Browsing by Subject "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 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 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 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 Dysfunctional Control of Coronary Blood Flow in Renovascular Hypertension(1999-06-01) Kline, Geoffrey Philip; Gwirtz, Patricia A.; Shi, Xiangrong; Raven, Peter B.Kline, Geoffrey Philip, Dysfunctional Control of Coronary Blood Flow in Renovascular Hypertension Doctor of Philosophy (Biomedical Sciences), June 1999, 98 pp, 2 tables, 10 figures, references, 142 titles. This study was designed to determine the effects of renovascular hypertension (RVH) on coronary vasoreactivity in conscious, chronically instrumented dogs. Six dogs were instrumented to measure left ventricular pressure, +dP/dtmax, heart rate, mean aortic pressure, circumflex blood flow (CBF), and cardiac output. In order to examine endothelial-dependent and independent coronary vasodilation, intracoronary injections of actylcholine (Ach), bradykinin (BDK), and sodium nitroprusside (SNP) were studied before and after induction of RVH in the presence and absence of nitric oxide (NO) blockade. After RVH, resting CBF was significantly reduced (P [less than] 0.05). In the normotensive state, NO-blockade significantly reduced the coronary vasodilation to Ach and BDK (P [less than] 0.05), but not SNP. After RVH, the coronary vasodilation to Ach, BDK, and SNP were reduced (P[less than] 0.05). After RVH, NO-blockade further reduced the coronary vasodilation to BDK (P [less than] 0.05), but not Ach. Thus, RVH resulted in an impairment of both endothelial-dependent and –independent coronary vasodilation. It also appears that during RVH the endothelium retains the ability to produce/release NO to some, but not all, stimuli. In order to examine the possibility that β-adrenergic mediated coronary vasodilation is impaired after RVH, intracoronary injections of norepinephrine (NE), isoproterenol (ISO), and terbutaline (TRB) were administered. These drugs all caused dose dependent increases in CBF before and after RVH. After RVH, the coronary vasodilatory responses to NE, ISO and TRB were significantly reduced (P [less than] 0.05). β1-blockade with intracoronary atenolol (1 mg) reduced the ISO-induced increases in CBF and had no effect on TRB responses (P [less than] 0.05). β2-blockade with intracoronary ICI-118,551 (1 mg) reduced the ISO-induced coronary vasodilation and abolished TRB responses (p[less than] 0.05). During β2-blockade, ISO-induced increases in CBF were not different after RVH. Therefore, these data indicate that β1-adrenergic mediated coronary vasodilation is preserved after RVH, whereas, β2-mediated is not. We conclude that 1) RVH results in an impairment of both endothelial-dependent and –independent coronary vasodilation; 2) RVH results in an impairment of β2-adrenergic mediated coronary vasodilation.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 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 Inhibitory Rib-Raising and Microneurographic Measurement of Sympathetic Nervous System Activity(2007-05-01) Kinzler, Damien W.; Michael Smith; Russell Gamber; Hollis KingThe clinical effectiveness of osteopathic manipulative therapy (OMT) techniques that are designed to address the autonomic nervous system (ANS) are untested to current research standards. As the concept of “autonomic imbalance” is frequently ascribed as the etiology of various pathologic conditions, it is paramount to undertake basic research into not only efficacy but also possible mechanistic actions and origins. Osteopathic physicians often utilize treatment regimens and techniques for which the given mechanism of action is simply attributed to “balancing the autonomics”. This intuitive concept may finally be at the threshold where enough basic science exists to justify clinical investigations. Osteopathic manual manipulative techniques have shown effectiveness in the treatment of various musculoskeletal conditions and have been shown to lower perceived pain; supporting the use of manual therapy as an effective treatment modality. A brief review yields the following within just the last four years: Eisenhart showed positive range-of-motion outcomes after ankle sprain in the emergency department. Biondi reviews the usefulness of cervical manipulation for tension headache and McReynolds demonstrated an equivalent decrease in acute neck with OMT versus intramuscular ketolac in an emergency department setting, although the dosing was not maximal. German researchers have shown effectiveness in chronic epicondylopathia humeri radialis and research has led to the demonstration of lowered post-operative pain in hip or knee arthroplasty. There has also been decreased post-operative pain medication reported in hysterectomy when compared with a control group. OMT has demonstrated a decrease in fibromyalgia symptoms when used with standard care over standard care alone. Low back pain, perhaps the most extensively studied diagnosis in which OMT has been evaluated, has reported numerous positive outcomes including lower levels of narcotic use and decreased pain in both double-blinded and meta-analysis studies, although there is still considerable debate within this area. There has also been favorable outcomes associated with the management of gain in Parkinson’s disease