Academic literature on the topic 'Metabolic responses'
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Journal articles on the topic "Metabolic responses"
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Hunt, I. K., S. Martin, and R. K. Hetzler. "METABOLIC RESPONSES TO SKATEBOARDING." Medicine & Science in Sports & Exercise 35, Supplement 1 (May 2003): S155. http://dx.doi.org/10.1097/00005768-200305001-00858.
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LISTER, GEORGE. "Metabolic responses to hypoxia." Critical Care Medicine 21, Supplement (September 1993): S340. http://dx.doi.org/10.1097/00003246-199309001-00022.
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Bradshaw, D. J. "Metabolic Responses in Biofilms." Microbial Ecology in Health and Disease 8, no. 6 (January 1995): 313–16. http://dx.doi.org/10.3109/08910609509140112.
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Evans, W. J. "Metabolic responses to exercise." Aging Clinical and Experimental Research 7, no. 6 (December 1995): 471. http://dx.doi.org/10.1007/bf03324371.
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Hooper, SB. "Fetal metabolic responses to hypoxia." Reproduction, Fertility and Development 7, no. 3 (1995): 527. http://dx.doi.org/10.1071/rd9950527.
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It has been known for may years that hypoxaemia in the fetus induces a number of biophysical, cardiovascular, endocrine and metabolic responses by the fetus, some of which are not sustained if the period of hypoxaemia is extended. For instance, fetal breathing and body movements and the circulating concentrations of many of the stress-related hormones return to control levels during prolonged periods of hypoxaemia. In particular, circulating fetal blood glucose concentrations gradually return to control levels, after an initial increase. The initial increase is primarily due to a catecholamine-mediated increase in glucose production from glycogen stores leading to a marked reduction in glycogen content. During prolonged periods of hypoxaemia, however, the decrease in fetal blood glucose concentrations is principally due to a decrease in the activity of the major enzymes responsible for glycogenolysis and not to a total depletion of glycogen stores. It is suggested that the decrease in enzyme activity could be due to a prostaglandin E2-mediated antagonism of catecholamine-activated glycogenolysis. In contrast, fetal blood lactate concentrations increase to a plateau after 4-5 h of hypoxaemia and remain at this elevated level for the duration of the hypoxaemia. Circulating lactate concentrations do not increase further, despite production by hypoxic tissues remaining high, due to an increase in lactate clearance by the placenta; under normal conditions the placenta releases lactate into the fetal circulation. It is considered that many of these changes are important adaptive responses which allow the fetus to survive in a sub-optimal intrauterine environment.
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Kang, Jie, Emily Raines, Joseph Rosenberg, Nicholas Ratamess, Fernando Naclerio, and Avery Faigenbaum. "Metabolic Responses During Postprandial Exercise." Research in Sports Medicine 21, no. 3 (June 18, 2013): 240–52. http://dx.doi.org/10.1080/15438627.2013.792088.
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Martini, Wenjun. "Fibrinogen metabolic responses to trauma." Scandinavian Journal of Trauma, Resuscitation and Emergency Medicine 17, no. 1 (2009): 2. http://dx.doi.org/10.1186/1757-7241-17-2.
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Hill, Andrew G., Jonathan Siegel, Jan Rounds, and Douglas W. Wilmore. "Metabolic Responses to Interleukin-1." Annals of Surgery 225, no. 3 (March 1997): 246–51. http://dx.doi.org/10.1097/00000658-199703000-00002.
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Noy, Yael, and David Sklan. "Metabolic Responses to Early Nutrition." Journal of Applied Poultry Research 7, no. 4 (December 1998): 437–51. http://dx.doi.org/10.1093/japr/7.4.437.
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TRACEY, KEVIN J., and ANTHONY CERAMI. "Metabolic Responses to Cachectin/TNF." Annals of the New York Academy of Sciences 587, no. 1 (June 1990): 325–31. http://dx.doi.org/10.1111/j.1749-6632.1990.tb00173.x.
Full textDissertations / Theses on the topic "Metabolic responses"
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Holmbäck, Ulf. "Metabolic and Endocrine Responses to Nocturnal Eating." Doctoral thesis, Uppsala universitet, Institutionen för medicinska vetenskaper, 2002. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-2956.
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An increasing amount of people have their work hours displaced to the night and there are indications that shift work and other irregular working schedules are associated with an increased risk of developing the metabolic syndrome and other pathological conditions. It is therefore important to address the consequences of eating at irregular hours, especially nighttime. Papers I-III refer to a study in which 7 males were given a high-carbohydrate diet (HC) or a high-fat diet (HF), using a cross-over design. Subjects were kept awake for 24 h and food was provided as 6 equally spaced isocaloric meals. Higher energy expenditure and non-esterified fatty acids (NEFA) concentration, as well as lower glucose and triacylglycerol (TAG) concentrations were observed with the HF-diet, compared to the HC-diet. With the HF-diet, fat oxidation, heat release, heart rate, glucose, NEFA and TAG concentrations differed depending on time of day. The highest postprandial TAG concentrations were seen after the 04.00 meal with both diets. Insulin and leptin responses to meal intake differed with respect to diet and time of day. Time of day affected glucagon, thyroid stimulating hormone, free thyroxin, total triiodothyronine (tT3), cortisol, chromogranin A and pancreatic polypeptide (PP) concentrations. PP’s postprandial increase was greater during 08.00 – 16.00 compared to 20.00 – 08.00. Furthermore, the subjects felt less irritated when eating the HF-diet but hunger was not related to macronutrient composition. Hunger and thirst decreased throughout the 24 h period despite constant activity and energy intake; and were correlated with several endocrine and metabolic variables. In paper IV 7 males were studied twice during 24-h either given 6 isocaloric meals throughout the 24-h period, or 4 isocaloric meals from 08.00 to 20.00, followed by a nocturnal fast. Energy expenditure, glucose, TAG, insulin and glucagon concentrations were lower; and NEFA concentrations were higher during the nocturnal fast compared to nocturnal eating; although no 24 h differences between the protocols were apparent. The subjects were more passive during the fasting period compared to when food was given. Stepwise regression showed that correlations between metabolic variables and hormones differed between daytime and nighttime. The decreased evening/nocturnal responses of cortisol and PP to meal intake suggest that nocturnal eating might have health implications and that the body reacts unfavorably to nocturnal eating. Smaller meals around the clock, however, showed marginally better effects on postprandial TAG concentrations and mental energy compared to larger meals during daytime. Further studies (long term) are needed before dietary guidelines can be given to shift workers, especially regarding the impact of nocturnal eating on gastrointestinal response and cortisol.
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Drust, Barry. "Metabolic responses to soccer-specific intermittent exercise." Thesis, Liverpool John Moores University, 1997. http://researchonline.ljmu.ac.uk/5574/.
