solaros
oczywiscie wiecej jest badan pokazujacych brak jakichkolwiek efektow na wzrost sily i masy miesniowej,czy lepszej regeneracji - przy dawkach rzedu 0,3-0,9g/kgmc
ale tak samo brak jakiejkolwiek toksycznosci tak olbrzymich dawek
Z tym ze spozywanie 90g glutaminy - ze wzgledow czysto ekonimicznych - mija sie z celem.
Jest kilka badan swiadczacych o pozytywnym dzialaniu glutaminy - ale nie stricte masa/sila/regeneracja:
to juz (chyba) widziales:
Glutamine prevents downregulation of myosin heavy chain synthesis and muscle atrophy from glucocorticoids
'.....In conclusion, these data show that glutamine infusion is effective therapy in counteracting glucocorticoid-induced muscle atrophy. Atrophy attenuation appears related to maintaining muscle glutamine levels, which in turn may limit the glucocorticoid-mediated downregulation of MHC synthesis'
http://www.ncbi.nlm.nih.gov/pubmed/7733273
obniza poziom kortyzolu (u sczorow traktowanych glukokortykoidami)
****************************
kolejna sprawa - wzmocnienie systemu odpornosciowego:
Glutamine Alimentation in Catabolic State
Glutamine should be reclassified as a conditionally essential amino acid in the catabolic state because the body’s glutamine expenditures exceed synthesis and low glutamine levels in plasma are associated with poor clinical outcome. After severe stress, several amino acids are mobilized from muscle tissue to supply energy and substrate to the host. Glutamine is one of the most important amino acids that provide this function. Glutamine acts as the preferred respiratory fuel for lymphocytes, hepatocytes and intestinal mucosal cells and is metabolized in the gut to citrulline, ammonium and other amino acids. Low concentrations of glutamine in plasma reflect reduced stores in muscle and this reduced availability of glutamine in the catabolic state seems to correlate with increased morbidity and mortality. Adding glutamine to the nutrition of clinical patients, enterally or parenterally, may reduce morbidity. Several excellent clinical trials have been performed to prove efficacy and feasibility of the use of glutamine supplementation in parenteral and enteral nutrition. The increased intake of glutamine has resulted in lower septic morbidity in certain critically ill patient populations. This review will focus on the efficacy and the importance of glutamine supplementation in diverse catabolic states.
http://jn.nutrition.org/content/131/9/2569S.short
******************************************
Having a glutamine deficiency will lower the levels of our protective T cells and reduce the ability of macrophages to kill viruses and bacteria
Hack, V., Weiss, C., Friedmann, B., Suttner, S., Schykowski, M., Erge, N., Benner, A., Bartsch, P., and Droge, W. (1997). Decreased Plasma glutamine level and CD4+ T-cell number in response to 8 weeks of anaerobic training. American Journal of Physiology. 272: 788-95
Does glutamine have a role in reducing infections in athletes?
There is an increased risk of infections in athletes undertaking prolonged, strenuous exercise. There is also some evidence that cells of the immune system are less able to mount a defence against infections after such exercise. The level of plasma glutamine, an important fuel for cells of the immune system, is decreased in athletes after endurance exercise; this may be partly responsible for the apparent immunosuppression which occurs in these individuals. We monitored levels of infection in more than 200 runners and towers. The levels of infection were lowest in middle-distance runners, and highest in runners after a full or ultramarathon and in elite rowers after intensive training. In the present study, athletes participating in different types of exercise consumed two drinks, containing either glutamine (Group G) or placebo (Group P) immediately after and 2 h after exercise. They subsequently completed questionnaires (n = 151) about the incidence of infections during the 7 days following the exercise. The percentage of athletes reporting no infections was considerably higher in Group G (81%, n = 72) than in Group P (49%, n = 79, p < 0.001).
http://www.ncbi.nlm.nih.gov/pubmed/8803512
******************************
odnosnie glikogenu:
Stimulatory effect of glutamine on glycogen accumulation in human skeletal muscle.
To determine whether glutamine can stimulate human muscle glycogen synthesis, we studied in groups of six subjects the effect after exercise of infusion of glutamine, alanine+glycine, or saline. The subjects cycled for 90 min at 70-140% maximal oxygen consumption to deplete muscle glycogen; then primed constant infusions of glutamine (30 mg/kg; 50 mg.kg-1.h-1) or an isonitrogenous, isoenergetic mixture of alanine+glycine or NaCl (0.9%) were administered. Muscle glutamine remained constant during saline infusion, decreased 18% during alanine+glycine infusion (P < 0.001), but rose 16% during glutamine infusion (P < 0.001). By 2 h after exercise, muscle glycogen concentration had increased more in the glutamine-infused group than in the saline or alanine+glycine controls (+2.8 +/- 0.6, +0.8 +/- 0.4, and +0.9 +/- 0.4 mumol/g wet wt, respectively, P < 0.05, glutamine vs. saline or alanine+glycine). Labeling of glycogen by tracer [U-13C]glucose was similar in glutamine and saline groups, suggesting no effect of glutamine on the fractional rate of blood glucose incorporation into glycogen. The results suggest that, after exercise, increased availability of glutamine promotes muscle glycogen accumulation by mechanisms possibly including diversion of glutamine carbon to glycogen.
http://www.ncbi.nlm.nih.gov/pubmed/7653548
Interaction between glutamine availability and metabolism of glycogen, tricarboxylic acid cycle intermediates and glutathione.