and preliminary work has shown the efficacy in treatment of carpal tunnel syndrome. Most of the aforementioned musculoskeletal conditions are not amenable to traditional therapies and have a high-cost burden on the economy. Traditional treatments generally have a “wait and see” approach combined with analgesics which may not cause harm, but hampers quality of life and income in the interim. The cost effectiveness of OMT is still in the preliminary stages, but there is evidence supporting a superior cost benefit ratio when compared to standard care and since many of these conditions have no other proven treatment modality available patients will often try anything over nothing. The evaluation of OMT addressing clear autonomic dysfunction is limited. This study closes a small part of that gap by examining the proposed physiologic mechanism of OMT and its’ interaction with the ANS. Small studies have documented changes, namely heart rate variability, in autonomic processes in healthy individuals while other, older studies have found benefit in clinical variables. With few exceptions however, most of these studies lacked a particular technique protocol. Operators were free to use whatever intervention that they chose and most of these studies were not performed under rigorous testing methods with a randomized design. The technique that was evaluated (inhibitory rib-raising) has a documented history from the origins of osteopathic medicine in the United States, and is currently taught to students in osteopathic medical schools as part of their medical education curriculum. Rib-raising is most often taught to enhance the mechanical motion of the ribs, but other paradigms utilize this technique to either enhance or inhibit sympathetic nervous system (SNS) activity. The evaluation of inhibitory rib-raising or its’ proposed mechanism of action has never been rigorously scrutinized to modern scientific standards. The current study was designed to address that gap with both direct and indirect measurement of SNS variable in healthy individuals with the hypothesis that there would be a time-dependent, graded reduction in measured sympathetic nervous system activity (MSNA) in healthy individuals undergoing cold-pressor stimulus.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 Post-Apneic Symathoinhibition in Humans(2002-08-01) Swift, Nicolette Muenter; Michael Smith; David Barker; John R BurkMuenter Swift, Nicolette, Mechanisms of Post-Apneic Sympathoinhibition in Humans. Doctor of Philosophy (Biomedical Sciences), August, 2002, 110 pp., 14 figures, references. Apnea is accompanied by a concomitant rise in arterial pressure and muscle sympathetic nerve activity (MSNA), the latter primarily due to chemoreflex stimulation and possibly the lack of sympathoinhibitory input from pulmonary stretch receptors. The progressive sympathoexcitation during apnea suggests a possible overriding of arterial baroreflex sympathoinhibitory input to sympathoregulatory centers by apnea-induced sympathoexcitatory mechanisms. Nevertheless, it is unknown whether apnea attenuates baroreflex control of MSNA. Apnea termination is accompanied by a profound and immediate sympathoinhibition, the mechanisms of which are unclear; however, potential mediators include normalization of blood gases (i.e. chemoreflex unloading), the lung inflation reflex, and arterial baroreflex stimulation. Therefore, the purpose of the current studies was to: i) determine the contribution of chemoreflex unloading to post-apneic sympathoinhibition, ii) determine the contribution of the lung inflation reflex to post-apneic sympathoinhibition, and iii) determine whether carotid baroreflex control of MSNA is altered by apnea and its termination. The first study compared MSNA during post-apneic administration of room air versus a gas mixture designed to maintain the subjects’ end-apneic alveolar gas levels. Regardless of post-apneic gas administration, post-apneic MSNA was at or below baseline pre-apneic levels; thus; chemoreflex unloading does not contribute to post-apneic sympathoinhibition. Furthermore, quantification of post-apneic MSNA associated only with the low lung volume phase of respiration, when sympathoinhibitory input from the lung inflation reflex is minimal, demonstrated that post-apneic sympathoinhibition persists even during the low lung volume phase of respiration, when sympathoinhibitory input from the lung inflation reflex is minimal, demonstrated that post-apneic sympathoinhibition persists even during the low lung volume phase of respiration. Therefore, the lung inflation reflex does not appear to be the primary mediator of post-apneic sympathoinhibition. The second study utilized neck suction (NS) and neck pressure (NP) to assess carotid baroreflex function during and following sleep apnea. The sympathoinhibitory response to -60 Torr NS was maintained throughout apnea; conversely, the sympathoexcitatory response to +30 Torr NP was attenuated for nearly one minute post-apnea. Thus, carotid baroreflex control of MSNA is not altered by apnea but is transiently attenuated by apnea termination. We propose that the carotid baroreflex-MSNA function curve resets rightward and upward during apnea. Return of the function curve to baseline upon apnea termination may partly explain the reduced MSNA response to NP post-apnea.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.