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The amino acid imbalance hypothesis should explain the fatigue originating in the brain during sustained exercise or over-training as a branched-chain (BCAA)/aromatic amino acids (AAA) imbalance with increased brain tryptophan uptake and 5-hydroxytryptamine synthesis. The serum amino acid profile was determined in 9 ultra-triathletes before and after completing the 1993 Colmar ultra-triathlon to additionally analyse the extent of this amino acid imbalance during such an extreme prolonged contest lasting more than 23 hours. The summed serum concentration of 25 amino acids decreased by 18% from 3962 +/- 846 to 3255 +/- 694 umol.l-1 likely reflecting a catabolic state of the organism with a decrease in 18 individual amino acids by 9-56%, an increase in cystine (+38%), methionine (+24%), tyrosine (+10%), phenylalanine (+12%), free tryptophan (+74%), and constant glutamine, leucine and total tryptophan levels. Since plasma volume increased by approximately 7.6% with a 3.3 kg body mass decrease in the athletes during the ultra triathlon, a decrease in intra-cellular water with an extra-cellular fluid increase is hypothesized. This decrease in cellular hydration state is seen as a protein-catabolic signal.

To test the overtraining-related "imbalanced amino acid hypothesis" (19), the influence of an unaccustomed average 103 %.4 wk-1 increase in training mileage (ITV) on performance and on serum levels of individual amino acids (AAs) was examined in distance runners and controlled by an unaccustomed average 152%.4 wk-1 increase in tempo-pace and interval runs (ITI). Two mmol.l-1 lactate performance (2 LP) increased, 4 LP stagnated and total running distance (TD) decreased in the incremental test during ITV--which may indicate an ITV-dependent overtraining--in contrast to an ITI-related increase in 2 LP, 4 LP and TD. The summed serum AAs decreased in ITV (2744 +/- 534 vs 2933 +/- 663 umol.l-1; p < 0.05) in contrast to an ITI-related increase (3541 +/- 657 vs 3252 +/- 885 umol.l-1; p < 0.05) with an average 29% higher final summed AAs concentration during ITI (p < 0.05). During ITV 12 individual AAs decreased by 6-17%, 8 remained constant and 3 increased (Cys, Met, fTrp) by 6-19%, as opposed to an ITI-related increase in 16 AA by 6-55%. The observed ITV-related changes in serum AAs profile were smaller than after completing contests as a marathon, a 100 km-run or an ultra-triathlon. It may be concluded that the observed small changes in AAs profile or AAA/BCAA and AA/LNAA ratios only represent an epiphenomenon without recognizable influence on incremental test performance, since increases in fTrp/LNAA ratios (+28% in ITV vs +45% in ITI) were found to be related both to performance impairment (ITV) and improvement (ITI).

Zinc supplementation is beneficial in some clinical conditions. Histidine has been shown to improve zinc absorption in animals. To test its influence on zinc absorption in humans, we studied the bioavailability of zinc from zinc-histidine complexes as compared to zinc sulfate in 10 healthy volunteers. Ingestion of zinc complexed with histidine at a ratio of 1:2 or 1:12 increased serum-zinc concentration 25% more than ingestion of zinc sulfate. Calculated uptake was 30-40% increased with zinc histidine over zinc sulfate. Urinary excretion was not different with any preparation. Application of 15 mg zinc as zinc histidine 1:2 gave an identical serum-zinc response as 45 mg zinc taken as zinc sulfate. Zinc histidine complexes are better absorbed than zinc sulfate in humans.

