GLUTAMINA -badania naukowe, czyli przeznacz pieniądze na co innego ;)

Ja frazę: uważa się, że niektóre z nich są nieaktywne (zostały 'uśpione' w efekcie adaptacji do określonych źródeł pożywienia), przez co komórka ludzka nie produkuje kilku aminokwasów lub produkuje je w ilościach trudnych do oznaczenia czy obserwacji aktywności danego szlaku metabolicznego. - jako komunikat iz ewentualna produkcja niektórych aminokwasów w org ludzkim jest ilosciowo nieistotna/symboliczna.


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Co do sterydów anabolicznych - to nie mogę się zgodzić niestety, bo widziałem badania które przeczą Twoim założeniom (iz popwodowały wzrost masy.siły jedynie u wyczynowych sportowców). Stąd jak mówię - Twoja analogia jest moim zdaniem jest chybiona.


Effect of testosterone on muscle mass and muscle protein synthesis

R. C. Griggs, W. Kingston, R. F. Jozefowicz, B. E. Herr, G. Forbes and D. Halliday
Department of Neurology, University of Rochester School of Medicine and Dentistry, New York 14642.

We have studied the effect of a pharmacological dose of testosterone enanthate (3 mg.kg-1.wk-1 for 12 wk) on muscle mass and total-body potassium and on whole-body and muscle protein synthesis in normal male subjects. Muscle mass estimated by creatinine excretion increased in all nine subjects (20% mean increase, P less than 0.02); total body potassium mass estimated by 40K counting increased in all subjects (12% mean increase, P less than 0.0001). In four subjects, a primed continuous infusion protocol with L-[1-13C]leucine was used to determine whole-body leucine flux and oxidation. Whole-body protein synthesis was estimated from nonoxidative flux. Muscle protein synthesis rate was determined by measuring [13C]leucine incorporation into muscle samples obtained by needle biopsy. Testosterone increased muscle protein synthesis in all subjects (27% mean increase, P less than 0.05). Leucine oxidation decreased slightly (17% mean decrease, P less than 0.01), but whole-body protein synthesis did not change significantly. Muscle morphometry showed no significant increase in muscle fiber diameter. These studies suggest that testosterone increases muscle mass by increasing muscle protein synthesis.

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Recent studies of human steroid use have revealed that steroid use increases muscle cross-sectional area and mass, largely due to increases in protein synthesis, and muscle fiber hypertrophy attributable to an increased number of satellite cells and myonuclei per unit area. These biochemical and cellular effects on skeletal muscle morphology translate into increased power and work during weight-lifting and enhanced performance in burst, sprinting activities.

*(Steroid use and human performance: Lessons for integrative biologists. Jerry F. Husak and Duncan J. Irschick{dagger}

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Testosterone restores sex drive and boosts muscle mass, making it central to 2 of society’s rising preoccupations: perfecting the male body and sustaining the male libido. The anabolic effects of AAS have been questioned for decades, but recent scientific investigation of supraphysiologic doses supports the efficacy of these regimens. Testosterone has potent anabolic effects on the musculoskeletal system, including an increase in lean body mass, a dose-related hypertrophy of muscle fibers, and an increase in muscle strength. For athletes requiring speed and strength and men desiring a cosmetic muscle makeover, illegal steroids are a powerful lure, despite the risk of subjective side effects.

*Current Concepts in Anabolic-Androgenic Steroids. Nick A. Evans, MD


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The Mechanisms of Androgen Effects on Body Composition: Mesenchymal Pluripotent Cell as the Target of Androgen Action

1. Shalender Bhasin,
2. Wayne E. Taylor,
3. Rajan Singh,
4. Jorge Artaza,
5. Indrani Sinha-Hikim,
6. Ravi Jasuja,
7. Helen Choi and
8. Nestor F. Gonzalez-Cadavid

+ Author Affiliations

1.
Division of Endocrinology, Metabolism, and Molecular Medicine, Charles R. Drew University of Medicine and Science, Los Angeles, California.

* Received July 23, 2003.
* Accepted August 5, 2003.

