This thesis is concerned with the role of 'central command' in cardiorespiratory control during exercise and the peripheral autonomic modulation of cardiac excitability. Chapter One reviews the background to the work in the thesis. The cardiorespiratory and autonomic changes occurring during exercise and the ways in which they are brought about are discussed. This is followed by a review of some pathological changes in autonomic activity and the ways in which they might be arrhythmogenic. Chapter Two details the experimental techniques used in the thesis and discusses their theoretical background. Chapter Three studies the cardiorespiratory responses to imagination of exercise under hypnosis. This results in hyperventilation, hypocapnia and an increase in heart rate. In contrast, no cardiorespiratory changes are seen when the same protocol is repeated in the awake state. The response to imagined exercise under hypnosis is not affected by maintaining isocapnia. A powerful drive to breathe arising from higher centres, that is independent of peripheral muscular feedback, is elicited when 'exercise' is imagined under hypnosis. Chapter Four investigates the neural correlates of imagined exercise under hypnosis using positron emission tomography to see if they are the same as those classically implicated in 'central command' during exercise. Activation of 'motor' areas occurs, including the supplementary motor area, primary motor cortex for breathing, premotor area, thalamus, basal ganglia and cerebellum. The insular cortex, right dorsolateral prefrontal cortex and posterior parietal cortices are also activated. These activations are similar to those previously reported during actual exercise, but occur in the absence of peripheral feedback that accompanies actual exercise and may therefore reflect 'central command'. Chapter Five studies the responses to altered perception of work rate during actual exercise using hypnotic suggestions. If exercising hypnotised subjects are told that the work rate has increased (when it hasn't), they hyperventilate, become hypocapnic and heart rate increases, suggesting a partial uncoupling of 'central command' from peripheral feedback. Chapter Six investigates the cardiovascular effects of electrical stimulation of the thalamus and midbrain in awake man to determine the role of subcortical areas in cardiovascular control. High-frequency stimulation of the thalamus, subthalamic nucleus and substantia nigra results in increases in heart rate and blood pressure, whereas stimulation of the globus pallidus has no effect. In patients with implanted stimulating electrodes, chronic high-frequency electrical stimulation does not affect baroreflex sensitivity, heart rate variability or blood pressure variability. Chapter Seven characterises the cardiac electrophysiological consequences of sympathetic imbalance using multi-electrode array mapping techniques in the pig heart in vivo. A novel potential arrythmogenic mechanism of noradrenaline is also investigated in two in vitro preparations. Chapter Eight presents a brief summary of the findings in the thesis and discusses future research directions.

Typescript. / Thesis (Ph. D.)--University of Hawaii at Manoa, 1979. / Bibliography: leaves 86-97. / Microfiche. / xii, 97 leaves ill. 29 cm

Thesis (Ph. D.)--University of Hawaii at Manoa, 1995. / Includes bibliographical references (leaves 96-106). / Microfiche. / xxii, 106 leaves, bound 29 cm

Typescript. / Bibliography: leaves 172-181. / x, 181 leaves ill

The overarching aim of this thesis was to examine factors that affect post-exercise glycaemia and contribute to minimising the risk of hypoglycaemia after exercise. An inability to regulate circulating insulin concentrations is considered the primary gluco-regulatory defect within T1DM. Therefore, the aim of chapter 3 was to examine the effects of pre-exercise rapid-acting insulin reductions on blood glucose responses before and after running in T1DM individuals, to test the hypothesis that reducing pre-exercise insulin dose may help preserve post-exercise glycaemia. The results demonstrate that a 75% reduction to pre-exercise rapidacing insulin dose best preserved blood glucose before and after exercise, without increasing the risk of ketoacidosis, and reduced the risk of hypoglycaemia in free living conditions for 24 hours following running. An important factor determining blood glucose concentrations and subsequent patterns of fuel oxidation is the rate of appearance of carbohydrate into the circulation. Potentially, low GI carbohydrates may raise blood glucose less and increase the percentage contribution of lipids as a fuel because of a slower digestion. Therefore, the aim of chapter 4 was to examine the metabolic and blood glucose responses to ingestion of a high or low GI carbohydrate, combined with a 75% reduced insulin dose, before, during and for 24 hours after running. The results demonstrate that compared to a high GI carbohydrate, the low GI carbohydrate increased blood glucose concentrations less before exercise and maintained blood glucose better for 24 hours after running, via lower carbohydrate and higher lipid oxidation rates during the latter stages of running. After manipulating both the insulin dose and the pre-exercise carbohydrate GI, to improve post-exercise blood glucose concentrations, the timing of the ingestion of carbohydrate (alongside a reduced insulin dose) before exercise is an important factor which may further refine these strategies. Therefore, chapter 5 examined the metabolic and blood glucose responses to alterations in the timing of carbohydrate feeding and insulin administration prior to running. Our results demonstrated that administration of both a reduced rapid-acting insulin dose and low GI carbohydrate 30 minutes before exercise improved glycaemia for 24 hours after running, by reductions in carbohydrate oxidation, leading to increased carbohydrate availability post-exercise.

