Thesis (Ph. D.)--University of Missouri-Columbia, 2002. / Typescript. Vita. Includes bibliographical references (leaves 80-89). Also available on the Internet.

The aim of the present thesis was to examine the potential for acute carbohydrate-protein (CHO-P) ingestion to enhance performance and recovery from exercise designed to simulate the demands of multiple-sprint sports (MSSs). Chapter 3 of the thesis explored the inter- and intra-day reliability and concurrent validity of non-motorised treadmill ergometry (NMT) for the assessment of short-distance sprint performance [i.e. 10-30 m). There were no significant mean differences between NMT variables recorded on the same day or between days. Ratio limits of agreement indicated that the best agreement was in 20 [1.02 */-=- 1.09) and 30 m [1.02 */* 1.07) sprint times, peak [1.00 */T 1.06) and mean (0.99 */+ 1.07) running speed and step length (0.99 */-=- 1.09) and frequency (1.01 */+ 1.06). The poorest agreement was observed for time to peak running speed (1.10 */* 1.47). Significant differences were observed between NMT and over-ground sprint times across all distances, with times being lower (faster) by approximately 25-30% over-ground. The correlations between NMT and over-ground variables were generally modest (r5 = 0.44 - 0.67), and optimal for time to cover 30 m on Day 2 (rs = 0.8). Chapter 4 sought to examine the efficacy of CHO-P ingestion during 4 h of recovery from the Loughborough Intermittent Shuttle Test (LIST) when compared to CHO matched for energy (ISOEN) or CHO (ISOCHO) in a typical CHO beverage. There were significant increases over time in muscle soreness, and reductions in extensor and flexor peak torque (by approximately 9%, 9% and 8%, and 13 %, 13% and 11% at 60 deg-s-1) and jump performance (10%, 7% and 5%) with the ingestion of CHO-P, ISOEN and ISOCHO, respectively. Beverage type x time interactions were not significant for any of these variables, indicating that changes in each variable were similar for all groups. Decrements in sprint performance assessed on the NMT were typically small and not different between beverage types (<4%), although sprint times over 20 and 30 m remained elevated for 48 h post-exercise. Accordingly, Chapter 4 provided no clear evidence for a benefit of ingesting CHO-P in the hours after exercise to enhance recovery of muscle function and selected performance variables following MSS activity. Chapters 5 and 6 of the thesis aimed to examine the effect of CHO-P ingestion during simulated MSS exercise. In Chapter 5, it was observed that sprint times, HR and gut fullness increased over the course of the LIST, with no influence of consuming each of the different beverages. In contrast, there was a main effect of time (P < 0.001), and drink (P = 0.042) observed for RPE, which was lower (P < 0.001) during the LIST in the CHO-P condition (16.9 ± 1.4) than in either the ISOCHO (17.8 ± 1.1) or ISOEN (17.7 ± 1.3). However, time to exhaustion was not different (P = 0.29) between CHO-P (468.3 ± 268.5 s), ISOCHO (443.4 ± 286.3 s) and ISOEN (446.2 ± 282.08 s), although these times did equate to a non-significant mean improvement of 4% in the CHO-P trial. Chapter 6 demonstrated that during a modified version of the LIST with two self-regulated blocks of exercise intensity, participants had a higher average speed (8.1 ± 0.3 cf. 7.9 ± 0.5 knvlr1) during the final (self-regulated) 15 min block of the LIST in the CHO-P condition compared to CHO. Whilst the mechanisms for such an improvement are not certain, the attenuated rise in RPE observed in Chapter 5, and increased blood urea concentration observed in Chapter 6, with CHO-P ingestion may suggest altered central fatigue and/or increased protein oxidation enhances performance during MSSs.

