joan F. Carroll; Susan FranksTaylor, Sara A., The effect of exercise training on behavior and oxidative stress in aging mice. Doctor of Philosophy (Biomedical Sciences), August 2005, 136 pp., 17 figures, bibliography, 97 titles. Purpose: Accrued oxidative damage to brain tissue is a proposed mechanism of cognitive deficits observed in aging. In mammalian tissue, it is hypothesized that a balance normally exists between pro-oxidants (reactive oxygen/nitrogen species) and endogenous antioxidant enzymes that are able to inhibit the activity of reactive oxygen/nitrogen species. As long as this balance is maintained, oxidative damage is moderated, but if the production of pro-oxidants becomes excessive or if the activity of antioxidants lags, oxidative stress and ultimately oxidative damage to tissues may result. It is the hypothesis of this project that exercise training is able to prevent decreased antioxidant activity in brain tissue, produce a favorable shift in the pro-oxidant/antioxidant balance, and thus moderate oxidative damage in the aging mice brain. Methods: 3 and 20 month old C57BL/6 mice were either subjected to 8 weeks of treadmill exercise followed by 3 weeks of concurrent exercise and behavior testing, or else they were age-matched, non-exercised controls. Mice were tested on multiple behavioral tasks that tested sensorimotor learning as well as tasks that required utilization of various component of cognitive learning. After exercise and behavior testing regimens were completed, biochemistry assays for protein oxidative damage as well as for antioxidant enzyme activity were performed on several brain regions. Results: It is a finding of the study that moderate, short-term exercise initiated in aged C57BL/6 mice resulted in increased fitness in the aged mice to the same degree as observed in young mice, improved some psychomotor skills, including bridge-walking and reaction time, and improved age-impaired spatial memory performance. Moreover, exercise training showed a lack of effect on oxidative damage in all brain regions, increased activity of glutathione peroxidase in the cerebellum and striatum of young, but not aged mice, and it increased the activity of catalase in the cortex of aged mice. Conclusions: The data presented in this project shows that exercise does moderate some age associated cognitive deficits, and the findings do not preclude the possibility that exercise produces this effect by reducing accrued oxidative damage that occurs with aging.Item The Effect of Fitness on Cardiac Work with and without Metoprolol(2008-07-01) Hawkins, Megan Nicole; Peter Raven; Michael Smith; Robert MalletHawkins, Megan Nicole, The Effect of Fitness on Cardiac Work with and without Metoprolol. Doctor of Philosophy (Biomedical Science), July 2008; 128 pp; 3 tables; 17 figures; bibliography. Chronic endurance exercise adaptations of the cardiovascular and skeletal muscle systems. The mechanisms by which these adaptations occur, and their effect on the physiological response to exercise, have not been fully elucated. In addition, the classic concept of the role of maximal oxygen consumption (Vo2max) as a parametric index of cardiorespiratory capacity has been questioned. Therefore the purpose of the investigations presented within this dissertation was to: i)retrospectively analyze 156 incremental exercise stress tests and supramaximal exercise tests to verify that VO2 does indeed attain a maximal value; ii)evaluate the effects of cardioselective beta-adrenergic blockade on the ability to maintain cardiac work in average trained and endurance exercise trained subjects during moderate (45% VO2max) and heavy (70% Vo2max) intensity cycling exercise; and iii) determine the effect of aerobic fitness on resting and peak leg vascular conductance and the change in central blood volume observed during the onset of cycling exercise. In the first investigation we demonstrated that highly trained runners capable of maintaining supramaximal workloads achieved a VO2 that rarely exceeded the VO2max value obtained during an incremental exercise stress test. In the second investigation we demonstrated that acute β1-adrenergic receptor (βAR) inhibition reduced cardiac output, cardiac work and cardiac efficiency in endurance trained athletes during moderate and heavy intensity exercise. However, in average trained individuals these same variables were not affected during moderate exercise intensity, but were reduced at heavy intensity exercise. We concluded that βAR blockade impaired the more efficient Frank-Starling mechanism in endurance trained athletes but remained functional in average trained subjects during moderate exercise intensities. In the third investigation we demonstrated that endurance athletes responded to the onset of exercise with a larger increase in central blood volume than average trained individuals. In addition, resting and post-ischemic leg blood glow and leg vascular conductance were greater in the exercise training-induced adaptations of the skeletal muscle vasculature resulted in larger conductance capacity of the working muscle in response to increases in oxygen demand and enabled a greater increase in muscle blood flow from rest to exercise.Item The Use of Osteopathic Palpatory Findings in Screening for Nephropathy in Type 2 Diabetes Mellitus: A Pilot Study(2008-05-01) Curlee, Laura Denise; John Licciardone; Hollis King; Roberto CardarelliCurlee, Laura D., The Use of Osteopathic Palpatory Findings in Screening for Neuropathy in Type 2 Diabetes Mellitus: A Pilot Study. Master of Science, May, 2008, 100 pp., 6 tables, 9 illustrations, bibliography, 40 titles. Viscerosomatic reflexes result in somatic dysfunction, which manifests as palpatory TART changes. There are two hypotheses of this study: palpatory findings will be associated with diabetes and will be associated with renal disease. An osteopathic predoctoral fellow conducted a palpatory exam on each subject at the level of T10-L2, to feel for TART changes. The results from the palpatory exam were recorded in SPSS for statistical analysis. Descriptive statistics, chi square and risk assessment were conducted. There were no statistically significant findings. Results demonstrated possible associations between type 2 diabetes mellitus and race, and tissue texture changes with control groups. Restriction of motion was found to have no difference amongst control and disease groups.