The impact of acute resistance exercise (RE) on glycaemia in type 1 diabetes (T1DM) individuals is poorly understood. Yet, such knowledge would have great use in improving our understanding of blood glucose control during and after the performance of RE. Increasing research in this area might help minimise complications associated with blood glucose vulnerability and potentially maximise health benefits related to RE which are known to be obtained by people without diabetes. The overarching aim of this thesis was to examine the impact of acute RE on glycaemia in T1DM individuals, and promote confidence in people with T1DM to partake in this form of exercise and lead a more physically active lifestyle. Exercise volume, or the total weight lifted during a RE session, is a primary component in the design of a RE session. Therefore, Chapter 3 examined the acute impact of manipulating RE session volume in T1DM individuals. The results demonstrate that exercise volume is an important factor in determining the blood glucose responses to RE; specifically, blood glucose concentrations rose above rest for one hour after one and two sets of similar intensity RE, but this exercise-induced hyperglycaemia was attenuated by increasing the volume of exercise by addition of a similar intensity third set of RE. Additionally, performing morning RE after an overnight fast and in the absence of rapid-acting insulin, did not induce acute hypoglycaemia, ketoacidosis or raise a marker of muscle damage, but caused metabolic acidosis in a dose-dependent fashion. Exercise intensity is a characteristic that is integral to the design of a RE session, and this characteristic might play a role in explaining the exercise-induced hyperglycaemia caused by the thirty minute (two-set) RE sessions in Chapter 3. The aim of Chapter 4 was to examine the impact of manipulating exercise intensity in T1DM individuals. The findings from this study demonstrate that performing a low intensity RE session evoked a similar magnitude of post-exercise hyperglycaemia and metabolic acidosis than a higher intensity RE session, when sessions were matched for total weight lifted. In an attempt to alleviate the consistent exercise-induced hyperglycaemia presented by the two-set RE session, the aim of Chapter 5 was to implement a modified algorithm that delivers an individualized dose of rapid-acting insulin after morning RE, to counter acute post-exercise hyperglycaemia in T1DM individuals. The results demonstrate that post-exercise rapid-acting insulin injection delivered by means of an algorithm resulted in reductions to post-RE hyperglycaemia without the occurrence of hypoglycaemia during two hours after exercise. However, during the subsequent twenty hours of freely living conditions, T1DM individuals remained unprotected from post-exercise hypoglycaemia as per a control condition. Overall, the findings of this thesis underpin some important factors that determine the glycaemic and metabolic responses to acute performance of RE, which may facilitate the better management of blood glucose around this form of exercise, in T1DM individuals.

The purpose of this study was to examine the effectiveness of behavioural self-control and relapse prevention strategies for increasing adherence in obese women during a 12 week supervised walking programme and in a six month unsupervised maintenance period. Fifty female volunteers aged 18-60 years who were inactive during the previous six months were matched on the variables of age and oxygen pulse and assigned to one of three groups. Each group participated in a 12 week supervised walking programme at the University of Victoria. Group one (n = 16) was exposed to the Behavioural Self-Control intervention (BSC). Group two (n = 17) was exposed to the Relapse Prevention intervention (RP). The control group (C, n = 17) received no intervention. The participants were expected to attend a minimum of three supervised sessions per week at which attendance was recorded and then participate in an unsupervised "4th Day Walk". Adherence to the 4th day walk was self-reported, as was adherence during the maintenance period. Fitness was evaluated three times during the study: (1) pre-intervention, (2) post intervention (3 months), and (3) post maintenance (6 months). Each fitness assessment included anthropometry and a submaximal treadmill aerobic fitness test to evaluate fitness changes and provide confirmation of self-reported adherence. Average adherence to the walking during the supervised programme was 75.38%, with 80% of the subjects completing the programme. Adherence to walking during maintenance declined from 73.17% in the first month to 50.87% in the sixth, with 60% of the individuals remaining involved at 9 months. No significant differences in overall program adherence or number and distribution of drop-outs were found. Significant differences were found when the final six weeks of the supervised programme were analysed separately, F(2,27) = 4.60, p<.02. The BSC group had significantly higher adherence than the RP group during this period. Overall adherence during maintenance was significantly different among groups, F(2,27) = 4.85, p<.02. The BSC group had significantly greater adherence than the C group. Physiological measures demonstrated that fitness increased during the programme and was maintained during the maintenance period for all groups. Rates of adherence, measured as either attendance or drop-out, were comparable to those reported for normal weight populations. The BSC intervention in an educational skill-based setting appeared to be an effective means of maintaining exercise behaviour over nine months. The RP intervention was no more effective than no intervention. The high levels of adherence obtained during this programme support the increasing use of exercise in the treatment of obesity. / Graduate

No description available.