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The intermittent exercise pattern associated with soccer makes analysis of the demands of the sport more complex than in many individual sports. The aim in this thesis was to determine the physiological and metabolic responses to soccer-specific exercise. The demands associated with elite level match-play were evaluated by techniques of motion-analysis. Laboratory based soccer-specific intermittent exercise protocols were then devised to determine the physiological strain associated with soccer and investigate the effects of increased ambient temperature and whole body pre-cooling on performance. The work-rate profiles of elite South American soccer players and English Premier League players, performing in international and club level respectively, were determined. English Premier League players covered a greater total distance during a game than the South American players (P< 0.05). Differences were found for the total distance covered for playing positions with midfield players covering larger distances than forwards. Defenders covered a greater distance jogging backwards than forward players with forwards sprinting a greater distance than defenders. Work-rate was reduced in the second half of the game for all player. The total distance covered by the international players was done mainly at submaximal intensities. High intensity exercise was infrequent and bouts were of short duration. No significant correlations were observed between the work-rate profile and anthropometric charactersitics of individuals. The use of the doubly-labelled water technique to indicate the energy expenditure during soccer match-play was investigated. The doubly-labelled water technique cannot determine energy expenditure during a soccer match as the rate of turnover of the isotopes is too small to allow the accurate estimation of energy expended. Laboratory based soccer-specific intermittent protocols elicited physiological responses that were similar in magnitude and pattern to soccer match-play. Physiological demands fluctuated with exercise intensity during intermittent exercise. Oxygen consumption and heart rate were not significantly different during soccer-specific intermittent exercise and steady-rate exercise at the same average intensity. Rectal temperature did not differ significantly between the two protocols, although intermittent exercise performance resulted in a greater rise in rectal temperature as the protocol progressed (P< 0.05). Sweat production did not differ significantly between the two exercise sessions, though the rating of perceived exertion was significantly higher (P< 0.05), for the session as a whole, during intermittent exercise. Intermittent exercise performance at 26 ° C did not result in significant increases in the physiological, metabolic or thermoregulatory responses when compared to intermittent exercise at 20 ° C. The physiological and metabolic responses were also similar when intermittent exercise was performed after a whole body pre-cooling manoeuvre. Rectal temperature was lowered by the pre-cooling strategy prior to exercise (- 0.6 ± 0.6 ° C, P< 0.05). Rectal temperature during exercise was only significantly lower after pre-cooling than during exercise at 26 ° C. No significant differences were observed in rectal temperature during exercise between the normal and pre-cooled condition. The increase in rectal temperature during the second half of the protocol was significantly greater than the increase observed at 26 ° C or under normal conditions. This may be a consequence of an altered thermoregulatory response due to the pre-cooling manouvre. In conclusion, the work-rate demands of soccer seem to be predominantly aerobic in nature with anaerobic bouts and the performance of specific match activities increasing the demands placed on players. The demands of intermittent exercise are not significantly different from continuous work performed at the same average intensity though there is tentative evidence for a decrease in the efficiency of the thermoregulatory system during intermittent work. No adverse effects upon intermittent exercise performance were noted under conditions of moderate heat stress, while any thermoregulatory benefits of whole body pre-cooling during intermittent work are probably only transient.
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Steel, Helen Carolyn. "Metabolic responses to in vitro zinc supplementation." Thesis, Rhodes University, 1994. http://hdl.handle.net/10962/d1004101.
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The present study was carried out to determine the effects and possible mechanism of action of zinc supplementation on the in vitro growth of malignant murine melanoma (B16) and non-malignant monkey kidney (LLCMK) cells. Cell culture studies showed that zinc supplementation significantly inhibited B16 growth at all the concentrations studied (1, 3, 5 and lOμg/ml). Zinc was also found to inhibit the growth of the LLCMK cells, although to a lesser extent than the B16 cells. Possible evidence of mobilisation of the essential fatty acids from the membrane phospholipid stores was noted in both cell types. This effect was, however, greater in the B16 cells. Δ⁶-desaturase activity was found to be significantly lower in the B16 cells than in the LLCMK cells (p ≥ 0.05). Zinc supplementation resulted in an increase in the enzymes activity in the LLCMK cells and, at high concentrations, in the B16 cells. An estimation of elongase and Δ⁶-desaturase activity with zinc supplementation indicated that zinc had little or no effect on the activity of these enzymes. B16 cells were found to have higher levels of free radicals than the LLCMK cells. Zinc supplementation resulted in increased free radical formation in the B16 cells, while no effect was observed in the LLCMK cells. Lipid peroxidation increased in both cell types with increased zinc concentrations. The observed effect of zinc supplementation on cell growth may involve these elevated levels of lipid peroxides. CycIo-oxygenase activity was found to be greater in the B16 cells than the LLCMK cells. The activity of the enzyme increased with higher concentrations of zinc (lOμg/ml) in both cell types. Prostaglandin E, levels were found to be lower in the B16 cells compared to the LLCMK cells. The levels of prostaglandin E, in both cell types appeared to be dependent on the levels of the polyunsaturated fatty acid precursors to the prostaglandins. Zinc was found to inhibit the activity of the enzyme adenylate cyclase in both cell types. The cAMP levels in the LLCMK cells were also found to decrease with zinc supplementation. In the case of the B16 cells, cAMP levels increased at low concentrations of zinc despite a decrease in adenyl ate cyclase activity, suggesting a possible inhibition of cAMP phosphodiesterase activity at these concentrations of zinc. It is concluded that although zinc supplementation does have an effect on cell growth, this effect is not mediated through the activation of adenylate cyclase by the prostaglandins resulting in elevated levels of cAMP. A possible mechanism involving lipid peroxidation is proposed.
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Weber, Clare L., and n/a. "Metabolic Responses to Supramaximal Exercise and Training: A Gender Comparison." Griffith University. School of Physiotherapy and Exercise Science, 2003. http://www4.gu.edu.au:8080/adt-root/public/adt-QGU20030407.155407.
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The primary aim of this thesis was to investigate the gender-specific responses to supramaximal cycling and to examine the changes in anaerobic and aerobic metabolism that occur in response to high-intensity interval training (HIT). All subjects in the present experiments were untrained, healthy young adults aged between 18 and 35 yr. Cycle ergometry was used for all experimental test procedures and training programs. The accumulated oxygen (AO2) deficit was used to quantify the production of adenosine triphosphate (ATP) via anaerobic metabolism during supramaximal cycling. In addition, pulmonary oxygen uptake measured at the onset of exercise was described using mathematical modeling to determine the rate response of the aerobic energy system during exercise. The purpose of experiment one was to examine the test-retest reliability of the maximal accumulated oxygen deficit (MAOD) measured at 110% and 120% of peak oxygen uptake for cycling in seven untrained male and seven untrained female subjects. After one familiarization trial, all subjects performed two MAOD tests at a power output corresponding to 110% and two tests at 120% of peak oxygen uptake in random order. MAOD was calculated for each subject as the difference between the estimated AO2 demand and the AO2 uptake measured during the exercise bout. The mean±standard error time to exhaustion (TE) for the group was not significantly different between trial one (226±13 s) and trial two (223±14 s) of the 110% test. Likewise, the difference in the TE between trial one (158±11 s) and trial two (159±10 s) was not significant for the 120% test. The intra-class correlation coefficients for the TE were 0.95 for the 110% test and 0.98 for the 120% test. The mean MAOD value obtained in trial one (2.62±0.17 L) was not significantly different from the mean value obtained in trial two (2.54±0.19 L) for the 110% test. Additionally, the mean values for the two trials did not differ significantly for MAOD (2.64±0.21 L for trial one and 2.63±0.19 L for trial two) in the 120% test. The intra-class correlation coefficients for MAOD were 0.95 for the 110% test and 0.97 for the 120% test. All intra-class correlation coefficients were significant at p < 0.001. When conducted under standardized conditions, the determination of MAOD for cycling was highly repeatable at both 110% and 120% of peak oxygen uptake in untrained male and female subjects. The results observed in experiment one suggest that the MAOD may be used to compare the anaerobic capacity (AC) of men and women and to examine changes in the contribution of the anaerobic energy systems before and after training. Experiment two examined the gender-specific differences in MAOD before and after 4 and 8 wk of HIT. Untrained men (n=7) and women (n=7) cycled at 120% of pre-training peak oxygen uptake to exhaustion (MAOD test) pre-, mid-, and post-training. A post-training timed test was also completed at the MAOD test power