This study investigated the effects of progressive dehydration by 1.5-2.0% body mass (BM) (NF) on core temperature (Tc), heart rate (HR), on-ice performance, and mental fatigue during a 70-min scrimmage, compared to maintaining BM with a carbohydrate-electrolyte solution (CES). Compared to CES, Tc was significantly higher throughout the scrimmage in NF. Players in NF had reduced mean skating speed and time at high effort between 30-50 min of the scrimmage. Players in NF committed more puck turnovers and completed a lower percentage of passes in the last 20 min of play. Post-scrimmage shuttle skating time was higher in NF. Hockey fatigue questionnaire total score and Profile of Mood States fatigue score was higher in NF. The results indicate that mild dehydration compared to maintaining BM with a CES resulted in increased Tc, decreased skating and puck handling performance, and increased mental fatigue during an ice hockey scrimmage. / Gatorade Sports Science Institute, Natural Sciences and Engineering Research Council of Canada

The synthesis of the three 6”-deoxy-6”-thio glycolipid analogues β-D-Gal-(1→6)-β-D-Gal-(1→4)-β-D-Glu-(1→OCH2)-[1,2,3]-triazole-1-dodecane, β-D-Gal-(1→4)-β-D-Glu-(1→4)- β-D-Glu-(1→OCH2)-[1,2,3]-triazole-1-dodecane and β-D-Gal-(1→4)-β-D-Glu-(1→4)-β-D-Glu-(1→OCH2)-[1,2,3]-triazole-1-octadecane is presented here. Glycosylation at position O-4’ of a propargyl cellobioside glycosyl acceptor and position O-6’ of a propargyl lactoside glycosyl acceptor with a 6-thio-6-deoxy galactosyl donor gave rise to two unique trisaccharides that in turn underwent copper-catalyzed azide-alkyne cycloadditions with either 1-azidododecane or 1-azidooctadecane. The potential for each of these analogues to function as tethers of lipid bilayers to Au(111) was assessed primarily by differential capacitance experiments. Deposition of a bilayer of DMPC/cholesterol (70:30) by Langmuir-Blodgett (LB) transfer followed by Langmuir-Schaefer (LS) touch to a self-assembled monolayer of the O-6’ linked analogue, diluted with 1-β-D-thioglucose, failed. This led to simplifying the target architecture to diagnose the quality of the monolayers. A monolayer of the known monosaccharide 1-octadecane-4-(6-thio-β-D-galacto-pyranosyloxymethyl)-[1,2,3]-triazole1 prepared by LB transfer was found to support a lipid monolayer deposited by LS touch and this bilayer had the lowest minimum capacitance observed of 0.9 µF/cm2. An attempt to produce a bilayer by the same method using the trisaccharide bearing the C-18 alkane chain failed and this was attributed to high water solubility, which gave rise to poor organization at the air-water interface. A self-assembled monolayer of this variant went forward to produce a poor quality bilayer with a minimum capacitance of 7.1 µF/cm2, which was the lowest value obtained for the trisaccharide series of analogues. / Natural Sciences and Engineering Research Council of Canada (NSERC)

Four analogues of the Lewis X trisaccharide antigen (β-D-Galp(1→4)[α-L-Fucp(1→3)]-D-GlcNAcp) in which the galactosyl residue is modified at O-4 as a methyloxy, deoxychloro, deoxyfluoro or deoxy were synthesized. The preparation of the modified 4-OMe, 4-Cl, 4-F and 4-H trichloroacetimidate galactosyl donors is described as well as their use in the glycosylation of an N-acetylglucosamine glycosyl acceptor. The resulting disaccharides were deprotected at O-3 of the glucosamine residue and fucosylated giving access to the desired protected Lewis X analogues. One step global deprotection (Na/NH3) of the protected 4”-methoxy and 4”-deoxy analogues, and two step deprotections (removal of a p-methoxybenzyl with DDQ, then Zemplén deacylation) of the 4”-deoxychloro and 4”-deoxyfluoro protected Lex analogues gave the desired compounds in good yields. The relative binding energies of the 4” manipulated Lewis X methyl glycoside analogues for anti-Lewis X mAb SH1 were determined using competitive ELISA procedures. The binding experiments revealed that substitution of the 4” site with a deoxychloro, deoxyfluoro or deoxy function had a large differential change in the free energy of binding; yet they did not completely abolish cross reactivity with native Lewis X. Substitution with a methyloxy function eliminated recognition by anti-Lewis X monoclonal antibody SH1. / NSERC

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No description available.

