5 resultados para Acari, biomass, wet mass

em Deakin Research Online - Australia


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This study investigated the effect of reduced acetylcarnitine availability on oxidative metabolism during the transition from rest to steady-state exercise. Eight male subjects completed two randomised exercise trials at 68 % of the peak rate of O2 uptake (V̇O2,peak). On one occasion subjects ingested 1 g (kg body mass)−1 glucose 75 min prior to exercise (CHO), whereas the other trial acted as a control (CON). Muscle samples were obtained pre- and 75 min post-ingestion, and following 1 and 10 min of exercise. Plasma glucose and insulin were elevated (P < 0.05), and plasma free fatty acids (FFA) were lower at the onset of exercise in CHO. Acetylcarnitine (CON, 4.8 ± 1.8; CHO, 1.5 ± 0.9 mmol (kg dry mass (d.m.))−1, P < 0.05) and acetyl CoA (CON, 13.2 ± 2.3; CHO, 6.3 ± 0.6 μmol (kg d.m.)−1, P < 0.05) were lower at rest, whereas pyruvate dehydrogenase activation (PDHa) was greater in CHO compared with CON (CON, 0.78 ± 0.07; CHO, 1.44 ± 0.19 mmol min−1 (kg wet mass (w.m.))−1). Respiratory exchange ratio (RER) was significantly elevated during exercise in CHO. The acetyl groups increased at similar rates at the onset of exercise (1 min) and there was no difference in substrate phosphorylation as determined from lactate accumulation and phosphocreatine degradation between trials. Subsequently, oxidative metabolism during the transition from rest to steady-state exercise was not affected by prior carbohydrate ingestion. Although exercise resulted in the rapid activation of PDH in both trials, PDHa was greater at 1 min in CHO (CON, 2.36 ± 0.22; CHO, 2.91 ± 0.18 mmol min−1 (kg w.m.)−1). No differences in muscle metabolite levels and PDHa were observed after 10 min of moderate exercise between trials. In summary, at rest, carbohydrate ingestion induced multiple metabolic changes which included decreased acetylcarnitine availability and small increases in PDHa. The prior changes in PDHa and acetylcarnitine availability had no effect on substrate phosphorylation and oxidative metabolism at the onset of exercise. These data suggest that acetylcarnitine availability is unlikely to be the site of metabolic inertia during the transition from rest to steady-state moderate intensity exercise.

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Fasting forces adaptive changes in whole body and skeletal muscle metabolism that increase fat oxidation and decrease the oxidation of carbohydrate. We tested the hypothesis that 40 h of fasting would decrease pyruvate dehydrogenase (PDH) activity and increase PDH kinase (PDK) isoform mRNA expression in human skeletal muscle. The putative transcriptional activators of PDK isozymes, peroxisome proliferator-activated receptor-α (PPAR-α) protein, and forkhead homolog in rhabdomyosarcoma (FKHR) mRNA were also measured. Eleven healthy adults fasted after a standard meal (25% fat, 60% carbohydrate, 15% protein) with blood and skeletal muscle samples taken at 3, 15, and 40 h postprandial. Fasting increased plasma free fatty acid, glycerol, and β-hydroxybutyrate concentrations and decreased glucose and insulin concentrations. PDH activity decreased from 0.88 ± 0.11 mmol acetyl-CoA · min-1 · kg wet muscle wt-1 at 3 h to 0.62 ± 0.10 (P = not significant) and 0.39 ± 0.06 (P < 0.05) mmol · min-1 · kg wet mass-1 after 15 and 40 h of fasting. Although all four PDK isoforms were expressed in human skeletal muscle, PDK-2 and -4 mRNA were the most abundant. PDK-1 and -3 mRNA abundance was ~1 and 15% of the PDK-2 and 4- levels, respectively. The 40-h fast had no effect on PDK-1, -2, and -3 mRNA expression. PDK-4 mRNA was significantly increased ~3-fold after 15 h and ~14-fold after 40 h of fasting. Skeletal muscle PPAR-α protein and FKHR mRNA abundance were unaffected by the fast. The results suggest that decreased PDH activation after 40 h of fasting may have been a function of the large increase in PDK-4 mRNA expression and possible subsequent increase in PDK protein and activity. The changes in PDK-4 expression and PDH activity did not coincide with increases in the transcriptional activators PPAR-α and FKHR.

