Thesis--PlanA (M.S.)--University of Wisconsin--Stout, 2001. / Includes bibliographical references.

The purpose of this study was to examine the effects of a 4% lean body weight dehydration with two levels of rehydration for four hours on the changes in physical work capacity and blood glucose. Further, the study examined the effects on volume STPD, V02, R.Q. and true 02 during the physical work capacity test. A total of 7 university-aged males were involved in the experiment as subjects. Each subject was tested in two experimental conditions, i.e. 50% rehydration and 100% rehydration, on two separate days. Each set of tests consisted of blood samples drawn from the finger tip, a physical work capacity test with expiratory gas collection. Six sets of tests were distributed as follows: one at 6 A.M., and one half an hour after dehydration. The four other sets were hourly separated. The rehydration consisted of intake of tomato juice given after the set of tests 2, 3, 4 and 5. The amount given was equally subdivided and depended on the experimental condition. Analysis of variance indicated significant changes ever time for all dependent variables, except V02; significant changes between level of rehydration for weight, and significant changes for the level of rehydration by time interaction for true 02 and weight. There was no significant individual simple correlation coefficient between blood glucose and physical work capacity for each experimental condition. There was a mean decrease of 30% in physical work capacity after heat dehydration and only 40% of the loss was recovered without significant difference between experimental conditions. Gas exchange was also affected. The volume STPD increased after dehydration, true 02 decreased after dehydration and a better recovery showed up in the 50% rehydration condition. The R.Q. parameter, in fact, did not indicate significant changes but there was a slight decrease after dehydration. The level of blood glucose decreased after dehydration tut there was an increase in the middle of rehydration, even with the expected increase in blood volume, from the liquid intake. This suggested a very high level of gluconeogenesis on those last hours, probably due to glucocorticoid hormone action. / Education, Faculty of / Curriculum and Pedagogy (EDCP), Department of / Graduate

Thesis (M.S.)--Purdue University, 2003. / Includes bibliographical references (leaves 60-63).

No description available.

No description available.

No description available.

There is no abstract available for this thesis. / Department of Family and Consumer Sciences

Thesis (M.S.)--Virginia Polytechnic Institute and State University, 1990. / Vita. Abstract. Includes bibliographical references (leaves 68-73). Also available via the Internet.

Plant seeds, yeasts, bacterial spores, rotifers, and other organisms are capable of suspending their metabolism and entering a state of latency when dehydrated. These organisms may maintain this state for extremely long periods of time, yet upon rehydration resume normal metabolism, without evidence of severe membrane disruption. With many of these organisms, the ability to survive dehydration has been correlated to the production of large amounts of carbohydrates, including glycerol, glycogen and the disaccharide trehalose. Trehalose has been shown to protect isolated sarcoplasmic reticulum microsomes and phospholipid vesicles from dehydration damage, implying that the site of protective action of trehalose and other carbohydrates is the lipid portion of membranes. In this thesis, the effects of carbohydrate composition, vesicle size, and lipid composition on the protection of liposomes from dehydration was investigated, as was the structure of the solid lipid-trehalose complex. Electron microscopy of dried liposomes indicated that vesicles protected with trehalose remain essentially intact even when dry, while vesicles not protected by sugar are severely disrupted by drying . ³¹-P and ¹³-C NMR results suggested that the lipid of protected vesicles is in a similar phase as that of unprotected vesicles, and that this state is similar to powdered anhydrous phospholipid. Using carboxyfluorescein as a probe, it was demonstrated that trehalose, other sugars can prevent vesicle disruption upon dehydration. Different lipid compositions of the liposomes showed nearly identical behavior, with the exception of vesicles composed of dipalmitoylphosphatidylcholine and egg phosphatidylcholine, which showed greater and lower stability to dehydration respectively. Light scattering experiments indicated that a wide variety of carbohydrate and lipid vesicle combinations can withstand dehydration and maintain their original size when protected by sugars. The implications of these results in the development of liposomes as pharmaceuticals are discussed, and a hypothesis is advanced regarding the role of carbohydrates in the preservation of dry lipid membranes. / Medicine, Faculty of / Biochemistry and Molecular Biology, Department of / Graduate

This thesis set out to answer 4 major questions: 1) Do elite hockey players arrive for a game hydrated and do they consume enough fluid to prevent dehydration over the course of a game? 2) Is hydration status repeatable between days and can an athlete who arrives dehydrated prior to training or competition become hydrated in the time before the start of activity? 3) What is the extent of dehydration (%body mass (BM) loss) necessary to change substrate oxidation and skeletal muscle metabolism during exercise in male and female subjects? 4) Will progressive dehydration have a negative effect on endurance performance? The first study evaluated the pre-game hydration status, sweat loss and fluid intake patterns of elite male junior ice hockey players during a game. Sweat loss was 3.2 ± 0.2L and exceeded net fluid intake (2.1 ± 0.1L). Mean BM loss was 1.3 ± 0.3%, but 8 out of 24 players lost between 1.8 - 4.3% BM. Despite abundant opportunities to hydrate during a hockey game, 33% of players did not drink enough to prevent sweat losses of ≥2% BM. The second study investigated 1) the day-to-day variability of morning urine specific gravity (USG) and consuming 600mL of water on the hydration status of hydrated and dehydrated (USG>1.020) subjects, and 2) the effects of consuming water or carbohydrate electrolyte solutions (CES) on hydration status of dehydrated subjects. Morning USG and hydration responses to the ingestion of 600mL of water were repeatable and mildly dehydrated subjects could reach euhydration within 45min after ingesting any type of fluid with no added effect of a CES. The next two studies (3 & 4) investigated the effects of mild progressive dehydration during 120min of exercise at ~65% VO2peak on whole body substrate oxidation and skeletal muscle metabolism, as well as cardiovascular, thermal, and mental responses in recreationally active, hydrated females and males. In both studies, muscle glycogenolysis was increased in the initial 60min of exercise in the dehydrated state when BM loss were ≤1%. Increased glycogenolysis appeared due to increases in core temperature during progressive dehydration as there were no differences in plasma epinephrine or the energy status of the cell (free ADP or AMP) between trials. Normal changes in physiological parameters accompanying exercise in a hydrated state were exacerbated with progressive mild dehydration. The final study determined the impact of dehydration on cycling performance. Active males cycled at ~65% VO2peak for 90min followed by a time trial (TT: 6 kJ/kg BM) with fluid to replace sweat losses (HYD) or without fluid (DEH). DEH subjects began the 90 min trial 0.6% dehydrated and progressively became more dehydrated with a BM loss of 1.4% at 45min, 2.3% at 90min, and 3.1% post-TT. TT performance was significantly compromised with ~2-3% BM loss (HYD 32 ± 4 vs. DEH 36 ± 3 min).