Thesis (M.S.)--University of Michigan, 1980.

Thesis (M.S.)--University of Michigan, 1980.

<p>The present thesis examined the acute and chronic (training) hemodynamic responses to the unique exercise stimulus of high-intensity "sprint" interval exercise or training (SIT). Previous research has characterized the muscle metabolic and exercise performance adaptations to both short and medium term SIT, however the cardiovascular adjustments and adaptations have not been examined. As part of this thesis two studies were designed to permit evaluations of the chronic cardiovascular responses to a six-week SIT intervention protocol, while two separate studies examined the acute impact of a sprint exercise session on indices of vascular structure and function. Comparisons were made between the SIT and traditional endurance exercise training (ET) in the two exercise training studies, while comparisons were made between a single sprint and that of multiple sprints in the acute exercise studies. The subject population examined in this research was young healthy participants.</p> <p>Our general hypothesis regarding the training adaptations was that similar changes of artery stiffness, vascular endothelial function, blood flow kinetics and oxygen uptake kinetics would occur following SIT compared to ET. Regarding the acute effects of a sprint exercise, we expected arterial stiffness to decrease in the exercising limbs and increase in the central arteries, similar to the responses observed previously immediately following endurance exercise, while we hypothesized that endothelial function would be decreased immediately following the exercise session because of the intense nature of the exercise. The overarching hypothesis guiding these specific hypothesis is that we believe that individual bouts of exercise impact on the arterial wall through the generation of a shear stimulus related to cyclic increases in blood flow and blood pressure. In the short-term the acute response of the artery depends on the composition of the arterial wall and the local stimulus. Over time, functional and structural adjustments occur to normalize the impact of shear forces.</p> <p>Training adaptations in vascular structure and function to SIT were similar to those observed with ET. Both exercise training methods stimulated improved peripheral artery stiffness and endothelial function. The rate of increase in oxygen uptake (kinetic response) was not improved with either training method. However, estimated myocardial demand was reduced with ET but not SIT, which indicates more favourable adaptation in central hemodynamics with ET.</p> <p>Acute sprint exercise markedly reduced peripheral artery stiffness in the exercised limbs well into recovery (~45 minutes), which may benefit central hemodynamics after exercise completion. Sprint exercise also acutely decreased endothelial function, likely because of high oxidative stress generated during the exercise bout and may provide the ideal stimulus for endothelial adaptation.</p> <p>In summary, this thesis highlights the chronic and acute effects of sprint interval exercise and training in young health individuals. The notion that sprint interval exercise provides equivalent benefits to the cardiovascular system as endurance exercise may be true in the peripheral circulation. However, further study focusing is required before the general acceptance of more favorable central hemodynamic effects from endurance exercise training.</p> / Thesis / Doctor of Philosophy (PhD)

Studienziel: Untersuchung der Dosis-Wirkung von inhalativem Stickstoffmonoxid (NO) bei Patienten mit schwerem akuten Lungenversagen (ARDS) und der diese Wirkung beeinflussenden Faktoren. Design: Prospektive, offene Beobachtungsstudie. Setting: Universitäts-Klinikum. Intensivstation. Patienten: 26 Intensivpatienten mit hohem pulmonal-vaskulärem Druck (PAP) bei zugrunde liegendem ARDS. Behandlung: Patienten mit ARDS wurden einer Therapie mit konventioneller Beatmung und Beimischung von inhalativem NO zugeführt. Das Protokoll sah die Applikation von NO in steigender Dosierung von 0,01 parts per million (ppm), 0,01 ppm, 1, 10 und 100 ppm vor. Zischen den Messungen wurden für 15 bis 20 Minuten Nullmessungen durchgeführt. Ein Anstieg des pulmonal-areriellen Sauerstoffdrucks (Pao2) um 20% wurde als "Responding" definiert. Messungen: Es wurden die Parameter des pulmonalen Gasaustausches wie PaO2, PaCo2 und CaO2 gemessen. Des Weiteren wurden die Werte für den mittleren systemischen Blutdruck (AP), den mittleren pulmonal-arteriellen Druck (PAP), den systemischen Widerstand (SVR), den pulmonalvaskulären Widerstand (PVR), die Herzfrequenz (HR), den Herzindex (CI), das Herz-Zeit-Volumen (HZV), den Wedgedruck (PCWP) und die venöse Beimischung registriert. Ergebnisse: NO verursachte einen dosisabhängigen Anstieg des Pao2 von 0,01 bis 10 ppm (p / STUDY OBJECTIVE: To determine the dose responsiveness to nitric oxide in adult patients with acute respiratory distress syndrom (ARDS), especially in those patients with pulmonary hypertension. To find factors influencing the response to NO. DESIGN: Prospective, open, nonblinded observation study. SETTING: University teaching hospital. PATIENTS: 26 ICU patients suffering from ARDS demonstrating pulmonary hypertension. INTERVENTIONS: Patients with severe acute respiratory distress syndrome received inhalation therapy with NO. Inhaled NO was sequentially titrated from 0,01 parts per million to 0,1 ppm, 1, 10, and 100 ppm at 15-minute intervals followed by a 15 to 20 min OFF interval. Changes in hemodynamics and gas exchange were monitored. An increase of at least 20 % in the oxygenation index was considered as a therapeutic response. MEASUREMENTS: Heart rate, mean arterial pressure, mean pulmonary arterial pressure, pulmonary vascular resistance (PVR), peripheral vascular resistance, cardiac index,rigt to left shunting , venous admixture and right ventricular ejection fraction were monitored throughout the study, as well as the Pao2, Cao2 and PaCo2. RESULTS: 26 patients received inhaled NO. Nitric oxide induced a dose-dependent increase in Pao2 for inspiratory nitric oxide concentrations ranging between 0.01 and 10 ppm (p