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D Merino

Publications and source records attributed to D Merino.

29 records · Page 2Linked to original sources

Hormonal and metabolic response to physical exercise, fasting and cold exposure in the rat. Effects on ketogenesis in isolated hepatocytes.

Four groups of rats were subjected to the following conditions: (1) 48 h fasting, (2) 48 h of 4 degrees C cold exposure, (3) 5 h treadmill running, (4) 48 h fasting with 4 degrees C cold exposure. The groups were compared to fed control rats in order to study hormonal and metabolic responses in blood and tissue samples. Isolated hepatocytes were used to evaluate the rate of ketogenesis. Decreases in liver glycogen and increases in blood free fatty acids (FFA) confirmed that glycogenolysis and lipolysis occur in these situations of metabolic stress. Increases in the glucagon/insulin plasma ratio were also noted. Plasma catecholamine levels were only enhanced after running and after cold exposure. Production of blood ketone bodies was stimulated more by running and by fasting than by cold exposure. The low ketone body production observed after cold exposure seems to be linked to increases liver glycogen levels and decreased FFA availability. Liver cells isolated after cold exposure exhibited higher ketogenesis than these isolated after running. This difference in ketogenic capacity could result both from the longer hormonal stimulation by high glucagon/insulin plasma ratios and from the metabolic state of the liver.

3-Hydroxybutyric Acid

Amphetamine and alpha-methyl-p-tyrosine affect the exercise-induced imbalance between the availability of tryptophan and synthesis of serotonin in the brain of the rat.

This study was performed to investigate the effects of exercise on the synthesis of dopamine (DA) and 5-hydroxytryptamine (5-HT) in the brain of the trained rat. The consequences on the relationships between these two systems were also examined. The sum of the levels of free 3,4-dihydroxyphenyl acetic acid (DOPAC) plus homovanillic acid (HVA) was increased by running and remained elevated throughout the first hour of recovery. Regional studies indicated that the levels of DA were increased in the midbrain, hypothalamus and hippocampus. In these areas, DOPAC showed little variation whereas HVA was largely increased. Administration of pargyline confirmed this increase in the metabolism of DA in hypothalamus and midbrain during running. Food deprivation and administration of tryptophan clearly revealed that running, despite increasing levels of tryptophan and 5-hydroxyindoleacetic acid in brain, reduced the central control of synthesis of 5-HT by tryptophan, probably by inhibiting tryptophan hydroxylase. To examine if such an alteration was caused by the running-induced activation of metabolism of DA in brain, compounds known to affect the activity of DA were used. Administration of amphetamine potentiated the relative inhibition of synthesis of 5-HT induced by running, while alpha-methyl-p-tyrosine prevented this effect of exercise. Haloperidol did not produce any significant change. It is concluded that the control of the synthesis of 5-HT in brain by the availability of tryptophan is altered during exercise and that the increased central catecholaminergic activity participates in such an alteration.

3,4-Dihydroxyphenylacetic Acid

Peripheral and central short-term effects of fusaric acid, a DBH inhibitor, on tryptophan and serotonin metabolism in the rat.

Fusaric acid (FA) administration to the rats promoted one hour later a large decrease in plasma total tryptophan (TRP), without affecting either plasma free TRP or lipolysis, as measured by plasma non esterified fatty acid concentration. The previous change was associated with hypoinsulinemia, hyperglycemia and increased plasma corticosterone level. Regression analysis revealed a significant correlation between brain TRP and the percentage of plasma TRP which was free (i.e. unbound to albumin), both increased by FA injection. The increase in brain TRP promoted an increased brain serotonin synthesis, as measured by the enhanced brain and CSF 5-HIAA levels. Valine pretreatment, which blocks TRP entry into the brain, completely prevented FA-induced brain TRP and brain 5-HIAA increases. These results suggest that the increased brain serotonergic turnover following FA treatment was due to a peripheral action of the drug upon TRP disposition. The latter effect may be caused (i) by in vivo peripheral alterations in catecholaminergic metabolism and (ii) by FA chemical structure since in vitro experiments revealed that FA was able to displace TRP binding to albumin, thus increasing the plasma free TRP pool.

Animals

Amino acid analysis demonstrates that increased plasma free tryptophan causes the increase of brain tryptophan during exercise in the rat.

Rats were trained to run on a horizontal treadmill for 2 h at 20 m/min. This activity considerably increased plasma free tryptophan (TRP) (+70%) but did not alter plasma total TRP levels and had little or no effect on plasma concentrations of the other large neutral amino acids (LNAAs) that compete with TRP for entry into the brain. Brain TRP levels increased by 80%. The only other brain LNAA to be affected by exercise was threonine, which rose moderately. The results indicate that increased plasma free TRP was specifically responsible for the increase of brain TRP after 2 h of exercise. Brain lysine was also increased whereas glycine, alanine, and gamma-aminobutyric acid were decreased. The differences between the present findings and those previously obtained following 2 h immobilization stress are discussed.