output, but this test was stopped at the TE achieved during the pre-training MAOD test. The 14.3±5.2% increase in MAOD observed in males after 4 wk of training was not different from the 14.0±3.0% increase seen in females (p > 0.05). MAOD increased by a further 6.6±1.9% in males and this change was not different from the additional 5.1±2.3% increase observed in females after the final 4 wk of training. Peak oxygen uptake measured during incremental cycling increased significantly (p < 0.01) in male but not in female subjects after 8 wk of training. Moreover, the AO2 uptake was higher in men during the post-training timed test compared to the pre-training MAOD test (p < 0.01). In contrast, the AO2 uptake was unchanged from pre- to post-training in female subjects. The increase in MAOD with training was not different between men and women suggesting an enhanced ability to produce ATP anaerobically in both groups. However, the increase in peak oxygen uptake and AO2 uptake obtained in male subjects following training indicates improved oxidative metabolism in men but not in women. It was concluded that there are basic gender differences that may predispose males and females to specific metabolic adaptations following an 8-wk period of HIT. Increases in AO2 uptake during supramaximal cycling demonstrated in men after training led to the hypothesis that peak oxygen uptake kinetics are speeded in male subjects with short-term HIT. It was suggested that training does not improve peak oxygen uptake kinetics in women as no change in AO2 uptake was found after 8 wk of HIT in female subjects. The purpose of experiment three was to examine peak oxygen uptake kinetics before and after 8 wk of HIT in six men and six women during cycling at 50% (50% test) and 110% (110% test) of pre-training peak oxygen uptake. A single-term exponential equation was used to model the peak oxygen uptake response (after phase I) during the 50% and 110% tests pre- and post-training. In addition, phase II and III of the peak oxygen uptake response during the 110% tests were examined using a two-term equation. The end of the phase I peak oxygen uptake response was identified visually and omitted from the modeling process. The duration of phase I determined during all experimental tests was not different between men and women and did not change with training in either group. Before training, men obtained a phase II peak oxygen uptake time constant (t2) of 29.0±3.3 s during the 50% test which was not different to the t2 of 28.8±2.2 s attained by women. In addition, the t2 determined during the 50% test was unchanged after 8 wk of HIT in both groups. The peak oxygen uptake kinetics examined during the 110% tests before training were well described by a single-term model in all male and female subjects. The t2 determined before training for the 110% test was significantly faster in men than in women. Furthermore, peak oxygen uptake was unchanged in female subjects and the t2 remained unaltered with 8 wk HIT (pre 45.5±2.2; post 44.8±2.3 s). In contrast, male subjects achieved a significantly higher peak oxygen uptake after training and the t2 determined for men during the 110% test was faster after training (36.4±1.6 s) than before training (40.1± 1.9 s). Improved model fits were obtained with the two-term equation compared to the single-term equation in two of the six male subjects during the 110% test post-training. It was found that the onset of the peak oxygen uptake slow component occurred at a mean time of 63.5±2.5 s and the t2 was reduced to 18.4±1.7 s. Using a Wilcoxon Signed Ranks z-test, the t2 described by the single-term equation in the remaining four subjects was determined to be significantly faster after training than before training, thus confirming the results obtained from the original group (n=6) of male subjects. End exercise heart rate (HREE) values obtained during the 50% and 110% tests were not different between men and women. During the 50% test, HREE values were unchanged, whereas HREE was significantly decreased during the 110% test after training in both groups. These data show that HIT might improve oxidative metabolism in men but not in women as reflected by a greater peak oxygen uptake and faster peak oxygen uptake kinetics during supramaximal work rates. We further suggest that the faster peak oxygen uptake kinetics demonstrated in men after training are probably not due to an improvement in cardiac function. Finally, the augmentation of oxidative metabolism during exercise after HIT in men might be dependent on the intensity of the exercise bout at which the peak oxygen uptake response is examined. The findings presented in this thesis suggest that MAOD is a reliable measure in both male and female subjects and can be used to monitor changes in anaerobic ATP production during supramaximal cycling. Moreover, these data suggest that 4 and 8 wk of HIT produce similar changes in anaerobic ATP generation in men and women. Finally, 8 wk of HIT results in the increase of peak oxygen uptake and AO2 uptake as well as the speeding of peak oxygen uptake kinetics during supramaximal cycling in male subjects. There was no evidence to suggest that oxidative metabolism was improved in women after short-term HIT. In conclusion, improvement in supramaximal exercise performances should be examined specifically for changes in the anaerobic and aerobic contributions to energy production. In addition, it is suggested that gender should be of primary consideration when designing exercise-training programs where improvement in both anaerobic and aerobic metabolism is required.
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Weber, Clare L. "Metabolic Responses to Supramaximal Exercise and Training: A Gender Comparison." Thesis, Griffith University, 2003. http://hdl.handle.net/10072/366993.
Full textAbstract:
The primary aim of this thesis was to investigate the gender-specific responses to supramaximal cycling and to examine the changes in anaerobic and aerobic metabolism that occur in response to high-intensity interval training (HIT). All subjects in the present experiments were untrained, healthy young adults aged between 18 and 35 yr. Cycle ergometry was used for all experimental test procedures and training programs. The accumulated oxygen (AO2) deficit was used to quantify the production of adenosine triphosphate (ATP) via anaerobic metabolism during supramaximal cycling. In addition, pulmonary oxygen uptake measured at the onset of exercise was described using mathematical modeling to determine the rate response of the aerobic energy system during exercise. The purpose of experiment one was to examine the test-retest reliability of the maximal accumulated oxygen deficit (MAOD) measured at 110% and 120% of peak oxygen uptake for cycling in seven untrained male and seven untrained female subjects. After one familiarization trial, all subjects performed two MAOD tests at a power output corresponding to 110% and two tests at 120% of peak oxygen uptake in random order. MAOD was calculated for each subject as the difference between the estimated AO2 demand and the AO2 uptake measured during the exercise bout. The mean±standard error time to exhaustion (TE) for the group was not significantly different between trial one (226±13 s) and trial two (223±14 s) of the 110% test. Likewise, the difference in the TE between trial one (158±11 s) and trial two (159±10 s) was not significant for the 120% test. The intra-class correlation coefficients for the TE were 0.95 for the 110% test and 0.98 for the 120% test. The mean MAOD value obtained in trial one (2.62±0.17 L) was not significantly different from the mean value obtained in trial two (2.54±0.19 L) for the 110% test. Additionally, the mean values for the two trials did not differ significantly for MAOD (2.64±0.21 L for trial one and 2.63±0.19 L for trial two) in the 120% test. The intra-class correlation coefficients for MAOD were 0.95 for the 110% test and 0.97 for the 120% test. All intra-class correlation coefficients were significant at p < 0.001. When conducted under standardized conditions, the determination of MAOD for cycling was highly repeatable at both 110% and 120% of peak oxygen uptake in untrained male and female subjects. The results observed in experiment one suggest that the MAOD may be used to compare the anaerobic capacity (AC) of men and women and to examine changes in the contribution of the anaerobic energy systems before and after training. Experiment two examined the gender-specific differences in MAOD before and after 4 and 8 wk of HIT. Untrained men (n=7) and women (n=7) cycled at 120% of pre-training peak oxygen uptake to exhaustion (MAOD test) pre-, mid-, and post-training. A post-training timed test was also completed at the MAOD test power output, but this test was stopped at the TE achieved during the pre-training MAOD test. The 14.3±5.2% increase in MAOD observed in males after 4 wk of training was not different from the 14.0±3.0% increase seen in females (p > 0.05). MAOD increased by a further 6.6±1.9% in males and this change was not different from the additional 5.1±2.3% increase observed in females after the final 4 wk of training. Peak oxygen uptake measured during incremental cycling increased significantly (p < 0.01) in male but not in female subjects after 8 wk of training. Moreover, the AO2 uptake was higher in men during the post-training timed test compared to the pre-training MAOD test (p < 0.01). In contrast, the AO2 uptake was unchanged from pre- to post-training in female subjects. The increase in MAOD with training was not different between men and women suggesting an enhanced ability to produce ATP anaerobically in both groups. However, the increase in peak oxygen uptake and AO2 uptake obtained in male subjects following training indicates improved oxidative metabolism in men but not in women. It was concluded that there are basic gender differences that may predispose males and females to specific metabolic adaptations following an 8-wk period of HIT. Increases in AO2 uptake during supramaximal cycling demonstrated in men after training led to the hypothesis that peak oxygen uptake kinetics are speeded in male subjects with short-term HIT. It was suggested that training does not improve peak oxygen uptake kinetics in women as no change in AO2 uptake was found after 8 wk of HIT in female subjects. The purpose of experiment three was to examine peak oxygen uptake kinetics before and after 8 wk of HIT in