Browsing by Subject "Exercise Science"
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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 Androgens and Cardiovascular Disease(1998-05-01) Dickerman, Rob D.; Walter J. McConathy; Thomas Yorio; Robert GracyDickerman, Rob D., Androgens and Cardiovascular Disease Doctor of Philosophy (Biomedical Sciences), May 1998; 111 pp; 10 tables, bibliography, 197 titles. Anabolic steroids are commonly used by many muscle and strength dependent athletes due to their ability to enhance the hypertrophic effects of resistance training. The use of anabolic steroids by bodybuilders appears to carry significant health risks, most commonly reported are sudden death, myocardial infarction and cardiomyopathy. To investigate the effects of anabolic steroids on cardiovascular risks, a study was designed to analyze the effects of androgens on lipoprotein levels and structure/function of the heart. For the study on lipid-related risk, twelve competitive bodybuilders were recruited for a comprehensive analysis of serum apolipoprotein A-I, B, total cholesterol, HDL-cholesterol, LDL-cholesterol, and testosterone. Serum total cholesterol, HDL- and LDL-cholesterol, apolipoproteins A-I and Be were significantly lower in androgen-users. Consistent with previous reports, androgens were associated with decreases in HDL-cholesterol and apolipoprotein A-I. However, androgens were also associated with reduced serum total cholesterol, LDL-cholesterol and apolipoprotein B. Despite the significantly higher total cholesterol/HDL-cholesterol ratio, the low levels of serum total cholesterol levels (percentile) in the androgen-users raises questions as to whether there is increased risk for cardiovascular disease and the exact role of androgens in cardiovascular risk. To investigate the effects of anabolic steroids in pathologic concentric left ventricular hypertrophy, the effects of androgens on left ventricular size and function were analyzed. Previous investigations conducted on left ventricular size and function have yielded inconclusive results. Problems existing in each of the previous investigations were small body mass, short length of myocardial exposure time to resistance training (years of training), significantly different body mass between steroid-users and steroid-free subjects and monitoring/reporting of steroid use. These problems may have contributed to the discrepancies between studies. Therefore, we selectively recruited eight competitive heavy weight drug-free bodybuilders and eight matched competitive weight bodybuilders on self-directed regimens of anabolic steroids for examination of left ventricular size and function via echocardiography. Increases in left ventricular posterior wall (LVPW) and ventricular septal thickness (VST) were apparent in the steroid-user group (p [less than] 0.05). Ratio of echocardiographic findings to body mass index (BMI) revealed a significantly smaller left ventricular and diastolic dimension (LVDEd/BMI, p [less than] 0.05) in the steroid-user. The smaller LVDEd in steroid-users is coupled with a significantly disproportionate septal and posterior wall thickness in steroid-users. There was no direct evidence of diastolic dysfunction. Thus it appears from these studies that androgens alter lipoproteins leading to a questionable increased risk for cardiovascular disease and may potentiate concentric left ventricular hypertrophy without affecting cardiac function.Item Arterial Baroreflex Control of Muscle Sympathetic Nerve Activity(2000-07-01) Fadel, Paul Joseph; Peter B. Raven; Michael Smith; Patricia GwirtzFadel, Paul Joseph, Jr., Arterial Baroreflex Control of Muscle Sympathetic Nerve Activity. Doctor of Philosophy (Biomedical Science), July 2000; 100 pp; 3 tables; 10 figures; bibliography. Arterial baroreflex control of sympathetic nerve activity is dependent on afferent nerve activity emanating from both the aortic and carotid baroreceptors. While several investigations have reported that the aortic baroreceptor reflex dominates in the baroreflex control of heart rate in humans, the role of carotid and the aortic baroreceptors in the control of sympathetic nerve activity remains unclear. In addition, the effect of exercise and long term endurance training on baroreflex-sympathetic nerve activity responses requires further definition. Therefore, the purpose of the investigations described within this dissertation was to: i) describe carotid baroreflex (CBR) control of muscle sympathetic nerve activity (MSNA) at rest and during exercise, ii) examine the relative contribution of the carotid and aortic baroreflexes to the overall arterial baroreflex control of MSNA during acute hypotension, and iii) determine the effect of fitness on arterial baroreflex control of MSNA. In the first investigation, we constructed stimulus-response relationships for CBR control of MSNA at rest and during dynamic arm cycling and demonstrated that carotid baroreflex control of MSNA was reset to function at the higher arterial pressures induced by exercise without a change in reflex sensitivity. Thus, we concluded that the carotid baroreflex control of MSNA was preserved during dynamic exercise. In the second investigation, acute hypotension was induced non-pharmacologically by releasing a unilateral arterial thigh cuff (300 Torr) following nine minutes of resting ischemia under two conditions: control (aortic and carotid baroreflex deactivation) and suction (aortic baroreflex deactivation alone). The application of neck suction to negate the CBR during cuff release caused a significant attenuation of the MSNA response and a greater decrease in mean arterial