After exhaustive exercise, intravenous or oral glutamine promoted skeletal muscle glycogen storage. However, when glutamine was ingested with glucose polymer, whole-body carbohydrate storage was elevated, the most likely site being liver and not muscle, possibly due to increased glucosamine formation. The rate of tricarboxylic acid (TCA) cycle flux and hence oxidative metabolism may be limited by the availability of TCA intermediates. There is some evidence that intramuscular glutamate normally provides alpha-ketoglutarate to the mitochondrion. We hypothesized that glutamine might be a more efficient anaplerotic precursor than endogenous glutamate alone. Indeed, a greater expansion of the sum of muscle citrate, malate, fumarate and succinate concentrations was observed at the start of exercise (70% VO2(max)) after oral glutamine than when placebo or ornithine alpha-ketoglutarate was given. However, neither endurance time nor the extent of phosphocreatine depletion or lactate accumulation during the exercise was altered, suggesting either that TCA intermediates were not limiting for energy production or that the severity of exercise was insufficient for the limitation to be operational. We have also shown that in the perfused working rat heart, there is a substantial fall in intramuscular glutamine and alpha-ketoglutarate, especially after ischemia. Glutamine (but not glutamate, alpha-ketoglutarate or aspartate) was able to rescue the performance of the postischemic heart. This ability appears to be connected to the ability to sustain intracardiac ATP, phosphocreatine and glutathione.
http://www.ncbi.nlm.nih.gov/pubmed/11533298
czolowi trenerzy/dietetycy etc. sugeruja (jesli juz mamy spozywac glutamine) to w okresie redukcyjnym - bardziej moze sie przydac - ale ze wzgledu na wzmocnienie odpornosci czy tez lepsza synteze glukozy
Zmieniony przez - solaros w dniu 2011-02-01 01:07:02
ale tak samo brak jakiejkolwiek toksycznosci tak olbrzymich dawek
Z tym ze spozywanie 90g glutaminy - ze wzgledow czysto ekonimicznych - mija sie z celem.
Jest kilka badan swiadczacych o pozytywnym dzialaniu glutaminy - ale nie stricte masa/sila/regeneracja:
to juz (chyba) widziales:
Glutamine prevents downregulation of myosin heavy chain synthesis and muscle atrophy from glucocorticoids
'.....In conclusion, these data show that glutamine infusion is effective therapy in counteracting glucocorticoid-induced muscle atrophy. Atrophy attenuation appears related to maintaining muscle glutamine levels, which in turn may limit the glucocorticoid-mediated downregulation of MHC synthesis'
http://www.ncbi.nlm.nih.gov/pubmed/7733273
obniza poziom kortyzolu (u sczorow traktowanych glukokortykoidami)
****************************
kolejna sprawa - wzmocnienie systemu odpornosciowego:
Glutamine Alimentation in Catabolic State
Glutamine should be reclassified as a conditionally essential amino acid in the catabolic state because the body’s glutamine expenditures exceed synthesis and low glutamine levels in plasma are associated with poor clinical outcome. After severe stress, several amino acids are mobilized from muscle tissue to supply energy and substrate to the host. Glutamine is one of the most important amino acids that provide this function. Glutamine acts as the preferred respiratory fuel for lymphocytes, hepatocytes and intestinal mucosal cells and is metabolized in the gut to citrulline, ammonium and other amino acids. Low concentrations of glutamine in plasma reflect reduced stores in muscle and this reduced availability of glutamine in the catabolic state seems to correlate with increased morbidity and mortality. Adding glutamine to the nutrition of clinical patients, enterally or parenterally, may reduce morbidity. Several excellent clinical trials have been performed to prove efficacy and feasibility of the use of glutamine supplementation in parenteral and enteral nutrition. The increased intake of glutamine has resulted in lower septic morbidity in certain critically ill patient populations. This review will focus on the efficacy and the importance of glutamine supplementation in diverse catabolic states.
http://jn.nutrition.org/content/131/9/2569S.short
******************************************
Having a glutamine deficiency will lower the levels of our protective T cells and reduce the ability of macrophages to kill viruses and bacteria
Hack, V., Weiss, C., Friedmann, B., Suttner, S., Schykowski, M., Erge, N., Benner, A., Bartsch, P., and Droge, W. (1997). Decreased Plasma glutamine level and CD4+ T-cell number in response to 8 weeks of anaerobic training. American Journal of Physiology. 272: 788-95
Does glutamine have a role in reducing infections in athletes?