six men and six women during cycling at 50% (50% test) and 110% (110% test) of pre-training peak oxygen uptake. A single-term exponential equation was used to model the peak oxygen uptake response (after phase I) during the 50% and 110% tests pre- and post-training. In addition, phase II and III of the peak oxygen uptake response during the 110% tests were examined using a two-term equation. The end of the phase I peak oxygen uptake response was identified visually and omitted from the modeling process. The duration of phase I determined during all experimental tests was not different between men and women and did not change with training in either group. Before training, men obtained a phase II peak oxygen uptake time constant (t2) of 29.0±3.3 s during the 50% test which was not different to the t2 of 28.8±2.2 s attained by women. In addition, the t2 determined during the 50% test was unchanged after 8 wk of HIT in both groups. The peak oxygen uptake kinetics examined during the 110% tests before training were well described by a single-term model in all male and female subjects. The t2 determined before training for the 110% test was significantly faster in men than in women. Furthermore, peak oxygen uptake was unchanged in female subjects and the t2 remained unaltered with 8 wk HIT (pre 45.5±2.2; post 44.8±2.3 s). In contrast, male subjects achieved a significantly higher peak oxygen uptake after training and the t2 determined for men during the 110% test was faster after training (36.4±1.6 s) than before training (40.1± 1.9 s). Improved model fits were obtained with the two-term equation compared to the single-term equation in two of the six male subjects during the 110% test post-training. It was found that the onset of the peak oxygen uptake slow component occurred at a mean time of 63.5±2.5 s and the t2 was reduced to 18.4±1.7 s. Using a Wilcoxon Signed Ranks z-test, the t2 described by the single-term equation in the remaining four subjects was determined to be significantly faster after training than before training, thus confirming the results obtained from the original group (n=6) of male subjects. End exercise heart rate (HREE) values obtained during the 50% and 110% tests were not different between men and women. During the 50% test, HREE values were unchanged, whereas HREE was significantly decreased during the 110% test after training in both groups. These data show that HIT might improve oxidative metabolism in men but not in women as reflected by a greater peak oxygen uptake and faster peak oxygen uptake kinetics during supramaximal work rates. We further suggest that the faster peak oxygen uptake kinetics demonstrated in men after training are probably not due to an improvement in cardiac function. Finally, the augmentation of oxidative metabolism during exercise after HIT in men might be dependent on the intensity of the exercise bout at which the peak oxygen uptake response is examined. The findings presented in this thesis suggest that MAOD is a reliable measure in both male and female subjects and can be used to monitor changes in anaerobic ATP production during supramaximal cycling. Moreover, these data suggest that 4 and 8 wk of HIT produce similar changes in anaerobic ATP generation in men and women. Finally, 8 wk of HIT results in the increase of peak oxygen uptake and AO2 uptake as well as the speeding of peak oxygen uptake kinetics during supramaximal cycling in male subjects. There was no evidence to suggest that oxidative metabolism was improved in women after short-term HIT. In conclusion, improvement in supramaximal exercise performances should be examined specifically for changes in the anaerobic and aerobic contributions to energy production. In addition, it is suggested that gender should be of primary consideration when designing exercise-training programs where improvement in both anaerobic and aerobic metabolism is required.Thesis (PhD Doctorate)
Doctor of Philosophy (PhD)
School of Physiotherapy and Exercise Science
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Bales, Juliana. "Metabolic signalling and neuroendocrine stress responses in pregnancy." Thesis, University of Edinburgh, 2007. http://hdl.handle.net/1842/29065.
Full textAbstract:
I investigated the relationship between the HPA axis and endocrine factors to adipose tissue storage and appetite regulation during late pregnancy in rats. The responsiveness of the hypothalamic neurones regulating ACTH and hence corticosterone responses to insulin induced hypoglycaemia (IIH) and the orexigenic peptides NPY, orexin and ghrelin were investigated. IIH increased ACTH secretion similarly I both virgin and pregnant rats. Unlike most stressors IIH did not stimulate parvocellular CRH mRNA expression in pPVN neurones but it did increase AVP mRNA expression. The responsiveness of the HPA axis to the orexigenic peptides ghrelin, orexin and NPY given by i.c.v. injection was markedly reduced during late pregnancy. This was at least partly a result of reduced activation of the pPVN neurones, as revealed by reduced stimulation of FOS expression in the pPVN compared with virgin rats given these peptides. ACTH secretory responses were also strongly attenuated in late pregnant rats. In contrast all three orexigenic peptides increased food intake to a similar level in both virgin and pregnant rats. Thus neuroendocrine stress responses to central administration of orexin, NPY and ghrelin are absent during late pregnancy whilst ingestive behavioural responses remain intact. Changes in brain circuitry regulating appetite during late pregnancy were shown by increased FOS activation in the lateral hypothalamic area (LHA), ventromedial hypothalamus (VMH) and dorsomedial hypothalamus (DMH). Supraoptic and magnocellular PVN oxytocin responses to centrally administered NPY were reduced during late pregnancy. Endogenous opioids are involved in the attenuation of HPA axis responses to orexin and NPY during late pregnancy since pre-treatment with the opioid receptor antagonist naloxone reinstated the ACTH response and restored CRH and AVP mRNA responses. Naloxone administration revealed that endogenous opioids facilitate NPY-induced feeding in both virgin and late pregnant rats, but more importantly in late pregnant rats. Naloxone restored a FOS response in the PVN and SON in response to NPY in late pregnant rats indicating that oxytocin neurone responses to NPY are suppressed by endogenous opioids. Basal blood glucose levels were lower in late pregnant rats than in virgins. Ghrelin increased blood glucose levels similarly in both virgin and pregnant rats, whilst NPY and orexin increased blood glucose in only the virgin rats. In conclusion, neuroendocrine stress responses to orexin, ghrelin and NPY are reduced in pregnant rats and this was shown for orexin and NPY to be due to endogenous opioid restraint. Endogenous opioid mechanisms have opposite effects on neuroendocrine stress responses and feeding, which will enhance energy availability for the fetuses at this time. Intact HPA axis responses to IIH will ensure continued glucose supply.
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Björklund, Glenn. "Metabolic and Cardiovascular Responses During Variable Intensity Exercise." Doctoral thesis, Mittuniversitetet, Institutionen för hälsovetenskap, 2010. http://urn.kb.se/resolve?urn=urn:nbn:se:miun:diva-11744.
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Previous research investigating endurance sports from a physiological perspectivehas mainly used constant or graded exercise protocols, although the nature ofsports like cross-country skiing and road cycling leads to continuous variations inworkload. Current knowledge is thus limited as regards physiological responses tovariations in exercise intensity. Therefore, the overall objective of the present thesiswas to investigate cardiovascular and metabolic responses to fluctuations inexercise intensity during exercise. The thesis is based on four studies (Studies I-IV);the first two studies use a variable intensity protocol with cardiorespiratory andblood measurements during cycling (Study I) and diagonal skiing (Study II). InStudy III one-legged exercise was used to investigate muscle blood flow duringvariable intensity exercise using PET scanning, and Study IV was performed toinvestigate the transition from high to low exercise intensity in diagonal skiing,with both physiological and biomechanical measurements. The current thesisdemonstrates that the reduction in blood lactate concentration after high-intensityworkloads is an important performance characteristic of prolonged variableintensity exercise while cycling and diagonal skiing (Studies I-II). Furthermore,during diagonal skiing, superior blood lactate recovery was associated with a highaerobic power (VO2max) (Study II). Respiratory variables such as VE/VO2, VE/VCO2and RER recovered independently of VO2max and did not reflect the blood lactate oracid base levels during variable intensity exercise during either cycling or diagonalskiing (Studies I-II). There was an upward drift in HR over time, but not inpulmonary VO2, with variable intensity exercise during both prolonged cyclingand diagonal skiing. As a result, the linear HR-VO2 relationship that wasestablished with a graded protocol was not present during variable intensityexercise (Studies I-II). In Study III, blood flow heterogeneity during one-leggedexercise increased when the exercise intensity decreased, but remained unchangedbetween the high intensity workloads. Furthermore, there was an excessiveincrease in muscular VO2 in the consecutive high-intensity workloads, mainlyexplained by increased O2 extraction, as O2 delivery and blood flow remainedunchanged. In diagonal skiing (Study IV) the arms had a lower O2 extraction thanthe legs, which could partly be explained by their longer contact phase along withmuch higher muscle activation. Furthermore, in Study IV, the O2 extraction in botharms and legs was at the upper limit during the high intensity workload with nofurther margin for increase. This could explain why no excessive increase inpulmonary VO2 occurred during diagonal skiing (Study II), as increased O2extraction is suggested to be the main reason for this excessive increase in VO2(Study III).
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Thorne, Stuart Douglas. "Hepatic responses to metabolic demand in the sheep." Thesis, University of Liverpool, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.388520.