To test the hypothesis that maternal glucose restriction (GR) would compromise small intestine (SI) growth and development, we used a diet induced model of IUGR. Pregnant rats and offspring were fed isoenergetic diets {0% (deficient), 12, 24% (restricted), 60% (adequate) glucose) from gestation day (gd) 0 through adolescence. SI tissue was collected at gd20, birth, 12--24h, postnatal day (pd) 7, 15, 21, 28, 35, 49 and in controls. GR affected pup weight at early timepoints, resulting in IUGR; beyond effects due to differences in body wt, GR compromised SI length at 12--24h and promoted SI growth during peak lactation (pd15; total and distal wts). Dietary glucose regulated in utero (gd20) expression of sodium-dependent glucose co-transporter (SGLT1) protein. Diet-induced precocious maturation of lactase and sucrase was observed in glucose deficient animals. In summary, there were periodic but no permanent effects of dietary glucose intake on gut growth and development.

Methylglyoxal (MG) is a reactive dicarbonyl compound mainly formed during glucose and fructose metabolism. Diabetic patients have increased plasma levels of MG. Our laboratory has shown that treatment with MG induces insulin resistance and type II diabetes in male Sprague-Dawley rats. However, the increases in endogenous MG level attained in different organs and its contribution to the pathogenesis of diabetes following the administration of either high glucose or high fructose diet have not been addressed. The present study aims to investigate whether the harmful effects induced by increased consumption of glucose and/or fructose is linked to increased MG generation. In vitro studies have suggested that L-arginine is an effective MG scavenger. Accordingly, another goal is to determine whether L-arginine pretreatment would scavenge MG under in vivo setting and reduce the harmful effects of hyperglycemia. MG and reduced glutathione (GSH) levels were determined in plasma and urine and in different organs of male Sprague-Dawley rats after 12 weeks of treatment with either high fructose or high glucose diet. GSH plays an important role in the degradation of MG and bears an inverse relationship with the levels of MG. The key results obtained suggest that both diets significantly increased blood pressure and plasma MG levels. A high fructose but not a high glucose diet, increased the plasma total cholesterol, triglycerides levels and total cholesterol/HDL ratio in parallel with the increases in MG and GSH levels in the liver. Increased MG levels seen in both aorta and mesenteric artery induced by high glucose or fructose diet was attenuated by pretreatment with L-arginine. These findings suggest that elevated MG level induced by treatment with high carbohydrate diets in both conduit (aorta) and resistance type (mesneteric artery) vessels may be linked to endothelial dysfunction seen in hyerglycemic/diabetic states. High glucose but not high fructose diet significantly increased MG levels in the pancreas. This observation is consistent with the well-known glucotoxicity caused by hyperglycemia in the pancreas. Taken together, these data provide the first evidence that elevated MG levels in certain organs/tissues following consumption of high fructose and/or glucose diet(s) may play a critical role in contributing to the metabolic abnormalities and the endothelial dysfunction that precedes the onset of macro and microvascular complications in either hyperglycemic and/or type II diabetic states. Interestingly, quenching of elevated MG levels in tissues by pretreamtent with L-arginine overcomes MG-induced vascular damage and endothelial dysfunction caused by high fructose and high glucose diet regimens.

This study determined outcomes of a low-carbohydrate (CHO) and moderate-CHO diet on weight loss, ketone production, and urinary calcium excretion in a convenience sample of 14 (ages 18-26, m=2, f=12) overweight students at a midwestern college for one month in a two-week, cross over study design. Results showed significant weight loss in subjects over time (p< .01). However, no significant difference between diet groups over time for weight loss was shown. Outcome of urine ketone production remained unaffected over time and between groups over time. A significant difference was noted in urinary calcium excretion within subjects over time (p=.035), yet not between groups over time. These findings suggest that weight loss may be due to a decrease in water and lean body mass from glycogen mobilization. Ketone production was unaffected possibly due to non-compliance with diet recommendations and small sample size of the study. Urinary calcium excretion increases may be attributed to higher protein intakes in participants on the modified-CHO diets, possibly allowing for a negative calcium balance in the body leading to premature osteoporosis. / Department of Family and Consumer Sciences