Abstract

Testosterone supplementation increases muscle mass primarily by inducing muscle fiber hypertrophy; however, the mechanisms by which testosterone exerts its anabolic effects on the muscle are poorly understood. The prevalent view is that testosterone improves net muscle protein balance by stimulating muscle protein synthesis, decreasing muscle protein degradation, and improving the reutilization of amino acids. However, the muscle protein synthesis hypothesis does not adequately explain testosterone-induced changes in fat mass, myonuclear number, and satellite cell number. We postulate that testosterone promotes the commitment of pluripotent stem cells into the myogenic lineage and inhibits their differentiation into the adipogenic lineage. The hypothesis that the primary site of androgen action is the pluripotent stem cell provides a unifying explanation for the observed reciprocal effects of testosterone on muscle and fat mass.

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Am J Physiol Endocrinol Metab. 2002 Jul;283(1):E154-64.
Testosterone-induced increase in muscle size in healthy young men is associated with muscle fiber hypertrophy.

Sinha-Hikim I, Artaza J, Woodhouse L, Gonzalez-Cadavid N, Singh AB, Lee MI, Storer TW, Casaburi R, Shen R, Bhasin S.

Division of Endocrinology, Metabolism, and Molecular Medicine, Charles R. Drew University of Medicine and Science, Los Angeles, California 90059, USA.

Administration of replacement doses of testosterone to healthy hypogonadal men and supraphysiological doses to eugonadal men increases muscle size. To determine whether testosterone-induced increase in muscle size is due to muscle fiber hypertrophy, 61 healthy men, 18-35 yr of age, received monthly injections of a long-acting gonadotropin-releasing hormone (GnRH) agonist to suppress endogenous testosterone secretion and weekly injections of 25, 50, 125, 300, or 600 mg testosterone enanthate (TE) for 20 wk. Thigh muscle volume was measured by magnetic resonance imaging (MRI) scan, and muscle biopsies were obtained from vastus lateralis muscle in 39 men before and after 20 wk of combined treatment with GnRH agonist and testosterone. Administration of GnRH agonist plus TE resulted in mean nadir testosterone concentrations of 234, 289, 695, 1,344, and 2,435 ng/dl at the 25-, 50-, 125-, 300-, and 600-mg doses, respectively. Graded doses of testosterone administration were associated with testosterone dose and concentration-dependent increase in muscle volume measured by MRI (changes in vastus lateralis volume, -4, +7, +15, +32, and +48 ml at 25-, 50-, 125-, 300-, and 600-mg doses, respectively). Changes in cross-sectional areas of both type I and II fibers were dependent on testosterone dose and significantly correlated with total (r = 0.35, and 0.44, P < 0.0001 for type I and II fibers, respectively) and free (r = 0.34 and 0.35, P < 0.005) testosterone concentrations during treatment. The men receiving 300 and 600 mg of TE weekly experienced significant increases from baseline in areas of type I (baseline vs. 20 wk, 3,176 +/- 186 vs. 4,201 +/- 252 microm(2), P < 0.05 at 300-mg dose, and 3,347 +/- 253 vs. 4,984 +/- 374 microm(2), P = 0.006 at 600-mg dose) muscle fibers; the men in the 600-mg group also had significant increments in cross-sectional area of type II (4,060 +/- 401 vs. 5,526 +/- 544 microm(2), P = 0.03) fibers. The relative proportions of type I and type II fibers did not change significantly after treatment in any group. The myonuclear number per fiber increased significantly in men receiving the 300- and 600-mg doses of TE and was significantly correlated with testosterone concentration and muscle fiber cross-sectional area. In conclusion, the increases in muscle volume in healthy eugonadal men treated with graded doses of testosterone are associated with concentration-dependent increases in cross-sectional areas of both type I and type II muscle fibers and myonuclear number. We conclude that the testosterone induced increase in muscle volume is due to muscle fiber hypertrophy.


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Testosterone-induced increase in muscle size in healthy young men is associated with muscle fiber hypertrophy.

Sinha-Hikim I, Artaza J, Woodhouse L, Gonzalez-Cadavid N, Singh AB, Lee MI, Storer TW, Casaburi R, Shen R, Bhasin S.

Division of Endocrinology, Metabolism, and Molecular Medicine, Charles R. Drew University of Medicine and Science, Los Angeles, California 90059, USA.