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Duncan, Benedict. "Metabolic responses to acute and prolonged hypoxic exposure." Thesis, University of Brighton, 2017. https://research.brighton.ac.uk/en/studentTheses/b7ceef66-97ca-4c21-b388-34da9d84ca87.
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This thesis examined the metabolic effects of acute and intermediate hypoxic exposure in humans, specifically, physiological mechanisms associated with weight loss. Namely; increased metabolic rate, changes in substrate oxidation, altered lipid metabolism and changes in taste. Study one assessed the validity and reproducibility of an online gas analyser in normobaric hypoxia [Fraction of inspired oxygen: 0.12 (FiO2:0.12) equivalent to approximately 4,500m] (n=nine; two females, seven males). The MetaMax3x demonstrates good reproducibility between repeated trials. Differences exist between the system and the gold standard Douglas Bag method for measures of oxygen uptake (percent differences of V̇O2; 21%), carbon dioxide production (V̇CO2; 10%) and minute ventilation (V̇E; 5%). The second study investigated the free fatty acid (FFA) and triglyceride (TAG) response to an acute (45 minutes) hypoxic exposure (FiO2: 0.12) (n=10; five females, five males). A greater resting metabolic rate (RMR) (+28 ± 6 kcal.hr-1 ) was observed, through increased carbohydrate (CHO) and fat oxidation. Increased plasma FFA (+54%) and TAG (+26%) were observed, highlighting metabolic perturbations from acute exposure. Study three investigated the metabolic responses to an acute (60 minute) hypoxic exposure (FiO2: 0.12) at rest and a subsequent bout of moderate exercise in normoxia following a high fat meal (n=eight males). Experimental trials included a lipid ingestion prior to a rest period at hypoxia or normoxia followed by moderate intensity exercise (60% heart rate reserve). Control trials consisted of the same protocol without lipid ingestion. Acute, severe hypoxia increased energy expenditure (EE), (+22 ± 11 kcal.hr-1 ) CHO and fat oxidation following exposure. A prior acute bout of severe hypoxia did not alter EE and substrate use during subsequent moderate intensity exercise. An exercise bout, postlipid ingestion, resulted in lower triglyceride concentration. No changes in Meteorin-like were observed throughout trials. These findings suggest that an increase in RMR occurs following a single resting hypoxic exposure and independently to Meteorin-like protein. The fourth study observed reductions in body mass (-2.36 ± 1.41 kg) and increases in CHO oxidation during an altitude stay in Peru (18 days, 3400 m) (n=10; five females, five males). The reduction in body mass (-1.89 ± 1.31 kg) was sustained four weeks post-return to sea-level. Salt, sweet and bitter taste sensations were reduced at 3,400 m compared to sea-level. No changes in self-reported appetite were observed throughout the testing period. Furthermore no changes in circulating Meteorin-like protein were observed upon return to sea-level at one and four weeks post-altitude stay. Study five investigated the blood lipid response to a high lipid meal consumed one and four weeks post-return to sea-level following an altitude stay (18 days, 3400 m) (n=10; five females, five males). No lasting postprandial effects were observed. It is likely that a time dependent effect of hypoxia exists with regards to postprandial blood lipid responses. Taken together acute and intermediate exposure to hypoxic conditions alter substrate oxidation with the potential to induce losses in body mass, independently to changes in Meteorin-like protein and self-reported appetite. Specifically, prolonged stay at moderate altitude results in a greater dependency on CHO use. Increases in RMR were observed during an acute severe bout of hypoxia, although this was not a consistent effect throughout prolonged exposure and should be further investigated. Altered taste during an altitude stay may influence food preferences, energy intake and subsequent changes in body mass and should be considered an area of future investigation. Higher circulating levels of FFA and TAG, demonstrates a metabolic perturbation from a single, acute severe hypoxic exposure.
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Parry, Sion A. "Metabolic responses to short-term high-fat overfeeding." Thesis, Loughborough University, 2017. https://dspace.lboro.ac.uk/2134/26916.
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The main aim of this thesis was to increase our understanding of the metabolic responses associated with short-term high-fat overfeeding. To this end, four separate studies are described in this thesis; each of which involved the provision of a high-fat, high-energy diet to young, healthy, lean individuals. The first of these experimental chapters (Chapter 2) determined the effects of a 7-day, high-fat (65%), high-energy (+50%) diet on postprandial metabolic and endocrine responses to a mixed meal challenge. This chapter demonstrates that 7-days of overfeeding impaired glycaemic control in our subject cohort but did not influence the response of selected gut hormones (acylated ghrelin, GLP-1 and GIP). In a mechanistic follow up study utilising stable isotope tracer methodology we then demonstrate that overfeeding-induced impairments in glycaemic control are attributable to subtle alterations in plasma glucose flux, rather than the overt tissue-specific adaptations (e.g. increased EGP, or reduced glucose disposal) that have previously been reported (Chapter 3). In an attempt to delineate the time-course of diet-induced impairments in glycaemic control, we then investigated the effects of 1-day of overfeeding (+80% energy with 73% of total energy coming as fat) (Chapter 4). Results demonstrate that a single day of overfeeding elicits responses which are comparable to 7-days of high-fat overfeeding; highlighting the rapidity with which excessive high-fat food intake can negatively influence glucose metabolism. In chapter 5 we utilised stable isotope tracer and muscle biopsy techniques to demonstrate that 7-days of high-fat overfeeding impairs glycaemic control but does not influence the fed-state mixed muscle protein fractional synthesis rate (FSR). In conclusion, the findings of this thesis demonstrate that while short-term high-fat overfeeding negatively influences whole-body glucose metabolism, skeletal muscle protein metabolism appears to be relatively unaffected in young, lean, healthy humans.
Books on the topic "Metabolic responses"
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Vitor, Cohen Ricardo, ed. Metabolic and systemic responses following interventional laparoscopy. Austin: R.G. Landes, 1994.
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G, Alscher Ruth, Wellburn Alan 1940-, and International Symposium on Air Pollutants and Plant Metabolism (3rd : 1992 : Blacksburg, Va.), eds. Plant responses to the gaseous environment: Molecular, metabolic, and physiological aspects. London: Chapman & Hall, 1994.
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Ferreira, R. M. B. The metabolic responses of plants to stress: With particular reference to protein turnover. Norwich: University of East Anglia, 1987.
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Wheeldon, Nigel Mark. Studies on the beta-adrenoceptor subtypes responsible for mediating cardiovascular and metabolic responses in man. Manchester: University of Manchester, 1993.
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Gottlieb-Vedi, Marianne. Circulatory and muscle metabolic responses to draught work of varying intensity and duration in Standardbred horses. Uppsala: Sveriges Lantbruksuniversitet, 1988.
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United States. National Aeronautics and Space Administration., ed. Studies of intercellular communication and intracellular metabolic responses by bone cells to simulated weightlessness: Final NASA report. [Washington, DC: National Aeronautics and Space Administration, 1997.
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Valberg, Stephanie. Skeletal muscle metabolic responses to exercise in the horse: Effects of muscle fibre properties, recruitment and fibre composition. Uppsala: Sveriges Lantbruksuniversitet, 1986.
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Mair, Jean Laura. Some metabolic responses of the brown trout, Salmo trutta, to exercise in acid freshwater containing sub-lethal levels of copper. Birmingham: University of Birmingham, 1995.
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Holm, Holmsen, ed. Platelet responses and metabolism. Boca Raton, Fla: CRC Press, 1987.
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Holm, Holmsen, ed. Platelet responses and metabolism. Boca Raton, Fla: CRC Press, 1986.
Find full textBook chapters on the topic "Metabolic responses"
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Leibel, Rudolph L., and Michael Rosenbaum. "Metabolic Responses to Weight Perturbation." In Research and Perspectives in Endocrine Interactions, 121–33. Berlin, Heidelberg: Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-642-13517-0_12.
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Gunst, Jan, Eva Boonen, and Greet Van den Berghe. "Endocrine Responses to Critical Illness." In Endocrine and Metabolic Medical Emergencies, 60–82. Oxford, UK: John Wiley & Sons, Ltd, 2018. http://dx.doi.org/10.1002/9781119374800.ch3.