BackgroundImmigrants to Germany and their children are at particular risk for tuberculosis (TB).Methods35 Patients (10 male/25 female aged 2 - 59 years (median 33 years) originating mostly from high incidence countries in Asia (19 [54.3%]) in Africa (14 [40.0%] and East Europe (2 [5.7%]), attended at the Tropical Medicine unit were analysed.ResultsPrimary clinical presentation was most frequently lymphadenitis (13 [37.1%]). other organs involved included bones (7 [20.0%]), central nervous system (5 [14.3%]), urogenital organs (3 [8.6%]), lung (3 [8.6%]), mediastinum, (2 [5.7%]) and abdomen (2 [5.7%]). ESR was abnormal in 21/28 (75.0%), CRP in 20/35 (57.1%), and protein electrophoresis in 22/26 (84.6%) cases. The tuberculin skin test was strongly positive in all 15 cases where the test had been performed. Tuberculosis interferon gamma release assay (TB-IGRA) was positive in all 35 cases (100%). PCR for nucleic acids of Mycobacterium (M.) tuberculosis complex was positive in only 7/20 (35.0%) cases. M. tuberculosis was identified in 32/35 (91.4%), M. bovis in 2 (5.7%) cases. 1 case was diagnosed clinically. All patients were negative for HIV. Typical histopathology was seen in the 29 cases, where biopsies had been taken. Chest-X-ray did not reveal specific pulmonary lesions in the majority of cases (22/35 [62.9%]). Diagnosis of TB was mostly delayed (4 to 299 weeks, [median 8]). The most frequent primary suspicion was a malignancy (17/35 [48.6%]) while TB was initially suspected in 5 cases only. Diagnosis of TB is impeded by its multifaceted presentation especially in immigrants.

Addition of phenylephrine to isolated perfused rat liver is followed by an increased 14CO2 production from [1-14C]glutamate, [1-14C]glutamine, [U-14C]proline and [3-14C]pyruvate, but by a decreased 14CO2 production from [1-14C]pyruvate. Simultaneously, there is a considerable decrease in tissue content of 2-oxoglutarate, glutamate and citrate. Stimulation of 14CO2 production from [1-14C]glutamate is also observed in the presence of amino-oxyacetate, suggesting a stimulation of glutamate dehydrogenase and 2-oxoglutarate dehydrogenase fluxes by phenylephrine. Inhibition of pyruvate dehydrogenase flux by phenylephrine is due to an increased 2-oxoglutarate dehydroxygenase flux. Phenylephrine stimulates glutaminase flux and inhibits glutamine synthetase flux to a similar extent, resulting in an increased hepatic glutamine uptake. Whereas the effects of NH4+ ions and phenylephrine on glutaminase flux were additive, activation of glutaminase by glucagon was considerably diminished in the presence of phenylephrine. The reported effects are largely overcome by prazosin, indicating the involvement of alpha-adrenergic receptors in the action of phenylephrine. It is concluded that stimulation of gluconeogenesis from various amino acids by phenylephrine is due to an increased flux through glutamate dehydrogenase and the citric acid cycle.

Glycerol, water, and urea transport were studied in the perfused rat liver. When hypertonic glycerol (100 mM) was infused into the perfused rat liver, rapid equilibration of glycerol between the extracellular and intracellular space occurred and only small effects of osmotic water fluxes on liver mass and extracellular ion concentrations were observed. However, when phloretin (0.2 mmol/l) was present, addition (or removal) of glycerol (100 mmol/l) induced within seconds a marked and transient decrease (or increase) of both liver mass and effluent Na+ and K+ concentrations, suggestive of transient osmotic water shifts out of and/or into the cells. These effects were observed with glycerol but not with infusion of 1,2-propanediol, 1,3-propanediol, or ethanediol (100 mmol/l). Calculation of permeability coefficients for hepatocytes in the perfused rat liver revealed that in the absence of a transmembrane glycerol concentration gradient the glycerol permeability was decreased from 0.146 +/- 0.005 (n = 14) to 0.055 +/- 0.016 microm/s (n = 4) in the presence of phloretin (200 microM). Water permeability was not affected by phloretin [0.146 +/- 0.005 under control conditions (n = 12) vs. 0.157 +/- 0.006 microm/s (n = 4) in the presence of phloretin]. Urea permeability was 0.131 +/- 0.008 microm/s (n = 5) and decreased to 0.061 +/- 0.003 microm/s in the presence ofphloretin. Glycerol and water permeability were inhibited in the presence of hypertonic glucose (200 mM) by 47 and 27%, respectively, but urea permeability was not affected by glucose.