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  • American Physiological Society  (4)
  • 2000-2004  (4)
  • 1
    Online Resource
    Online Resource
    Hypercortisolemia alters muscle protein anabolism following ingestion of essential amino acids
    American Physiological Society ; 2003
    In:  American Journal of Physiology-Endocrinology and Metabolism Vol. 284, No. 5 ( 2003-05-01), p. E946-E953
    Details
    In: American Journal of Physiology-Endocrinology and Metabolism, American Physiological Society, Vol. 284, No. 5 ( 2003-05-01), p. E946-E953
    Abstract: Debilitating injury is accompanied by hypercortisolemia, muscle wasting, and disruption of the normal anabolic response to food. We sought to determine whether acute hypercortisolemia alters muscle protein metabolism following ingestion of a potent anabolic stimulus: essential amino acids (EAA). A 27-h infusion (80 μg · kg −1 · h −1 ) of hydrocortisone sodium succinate mimicked cortisol (C) levels accompanying severe injury ( 〉 30 μg/dl), (C + AA; n = 6). The control group (AA) received intravenous saline ( n = 6). Femoral arteriovenous blood samples and muscle biopsies were obtained during a primed (2.0 μmol/kg) constant infusion (0.05 μmol · kg −1 · min −1 ) ofl-[ ring- 2 H 5 ]phenylalanine before and after ingestion of 15 g of EAA. Hypercortisolemia [36.5 ± 2.1 (C + AA) vs. 9.0 ± 1.0 μg/dl (AA)] increased postabsorptive arterial, venous, and muscle intracellular phenylalanine concentrations. Hypercortisolemia also increased postabsorptive and post-EAA insulin concentrations. Net protein balance was blunted (40% lower) following EAA ingestion but remained positive for a greater period of time (60 vs. 180 min) in the C + AA group. Thus, although differences in protein metabolism were evident, EAA ingestion improved muscle protein anabolism during acute hypercortisolemia and may help minimize muscle loss following debilitating injury.
    Type of Medium: Online Resource
    ISSN: 0193-1849 , 1522-1555
    URL: Article
    DOI: 10.1152/ajpendo.00397.2002
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2003
    detail.hit.zdb_id: 1477331-4
    SSG: 12
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  • 2
    Online Resource
    Online Resource
    Timing of amino acid-carbohydrate ingestion alters anabolic response of muscle to resistance exercise
    American Physiological Society ; 2001
    In:  American Journal of Physiology-Endocrinology and Metabolism Vol. 281, No. 2 ( 2001-08-01), p. E197-E206
    Details
    In: American Journal of Physiology-Endocrinology and Metabolism, American Physiological Society, Vol. 281, No. 2 ( 2001-08-01), p. E197-E206
    Abstract: The present study was designed to determine whether consumption of an oral essential amino acid-carbohydrate supplement (EAC) before exercise results in a greater anabolic response than supplementation after resistance exercise. Six healthy human subjects participated in two trials in random order, PRE (EAC consumed immediately before exercise), and POST (EAC consumed immediately after exercise). A primed, continuous infusion ofl-[ ring- 2 H 5 ]phenylalanine, femoral arteriovenous catheterization, and muscle biopsies from the vastus lateralis were used to determine phenylalanine concentrations, enrichments, and net uptake across the leg. Blood and muscle phenylalanine concentrations were increased by ∼130% after drink consumption in both trials. Amino acid delivery to the leg was increased during exercise and remained elevated for the 2 h after exercise in both trials. Delivery of amino acids (amino acid concentration times blood flow) was significantly greater in PRE than in POST during the exercise bout and in the 1st h after exercise ( P 〈 0.05). Total net phenylalanine uptake across the leg was greater ( P = 0.0002) during PRE (209 ± 42 mg) than during POST (81 ± 19). Phenylalanine disappearance rate, an indicator of muscle protein synthesis from blood amino acids, increased after EAC consumption in both trials. These results indicate that the response of net muscle protein synthesis to consumption of an EAC solution immediately before resistance exercise is greater than that when the solution is consumed after exercise, primarily because of an increase in muscle protein synthesis as a result of increased delivery of amino acids to the leg.
