Maximizing postexercise muscle glycogen synthesis: carbohydrate supplementation and the application of amino acid or protein hydrolysate mixtures.
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BACKGROUND: Postexercise muscle glycogen synthesis is an important factor in determining the time needed to recover from prolonged exercise. OBJECTIVE: This study investigated whether an increase in carbohydrate intake, ingestion of a mixture of protein hydrolysate and amino acids in combination with carbohydrate, or both results in higher postexercise muscle glycogen synthesis rates than does ingestion of 0.8 g*kg(-)(1)*h(-)(1) carbohydrate, provided at 30-min intervals. DESIGN: Eight trained cyclists visited the laboratory 3 times, during which a control beverage and 2 other beverages were tested. After the subjects participated in a strict glycogen-depletion protocol, muscle biopsy samples were collected. The subjects received a beverage every 30 min to ensure ingestion of 0.8 g carbohydrate*kg(-)(1)*h(-)(1) (Carb trial), 0.8 g carbohydrate*kg(-)(1)*h(-)(1) plus 0.4 g wheat protein hydrolysate plus free leucine and phenylalanine*kg(-)(1)*h(-)(1) (proven to be highly insulinotropic; Carb + Pro trial), or 1.2 g carbohydrate*kg(-)(1)*h(-)(1) (Carb + Carb trial). After 5 h, a second biopsy was taken. RESULTS: Plasma insulin responses in the Carb + Pro and Carb + Carb trials were higher than those in the Carb trial (88 +/- 17% and 46 +/- 18%; P < 0.05). Muscle glycogen synthesis was higher in both trials than in the Carb trial (35. 4 +/- 5.1 and 44.8 +/- 6.8 compared with 16.6 +/- 7.8 micromol glycosol units*g dry wt(-)(1)*h(-)(1), respectively; P < 0.05). CONCLUSIONS: Addition of a mixture of protein hydrolysate and amino acids to a carbohydrate-containing solution (at an intake of 0.8 g carbohydrate*kg(-)(1)*h(-)(1)) can stimulate glycogen synthesis. However, glycogen synthesis can also be accelerated by increasing carbohydrate intake (0.4 g*kg(-)(1)*h(-)(1)) when supplements are provided at 30-min intervals. (+info)
Synthesis rate of plasma albumin is a good indicator of liver albumin synthesis in sepsis.
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Plasma albumin is well known to decrease in response to inflammation. The rate of albumin synthesis from both liver and plasma was measured in vivo by use of a large dose of L-[(2)H(3)-(14)C]valine in rats injected intravenously with live Escherichia coli and in pair-fed control rats during the acute-phase period (2 days postinfection). The plasma albumin concentration was reduced by 50% in infected rats compared with pair-fed animals. Infection induced a fall in both liver albumin mRNA levels and albumin synthesis relative to total liver protein synthesis. However, absolute liver albumin synthesis rate (ASR) was not affected by infection. In plasma, albumin fractional synthesis rate was increased by 50% in infected animals compared with pair-fed animals. The albumin ASR estimated in the plasma was similar in the two groups. These results suggest that hypoalbuminemia is not due to reduced albumin synthesis during sepsis. Moreover, liver and plasma albumin ASR were similar. Therefore, albumin synthesis measured in the plasma is a good indicator of liver albumin synthesis. (+info)
Pyruvate overrides inhibition of PDH during exercise after a low-carbohydrate diet.