Administration of replacement doses of testosterone to healthy hypogonadal men and supraphysiological doses to eugonadal men increases muscle size. To determine whether testosterone-induced increase in muscle size is due to muscle fiber hypertrophy, 61 healthy men, 18-35 yr of age, received monthly injections of a long-acting gonadotropin-releasing hormone (GnRH) agonist to suppress endogenous testosterone secretion and weekly injections of 25, 50, 125, 300, or 600 mg testosterone enanthate (TE) for 20 wk. Thigh muscle volume was measured by magnetic resonance imaging (MRI) scan, and muscle biopsies were obtained from vastus lateralis muscle in 39 men before and after 20 wk of combined treatment with GnRH agonist and testosterone. Administration of GnRH agonist plus TE resulted in mean nadir testosterone concentrations of 234, 289, 695, 1,344, and 2,435 ng/dl at the 25-, 50-, 125-, 300-, and 600-mg doses, respectively. Graded doses of testosterone administration were associated with testosterone dose and concentration-dependent increase in muscle volume measured by MRI (changes in vastus lateralis volume, -4, +7, +15, +32, and +48 ml at 25-, 50-, 125-, 300-, and 600-mg doses, respectively). Changes in cross-sectional areas of both type I and II fibers were dependent on testosterone dose and significantly correlated with total (r = 0.35, and 0.44, P < 0.0001 for type I and II fibers, respectively) and free (r = 0.34 and 0.35, P < 0.005) testosterone concentrations during treatment. The men receiving 300 and 600 mg of TE weekly experienced significant increases from baseline in areas of type I (baseline vs. 20 wk, 3,176 +/- 186 vs. 4,201 +/- 252 microm(2), P < 0.05 at 300-mg dose, and 3,347 +/- 253 vs. 4,984 +/- 374 microm(2), P = 0.006 at 600-mg dose) muscle fibers; the men in the 600-mg group also had significant increments in cross-sectional area of type II (4,060 +/- 401 vs. 5,526 +/- 544 microm(2), P = 0.03) fibers. The relative proportions of type I and type II fibers did not change significantly after treatment in any group. The myonuclear number per fiber increased significantly in men receiving the 300- and 600-mg doses of TE and was significantly correlated with testosterone concentration and muscle fiber cross-sectional area. In conclusion, the increases in muscle volume in healthy eugonadal men treated with graded doses of testosterone are associated with concentration-dependent increases in cross-sectional areas of both type I and type II muscle fibers and myonuclear number. We conclude that the testosterone induced increase in muscle volume is due to muscle fiber hypertrophy.

PMID: 12067856 [PubMed - indexed for MEDLINE]

Zmieniony przez - faftaq w dniu 2010-03-31 22:55:09

Zmieniony przez - faftaq w dniu 2010-03-31 22:56:37

Short-term oxandrolone administration stimulates net muscle protein synthesis in young men.

Sheffield-Moore M, Urban RJ, Wolf SE, Jiang J, Catlin DH, Herndon DN, Wolfe RR, Ferrando AA.

Department of Surgery, University of Texas Medical Branch, and Shriners Burn Hospital for Children, Galveston 77550, USA. [email protected]

Short term administration of testosterone stimulates net protein synthesis in healthy men. We investigated whether oxandrolone [Oxandrin (OX)], a synthetic analog of testosterone, would improve net muscle protein synthesis and transport of amino acids across the leg. Six healthy men [22+/-1 (+/-SE) yr] were studied in the postabsorptive state before and after 5 days of oral OX (15 mg/day). Muscle protein synthesis and breakdown were determined by a three-compartment model using stable isotopic data obtained from femoral arterio-venous sampling and muscle biopsy. The precursor-product method was used to determine muscle protein fractional synthetic rates. Fractional breakdown rates were also directly calculated. Total messenger ribonucleic acid (mRNA) concentrations of skeletal muscle insulin-like growth factor I and androgen receptor (AR) were determined using RT-PCR. Model-derived muscle protein synthesis increased from 53.5+/-3 to 68.3+/-5 (mean+/-SE) nmol/min.100 mL/leg (P < 0.05), whereas protein breakdown was unchanged. Inward transport of amino acids remained unchanged with OX, whereas outward transport decreased (P < 0.05). The fractional synthetic rate increased 44% (P < 0.05) after OX administration, with no change in fractional breakdown rate. Therefore, the net balance between synthesis and breakdown became more positive with both methodologies (P < 0.05) and was not different from zero. Further, RT-PCR showed that OX administration significantly increased mRNA concentrations of skeletal muscle AR without changing insulin-like growth factor I mRNA concentrations. We conclude that short term OX administration stimulated an increase in skeletal muscle protein synthesis and improved intracellular reutilization of amino acids. The mechanism for this stimulation may be related to an OX-induced increase in AR expression in skeletal muscle.