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Tsintzas, Kostas, and Ian A. MacDonald. "Endocrine and Metabolic Responses to Exercise." In Type 1 Diabetes, 1–28. London: Springer London, 2012. http://dx.doi.org/10.1007/978-0-85729-754-9_1.
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Lowry, S. F. "Metabolic Responses to Anti-Cytokine Therapies." In Update in Intensive Care and Emergency Medicine, 333–46. Berlin, Heidelberg: Springer Berlin Heidelberg, 1993. http://dx.doi.org/10.1007/978-3-642-85011-0_19.
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Dubey, Gunjan, Neeraj Mishra, and Sheo Mohan Prasad. "Metabolic Responses of Pesticides in Plants and Their Ameliorative Processes." In Plant Responses to Xenobiotics, 57–95. Singapore: Springer Singapore, 2016. http://dx.doi.org/10.1007/978-981-10-2860-1_4.
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Rennenberg, Heinz, and Andrea Polle. "Metabolic consequences of atmospheric sulphur influx into plants." In Plant Responses to the Gaseous Environment, 165–80. Dordrecht: Springer Netherlands, 1994. http://dx.doi.org/10.1007/978-94-011-1294-9_9.
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Rittweger, Jörn. "Metabolic Responses to Whole-Body Vibration Exercise." In Manual of Vibration Exercise and Vibration Therapy, 143–53. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-43985-9_10.
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Thompson, G. A., K. J. Einspahr, S. Ho Cho, T. C. Peeler, and Martha B. Stephenson. "Metabolic Responses of Plant Cells to Stress." In Biological Role of Plant Lipids, 497–504. Boston, MA: Springer US, 1989. http://dx.doi.org/10.1007/978-1-4684-1303-8_111.
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Gál, I., E. Rőth, and J. Lantos. "Metabolic Responses to Open and Laparoscopic Cholecystectomy." In Cell Injury and Protection in the Gastrointestinal Tract, 323–33. Dordrecht: Springer Netherlands, 1997. http://dx.doi.org/10.1007/978-94-011-5392-8_32.
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Wilson, Thad E. "Cardiovascular and Metabolic Responses to Thermal Insults." In Theory and Applications of Heat Transfer in Humans, 433–61. Chichester, UK: John Wiley & Sons Ltd, 2018. http://dx.doi.org/10.1002/9781119127420.ch21.
Full textConference papers on the topic "Metabolic responses"
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Williamson, Rebecca C., Peter J. Sharer, Bruce W. Webbon, and Lisa R. Rendon. "Metabolic Responses to Simulated Extravehicular Activity." In International Conference On Environmental Systems. 400 Commonwealth Drive, Warrendale, PA, United States: SAE International, 1992. http://dx.doi.org/10.4271/921303.
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RIGHI, ISABELLA, MARA PATRICIA TRAINA CHACON MIKAHIL, ALEX CASTRO, Marcel Lopes Santos, and CLAUDIA R CAVAGLIERI. "TIME COURSE OF METABOLIC RESPONSES AFTER HIGH INTENSITY INTERVAL TRAINING (HIIT): METABOLOMIC STUDY." In XXV Congresso de Iniciação Cientifica da Unicamp. Campinas - SP, Brazil: Galoa, 2017. http://dx.doi.org/10.19146/pibic-2017-78707.
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Albers, G., J. Iwasaki, P. Mcerlean, P. Ogger, P. Ghai, T. Kohyratty, I. Udalova, C. Lloyd, and A. Byrne. "IRF5 regulates airway macrophage metabolic responses to viral challenge." In ERS Lung Science Conference 2020 abstracts. European Respiratory Society, 2020. http://dx.doi.org/10.1183/23120541.lsc-2020.76.
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Kammerer, Bernd, Daqiang Pan, Caroline Lindau, Simon Lagies, Stefan Günther, and Nils Wiedemann. "Mitochondrial metabolomics reveals compartment-specific metabolic responses in yeast cells." In The 2nd International Electronic Conference on Metabolomics. Basel, Switzerland: MDPI, 2017. http://dx.doi.org/10.3390/iecm-2-04981.
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Ward, Tom, Martin Lindley, Richard Ferguson, Rachael Evans, Sally Singh, Charlotte Bolton, Paul Greenhaff, and Michael Steiner. "Eccentric cycling for individuals with COPD: cardiorespiratory and metabolic responses." In ERS International Congress 2019 abstracts. European Respiratory Society, 2019. http://dx.doi.org/10.1183/13993003.congress-2019.pa518.
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Nizetic, Sandro, Nikolina Pivac, Filip Mustac, and Vlasta Zanki. "Monitoring of occupant metabolic responses with application of wearable sensors." In 2020 5th International Conference on Smart and Sustainable Technologies (SpliTech). IEEE, 2020. http://dx.doi.org/10.23919/splitech49282.2020.9243813.
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Lantz, Renee, and Bruce Webbon. "Measurement of Metabolic Responses to an Orbital-Extravehicular Work-Simulation Exercise." In Intersociety Conference on Environmental Systems. 400 Commonwealth Drive, Warrendale, PA, United States: SAE International, 1988. http://dx.doi.org/10.4271/881092.
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Kam, Yoonseok, Pamela M. Swain, and Brian P. Dranka. "Abstract A67: Bi-phasic metabolic responses to in situ macrophage activation." In Abstracts: AACR Special Conference on Tumor Immunology and Immunotherapy; October 1-4, 2017; Boston, MA. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/2326-6074.tumimm17-a67.
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Kastan, Michael B., Yasmine Valentin-Vega, Adam Brown, Peter Scarbrough, and Donald Fleenor. "Abstract PL04-02: ATM: Bridging DNA damage responses and metabolic regulation." In Abstracts: Thirteenth Annual AACR International Conference on Frontiers in Cancer Prevention Research; September 27 - October 1, 2014; New Orleans, LA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1940-6215.prev-14-pl04-02.
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Cao, Rui, Jun Li, Bo Ning, Naidi Sun, Tianxiong Wang, Zhiyi Zuo, and Song Hu. "Photoacoustic microscopy of cerebral hemodynamic and oxygen-metabolic responses to anesthetics." In SPIE BiOS, edited by Qingming Luo and Jun Ding. SPIE, 2017. http://dx.doi.org/10.1117/12.2251684.
Full textReports on the topic "Metabolic responses"
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Heaps, Cristine L., and Stefan H. Constable. The Metabolic and Thermoregulatory Responses of Rhesus Monkeys to Combined Exercise and Environmental Heat Load. Fort Belvoir, VA: Defense Technical Information Center, August 1993. http://dx.doi.org/10.21236/ada269756.
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Pickles, W. L., and G. A. Cater. Detecting plant metabolic responses induced by ground shock using hyperspectral remote sensing and physiological contact measurements. Office of Scientific and Technical Information (OSTI), December 1996. http://dx.doi.org/10.2172/641267.
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Kim, Su-Jong. Understanding Obesity and the Influence of Acculturation on Metabolic Responses in East Asian Populations in the United States. Fort Belvoir, VA: Defense Technical Information Center, August 2007. http://dx.doi.org/10.21236/ad1014003.
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Mosquna, Assaf, and Sean Cutler. Systematic analyses of the roles of Solanum Lycopersicum ABA receptors in environmental stress and development. United States Department of Agriculture, January 2016. http://dx.doi.org/10.32747/2016.7604266.bard.
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Drought and other abiotic stresses have major negative effects on agricultural productivity. The plant hormone abscisic acid (ABA) regulates many responses to environmental stresses and can be used to improve crop performance under stress. ABA levels rise in response to diverse abiotic stresses to coordinate physiological and metabolic responses that help plants survive stressful environments. In all land plants, ABA receptors are responsible for initiating a signaling cascade that leads to stomata closure, growth arrest and large-scale changes in transcript levels required for stress tolerance. We wanted to test the meaning of root derived ABA signaling in drying soil on water balance. To this end we generated transgenic tomato lines in which ABA signaling is initiated by a synthetic agonist- mandipropamid. Initial study using a Series of grafting experiments indicate that that root ABA signaling has no effect on the immediate regulation of stomata aperture. Once concluded, these experiments will enable us to systematically dissect the physiological role of root-shoot interaction in maintaining the water balance in plants and provide new tools for targeted improvement of abiotic stress tolerance in crop plants.