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The effects of carbohydrate deprivation on the regulation of pyruvate dehydrogenase (PDH) were studied at rest and during moderate-intensity exercise. An inhibitory effect of a chronic low-carbohydrate diet (LCD) on the active form of PDH (PDHa) mediated by a stable increase in PDH kinase (PDHK) activity has recently been reported (Peters SJ, Howlett RA, St. Amand TA, Heigenhauser GJF, and Spriet LL. Am J Physiol Endocrinol Metab 275: E980-E986, 1998.). In the present study, seven males cycled at 65% maximal O(2) uptake for 30 min after a 6-day LCD. Exercise was repeated 1 wk later after a mixed diet (MD). Muscle biopsies were sampled from the vastus lateralis at rest and at 2 and 30 min of exercise. At rest, PDHa activity (0.18 +/- 0.04 vs. 0.63 +/- 0.18 mmol x min(-1) x kg wet wt(-1)), muscle glycogen content (310.2 +/- 36.9 vs. 563.9 +/- 32.6 mmol/kg dry wt), and muscle lactate content (2.6 +/- 0.3 vs. 4.2 +/- 0.6 mmol/kg dry wt) were significantly lower after the LCD. Resting muscle acetyl-CoA (10.8 +/- 1.9 vs. 7.4 +/- 0.8 micromol/kg dry wt) and acetylcarnitine (5.3 +/- 1.4 vs. 1.6 +/- 0.3 mmol/kg dry wt) contents were significantly elevated after the LCD. During exercise, PDHa, glycogenolytic rate (LCD 5.8 +/- 0.4 vs. MD 6.9 +/- 0.2 mmol x min(-1) x kg dry wt(-1)), and muscle concentrations of acetylcarnitine, pyruvate, and lactate increased to the same extent in both conditions. The results of the present study suggest that inhibition of resting PDH by elevated PDHK activity after a LCD may be overridden by the availability of muscle pyruvate during exercise. (+info)
Inhibition of lipolysis causes suppression of endogenous glucose production independent of changes in insulin.
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We have shown that insulin controls endogenous glucose production (EGP) indirectly, via suppression of adipocyte lipolysis. Free fatty acids (FFA) and EGP are suppressed proportionately, and when the decline in FFA is prevented during insulin infusion, suppression of EGP is also prevented. The present study tested the hypothesis that suppression of lipolysis under conditions of constant insulin would yield a suppression of EGP. N(6)-cyclohexyladenosine (CHA) was used to selectively suppress adipocyte lipolysis during euglycemic clamps in conscious male dogs. FFA suppression by CHA caused suppression of EGP. Liposyn control experiments, which maintained FFA levels above basal during CHA infusion, completely prevented the decline in EGP, whereas glycerol control experiments, which maintained glycerol levels close to basal, did not prevent a decline in EGP. These controls suggest that the EGP suppression was secondary to the suppression of FFA levels specifically. A difference in the sensitivity of FFA and EGP suppression (FFA were suppressed approximately 85% whereas EGP only declined approximately 40%) was possibly caused by confounding effects of CHA, including an increase in catecholamine and glucagons levels during CHA infusion. Thus suppression of lipolysis under constant insulin causes suppression of EGP, despite a significant rise in catecholamines. (+info)
Effects of continuous and intermittent feeding on biliary lipid outputs in man: application for measurements of intestinal absorption of cholesterol and bile acids.
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Hepatic outputs of biliary lipids can be measured by intestinal perfusion techniques, either during constant infusion of liquid formula into the duodenum or through-out a 24-hour period during which time three meals are given along with an overnight fast. The purpose of this study was to compare these two methods for estimating secretion of biliary lipids. In 21 subjects, mean hourly outputs measured during continuous feeding were highly comparable to those during intermittent feeding, showing that the constant infusion technique gave valid estimations of overall daily secretion rates of biliary lipids. On the other hand, the intermittent mode of feeding showed phasic changes of outputs and composition of biliary lipids in response to feeding and fasting apart from total outputs over 24 hours. However, it takes longer to complete and requires the use of a meal marker. By combining the intestinal perfusion technique with measurements of fecal excretion of neutral steroids and bile acids, this method may be used to estimate absorption of cholesterol and bile acids from the intestine. Thus, these measurements allow quantification of a number of parameters of the enterohepatic circulation. (+info)
Folate dependence of hyperhomocysteinemia and vascular dysfunction in cystathionine beta-synthase-deficient mice.
