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Glycogen metabolism in meal-fed pyridoxine-deficient ratsMellor, Ruth Marie January 1973 (has links)
Pyridoxine-deficient rats are known to exhibit little, if any, weight gain; they also have decreased fat stores in comparison with their pair-fed controls. The defect in energy metabolism responsible for this phenomenon is not well understood at present. This study was undertaken
to investigate some aspects of glycogenesis and glycogenolysis in order to add to the present information on energy metabolism in the pyridoxine deficiency state. Meal-fed animals were used, in order to eliminate differences
due to the mode of feeding between the experimental and the pair-fed control animals.
Male weanling rats were fed a pyridoxine-deficient diet in one 2-hour daily meal, while the controls were pair-fed. This eliminated differences due to feeding frequency when these groups were compared with each other.
Aspartate amino-transferase and alanine aminotransferase
activities were assayed in liver and erythrocytes
in order to verify the presence of a pyridoxine deficiency state under the conditions used in this laboratory.
The activities of glycogen phosphorylase, the rate-limiting enxyme in glycogenolysis, and glycogen UDP-glucosyltransferase were assayed in liver and muscle. Glycogen storage in these tissues was also measured.
Finally, the incorporation of labelled carbon atoms into
blood glucose and liver glycogen following intraperitoneal
injection of L-alanine-¹⁴C was assayed.
Glycogen phosphorylase activity was reduced in pyridoxine-deficient animals. This defect was not accompanied by a concomitant increase in the deposition of glycogen. There was, therefore, the possibility of a decreased ability to form glycogen.
Glycogen UDP-glucosyltransferase activity was normal in muscle and elevated in liver indicating, if anything,
an unimpaired ability to synethesize glycogen from UDPG.
A trend towards a lesser incorporation of labelled carbon atoms into the blood glucose by the pyridoxine-deficient group appeared when the results were expressed as a percent of administered dose per ml. This became statistically significant when the data was expressed in terms of the circulating glucose pool. Although not at a statistically significant level, there was a greater incorporation of labelled carbon atoms into the liver glycogen of the pyridoxine-deficient group.
It appeared from these findings that the defect in energy metabolism in pyridoxine deficiency may be the result of a reduced availability of carbon skeletons and occurred prior to the formation of glycogen. Further study in this area is necessary to reveal the exact point at which energy loss occurred. / Land and Food Systems, Faculty of / Graduate
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Studies on glycogen in the nervous systems of Haemopis sanguisuga (L) and Planorbis corneus (L)Seal, L. H. January 1986 (has links)
No description available.
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In vivo '1'3C spectroscopy at 3 TeslaBingham, Kathryn Ruth January 1998 (has links)
No description available.
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Muscle glycogen depletion during maximal isokinetic contractionsBenham, David W. January 1978 (has links)
The intent of this investigation was to determine the effects of contractile velocity on muscle glycogen depletion patterns during maximal isokinetic contractions.Three physically active male subjects performed maximal knee extensions and flexions using the Cybex II. Work was performed with one leg at a contractile volecity of 60 degs./sec. (1.05 rads./sec.) and the other at 300 degs./sec. (5.23 rads./sec.). Histochemical data was collected from muscle samples taken from the vastus lateralis m. of each leg. Gylcogen depletion patterns were later observed from a periodic-acid Schiffs stain (PAS) on the muscle sections. Additional muscle samples were freeze-dried for single fiber evaluation, of glycogen content. Both fast twitch (FT) and slow twitch (ST) muscle fibers were depleted of glycogen equally during each of the contractile velocities. Observations from FAS staining suggest that most of the FT fibers were depleted before the ST fibers. The results of this study indicate that the glycogen depletion pattern is independent of the velocity of contraction. This study also supports previous investigations in suggesting that the intensity of muscular contraction is one of the major determinants of the glycogen depletion pattern.