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The effects of supraphysiologic doses of testosterone on muscle size and strength in normal men.

Bhasin S, Storer TW, Berman N, Callegari C, Clevenger B, Phillips J, Bunnell TJ, Tricker R, Shirazi A, Casaburi R.

Department of Medicine, Charles R. Drew University of Medicine and Science, Los Angeles, CA 90059, USA.

Comment in:

* N Engl J Med. 1996 Jul 4;335(1):52-3.

BACKGROUND: Athletes often take androgenic steroids in an attempt to increase their strength. The efficacy of these substances for this purpose is unsubstantiated, however. METHODS: We randomly assigned 43 normal men to one of four groups: placebo with no exercise; testosterone with no exercise; placebo plus exercise; and testosterone plus exercise. The men received injections of 600 mg of testosterone enanthate or placebo weekly for 10 weeks. The men in the exercise groups performed standardized weight-lifting exercises three times weekly. Before and after the treatment period, fat-free mass was determined by underwater weighing, muscle size was measured by magnetic resonance imaging, and the strength of the arms and legs was assessed by bench-press and squatting exercises, respectively. RESULTS: Among the men in the no-exercise groups, those given testosterone had greater increases than those given placebo in muscle size in their arms (mean [+/-SE] change in triceps area, 424 +/- 104 vs. -81 +/- 109 square millimeters; P < 0.05) and legs (change in quadriceps area, 607 +/- 123 vs. -131 +/- 111 square millimeters; P < 0.05) and greater increases in strength in the bench-press (9 +/- 4 vs. -1 +/- 1 kg, P < 0.05) and squatting exercises (16 +/- 4 vs. 3 +/- 1 kg, P < 0.05). The men assigned to testosterone and exercise had greater increases in fat-free mass (6.1 +/- 0.6 kg) and muscle size (triceps area, 501 +/- 104 square millimeters; quadriceps area, 1174 +/- 91 square millimeters) than those assigned to either no-exercise group, and greater increases in muscle strength (bench-press strength, 22 +/- 2 kg; squatting-exercise capacity, 38 +/- 4 kg) than either no-exercise group. Neither mood nor behavior was altered in any group. CONCLUSIONS: Supraphysiologic doses of testosterone, especially when combined with strength training, increase fat-free mass and muscle size and strength in normal men.



i pełen text: http://content.nejm.org/cgi/content/full/335/1/1

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Abstrah**ąc od dobitnich dowodów kolegów z działu doping, moim zdaniem istnieje wystarczająca ilośc danych zrodłowych by uznać iz stosowanie sterydów androgennych może być przydatne w sporcie tak wyczynowym, jak i amatorskim. Od lat 80 (kiedy to pojawiała sie seria badań która ponoć podważała efektywnosc SAA w sporcie) wiele nowych badan objawiających anaboliczne wlasciwosci SAA jak powyżej widać sie pojawiło...



Zmieniony przez - faftaq w dniu 2010-03-31 23:25:39

Faftag, to nie moja teza, tylko autorów podręcznika DOPING (PZWL). Dlatego właśnie posłużyłem się cytatem!

Ale nieuważnie przeczytałeś ten cytat, jak również - przyznaję - jest on jedynie wycinkiem obszernej całości. Nikt nie polemizuje z dawno ustaloną, anaboliczną aktywnością sterydów, której dowodzą też wrzucone przez Ciebie badania, tylko z przełożeniem tej aktywności na wynik sportowy (o tym mówią właśnie autorzy DOPINGU). Nie mam czasu dokładnie analizować tych abstraktów - ale na pierwszy rzut oka widzę, że takie wnioski nie wyłaniają się z nich jednoznacznie (chyba tylko z jednej pracy). A autorom tej pozycji chodziło właśnie o niezwykle skromną liczbę takich, jednoznacznych i przekonywujących dowodów, świadczących o wpływie sterydów anabolicznych poprawę wyników sportowych.

A co do aminokwasów egzogennych... Znaczenie dla organizmu człowieka ma na pewno endogenna synteza argininy, histydyny i BCAA. Co do pozostałych - brakuje oceny tego zjawiska, ale - faktycznie - możemy uznać ten problem za marginalny.