The purpose of this study was to examine differences in 2,3-diphospho-glycerate concentrations among groups of smokers and nonsmokers, to determine relationships between 2,3-DPG concentrations and other blood parameters affecting oxygen transport, and to examine the effects of acute exercise on 2,3-DPG concentrations. Antecubital venous blood from each subject, before and after exercise, was analyzed for 2,3-DPG, hematocrit, hemoglobin and blood pH. Mean corpuscular hemoglobin concentration (MCHC) was calculated by dividing hemoglobin by hematocrit. Forty university-aged males constituted the sample population. Each subject was assigned to one of five groups, eight subjects per group, based on his status in relation to the variables of physical activity and cigarette smoking. The task consisted of one hour of exercise on a bicycle ergometer at a work rate producing a heartrate of approximately 150 beats per minute (70 per cent of maximal aerobic capacity). Blood samples were taken immediately prior to and immediately following the bout of exercise. A 12 hour fast preceded the work phase of the experiment. The hypotheses were: highly fit subjects have significantly higher 2,3-DPG concentrations and sedentary subjects have significantly lower 2,3-DPG concentrations than moderately fit subjects; smokers have significantly higher 2,3-DPG levels than nonsmokers; exercise produces significant increases in 2,3-DPG; negative relationships exist between 2,3-DPG levels and hemoglobin levels as well as between pre exercise 2,3-DPG levels and change of 2,3-DPG as a result of exercise. A priori orthogonal comparisons of pre exercise red cell 2,3-DPG levels indicated that differences between groups were not significant, i.e. highly fit groups did not demonstrate 2,3-DPG levels significantly higher, nor did sedentary groups demonstrate 2,3-DPG levels significantly lower than moderately fit groups. A definite trend towards higher 2,3-DPG levels was observed as training intensity increased, indicating that the hypothesis of physical training producing an increase in 2,3-DPG levels should not be totally rejected. Demonstration of differences in the carrying capacity of the blood, as reflected by differences in MCHC, hemoglobin and hematocrit, between groups appeared to be related to the trend observed in 2,3-DPG levels. Differences between smokers and nonsmokers in relation to 2,3-DPG concentrations were not significant,indicating that the hypoxia produced through cigarette smoking is not an important stimulator of 2,3-DPG production. Multivariate analysis of results indicated that 2,3-DPG levels were not significantly increased as a result of one hour of exercise at 70 per cent of maximal aerobic capacity. This is indicative of a slow-acting response mechanism affecting 2,3-DPG production, which requires more than one hour, or a more severe stress, to produce a physiological beneficial effect on oxygen transport by the blood. A significant negative correlation was observed between pre exercise levels of 2,3-DPG and hemoglobin levels. This was also reflected in the significant negative correlation between 2,3-DPG and hematocrit and 2,3-DPG and MCHC. A negative correlation was also observed between the change in 2,3-DPG and the change of MCHC that occurred as a result of exercise. The results are interpreted as showing a compensatory effect of 2,3-DPG in producing increased unloading of oxygen when the carrying capacity of the blood is reduced through a reduction in hemoglobin levels. An intimate relationship between 2,3-DPG and MCHC, tending to produce homeostasis in the position of the oxygen dissociation curve of hemoglobin, has been postulated. Changes in 2,3-DPG as a result of exercise were not related to the pre exercise concentration of 2,3-DPG indicating that change of 2,3-DPG is not significantly affected by the amount of 2,3-DPG present before physical activity is initiated. / Education, Faculty of / Curriculum and Pedagogy (EDCP), Department of / Graduate

The experiment was designed to demonstrate the effects of exercise and confinement on the calcium metabolism of rats. A subsidiary purpose was to determine if any such effects are mediated by a humoral agent. Twenty-four male Sprague Dawley rats were divided into three groups. One group was exercised in motorized activity cages for one hour per day five days per week; one group was confined in small individual metabolism cages for 26 days and in body holders for 12 days; one group was housed in individual metabolism cages and served as controls. Half of the rats of each of the above three groups received 2 ml whole blood from rats similarly treated (exercised, confined or control), on each of the last five days of the experiment. Thus the exercised rats received blood from confined rats, the confined rats received blood from exercised rats and the control rats received blood from control rats. A calcium balance study was carried out for the last 26 days of the 38 day experiment and a calcium-45 balance study was carried out for the last six hours of the experiment. Thus the following specific parameters of calcium metabolism were measured: calcium balance, per cent calcium utilization, food intake, faecal calcium, urinary calcium, total carcass calcium, femur calcium, calcium-45 absorption and femur calcium-45. The entire experiment was performed twice and the data analyzed using a randomized complete block design analysis of variance. The exercise or confinement did not significantly alter the calcium metabolism of the male Sprague Dawley rat under the conditions of this study. Two possible conclusions were discussed. Either this experiment casts some doubt on the current concepts regarding immobilization and osteoporosis, or that the humane conditions adopted in this study did not successfully immobilize the rats. The present experiment also suggests that regular vigorous exercise may not affect the calcium metabolism of the rat to a greater extent than normal activity or mild exercise. No conclusions could be drawn about the role of the blood in regulating or controlling the effects of exercise or confinement on calcium metabolism. / Medicine, Faculty of / Cellular and Physiological Sciences, Department of / Graduate