An adequate supply of oxygen (02) is essential to the survival of all higher organisms. The mammalian carotid body, located at the common carotid artery senses blood levels of 0 2, carbon dioxide (C02) and acidity. Glomus cells, or type I cells in the carotid body are the main 0 2-sensors which regulate blood p02 via reflex control of ventilation. The carotid body secretes multiple neurotransmitters including dopamine (DA), which is potentiated during low p02 levels and is thought to modulate sensory signaling by apposing afferent nerve fibers. Catecholamine (CA) release is also critical for the animal's ability to survive hypoxic stress associated with the birthing process and the transition to extrauterine life. However, the source for this CA release (primarily epinephrine; EPI) is from adrenal chromaffin cells. The primary 02-sensor in both adrenal chromaffin cells and carotid body type I cells is unknown. One potential candidate is the cytochrome b55s/NADPH oxidase complex that generates the respiratory burst in phagocytes. To test this hypothesis, cultured adrenal medulla chromaffin cells and intact carotid bodies from wild type (WT) and oxidase deficient (OD) mice (knockout gp91 phox, the glycoprotein subunits in the NADPH oxidase complex) were investigated. High performance liquid chromatography and immunocytochemistry were used to quantify amine release in these two chemoreceptors following exposure to hypoxia. Both WT and OD chromaffin cells and carotid bodies responded to the hypoxic challenge with increased monoamine secretion. Norepinephrine and epinephrine were the principal amines released from chromaffin cells, compared to dopamine and serotonin from carotid bodies. These findings suggest that NADPH oxidase is not the primary 02- sensor in either chemosensory system. Quantification of monoamine secretion in intact carotid body from mouse and rat was also compared under basal conditions and after exposure to hypoxia and acid/hypercapnia (pH 7.10). Significantly larger amounts of basal serotonin was secreted from mouse carotid body as compared to the rat. Interestingly, serotonin release was potentiated by hypoxia in mouse carotid body, but this was not observed in the rat. Additionally, ratio of basal level serotonin-to-dopamine secretion was significantly higher in mouse than rat CB. Surprisingly, acid/hypercapnic (pH 7.1 0) had no detectable effect on amine secretion from either mouse or rat carotid body. / Thesis / Master of Science (MSc)

In these experiments, we tested the hypothesis that sympathetic escape in skeletal muscle is mediated through a fall in parenchymal cell oxygen levels following blood flow reduction. This hypothesis predicts that if the fall in parenchymal cell PO₂ during stimulation can be minimized, escape should be reduced. To test this prediction, we studied the behavior of superficial arterioles of the cat sartorius muscle during 3 minutes of sympathetic nerve stimulation. The muscle was covered with silicone oil equilibrated with 0%, 5% and 10% oxygen. During stimulation under 0% oxygen, 90% of visible arterioles showed a significant secondary relaxation (escape). The relaxation averaged 55% of the initial constriction. Under 5% oxygen, resting arteriolar diameter was reduced by an average of 12% and escape was significantly reduced throughout the arteriolar network. Under 10% ambient oxygen, there was an additional 5% reduction in resting diameter and a further reduction of escape. Escape was not attenuated when control diameter was reduced to the same degree with arginine vasopressin, suggesting that the effect of oxygen was specific rather than secondary to an increase in vascular tone. The above observations are also consistent with the hypothesis that escape is mediated through a fall in vascular wall PO₂. To evaluate this possibility, periarteriolar and parenchymal tissue PO₂ were measured with oxygen microelectrodes during sympathetic stimulation under 0% and 10% oxygen suffusion of the muscle. In the proximal arterioles, the periarteriolar PO₂ during control and during stimulation was identical under 0% and 10% oxygen yet escape was reduced by 75% under 10% oxygen. Similarly, escape was reduced 90% in the distal arterioles under 10% oxygen but periarteriolar PO₂ was very nearly the same as that measured under 0% oxygen. In contrast, mean parenchymal tissue PO₂ fell to low levels during stimulation under 0% oxygen but did not fall below normal levels during stimulation under 10% oxygen. These findings argue against the hypothesis that a fall in vascular wall PO₂ is responsible for escape. The findings are consistent with the hypothesis that sympathetic escape in skeletal muscle is mediated through a fall in parenchymal cell PO₂. (Abstract shortened with permission of author.)

No description available.

There has been an interest in the kinetics of the V02 response during exercise at various intensities. However, most studies focus on the response of submaximal intensities whereas few studies have examined V02 kinetics at severe intensities. The purpose of this study was to evaluate the effect of exercise intensity on V02 kinetics over a range of severe intensities.

Bibliography: leaves 162-174.