    Type of Medium: Online Resource
    ISSN: 0193-1849 , 1522-1555
    URL: Article
    DOI: 10.1152/ajpendo.2001.281.2.E197
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2001
    detail.hit.zdb_id: 1477331-4
    SSG: 12
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  • 3
    Online Resource
    Online Resource
    An oral essential amino acid-carbohydrate supplement enhances muscle protein anabolism after resistance exercise
    American Physiological Society ; 2000
    In:  Journal of Applied Physiology Vol. 88, No. 2 ( 2000-02-01), p. 386-392
    Details
    In: Journal of Applied Physiology, American Physiological Society, Vol. 88, No. 2 ( 2000-02-01), p. 386-392
    Abstract: This study was designed to determine the response of muscle protein to the bolus ingestion of a drink containing essential amino acids and carbohydrate after resistance exercise. Six subjects (3 men, 3 women) randomly consumed a treatment drink (6 g essential amino acids, 35 g sucrose) or a flavored placebo drink 1 h or 3 h after a bout of resistance exercise on two separate occasions. We used a three-compartment model for determination of leg muscle protein kinetics. The model involves the infusion of ring- 2 H 5 -phenylalanine, femoral arterial and venous blood sampling, and muscle biopsies. Phenylalanine net balance and muscle protein synthesis were significantly increased above the predrink and corresponding placebo value ( P 〈 0.05) when the drink was taken 1 or 3 h after exercise but not when the placebo was ingested at 1 or 3 h. The response to the amino acid-carbohydrate drink produced similar anabolic responses at 1 and 3 h. Muscle protein breakdown did not change in response to the drink. We conclude that essential amino acids with carbohydrates stimulate muscle protein anabolism by increasing muscle protein synthesis when ingested 1 or 3 h after resistance exercise.
    Type of Medium: Online Resource
    ISSN: 8750-7587 , 1522-1601
    URL: Article
    DOI: 10.1152/jappl.2000.88.2.386
    RVK:
    WA 15000
    RVK:
    XA 52094
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2000
    detail.hit.zdb_id: 1404365-8
    SSG: 12
    SSG: 31
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  • 4
    Online Resource
    Online Resource
    Role of TNF-α in gut mucosal changes after severe burn
    American Physiological Society ; 2002
    In:  American Journal of Physiology-Gastrointestinal and Liver Physiology Vol. 283, No. 3 ( 2002-09-01), p. G703-G708
    Details
    In: American Journal of Physiology-Gastrointestinal and Liver Physiology, American Physiological Society, Vol. 283, No. 3 ( 2002-09-01), p. G703-G708
    Abstract: Gut epithelial cell death by apoptosis is increased in the gut epithelium after severe burn associated with mucosal atrophy. We hypothesized that tumor necrosis factor (TNF)-α-TNF receptor (TNFR) interaction activates apoptosis in small bowel mucosal cells after severe burn. C57BL6 mice received a 30% total body surface area scald burn and were treated with neutralizing anti-TNF-α. The proximal small bowel was assessed for mucosal atrophy. Proliferation and apoptosis of mucosal cells were assessed by proliferative cell nuclear antigen-immunostaining and terminal deoxyuridine nick-end labeling assay, respectively. Mucosal height and mucosal cell number decreased after burn. Anti-TNF-α-treated mice showed significantly less mucosal atrophy. Proliferation of intestinal cells was not changed with burn or anti-TNF-α treatment. An over threefold increase in apoptotic cell number was seen after burn, which was diminished by anti-TNF-α treatment. Changes in gut mucosal homeostasis after severe burn are affected, in part, by the activation of apoptosis by TNF-α-TNFR interaction.
    Type of Medium: Online Resource
    ISSN: 0193-1857 , 1522-1547
    URL: Article
    DOI: 10.1152/ajpgi.00149.2001
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2002
    detail.hit.zdb_id: 1477329-6
    SSG: 12
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