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Effects of fructose ingestion on muscle glycogen during prolonged exerciseHoopes, David G. January 1976 (has links)
Ten trained subjects were studied during and following exercise to determine the effects of fructose ingestion on muscle glycogen depletion and resynthesis. Three subjects cycled for anhour while the other six subjects completed a 3000-yard swim. The subjects ingested 12 grams of fructose before, 46 grams during, and 12 grams in the 30 minutes following the exercise. Muscle biopsies were obtained before, immediately after, and 12 hours post exercise. In -the cyclists, plasma glucose and insulin were also determined. The ingestion of fructose had no effect on the glycogen depletion during exercise. However, in the 12 hours following exercise, fructose ingestion resulted in a 41.4 mmole/kg-wet tissue increase in muscle glycogen. At the same time, the control period resulted in only a 9.53 mmole/kg-wet tissue increase in muscle glycogen. Plasma glucose and insulin levels increased during the fructose feeding. These data suggest that fructose ingestion during exercise has no effect in sparing muscle glycogen during work, but could significantly enhance the resynthesis of glycogen after work.
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Post-mortem glycolytic and physical changes in turkey breast muscleVanderstoep, John January 1971 (has links)
The concentration of glycolytic intermediates and co-factors in and pH values of P. superficlalis muscles from each of five 15 week-old and five 25 week-old White Cannon torn turkeys was measured at varying times between 0 and 180 min. post-mortem.
Different rates of post-mortem glycolysis were evident
among birds, independent of age. On the basis of ATP catabolism, pH and lactic acid accumulation, two groups categorized
as "fast-" and "slow-glycolyzing" were evident. The different rates of glycolysis could not be explained by qualitative
or quantitative differences in control of the glycolytic flux.
The patterns of change in concentration of intermediates
and co-factors expressed as mass action ratios suggested
that regardless of glycolytic rate, post-mortem glycolysis in turkey breast muscle is susceptible to control at the reactions
catalyzed by hexokinase, phosphofructo kinase, aldolase
and triosephosphate isomerase, glyceraldehyde phosphate dehydrogenase and phosphoglycerokinase and pyruvate kinase.
P. superficialis muscles from six 19 and six 27 week-old White Cannon torn turkeys were analyzed for ATP concentration at "0" and "60" min. post-mortem and muscle pH was determined during a three hour post-mortem period. The time required for excised muscle strips to achieve maximum contraction was determined
by periodic measurement of strip length.
Analysis of the data indicated a relationship between rate of ATP catabolism and time to maximum contraction. "Slow-" and "fast-glycolyzing" groups were evident and were independent
of age. The "slow-glycolyzing" group had a higher initial ATP concentration, a larger proportion of initial ATP remaining
at 60 min. and required a longer time for the muscle strips to achieve maximum contraction. / Land and Food Systems, Faculty of / Graduate
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Pre-exercise carbohydrate feedings and endurance performanceHargreaves, Mark January 1984 (has links)
Six men were studied to compare the effects of pre-exercise carbohydrate feedings on endurance performance and muscle glycogen utilization during exhaustive exercise. Trials consisted of a cycling ride to exhaustion at 757. of the subjects' maximal oxygen uptake preceded by the ingestion of either fructose (FRU), glucose (GLU), or sweet placebo (CON). No differences were observed between trials for oxygen uptake, respiratory exchange ratio, heart rate, or exercise time to exhaustion. Blood glucose was elevated (P<0.05) as a result of the glucose feeding, but fell rapidly with the onset of exercise, reaching a nadir of 4.02 + O.-'4 mmcl: i (mean + SE) at 15 min of exercise (P<0.05). Serum insulin also increased (P<0.05) following the glucose feeding: by 30 min of exercise, however, insulin had returned to pre-drink levels. No differences in blood glucose and insulin were observed between FRU and CON. Muscle glycogen utilization during the first 30 min of exercise (CON = 46.3 ± 82 mmol/kg w.w., FRU = 56.3 + 3, GLU = 50.0 + 4.9) and total glycogen use (CON = 93.4 + 11.1, FRU = 118.8 + 10.9, GLU = 99.5 + 4.3) was similar between trials (P>O.05). It was concluded that despite more stable blood glucose and insulin levels in FRU and CON, compared with GLU, this provided no advantage to endurance performance or muscle glycogen utilization.
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Methods for in vivo '1'3C magnetic resonance spectroscopyMann, Robert David January 1999 (has links)
No description available.