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Hyperhomocysteinemia is a risk factor for stroke, myocardial infarction, and venous thrombosis. Moderate hyperhomocysteinemia is associated with impaired endothelial function, but the mechanisms responsible for endothelial dysfunction in hyperhomocysteinemia are poorly understood. We have used genetic and dietary approaches to produce hyperhomocysteinemia in mice. Heterozygous cystathionine beta-synthase-deficient mice (CBS +/-), which have a selective defect in homocysteine transsulfuration, and wild-type (CBS +/+) littermates were fed either a control diet or a diet that is relatively deficient in folic acid for 6 wk. Plasma total homocysteine was 5.3 +/- 0.7 microM in CBS +/+ mice and 6.4 +/- 0.6 microM in CBS +/- mice (P = 0.3) given the control diet. Plasma total homocysteine was 11.6 +/- 4.5 microM in CBS +/+ mice and 25.1 +/- 3.2 microM in CBS +/- mice (P = 0.004) given a low-folate diet. In mice fed the control diet, relaxation of aortic rings in response to the endothelium-dependent vasodilator acetylcholine did not differ significantly between CBS +/+ mice and CBS +/- mice. In contrast, in mice fed a low-folate diet, maximal relaxation to acetylcholine was markedly impaired in CBS +/- mice (58 +/- 9%) compared with CBS +/+ mice (84 +/- 4%) (P = 0.01). No differences in relaxation to the endothelium-independent vasodilator sodium nitroprusside were observed among the four groups of mice. These data indicate that CBS-deficient mice are predisposed to hyperhomocysteinemia during dietary folate deficiency, and moderate hyperhomocysteinemia is associated with marked impairment of endothelial function in mice. (+info)
How do fiber-supplemented formulas affect antroduodenal motility during enteral nutrition? A comparative study between mixed and insoluble fibers.
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BACKGROUND: Fiber supplementation during enteral nutrition has been recommended, but the effect of soluble compared with insoluble fiber supplements on antroduodenal motility is unknown. OBJECTIVE: The objective of this study was to compare antroduodenal motor patterns in 8 healthy volunteers during and after gastric infusion of 3 different diets: a fiber-free diet, an insoluble-fiber diet, and a mixed-fiber diet (50% soluble fiber and 50% insoluble fiber). DESIGN: Manometric studies with the 3 different diets (2100 kJ) were performed in random order. Antroduodenal motility was monitored continuously for 6 h by using a pneumohydraulic system to calculate the number, amplitude, and duration of the pressure waves; the area under the curve (AUC); and the percentage of time occupied by motor activity before, during, and after each type of infusion. Variations in antral areas were measured by ultrasonography. RESULTS: The gastric motor response was significantly higher, whatever the diet, in the distal antral recording site than in the 2 more proximal sites. In the proximal but not the distal antrum, the number of waves, the AUC, and the percentage of time occupied by motor activity were higher (P: < 0.04) with the mixed-fiber than with the insoluble-fiber diet. No significant differences in variations of antral area were observed among the 3 diets. In the duodenum, motor variables were not significantly different among the 3 diets. CONCLUSIONS: A gastric infusion induced a greater motor response in the distal than in the proximal antrum. A mixed-fiber diet was associated with significantly greater proximal antral motility than was an insoluble-fiber diet. There was no significant difference among the 3 formulas in duodenal motor variables or in variations in antral area as measured by ultrasound. (+info)
Clinical and physiological consequences of rapid tryptophan depletion.
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We review here the rapid tryptophan depletion (RTD) methodology and its controversial association with depressive relapse. RTD has been used over the past decade to deplete serotonin (5-hydroxy-tryptamine, or 5-HT) in humans and to probe the role of the central serotonin system in a variety of psychiatric conditions. Its current popularity was stimulated by reports that RTD reversed the antidepressant effects of selective serotonin reuptake inhibitors (SSRIs) and monoamine oxidase inhibitors (MAOIs) in remitted patients with a history of depression but not in patients treated with antidepressants which promote catecholaminergic rather than serotonergic neurotransmission (such as tricyclic antidepressants or buproprion). However, RTD has inconsistent effects in terms of full clinical relapse in depressed patients. Pooling the data from all published reports, patients who are either unmedicated and/or fully remitted are much less likely to experience relapse (7 of 61, or approximately 9%) than patients who are recently medicated and partially remitted (63 of 133, or approximately 47%; although, the numbers here may reflect patient overlap between reports). Recently remitted patients who have been treated with non-pharmacological therapies such as total sleep deprivation, electroconvulsive therapy, or bright light therapy also do not commonly show full clinical relapse with RTD. We briefly review RTD effects in other psychiatric disorders, many of which are treated with SSRIs. There is accumulating evidence to suggest that RTD affects central serotonergic neurotransmission. Nevertheless, many questions remain about the ability of RTD to reverse the beneficial effects of SSRIs or MAOIs, or to induce symptoms in unmedicated symptomatic or asymptomatic patients. (+info)