Alanine

Effect of hypoxia on heart glycogen utilization during exercise.

An investigation was made into the effects of physical exercise upon heart glycogen change in rats exposed to decreased barometric pressure in hypobaric chamber simulating the effects of 3,000 m and 5,000 m altitude. Blood and cardiac tissue samples were examined after 1 h and 5 h of treadmill running at sea level and at 3,000 m, and after 1 h at 5,000 m. At sea level, cardiac glycogen level showed a classic biphasic evolution which was not affected by running. At 3,000 m, 1 h of running promoted an initial increase of 16% from control values, while a secondary decrease of 15% was measured after 5 h of running. Running for 1 h at 5,000 m induced a total depletion in cardiac glycogen level, the latter being depressed by 90% from control values. Free fatty acid (FFA) plasma level was increased by physical exercise at all barometric pressures, but the response was gradually enhanced by hypoxia. These data indicate that heart glycogen utilization during prolonged physical exercise is stimulated by acute altitude exposure, which suppresses the sparing effect observed at sea level upon dependence of enhanced FFA availability. The great differences in cardiac glycogen utilization support the views that enhanced glycogenolysis during hypoxia is promoted by different parameters, thus affecting various pathways. The slight decrease at 3,000 m suggests a moderate increase in anaerobic metabolism while the exhaustion observed after 1 h of running at 5,000 m indicates a decrease in cellular respiration response and enhanced heart anaerobic metabolism.

Animals

Metabolic effects of testosterone during prolonged physical exercise and fasting.

Previous studies have shown a decrease in plasma testosterone during prolonged physical exercise and 72 h fasting in rats. To determine whether this hormonal change has an influence upon energy metabolism, two experiments were carried out, in which the plasma levels of testosterone were elevated during prolonged physical exercise and fasting in male wistar rats. The effects of acute and chronic increases in the levels of circulating testosterone were studied, on the one hand after human chorionic gonadotropin (H.C.G.) injection, and on the other by prolonged testosterone perfusion with an osmotic minipump. Blood and tissue sampling were performed to evaluate blood glucose, alanine, and lactate, and tissue glycogen. The results in fed and rest control rats showed no changes in blood parameters under the effect of hypertestosteronemia but there was an increase in muscle glycogen after testosterone perfusion. In 72 h fasted rats both types of hypertestosteronemia were associated with a decrease in blood alanine and lactate ranging from 25% to 35%. Only testosterone perfusion was associated with higher concentrations of muscle glycogen. After 7 h of treadmill running, testosterone perfusion and H.C.G. injection induced a 35% decrease in blood alanine and a slight decrease in blood glucose, with no change in other parameters. Whereas an elevation in the level of testosterone can induce muscle glycogen compensation in the fed resting state, it cannot counteract the exhaustion of muscle glycogen during running.

Animals

Metabolic and hormonal response to short term fasting after endurance training in the rat.

The metabolic and hormonal response to short term fasting was studied after endurance exercise training. Rats were kept running on a motor driven rodent treadmill 5 days/wk for periods up to 1 h/day for 6 wk. Trained and untrained rats were then fasted for 24 h and 48 h. Liver and muscle glycogen, blood glucose, lactate, beta OH butyrate, glycerol, plasma insulin, testosterone and corticosterone were measured in fed and fasted trained and untrained rats. 48 h fasted trained rats show a lower level of blood lactate (1.08 +/- 0.05 vs 1.33 +/- 0.08 mmol/l-1 of blood glycerol (1 +/- 0.11 vs 0.84 +/- 0.08 mmol/l-1), and of muscle glycogen. There is a significant increase in plasma corticosterone in 48 h fasted trained rats from fed values. Plasma testosterone decreases during fasting, the values are higher in trained rats. Plasma insulin decreases during fasting without any difference between the two groups. These results show higher lipolysis, and decreased glycogenolysis in trained animals during 48 h fasting. The difference between the groups in steroid hormone response could reduce neoglucogenesis and muscle proteolysis in trained animals.

Animals

Effects of prolonged physical exercise and fasting upon plasma testosterone level in rats.

Prolonged physical exercise and fasting in male rats were studied to determine the effect of these two treatments on plasma testosterone level. Blood and tissue samples were drawn after 1 h, 3 h, 5 h, and 7 h treadmill running, and after 24 h, 48 h, and 72 h of fasting. Both treatments resulted in a significant fall in plasma testosterone, plasma luteinizing hormone (LH), plasma Insulin (IRI) and in liver and muscle glycogen stores. In the course of these two treatments the injection of a supra maximal dose of Human Chorionic Gonadotropin (HCG) produced a rise in plasma testosterone similar to that in control rats. This indicates that the decrease of plasma LH may be responsible for the decrease in plasma testosterone, which is time-related with the decrease in glycogen stores. The possible metabolic role of the decrease in plasma testosterone is discussed.

Animals