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The effect of carbohydrate ingestion on gastric emptying, glycogen metabolism, and exercise performanceMitchell, Joel Beach January 1988 (has links)
This study was undertaken to examine the effects of ingestion of different concentrations of carbohydrate (CHO) (H20, 6, 12, and 18 g/100ml- WP, CHO-6, CH0-12, and CH0--18, respectively) on gastric emptying, muscle glycogen metabolism, and performance. Ten trained male cyclists performed four trials of 105 min of continuous cycling at 70% of VO2max. In a fifth trial the subjects completed seven 15-min rides at 70% of VO2max with three min rest between each ride. In all five trials the submaximal rides were followed by an all-out, self-paced 15-min "performance" ride on an isokinetic ergometer (Fitron) interfaced with a computer which calculated the total work output. Every 15 min the men consumed approximately 150 ml (8.5 ml/kg/hr) of one of the four test solutions (in the intermittent trial the men consumed the CHO-12 solution). Blood samples were taken every 15 min for glucose and insulin determination. Muscle biopsies were obtained from the vastus lateralis at 0 and 105 min in the WP, and the CHO-12 continuous and intermittent trials. Biopsy samples were assayed for glycogen, and sectioned and stained for myosin ATPase and glycogen to determine single fiber depletion patterns. Gastric residue was determined by intubation following the performance ride. The volume of drink emptied in the CHO-12 and CHO-18 trials was significantly less compared to both the WP and CHO-6 trials, and the volume emptied in the CHO-18 trial was less than in the CHO-12. There were no differences in glycogen use between the water and the two CHO-12 trials. Single fiber depletion patterns showed a trend toward a greater depletion of type I fibers but were not influenced by CHO ingestion. Blood glucose was significantly elevated at 105 min in both CHO-12 and the CHO-18 trials compared to the WP trial. CHO oxidation in both CHO-12 and the CHO-18 trials was significantly higher in the performance ride. Work output in both the CHO-12 trials was significantly elevated compared to the WP. These data demonstrate that 12 and 18% CHO solutions retarded gastric emptying, but that adequate CHO was delivered to enable enhanced performance in the CHO-12 trials. The fact that glycogen sparing was not observed suggests that the improved performance may have been due to the maintenance of blood glucose. Single fiber depletion patterns did not explain the performance benefits observed with CHO ingestion. / Human Performance Laboratory
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Muscle glycogenolysis during weight-resistance exerciseRobergs, Robert A. January 1990 (has links)
Skeletal muscle glycogenolysis was investigated in eight subjects during both high (HI) (70% 1 RM) and low (LO) intensity (35% 1 RM) leg extension weight-resistance exercise. Total force application to the machine lever arm was determined and equated between trials via a strain gauge and computer interfaced system. After the sixth set, muscle glycogen degradation was similar in the HI and LO trials (46.9 ± 6.6 and 46.6 ± 6.0 mmol•kg-1 wet wt, respectively), with the LO trial characterized by almost double the repetitions (6.0 and 12.7 ± 1.1) and half the peak concentric torque per repetition (24.2 ± 1.0 and 12.4 ± 0.5). After the sixth set, muscle lactate accumulation was also similar (13.8 ± 0.7 and 16.7 ± 4.2 mmol•kg-1 wet wt for HI and LO trials, respectively). After two hours of passive recovery with no feedings, muscle glycogen storage during the HI and LO trials was 22.2 (±6.8) and 14.2 (±2.5) mmol•kg-1 wet wt, respectively These values represented glycogen synthesis rates of 11.1 (±3.4) and 7.1 (±1.3) mmol•kg-1 •hr-1 , and occurred without significant increases in blood glucose relative to resting concentrations. Optical absorbance measurement of PAS stained muscle sections revealed no differences in the glycogen content of fast (FT) and slow twitch (ST) fibers between trials. When data from each trial were combined, declines in absorbance were larger in FT than ST fibers after the sixth set (0.356 ± 0.048) than in slow twitch fibers (0.222 ± 0.039, p < 0.05). The increase in absorbanceduring the two hour recovery was also larger in FT than ST fibers (0.119 ± 0.024 and 0.055 ± 0.024, p < 0.05). When total force application was constant, muscle glycogenolysis was the same regardless of the intensity of resistance exercise. Glycogenolysis was greater in fast twitch fibers, as was glycogen storage during the immediate post-exercise recovery. The relatively high rate of glycogen synthesis after exercise may be evidence of glycogenesis from intramuscular metabolites. / Human Performance Laboratory
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