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Schaffer, Arthur A., D. Mason Pharr, Joseph Burger, James D. Burton, and Eliezer Zamski. Aspects of Sugar Metabolism in Melon Fruit as Determinants of Fruit Quality. United States Department of Agriculture, September 1994. http://dx.doi.org/10.32747/1994.7568770.bard.
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The cucurbit family, including melon, translocates the galactosyl-sucrose oligosaccharides, raffinose and stachyose, in addition to sucrose, from the source leaves to the fruit sink. The metabolism of these photoassimilates in the fruit sink controls fruit growth and development, including the horticulturally important phenomenon of sucrose accumulation, which determines melon fruit sweetness. During this research project we have characterized the complete pathway of galactosyl sucrose metabolism in developing fruit, from before anthesis until maturity. We have also compared the metabolic pathway in scurose accumulating genotypes, as compared to non-accumulating genotypes. Furthermore, we studied the pathway in different fruit tissues, in response to pollination, and also analyzed the response of the individual steps of the pathway to perturbations such as low temperature and leaf removal. The results of our studies have led to the conclusion that generally galactosyl-sucrose metabolism functions as a coordinately controlled pathway. In one case, as an immediate response to the absence of pollination, the activity of a single enzyme, UDPglu pyrophosphorylase, was drastically reduced. However, during young fruit development, sucrose accumulation, and in response to perturbations of the system, groups of enzymes, rather than single enzymes, respond in a concerted manner. Our research has characterized in detail the initial enzymes of galactosyl-sucrose metabolism, including the galactosidases, galactokinase and the UDPgal- and UDPglu pyrophosphorylases. We have discovered a novel alkaline a-galactoside which hydrolyzes both stachyose and reaffinose and thereby may have solved the dilemma of cytosolic-sucrose metabolism, since prior to this research there was no known alkaline a-galactosidase capable of hydrolyzing raffinose.
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Pell, Eva J., Sarah M. Assmann, Amnon Schwartz, and Hava Steinberger. Ozone Altered Stomatal/Guard Cell Function: Whole Plant and Single Cell Analysis. United States Department of Agriculture, December 2000. http://dx.doi.org/10.32747/2000.7573082.bard.
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Original objectives (revisions from original proposal are highlighted) 1. Elucidate the direct effects O3 and H2O2 on guard cell function, utilizing assays of stomatal response in isolated epidermal peels and whole cell gas exchange. 2. Determine the mechanistic basis of O3 and H2O2 effects on the plasma membrane through application of the electrophysiological technique of patch clamping to isolated guard cells. 3. Determine the relative sensitivity of Israeli cultivars of economically important crops to O3 and determine whether differential leaf conductance responses to O3 can explain relative sensitivity to the air pollutant: transfer of technological expertise to Israel. Background to the topic For a long time O3 has been known to reduce gas exchange in plants; it has however been unclear if O3 can affect the stomatal complex directly. Ion channels are essential in stomatal regulation, but O3 has never before been shown to affect these directly. Major conclusions, solution, achievements 1. Ozone inhibits light-induced stomatal opening in epidermal peels isolated from Vicia faba, Arabidopsis thaliana and Nicotiana tabacum in V. faba plants this leads to reduced assimilation without a direct effect on the photosynthetic apparatus. Stomatal opening is more sensitive to O3 than stomatal closure. 2. Ozone causes inhibition of inward K+ channels (involved in stomatal opening) while no detectable effect is observed o the outward K+ channels (stomatal closure). 3. Hydrogen peroxide inhibits stomatal opening and induces stomatal closure in epidermal peels isolated from Vicia faba. 4. Hydrogen peroxide enhances stomatal closure by increasing K+ efflux from guard cells via outward rectifying K+ channels. 5. Based on epidermal peel experiments we have indirectly shown that Ca2+ may play a role in the guard cell response to O3. However, direct measurement of the guard cell [Ca2+]cyt did not show a response to O3. 6. Three Israeli cultivars of zucchini, Clarita, Yarden and Bareqet, were shown to be relatively sensitive to O3 (0.12 ml1-1 ). 7. Two environmentally important Israeli pine species are adversely affected by O3, even at 0.050 ml1-1 , a level frequently exceeded under local tropospheric conditions. P. brutia may be better equipped than P. halepensis to tolerate O3 stress. 8. Ozone directly affects pigment biosynthesis in pine seedlings, as well as the metabolism of O5 precursors, thus affecting the allocation of resources among various metabolic pathways. 9. Ozone induces activity of antioxidant enzymes, and of ascorbate content i the mesophyll and epidermis cells of Commelina communis L. Implications, both scientific and agricultural We have improved the understanding of how O3 and H2O2 do affect guard cell and stomatal function. We have shown that economical important Israeli species like zucchini and pine are relatively sensitive to O3.
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Fait, Aaron, Grant Cramer, and Avichai Perl. Towards improved grape nutrition and defense: The regulation of stilbene metabolism under drought. United States Department of Agriculture, May 2014. http://dx.doi.org/10.32747/2014.7594398.bard.
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The goals of the present research proposal were to elucidate the physiological and molecular basis of the regulation of stilbene metabolism in grape, against the background of (i) grape metabolic network behavior in response to drought and of (ii) varietal diversity. The specific objectives included the study of the physiology of the response of different grape cultivars to continuous WD; the characterization of the differences and commonalities of gene network topology associated with WD in berry skin across varieties; the study of the metabolic response of developing berries to continuous WD with specific attention to the stilbene compounds; the integration analysis of the omics data generated; the study of isolated drought-associated stress factors on the regulation of stilbene biosynthesis in plantaand in vitro. Background to the topic Grape quality has a complex relationship with water input. Regulated water deficit (WD) is known to improve wine grapes by reducing the vine growth (without affecting fruit yield) and boosting sugar content (Keller et al. 2008). On the other hand, irregular rainfall during the summer can lead to drought-associated damage of fruit developmental process and alter fruit metabolism (Downey et al., 2006; Tarara et al., 2008; Chalmers et al., 792). In areas undergoing desertification, WD is associated with high temperatures. This WD/high temperature synergism can limit the areas of grape cultivation and can damage yields and fruit quality. Grapes and wine are the major source of stilbenes in human nutrition, and multiple stilbene-derived compounds, including isomers, polymers and glycosylated forms, have also been characterized in grapes (Jeandet et al., 2002; Halls and Yu, 2008). Heterologous expression of stilbenesynthase (STS) in a variety of plants has led to an enhanced resistance to pathogens, but in others the association has not been proven (Kobayashi et al., 2000; Soleas et al., 1995). Tomato transgenic plants harboring a grape STS had increased levels of resveratrol, ascorbate, and glutathione at the expense of the anthocyanin pathways (Giovinazzo et al. 2005), further emphasizing the intermingled relation among secondary metabolic pathways. Stilbenes are are induced in green and fleshy parts of the berries by biotic and abiotic elicitors (Chong et al., 2009). As is the case for other classes of secondary metabolites, the biosynthesis of stilbenes is not very well understood, but it is known to be under tight spatial and temporal control, which limits the availability of these compounds from plant sources. Only very few studies have attempted to analyze the effects of different environmental components on stilbene accumulation (Jeandet et al., 1995; Martinez-Ortega et al., 2000). Targeted analyses have generally shown higher levels of resveratrol in the grape skin (induced), in seeded varieties, in varieties of wine grapes, and in dark-skinned varieties (Gatto et al., 2008; summarized by Bavaresco et al., 2009). Yet, the effect of the grape variety and the rootstock on stilbene metabolism has not yet been thoroughly investigated (Bavaresco et al., 2009). The study identified a link between vine hydraulic behavior and physiology of stress with the leaf metabolism, which the PIs believe can eventually lead to the modifications identified in the developing berries that interested the polyphenol metabolism and its regulation during development and under stress. Implications are discussed below.
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Glazer, Itamar, Randy Gaugler, Yitzhak Spiegel, and Edwin Lewis. Host Adaptation in Entomopathogenic Nematodes: An Approach to Enhancing Biological Control Potential. United States Department of Agriculture, April 1996. http://dx.doi.org/10.32747/1996.7613023.bard.