pressure; thereby signifying the importance of the CBR in the control of MSNA and maintenance of arterial blood pressure. However, when the drop in carotid sinus pressure was counteracted with neck suction a significant MSNA response was noted, indicating the dominance of the aortic baroreflex control of MSNA. Furthermore, a comparison between high-fit (HF) and average fit (AF) subjects indicated that despite an augmented baroreflex control of MSNA, HF subjects exhibited a greater decrease in mean arterial pressure compared to AF subjects. Thus, it appeared that although the arterial baroreflex appropriately increased the MSNA response to hypotension, the regulation of blood pressure remained attenuated in the HF subjects. We contend that an impaired control of vasomotion hinders blood pressure regulation in high-fit subjects.Item Cardiorespiratory Fitness, Body Mass Index and All-Cause Mortality in Women, ACLS 1970-1994(1999-12-01) Braun, LeeAnn; Sally Blakley; Antonio A. ReneBraun, LeeAnn, Cardiorespiratory Fitness, Body Mass Index and All-Cause Mortality in Women, Aerobics Center Longitudinal Study, 1970-1994. Master of Public Health (Epidemiology), December, 1999, 44 p.p., 9 tables, references, 24 titles. Cardiorespiratory fitness and body mass index are related to morbidity and mortality (Manson, 1996). There is a preponderance of evidence supporting this relation in men (Gibbons, 1983; Blair, 1989, 1995, 1996; Lee, I, 1993; Barlow, 1995; Kampert, 1996; Dorn, 1997; Lee, C, 1999). The evaluation of the stated risk factors have been virtually unexplored in a cohort of women. The aim of this study is to evaluate whether higher levels of cardiorespiratory fitness attenuate the risk of all-cause mortality in overweight and obese women. In this prospective study, the study population consisted of 7572 women ages 20-89 years, who had a medical examination and achieved at least 85% of their age-adjusted maximal heart rate during a maximal treadmill test were followed for 69,979 woman-years. After adjustment for age, exam year, health status and smoking status, unfit women had a higher risk for all-cause mortality across BMI categories [RR 1.70 95% CI (1.18, 2.43)]. The benefits of cardiorespiratory fitness significantly decrease the risk of all-cause mortality in women as the concurrent consideration of cardiorespiratory fitness.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 Does Osteopathic Manipulative Treatment Improve Dyspnea and Exercise Tolerance Subjects with Stable Chronic Obstructive Pulmonary Disease?(2006-05-01) Pickett, Carolyn M.; Stoll, Scott; Cruser, des Anges; Licciardone, John C.Pickett, Carolyn M., D.O., M.S. Does Osteopathic Manipulative Treatment Improve Dyspnea and Exercise Tolerance in Subjects with Stable Chronic Obstructive Pulmonary Disease? Master of Science (Clinical Research and Education – OMM), May 2006, 54 pages, 10 tables, 4 figures, references 48 titles. Chronic Obstructive Pulmonary Disease (COPD) is the fourth leading cause of death globally and is projected to increase. This highly prevalent and costly disease causes reduced physical and social functioning, and none of the existing medications for COPD seem to modify long-term decline in lung function. COPD patients with the severe dyspnea have more deficits in the health status and energy. Reduced functional status has been significantly correlated with health related quality of life. Osteopathic Manipulative Treatment (OMT) has been suggested for treatment of COPD as early as 1902, some research indicates that OMT may improve dyspnea and exercise tolerance, yet there are few published studies on OMT and COPD. Study goals were to increase scientific knowledge about how OMT may immediately improve dyspnea and exercise tolerance in stable COPD following exertion. This RCT was approved by the Institutional Review Board at the University of North Texas Health Science Center (UNTHSC) in Fort Worth and funded by the Osteopathic Research Center (ORC) at UNTHSC. –Hypothesis 1: A single intervention of OMT will improve dyspnea in a stable COPD subject, as measured by response to the Borg scale with exertion, when compared to no treatment. –Hypothesis: a single intervention of OMT will improve exercise tolerance in a stable COPD subject, as measured by distance walked during the six-minute walk test, when compared to no treatment. Twenty-one subjects completed the trial, 10 in the OMT group and 11 in the no-treatment group. No significant differences were found in the Borg scale or 6MWT following OMT. This study is limited by a small sample size and single OMT intervention design; however, it does demonstrate the feasibility of this research at this institution and may lead to a larger, more definitive and funded clinical trial.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 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 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 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 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 Medical Gymnastics and Massage in General Practice(P. Blakiston's Son & Co., 1926-01-01) Dobbie, Mina; Arvedson, J.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 Physical Culture Classics: Building Vitality(E.R. Dumont, 1909-01-01) Fleming, WilliamItem Physical Culture Classics: Pertinant Statements by the Masters(E.R. Dumont, 1909-01-01) Fleming, WilliamItem Physical Culture Classics: Prevention and Cure of Disease by Natural Methods(E.R. Dumont, 1909-01-01) Fleming, WilliamItem Physical Culture Classics: Strength From Exercise and Diet(E.R. Dumont, 1909-01-01) McFadden, Bernarr; Treloar, Albert; Merrilles, Charles; Fleming, William