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Abstract. In applying a quantitative approach to the reproduction of Trygonoptera imitata, the present study contributes to understanding the wide diversity in the reproductive biology of the family Urolophidae and provides insights to help determine phylogenetic relationships. This localised species is taken as bycatch in several inshore fisheries and potentially impacted by a range of other anthropogenic pressures, including introduced species, particularly in shallow-water pupping areas.T. imitata can be characterised as a species of comparatively lowmatrotrophic histotrophy with an extended period of relatively large eggs in utero (5–8 months) followed by rapid growth of the embryos (4–6 months). The reproductive cycle is annual with parturition occurring during late-February–April, followed immediately by ovulation. Mean size-at-birth is ~225mm total length and there is a ~1000% gain in mean wet mass from egg (15 g) to full-term embryo in utero (150 g), the lowest reported for any viviparous batoid. Litter size increases with maternal length, reaching a maximum of seven, and sex ratio of embryos is 1 : 1. Maximum length and estimates of the maturity–ogive parameters l50 and l95 are similar for females and males.

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Urolophus bucculentus, the largest urolophid species found in southern Australia, exhibits a biennial reproductive cycle. Ovulation occurs during October to January followed by a 15–19 month period of gestation followed by parturition during April to May and a short rest period while the ovarian follicles continue to develop for subsequent ovulation. Male breeding condition peaks during April to June to coincide with the period of parturition. Urolophus bucculentus has the highest matrotrophic contribution reported for any urolophid species, with a mean wet mass gain from egg in utero (4 g) to full-term embryo in utero (250 g) of c. 6250% (maximum c. 7200%), and perhaps explains the biennial female reproductive cycle where 50% of females contribute to each year's recruitment. Litter size (one to five) increases with total length (LT). Females reach a longer maximum LT (LTmax) than do males (885 v. 660 mm). The LT at maturity for males and females at 50% mature (LT50) is c. 414 mm (63% of LTmax) for males and c. 502 mm (57% of LTmax) for females, length at maternity indicates that recruitment production occurs later in life at c. 632 mm LT (71% of LTmax).

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During their autumn migratory phase, thrush nightingales (Luscinia luscinia) previously starved for 2 d were allowed to refuel under three different ambient temperature conditions (-7 degrees, 7 degrees, and 22 degrees C). During the refueling period, as well as during the preceding control and starvation periods, food intake, body mass, and feces production were monitored. In addition, daily energy expenditure was measured during the refueling period. The compilation of the energy balance during the refueling period revealed an energy density of the deposited tissue of 33.6 kJ g-1. Assuming that the deposited tissue consists of fat and protein exclusively, with energy densities of 39.6 and 5.5 kJ g-1 wet mass, respectively, we estimated the deposited tissue to consist of 82% fat and 18% wet protein (6% dry protein and 12% water). Nitrogen balances during control, starvation, and refueling phases and during a period of prolonged and complete starvation indicated that 5% of the nutrient stores consisted of dry protein. Our results support recent findings that nutrient stores for migration often contain protein in addition to fat and consequently are 15%-25% less energy rich than pure fat stores. These proteins might be stored as muscle or other functional tissue and may be required to support the extra mass of the stores and/or reflect an incapacity of the metabolic machinery to catabolize far exclusively. Fuel deposition rate was positively related with ambient temperature, whereas food intake rate was unaffected by temperature. These results indicate that the rate of fuel deposition is limited by a ceiling in food intake rate; when this ceiling is reached, fuel deposition rate is negatively affected by daily energy expenditure rate. To a certain extent, the ceiling in food intake rate varies depending on feeding conditions over the previous days. These variations in food intake capacity probably reflect the building and breakdown of gut tissues and/or gut enzyme systems and might be insensible and not evolutionary adaptive. Significant energetic costs, however, are probably associated with the maintenance of gut tissues. It is therefore feasible that changes in digestive capacity are regulated and are directed at energy economization.