There is an increased risk of infections in athletes undertaking prolonged, strenuous exercise. There is also some evidence that cells of the immune system are less able to mount a defence against infections after such exercise. The level of plasma glutamine, an important fuel for cells of the immune system, is decreased in athletes after endurance exercise; this may be partly responsible for the apparent immunosuppression which occurs in these individuals. We monitored levels of infection in more than 200 runners and towers. The levels of infection were lowest in middle-distance runners, and highest in runners after a full or ultramarathon and in elite rowers after intensive training. In the present study, athletes participating in different types of exercise consumed two drinks, containing either glutamine (Group G) or placebo (Group P) immediately after and 2 h after exercise. They subsequently completed questionnaires (n = 151) about the incidence of infections during the 7 days following the exercise. The percentage of athletes reporting no infections was considerably higher in Group G (81%, n = 72) than in Group P (49%, n = 79, p < 0.001).
http://www.ncbi.nlm.nih.gov/pubmed/8803512
******************************
odnosnie glikogenu:
Stimulatory effect of glutamine on glycogen accumulation in human skeletal muscle.
To determine whether glutamine can stimulate human muscle glycogen synthesis, we studied in groups of six subjects the effect after exercise of infusion of glutamine, alanine+glycine, or saline. The subjects cycled for 90 min at 70-140% maximal oxygen consumption to deplete muscle glycogen; then primed constant infusions of glutamine (30 mg/kg; 50 mg.kg-1.h-1) or an isonitrogenous, isoenergetic mixture of alanine+glycine or NaCl (0.9%) were administered. Muscle glutamine remained constant during saline infusion, decreased 18% during alanine+glycine infusion (P < 0.001), but rose 16% during glutamine infusion (P < 0.001). By 2 h after exercise, muscle glycogen concentration had increased more in the glutamine-infused group than in the saline or alanine+glycine controls (+2.8 +/- 0.6, +0.8 +/- 0.4, and +0.9 +/- 0.4 mumol/g wet wt, respectively, P < 0.05, glutamine vs. saline or alanine+glycine). Labeling of glycogen by tracer [U-13C]glucose was similar in glutamine and saline groups, suggesting no effect of glutamine on the fractional rate of blood glucose incorporation into glycogen. The results suggest that, after exercise, increased availability of glutamine promotes muscle glycogen accumulation by mechanisms possibly including diversion of glutamine carbon to glycogen.
http://www.ncbi.nlm.nih.gov/pubmed/7653548
Interaction between glutamine availability and metabolism of glycogen, tricarboxylic acid cycle intermediates and glutathione.
After exhaustive exercise, intravenous or oral glutamine promoted skeletal muscle glycogen storage. However, when glutamine was ingested with glucose polymer, whole-body carbohydrate storage was elevated, the most likely site being liver and not muscle, possibly due to increased glucosamine formation. The rate of tricarboxylic acid (TCA) cycle flux and hence oxidative metabolism may be limited by the availability of TCA intermediates. There is some evidence that intramuscular glutamate normally provides alpha-ketoglutarate to the mitochondrion. We hypothesized that glutamine might be a more efficient anaplerotic precursor than endogenous glutamate alone. Indeed, a greater expansion of the sum of muscle citrate, malate, fumarate and succinate concentrations was observed at the start of exercise (70% VO2(max)) after oral glutamine than when placebo or ornithine alpha-ketoglutarate was given. However, neither endurance time nor the extent of phosphocreatine depletion or lactate accumulation during the exercise was altered, suggesting either that TCA intermediates were not limiting for energy production or that the severity of exercise was insufficient for the limitation to be operational. We have also shown that in the perfused working rat heart, there is a substantial fall in intramuscular glutamine and alpha-ketoglutarate, especially after ischemia. Glutamine (but not glutamate, alpha-ketoglutarate or aspartate) was able to rescue the performance of the postischemic heart. This ability appears to be connected to the ability to sustain intracardiac ATP, phosphocreatine and glutathione.
http://www.ncbi.nlm.nih.gov/pubmed/11533298
czolowi trenerzy/dietetycy etc. sugeruja (jesli juz mamy spozywac glutamine) to w okresie redukcyjnym - bardziej moze sie przydac - ale ze wzgledu na wzmocnienie odpornosci czy tez lepsza synteze glukozy
Zmieniony przez - solaros w dniu 2011-02-01 01:07:02
"Cóż jest trucizną?
Wszystko jest trucizną i nic nie jest trucizną, tylko dawka czyni, że dana substancja nie jest trucizną!".
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