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The overall objective of our research was to develop methods to match species of entomopathogenic nematodes against the insect pests which they would be best adapted to control. The underlying hypothesis for this work was that entomopathogenic nematodes should be most effective when used against insect species to which they are naturally adapted to parasitize. Toward this end, we undertook a number of related studies focusing primarily on nematode foraging strategies. We found that foraging strategies affected host associations directly and indirectly. Nematodes' responses to host cues, and the role of their sensory organs based on lectin binding, led to new approaches to determining host range for these parasites. Based on this work, we developed a laboratory bioassay of host recognition behavior designed to predict field results. We also determined that nematodes that forage in a stationary manner (ambushers) have a slower metabolic rate than do active forgers (cruisers), thus their infective stage juveniles are longer lived. This study helps predict the duration of field activity after application and may partially explain field distributions of natural populations of entomopathogenic nematodes. The common thread linking all of these studies was that they led to a deeper understanding of the associations between entomopathogenic nematodes and insects as hosts.
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Yahav, Shlomo, John McMurtry, and Isaac Plavnik. Thermotolerance Acquisition in Broiler Chickens by Temperature Conditioning Early in Life. United States Department of Agriculture, 1998. http://dx.doi.org/10.32747/1998.7580676.bard.
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The research on thermotolerance acquisition in broiler chickens by temperature conditioning early in life was focused on the following objectives: a. To determine the optimal timing and temperature for inducing the thermotolerance, conditioning processes and to define its duration during the first week of life in the broiler chick. b. To investigate the response of skeletal muscle tissue and the gastrointestinal tract to thermal conditioning. This objective was added during the research, to understand the mechanisms related to compensatory growth. c. To evaluate the effect of early thermo conditioning on thermoregulation (heat production and heat dissipation) during 3 phases: (1) conditioning, (2) compensatory growth, (3) heat challenge. d. To investigate how induction of improved thermotolerance impacts on metabolic fuel and the hormones regulating growth and metabolism. Recent decades have seen significant development in the genetic selection of the meat-type fowl (i.e., broiler chickens); leading to rapid growth and increased feed efficiency, providing the poultry industry with heavy chickens in relatively short growth periods. Such development necessitates parallel increases in the size of visceral systems such as the cardiovascular and the respiratory ones. However, inferior development of such major systems has led to a relatively low capability to balance energy expenditure under extreme conditions. Thus, acute exposure of chickens to extreme conditions (i.e., heat spells) has resulted in major economic losses. Birds are homeotherms, and as such, they are able to maintain their body temperature within a narrow range. To sustain thermal tolerance and avoid the deleterious consequences of thermal stresses, a direct response is elicited: the rapid thermal shock response - thermal conditioning. This technique of temperature conditioning takes advantage of the immaturity of the temperature regulation mechanism in young chicks during their first week of life. Development of this mechanism involves sympathetic neural activity, integration of thermal infom1ation in the hypothalamus, and buildup of the body-to-brain temperature difference, so that the potential for thermotolerance can be incorporated into the developing thermoregulation mechanisms. Thermal conditioning is a unique management tool, which most likely involves hypothalamic them1oregulatory threshold changes that enable chickens, within certain limits, to cope with acute exposure to unexpected hot spells. Short-tem1 exposure to heat stress during the first week of life (37.5+1°C; 70-80% rh; for 24 h at 3 days of age) resulted in growth retardation followed immediately by compensatory growth" which resulted in complete compensation for the loss of weight gain, so that the conditioned chickens achieved higher body weight than that of the controls at 42 days of age. The compensatory growth was partially explained by its dramatic positive effect on the proliferation of muscle satellite cells which are necessary for further muscle hypertrophy. By its significant effect of the morphology and functioning of the gastrointestinal tract during and after using thermal conditioning. The significant effect of thermal conditioning on the chicken thermoregulation was found to be associated with a reduction in heat production and evaporative heat loss, and with an increase in sensible heat loss. It was further accompanied by changes in hormones regulating growth and metabolism These physiological responses may result from possible alterations in PO/AH gene expression patterns (14-3-3e), suggesting a more efficient mechanism to cope with heat stress. Understanding the physiological mechanisms behind thermal conditioning step us forward to elucidate the molecular mechanism behind the PO/AH response, and response of other major organs. The thermal conditioning technique is used now in many countries including Israel, South Korea, Australia, France" Ecuador, China and some places in the USA. The improvement in growth perfom1ance (50-190 g/chicken) and thermotolerance as a result of postnatal thermal conditioning, may initiate a dramatic improvement in the economy of broiler's production.
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Fromm, Hillel, Paul Michael Hasegawa, and Aaron Fait. Calcium-regulated Transcription Factors Mediating Carbon Metabolism in Response to Drought. United States Department of Agriculture, June 2013. http://dx.doi.org/10.32747/2013.7699847.bard.
Full textAbstract:
Original objectives: The long-term goal of the proposed research is to elucidate the transcription factors, genes and metabolic networks involved in carbon metabolism and partitioning in response to water deficit. The proposed research focuses on the GTLcalcium/calmodulinbindingTFs and the gene and metabolic networks modulated by these TFs in Arabidopsis thaliana. The specific objectives are as follows. Objective-1 (USA): Physiological analyses of GTL1 loss- and gain-of-function plants under water sufficient and drought stress conditions Objective 2 (USA / Israel-TAU): Characterizion of GTL target genes and bioinformatic analysis of data to eulcidate gene-network topology. Objective-3 (Israel-TAU): Regulation of GTLmediated transcription by Ca²⁺/calmodulin: mechanism and biological significance. Objective-4 (Israel-BGU): Metabolic networks and carbon partitioning in response to drought. Additional direction: In the course of the project we added another direction, which was reported in the 2nd annual report, to elucidate genes controlling drought avoidance. The TAU team has isolated a few unhydrotropic (hyd) mutants and are in the process of mapping these mutations (of hyd13 and hyd15; see last year's report for a description of these mutants under salt stress) in the Arabidopsis genome by map-based cloning and deep sequencing. For this purpose, each hyd mutant was crossed with a wild type plant of the Landsberg ecotype, and at the F2 stage, 500-700 seedlings showing the unhydrotropic phenotype were collected separately and pooled DNA samples were subkected to the Illumina deep sequencing technology. Bioinformatics were used to identify the exact genomic positions of the mutations (based on a comparison of the genomic sequences of the two Arabidopsis thaliana ecotypes (Columbia and Landsberg). Background: To feed the 9 billion people or more, expected to live on Earth by the mid 21st century, the production of high-quality food must increase substantially. Based on a 2009 Declaration of the World Summit on Food Security, a target of 70% more global food production by the year 2050 was marked, an unprecedented food-production growth rate. Importantly, due to the larger areas of low-yielding land globally, low-yielding environments offer the greatest opportunity for substantial increases in global food production. Nowadays, 70% of the global available water is used by agriculture, and 40% of the world food is produced from irrigated soils. Therefore, much needs to be done towards improving the efficiency of water use by plants, accompanied by increased crop yield production under water-limiting conditions. Major conclusions, solutions and achievements: We established that AtGTL1 (Arabidopsis thaliana GT-2 LIKE1) is a focal determinant in water deficit (drought) signaling and tolerance, and water use efficiency (WUE). The GTL1 transcription factor is an upstream regulator of stomatal development as a transrepressor of AtSDD1, which encodes a subtilisin protease that activates a MAP kinase pathway that negatively regulates stomatal lineage and density. GTL1 binds to the core GT3 cis-element in the SDD1 promoter and transrepresses its expression under water-sufficient conditions. GTL1 loss-of-function mutants have reduced stomatal number and transpiration, and enhanced drought tolerance and WUE. In this case, higher WUE under water sufficient conditions occurs without reduction in absolute biomass accumulation or carbon assimilation, indicating that gtl1-mediated effects on stomatal conductance and transpiration do not substantially affect CO₂ uptake. These results are proof-of-concept that fine-tuned regulation of stomatal density can result in drought tolerance and higher WUE with maintenance of yield stability. Implications: Accomplishments during the IS-4243-09R project provide unique tools for continued discovery research to enhance plant drought tolerance and WUE.