Thesis (Ph. D.)--Florida State University, 2005. / Advisor: Dr. Richard Hyson, Florida State University, Program in Neuroscience. Title and description from dissertation home page (viewed Sept. 19, 2005). Document formatted into pages; contains ix, 64 pages. Includes bibliographical references.

Thesis (M. Sc.)--University of Hong Kong, 200.

Thesis (Ph. D.)--Ohio State University, 2007. / Title from first page of PDF file. Includes bibliographical references (p. 113-118).

The relative contribution of arteriovenous oxygen (A-V O2) difference to thermally-induced and activity-induced changes in metabolic rate (VO2) were delineated in the toad, B. marinus. In conjunction, the influence of rest and activity, temperature, and removal of the pericardia! sac on separation efficiency (Es) in the anuran ventricle was determined by direct measurement of arterial and venous percent oxygen saturation (% saturation), using a microsampling technique.

No description available.

While a great deal of research has been directed towards investigating the age-related decline in V02max, the effect of physical activity on the age-related decline in V02max has not been clearly established. Therefore, the purpose of this study was to examine the relationship between physical activity and the age-related decline in maximal oxygen consumption (VO2max) in apparently healthy individuals. In order to assess the effects of physical activity on the age-related decline in V02max, physiological data was obtained from 142 former participants (116 men and 26 women) (40 ± 8.0 years), in the Ball State University Adult Physical Fitness Program across an average of 12 ± 4.5 years. The subjects were divided into three physical activity group categories depending on their self-reported physical activity status at the time of the first and follow-up test. Those subjects who were sedentary at the first and last test were designated as SED-SED. Those who reported sedentary at the first test and active at the last test were designated as SEDACT and those who were physically active at the time of both tests were designated as ACT-ACT. The data from the analysis revealed that the rate of decline in V02mx expressed as change per year among adult men varied as a function of their reportedphysical activity habits. Those men designated as SED-SED and ACT-ACT experienced a statistically significant decline (p<0.05) in V02max during the follow-up period, while, those men designated as SED-ACT maintained their V°2max. The rates of the change in V02max (ml-kg- 1•min-1) for the men were -0.45, 0.03 and -0.22 ml•kg-l-min-1•yr1 for the SED-SED, SED-ACT and ACT-ACT groups respectively. The percent decline in V02max were 6%, 11% and 2% respectively. A statistical comparison of the rate of change among physical activity groups indicated a difference between the SED-SED and SED-ACT groups (p<0.05). Within the limitations of this study, these data suggested that there was no statistically significant difference in the rate of change in V02max (ml•kg-1•min-1-yr1) between the SED-SED and ACT-ACT physical activity groups. However, when presented as percent change per decade, the decline for those men who were sedentary at both time points was twice that of those men who reported an active lifestyle at both time points. Although the rates of change were not different for the SED-SED and ACT-ACT physical activity groups, those men with a physically active lifestyle maintained their aerobic power advantage as compared to sedentary men who remained sedentary. Furthermore, sedentary men who took up an active lifestyle had offset the decline in V02max (ml•kg-1•min-1) attributed to physical inactivity.The rates for the change in V02max (ml•kg-1•min-1-yr1) for the women were -0.36, 0.20 and -0.21 (ml•kg-1•min-1-yr1) for the SED-SED, SED-ACT and ACT-ACT groups respectively. While these changes were similar in direction and magnitude to those observed for the men, there were no statistically significant differences among the female groups (p>0.05). Therefore the results from the present study were inconclusive for women possibly due to the low sample size (n=26). / School of Physical Education

The purpose of this study was to evaluate the effect of mode and intensity on VO2 kinetics in the severe intensity domain. Seventeen participants completed 3-7 tests each on a cycle ergometer and treadmill. For each test, Tfatigue, VO2max, Tmean response, VO2GAIN, TVO2max and T@VO2max were determined. Linear regression techniques were used to describe the relationship between TVO2max and Tfatigue . VO2max values were higher in running. The VO2 response profile was faster for running than cycling and faster at higher intensities. The faster VO2 response in running may be associated with larger active muscle mass or differences in muscle activation patterns. The faster response at higher intensities may suggest that VO2 response is driven by O2 demand.

The purpose of this study was to describe mathematically the oxygen uptake kinetics during cycle ergometry, and to examine the effect of intensity on the kinetic responses within the severe domain. Sixteen volunteers performed a series of exercise tests at a range of intensities selected to elicit fatigue in ~3 to 10 min. A simple mono-exponential model effectively described the response across all intensities. There was a positive correlation between the response time and the time to fatigue, demonstrating that the maximal oxygen uptake was achieved faster at higher intensities within the severe domain. Models incorporating two components effectively described the responses only in tests lasting 8 min or more. It was concluded that there is a second, slow component in the oxygen uptake response only at the lower intensities within the severe domain.

The purpose of this study was to predict VO2pak using ratings of perceived exertion (RPE), heart rate (HR), and percent fat (PFAT). Subjects were males (n= 60) (PFAT, M SD = 14.4 6.1) and females (n= 67) (PFAT, M SD = 23.4 4.9) with ages ranging from 18 to 33 years. Subjects performed an incremental cycle ergometer protocol and RPE, HR and Vo2 were measured at each stage until VO2 ak was achieved. Mean RPE and HR at the submaximal workload of 100 watts were, (RPE100) M= 12.7 2.6 and (HR100) M= 146.924.7 respectively. Correlations (p< .001) with VO2p. were -.75 (PFAT), -.66 (HR100), -.67 (FIPE100). The multiple correlation using PFAT, HR100, and RPE100 as predictors of VO2pak was .83 (SEE= 5.28 ml-kg BW'smin"). Each predictor contributed to the correlation (p<.01). The results indicate that PFAT combined with exercise responses of RPE and HR provide valid estimates of VO2peak with a relatively small SEE.

An organisms’ diet represents an exogenous influence that often yields colossal effects on long-term health and disease risk. The overconsumption of dietary sugars for example, has contributed to significant increases in obesity and type-2 diabetes; health issues that are costly both economically and in terms of human life. Individuals who are obese or are type-2 diabetic often have compromised oxygen delivery and an increased vulnerability to oxygen-deprivation related complications, such as ischemic strokes, peripheral arterial disease and myocardial infarction. Thus, it is of interest to identify the molecular changes glucose supplementation or hyperglycemia can induce, which ultimately compromise oxygen deprivation responses. By utilizing the Caenorhabditis elegans genetic model system, which is anoxia tolerant, I determined that a glucose-supplemented diet negatively impacts responses to anoxia and that the insulin-like signaling pathway, through fatty acid and ceramide biosynthesis and antioxidant activity, modulates anoxia survival. Additionally, a glucose-supplemented diet induces lipid accumulation. Use of RNA-sequencing analysis to compare gene expression responses in animals fed either a standard or glucose-supplemented diet revealed that glucose impacts the expression of genes involved with multiple cellular processes including lipid and carbohydrate metabolism, stress responses, cell division, and extracellular functions. Several of the genes we identified are homologous to human genes that are differentially regulated in response to metabolic diseases, suggesting that there may be conserved gene expression responses between C. elegans supplemented with glucose and a diabetic and/or obese state observed in humans. These findings support the utility of C. elegans to model specific aspects of the T2D disease process (e.g., glucose-induced sensitivity to oxygen deprivation) and identify potentially novel regulators of common complications seen in hyperglycemic and T2D patients (e.g., macrovascular complications).