Znaczenie dla organizmu człowieka ma na pewno endogenna synteza argininy, histydyny - dlatego są to aminokwasy względnie egzogenne.

Co do BCAA - to nigdy o tym nie slyszałem.

W kwestii dopingu, to kilka wklejonych przeze mnie tekstów odnosi sie wlasnie do tezy którą postawiłes / zacytowales.

chocby:

Testosterone restores sex drive and boosts muscle mass, making it central to 2 of society's rising preoccupations: perfecting the male body and sustaining the male libido. The anabolic effects of AAS have been questioned for decades, but recent scientific investigation of supraphysiologic doses supports the efficacy of these regimens. Testosterone has potent anabolic effects on the musculoskeletal system, including an increase in lean body mass, a dose-related hypertrophy of muscle fibers, and an increase in muscle strength. For athletes requiring speed and strength and men desiring a cosmetic muscle makeover, illegal steroids are a powerful lure, despite the risk of subjective side effects.


oza tym, dla mnie wnioski z powyzszych badań sa dośc jednoznaczne

Wiem, że o endogennej syntezie BCAA nie słyszałeś, dlatego zacytowałem właśnie BIOCHEMIĘ HARPERA.

A co do sterydów...
Jasne...! Dla mnie też wnioski z badań sterydów były zawsze jednoznaczne. Widać jednak, że nie dla wszystkich autorów, co znakomicie obrazuje przykład - 'szklanki do połowy pełnej i od połowy pustej'.

A, Faftag... Nie bardzo mam teraz czas na dłuższe epistoły, ale jak chcesz poczytać więcej o znaczeniu endogennej syntezy BCAA dla gospodarki azotowej czy fizjologii wysiłku, to na pewno znajdziesz masę informacji w internecie. Wklep w google któreś z tych haseł:

branched chain alpha keto analogues

branched chain alpha keto acids

ketoisocaproic acid

Metabolism of alpha-ketoisocaproic acid in isolated perfused liver of cirrhotic rats

F. Blonde-Cynober, F. Plassart, J. P. de Bandt, C. Rey, S. K. Lim, N. Moukarbel, F. Ballet, R. Poupon, J. Giboudeau and L. Cynober
Laboratoire de Biochimie A, Institut National de la Sante et de la Recherche Medicale U 402, Paris, France.

To determine the hepatic fate of alpha-ketoisocaproate (KIC) in cirrhosis, six groups of isolated rat livers were perfused with 0, 0.5, 1 (with or without alpha-[1-14C]KIC), 2, and 5 mM KIC; control livers from healthy rats were studied in parallel under similar conditions. KIC was rapidly removed by the normal livers, whereas uptake was lower in the cirrhotic livers at all concentrations tested (at 2 mM, 4.04 +/- 0.33 vs. 6.32 +/- 0.58 mumol/min; P < or = 0.05). The transamination pathway, evaluated by leucine exchanges, was more important in the cirrhotic livers (25.4 vs. 6.8% in controls at 2 mM). The incorporation of alpha-[1-14C]KIC in proteins of cirrhotic liver was increased compared with controls (0.25 +/- 0.04% of alpha-[1-14C]KIC was incorporated in proteins excreted in perfusate vs. 0.20 +/- 0.04 in controls; P < or = 0.05). In addition, a line of evidence suggests that glutamine rather than glutamate is the N donor for leucine synthesis from KIC. The decarboxylation pathway evaluated by beta-hydroxybutyrate production and by 14CO2 release from alpha-[1-14C]KIC was reduced, respectively, by 40-85% (according to KIC dose) and by 24% at 90 min in cirrhotic livers compared with healthy livers. These results indicate a dramatic modification of KIC metabolism in the cirrhotic liver; its uptake by the liver is decreased and its incorporation into proteins is increased via an enhancement of transamination to leucine, probably as a consequence of an inhibition of branched-chain keto acid dehydrogenase

A coś takiego miałem akurat pod ręką.

Effect of alanyl-glutamine on leucine and protein metabolism in irradiated rats.

Holecek M, Skopec F, Sprongl L, Mráz J, Skalská H, Pecka M.