Elite milers, Sir Roger Bannister and Joseph Falcon, have stated that the consumption of carbonated beverages hinders the performance of aerobic events. Oxygen transport is purportedly impaired by the consumption of carbonated beverages. The research on carbonated beverages has been limited to the effects on the digestive system, gastric emptying, and thermal heat stress in animals. The purpose of this study was to investigate the effects of consuming 28 ounces of carbonated beverages per day, for three weeks, on arterial oxygen saturation (Sa0₂), serum hemoglobin concentrations (Hb), and maximal oxygen consumption (VO₂max) in experienced cyclists. Nine competitive cyclists and triathletes (aged 19-24 years, M = 21.67 years), with average weights and percent body fat of 76.51 kg and 11.4 percent respectively, were randomly assigned to a three week period of consuming 28 ounces of carbonated water or a three week period of no carbonated beverages. At the end of each three week period, a 5 c.c. blood sample was taken for Hb determination and the subjects performed a test of maximal oxygen consumption on a cycle ergometer while Sa0₂ was being monitored. The groups then crossed-over with respect to their treatment, and after another three week period, the same variables were measured. The Student's t statistic was used to compare Sa0₂, Hb, and VO₂max. The results showed no significant differences between the carbonated period (C) and the noncarbonated period (NC) in Sa0₂ (94.00 vs 93.22 %, p= 0.21), Hb (13.71 vs 14.12 g/dl, p= 0.11), and VO₂max (4.63 vs 4.65 Imin, p= 0.92). From this study, it appears that the consumption of carbonated beverages does not affect the variables associated with the oxygen carrying capacity of blood (Sa0₂ and Hb) or the test of aerobic performance (V0₂max) / Graduation date: 1992

published_or_final_version / Sports Science / Master / Master of Science in Sports Science

Caenorhabditis elegans clk-1(qm30) and isp-1(qm150) mutants exhibit highly pleiotropic phenotypes that include slow development and long lifespan. clk-1(qm30) and isp-1(qm150) correspond to loss of function mutations in genes necessary for ubiquinone biosynthesis and complex III electron transport, respectively. Previous research has lead to the hypothesis that altered levels of cellular reactive oxygen species (ROS) may underlie clk-1(qm30) and isp-1(qm150) mutant phenotypes. To test this hypothesis RNA interference (RNAi) by feeding was used to indirectly alter cellular ROS levels by knocking down genes that encode ROS detoxification enzymes. Specifically, genes that detoxify ROS using glutathione or thioredoxin, both of which are important cellular thiol-redox molecules, were knocked down to examine the role of ROS in determining clk-1(qm30) and isp-1(qm150) lifespan, post-embryonic development, and germline development. In summary, knocking down ROS detoxification genes does not severely appear to affect the phenotypes that were studied. ROS detoxification gene knockdowns consistently induced mild decreases in wild type, clk-1(qm30), and isp-1(qm150) lifespan. However, knocking down NAD+-dependent isocitrate dehydrogenases, which are not closely involved in ROS detoxification, similarly affected lifespan, indicating that decreases are not specific to ROS detoxification. Of note, knocking down gcs-1, which is required for glutathione biosynthesis, induced lethal intestinal abnormalities in wild type, c1k-1(qm30), and isp-1(qm150) worms. Overall, findings do not support that low ROS underlies the clk-1(qm30) and isp-1(qm150) mutant phenotypes.

Eleven male triathletes were studied to determine the relationships between selected metabolic measurements and triathlon performance. Measurements were made for oxygen consumption (V02), pulmonary ventilation (Ve) and heart rate (HR) during submaximal and maximal 400-yd freestyle swimming (FS), cycle ergometry (CE) and treadmill running (TR). Submaximal workloads were 1 m/sec for swimming, 200 watts for cycling and 7.5 mph for running. The mean (1/min) was significantly (P<0.05) lower during 1/min) than CE (4.68 1/sin) or TR (4.81 1/min). cycling and running performance times during the (1.2 mile swim, 56 mile cycle, 13.1 mile run) were to have a low relationship to V0z max (ml/kg/min) -0.32 and -0.55, respectively. The V0z max when expressed as 1/min was found to significantly (P<0.05) related to cycling time (r=-0.70). However, at a selected workload the %VO2 max was found to be highly related to swimming (0.91), cycling (0.78) and running (0.86) performance times. Maximal HR (bts/min) was also observed to be significantly (P<0.05) lower during FS (163) than CE (176) or TR (183). Running and cycling times in the triathlon were highly correlated (P<0.05) to overall triathlon performance times, 0.97 and 0.81, respectively, whereas swimming was found to be less a contributor to the athlete's final time, r=0.30. This study suggests that economy of effort is of greater importance to a triathlete's performance than their maximal oxygen uptake.

It has been suggested that children are less likely than adults to demonstrate a plateau in oxygen uptake (V02) at maximal exercise. However, there has been no direct comparison. Therefore, the purpose of this study was to compare boys and men in achievement of plateau as well as the secondary criteria for maximal effort: heart rate (HR), respiratory exchange ratio (RER), and blood lactate (BLa). Seventeen boys (10.7 ±v 0.6 yrs) and 21 men (22.5 ± 2.0 yrs) completed a practice exercise test and a graded exercise test in order to determine VO2max and achievement of the criteria. The men also completed a second graded exercise test at a faster speed to determine if speed may affect plateau achievement. Comparisons indicated that, except for the BLa criterion, men and boys have similar rates of achievement. In addition, speed does not seem to play a role in criteria achievement. However, due to a small sample size, these results should be viewed with caution. / School of Physical Education