Department of Physiology, Charles University Medical Faculty, Hradec Králové, Czech Republic. [email protected]

The mechanism by which glutamine produces a favorable effect in the treatment of sepsis, injury, burns and abdominal irradiation is not completely understood. The main aim of this study was to evaluate the effect of alanyl-glutamine (AlaGln) administration on the metabolism of proteins in irradiated rats. The rats were exposed to whole-body irradiation (8Gy) and then fed intragastrically with a mixture of glucose and amino acids either with AlaGln or without AlaGln. At 48 hours after irradiation, parameters of whole-body protein metabolism and DNA synthesis in intestinal mucosa were investigated using a primed, continuous infusion of [1-14C]leucine and [3H]thymidine. In addition, we evaluated the effect of irradiation and AlaGln on gut morphology, blood count and amino acid concentrations in blood plasma and skeletal muscle. Control rats were not irradiated but were given identical treatment. An increase in whole-body leucine oxidation, and insignificant changes in whole-body proteolysis and in protein synthesis were observed after irradiation. In irradiated rats we observed a decrease in muscle glutamine concentration, a decrease in protein synthesis in jejunum, colon and heart, and an increase in synthesis of proteins of blood plasma and spleen. Morphological examination and measurement of DNA synthesis failed to demonstrate any favorable effect of AlaGln supplementation on irradiated gut. However, administration of AlaGln resulted in a decrease in whole-body proteolysis and leucine oxidation which caused an increase in the fraction of leucine incorporated into the pool of body proteins. We conclude that the data obtained demonstrate that irradiation induces metabolic derangement associated with increased oxidation of essential branched-chain amino acids (valine, leucine and isoleucine) and that these disturbances can be ameliorated by administration of AlaGln.

PMID: 12025876 [PubMed - indexed for MEDLINE]

I dość ciekawe:



Nutrition. 2002 Feb;18(2):130-3.
Relation between glutamine, branched-chain amino acids, and protein metabolism.

Holecek M.

Department of Physiology, Charles University School of Medicine, Hradec Králové, Czech Republic. [email protected]

The branched-chain amino acids (BCAAs; valine, isoleucine, and leucine) are the major nitrogen source for glutamine and alanine synthesis in muscle. Synthesis of glutamine, alanine, and BCAA use is activated in critical illnesses such as in sepsis, cancer, and trauma. The use of glutamine often exceeds its synthesis, resulting in the lack of glutamine in plasma and tissues. In critical illness, resynthesis of BCAA from branched-chain keto acids is activated, particularly in hepatic tissue. The BCAA released to circulation may be used for protein synthesis or synthesis of alanine and glutamine. Glutamine and/or alanine infusion has an inhibitory effect on the breakdown of body proteins and decreases BCAA catabolism in postabsorptive control, endotoxemic, and irradiated rats. Decreased protein breakdown also was observed when glutamine synthesis was activated by ammonia infusion. In conclusion some favorable effects of BCAA supply can be explained by its role in the synthesis of glutamine and some positive effects of glutamine exogenous supply can be explained by its effect on metabolism of BCAA.



Szkoda ze zdecydowana wiekszosc publikacji odnosi się do mocno nadwatlonych zdrowotnie szczurów. Mechanizm sam w sobie jednak interesujący. Z drugiej jednak strony - nawet jesli wizerunek glutaminy wzbogaci się o w/w wnioski, to raczej ewidentnie skłaniałbym się ku suplementacji BCAA/Leucyną w kontescie uzuełniania puli glutainy (plus - pozostale realne czy domniemane korzysci ze stosowania BCAA), niż stosowania glutaminy, (cały czas staram się odnisc wnioski do realiów praktycznych).

Relacje pomiędzy BCAA i glutaminą są ciekawe, ale i daleko bardziej złożone. Obejmują bowiem nie tylko transaminację, ale również aktywację i inhibicję kinaz szlaku PKB i MAPK - a co za tym idzie - regulację anabolizmu i katabolizmu białek.

Ustalenie tych relacji przekłada się też na praktykę. Zauważ, że ostatnio zaznaczył się w produkcji supli nowy trend... Teraz już rzadko producenci wypuszczają czystą glutaminę czy BCAA, tylko częściej - BCAA z dodatkiem glutaminy lub glutaminę z dodatkiem leucyny.

Tylko, faktycznie, przydałyby się jeszcze jakieś badania na sportowcach - potwierdzające, że takie suple spełniają pokładane w nich oczekiwania.